Pharm Final STEP 1

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They act as purine antagonists and inhibit de novo purine synthesis and block formation of AMP and GMP (6-thiopurine is specific for decreasing GMP concentration) ALL 6-MP is metabolized by xanthine oxidase so the amount of drug being administered needs to be reduced if the patient is also taking allopurinol. 6-thioguanine does not have this interaction with allopurinol

6-mercaptopurine (6-MP) and 6-thioguanine have the same mechanism of action. What is it? What do they treat? What is the difference between these drugs?

Acetaminophen

95% is glucoronylated or sulfated. 5% is metabolized by CYP2E1 to NAPQI, which, if not detoxified by conjugation by glutathione, may accumulate and is highly toxic to liver tissues.

Prilocaine

A large dose of which local anesthetic can lead to the accumulation of ο-toluidine which is capable of oxidizing hemoglobin to methemoglobin?

A protease inhibitor (-navir)

A patient being treated for HIV presents with a cushingoid appearance including a buffalo hump, central obesity, breast enlargement, etc. What drug type is this patient likely being treated with that is causing this problem?

Gemcitabine It is a cytidine analog that competes with cytidine, gets incorporated into the DNA, and inhibits chain elongation. Myelosuppression

A patient has been diagnosed with pancreatic cancer. What anti-cancer drug would they be given? What is its mechanism of action? What is its adverse effects?

Elevated creatine phosphokinases. If this occurs it is recommended to discontinue co-administrtion of statins.

A patient is being treated with daptomycin. What should we monitor for?

1. 1. Nucleoside analog that lacks a 3' OH group which leads to termination of DNA elongation and competitive inhibitor of reverse transcriptase 2. Use to treat HIV 3. 5% of patients develop a hypersensitivity reaction for which they should never be rechallenged againsts

Abacavir 1. Mechanism of action 2. Use 3. Adverse effects

1. Monoclonal antibody against the glycoprotein GPIIb/IIIa 2. Used to prevent clotting -mab means it is a monoclonal antibody. It begins with ab and it acts on GPIIB/IIIA. This is found on platelets and encourages platelet aggregation so inhibition of these receptors would prevent primary clotting from occuring

Abciximab 1. Mechanism of action 2. Use How can you remember the MOA and the function of this drug?

1. Competitive inhibitor of α-glucosidases which are required for breaking down starch and disaccharides 2. Used in the treatment of type 2 DM and cause modest reductions in fasting plasma glucose levels and HbA1c 3. Reversible hepatic enzyme elevation so it should be used with caution in the presence of hepatic disease Liver function should be monitored in these patients

Acarbose 1. Mechanism of action 2. Use 3. Adverse effects How should patients taking this drug be monitored?

Metformin There is a small risk of potentially fatal lactic acidosis.

According to the American Diabetes Association, what its he recommended first-line agent in the treatment of type 2 diabetes mellitus? What is a serious adverse effect of this drug?

Analgesic and antipyretic drug with no anti-inflammatory or anti-platelet effects. Not as monotherapy as it has no anti-inflammatory effect but it can be used as an adjunct to anti-inflammatory therapy. Acetylcysteine

Acetaminophen What effects does this drug have on analgesia, fever, inflammation, and platelet aggregation? Can this drug be used for RA? What should be given to patients who have overdosed on this drug?

1. A sulfhydryl donor 2. Used to treat acetaminophen overdose

Acetylcysteine 1. Mechanism of action 2. Use

1. Nucleoside/nucleotide analog that is monophosphorylated by viral thymidine kinase enzymes and then di- and triphosphorylated by host cell enzymes and is inserted into the DNA causing chain termination and inhibition of viral DNA polymerase 2. Treatment of choice for HSV encephalitis, with activity against most herpes viruses (1-4) and commonly used for genital herpes infections and as prophylaxis in immunocompromised transplant patients. 3. Depends on route of administration. Local skin irritation (topical) headache, diarrhea, N&V (oral) and acute renal failure (IV) whose risk can be minimized by slow infusion and proper hydration CMV is resistant at clinically achievable levels of this drug because CMV doesn't code for the required thymidine kinase

Acyclovir 1. Mechanism of action 2. Use 3. Adverse effects What herpes virus is this drug not able to combat and why?

1. TNFα inhibitor 2. Used to treat IBD

Adalimumab 1. Mechanism of action 2. Use

1. IgG1 anti-TNF monoclonal antibody which binds to TNFα and prevents its interaction with TNF receptors which down regulates macrophages and T-cell function. 2. Used to treat RA Fully human

Adalimumab 1. Mechanism of action 2. Use Is this Ab human or chimeric? If chimeric what is it mixed with?

Fenoldopam

Adrenergic Agonist - Direct D1-Agonist Selectively leads to peripheral vasodilation in some vascular beds. Should be administered by continuous IV infusion. Bolus should not be used. Used for in-hospital, short-term management of severe hypertension.

Dopamine

Adrenergic Agonist - Direct Endogenous Catecholamine Activates dopamine receptors and alpha and beta receptors. Substrate for both MAO and COMT. Ineffective when given orally. Increases blood pressure (beta1) and kidney perfusion(D1). Used to treat shock. Preferred to norepinephrine.

Norepinephrine

Adrenergic Agonist - Direct Endogenous Catecholamine Interacts with both alpha and beta receptors. At therapeutic doses, alpha receptor is most affected. Potent agonist at alpha receptors(but not as potent as epinephrine), and little action on beta-2 receptors. Actions - vasoconstriction(alpha1), increases both systolic and diastolic pressures. Unlike epinephrine, does not cause vasodilation with small doses, is not an effective "hormone"(no hyperglycemia/lipolysis). Used to treat shock because it increases vascular resistance and therefore BP, but also decreases kidney blood flow(dopamine is better. Note: If pre-treated with atropine, effect is tachycardia due to blocked transmission of vagal effects from atropine.

Phenoxybenzamine

Adrenergic Antagonist alpha-Antagonist - Non-selective Haloalkylamine. Alkylates and irreversibly blocks alpha receptors. Closely related chemically to nitrogen mustards. Also blocks H1, muscarinic, and serotonin receptors, and inhibits NE reuptake. Actions - prevents vasoconstriction of peripheral blood vessels, provoking tachycardia, but is no longer used for this purpose. Used in management of pheochromocytoma, pre-operatively to help control hypertension and sweating. beta-blockers should not be given before establishin effective alpha blockade, or blood pressure could be elevated. Adverse - postural hypotension, nasal stuffiness, nausea, vomitin, ejaculation inhibtion, and may induce tachycardia.

Phentolamine

Adrenergic Antagonist alpha-Antagonist - Non-selective Reversibly blocks alpha1 and alpha2 receptors. Actions - postural hypotension, cardiac stimulation and tachycardia, can trigger arrhythmias and anginal pain. Used to prevent or control hypertensive episodes in a patient with pheochromocytoma before and during surgery, to diagnose pheochromocytoma, to prevent dermal necrosis, in hypertensive crisis associated with stimulant drug overdose, sudden withdrawal of antihypertensive drugs, or from interaction between MAOI and tyramine or other sympathomimetic amines. All alpha-blockers reverse the alpha effects of epinephrine, but not the beta effects(ie. vasoconstriction is decreased, but not vasodilation, resulting in systemic blood pressure decrease.)

Labetalol

Adrenergic Antagonist alpha1 & beta-Antagonist Competitive. Substantially more potent as beta, than alpha. Given orally for chronic hypertension, and IV for hypertensive emergencies. Used in the management of hypertension. Adverse - orthostatic hypotension and dizziness. Also, associated with hepatic injury.

Carvedilol

Adrenergic Antagonist alpha1 & beta-Antagonist Substantially more potent as beta, than alpha. Also, has antioxidant properties. Used in hypertension and congestive heart failure.

Prazosin

Adrenergic Antagonist alpha1-Antagonist Prototype of alpha1-antagonists. Relaxes both arterial and venous smooth muscle. May also act on CNS to suppress sympathetic outflow. Also slightly decreases LDL and TAGs, while increasing HDL. Used for treatment of hypertension(but not drug of choice).

Tamsulosin

Adrenergic Antagonist alpha1-Antagonist Selective to alpha1A-receptors, which predominates in genitourinary smooth muscle, causing no effects on blood pressure. Less likely to cause orthostatic hypotension than the other alpha1 antagonists. Male sexual function not as severely affected as by non-selective alpha antagonists. Used to treat BPH. Adverse - dizziness, lack of energy, nasal congestion, headache, drowsiness, orthostatic hypotension. Typically administered with a diuretic because of tendency to retain sodium and fluid.

Doxazosin

Adrenergic Antagonist alpha1-Antagonist Structural analog of Prazosin. Has longer half-life than prazosin, allowing less frequent dosing. Used for hypertension and BPH.

Terazosin

Adrenergic Antagonist alpha1-Antagonist Structural analog of Prazosin. Has longer half-life than prazosin, allowing less frequent dosing. Used for hypertension and BPH.

Yohimbine

Adrenergic Antagonist alpha2-Antagonist Originally used to treat erectile dysfunction, but phosphodiesterase type 5 inhibitors have replaced it. Used to reverse the antihypertensive effects of alpha2 agonist such as clonidine.

1. Inhibits microtubule synthesis and glucose uptake which inhibits ATP production and leads to worm immobization and death 2. Used to treat custodial infestations and use as the drug of choice for toxocariasis

Albendazole 1. Mechanism of action 2. Use

1. Recombinant IL-2 which activates T lymphocytes and NK cells 2. Used in the treatment of renal cell cancer

Aldesleukin 1. Mechanism of action 2. Use

1. They inhibit osteoclastic activity by decreasing farnesyl pyrophosphate synthesis by disrupting the mevalonate pathway leading to decreased osteoclast H+ ATPase function leading to reduced resorption and formation of hydroxyapatite 2. Used to treat osteoporosis, malignancy associated with hypercalcemia, and Paget's disease of the bone.

Alendronate 1. Mechanism of action 2. Use

1. Strong µ receptor agonist 2. Seldom used to treat pain

Alfentanil 1. Mechanism of action 2. Use

-cillin Gram-positive bacteria are greatly effected by penicillin because their cell wall is easily crossed by the drug to act on PBPs. Gram-negative bacteria are also affected but to a lesser extent as a result of the requirement of penicillin to enter the cell via porins.

All of the penicillin drugs end in what? In general, what is the effect of the penicillin drugs on gram-positive and gram-negative bacteria?

Alkylating agents that alkylate the N7 position of guanine causing cross-linking of DNA. -platin (Cisplatin, carboplatin, and oxaliplatin) As part of the BEP treatment for testicular cancer. Neurotoxicity (which can lead to cochlear nerve damage and deafness), nephrotoxicity, and severe nausea and vomiting so patients should be pre-treated with anti-emetics. Carboplatin and oxaliplatin have a more acceptable toxicity profile with less neurotoxic effects and less emetogenic effects but they cause more myelosuppression than cisaplatin.

All of the platinum compound are what sort of anti-cancer drugs? What do they all end in? Cisplatin is used as treatment for what cancer? What important adverse effects should you remember for these drugs? What is the difference between cisplatin and the other platinum compounds carboplatin and oxaliplatin?

They start with Gli/Gly and end in -ide. The second generation drugs are more potent and lack some of the adverse effects. As a result, they have mostly replaced the first-generation agents Blocks the ATP-sensitive K+ channel in the beta cell membrane which leads to increased secretion of insulin Potentiation of the action of vasopressin leading to an apparent SIADH condition.

All of the second generation sulfonylurea drugs have what in their name? What is the difference between the first and second generation sulfonylurea drugs? What is the mechanism of action of these drugs? What is an interesting adverse effect seen with these drugs that most commonly occurs with Chlorpropamide?

-relix Soma- -opressin -tropin

All the GnRH receptor antagonists end in what? All the growth hormone analogs start with what? All the vasopressin agonists end in what? Allt he ACTH analogs end in what?

1. A purine analog that acts as an inhibitor of xanthine oxidase 2. Used to treat chronic gout by lowering uric acid plasma concentration It causes the dissolution of tophi. The attacks may increase because of the mobilization of the tissue stores of uric acid. By administering NSAIDs or colchicine during the first 4-6 months of allopurinol therapy to reduce the change of an acute attack of gout.

Allopurinol 1. Mechanism of action 2. Use What does this drug do to tophi? How can this affect the attacks of acute gouty arthritis? How can this be prevented?

1. 5-HT3 receptor antagonist which acts in the gut. 2. Used to treat IBS-D (recommended for severe diarrhea associated IBS) 3. Ischemic colitis (rare)

Alosetron 1. Mechanism of action 2. Use 3. Adverse effects

Clindamycin and primaquine Dapsone and trimethoprim Atovaquone by itself Pentamidine by itself Prednisone

Although Co-trimoxazole is the drug of choice for the treatment of Pneumocystis jirovecii pneumonia there are alternative treatments for patients who can't take this drug. What is the proper combination of the following drugs to treat this condition? Atovaquone, Dapsone, Clindamycin, Primaquine, Trimethoprim, Pentamidine Patients with moderate to severe disease should also be given what?

Respiratory depression Supportive care No, because the stimulates could trigger seizures

Although anti epileptic drugs are commonly taken in intentional drug overdoses they are rarely lethal. What its he most dangerous side effect of a large overdose on these drugs? What is the treatment of overdose? Should these patients be given stimulants to reverse the actions of the overdosed drugs?

Diltiazem

Anti-Anginals Calcium Channel Blocker - Benzothiazepine Anti-anginal effects from increase in oxygen supply and decrease in oxygen demand. Also able to dilate coronary artieries, preventing/reversing coronary vasospasm in Prinzmetal's. Given orally. Intermediate selectivity for vascular calcium channels. Actions - Block voltage-gated L-type Ca2+ channels on vascular smooth muscle, cardiac myocytesb, and cardiac nodal tissue, reducing intracellular calcium. This causes vasodilation, and decreased contractility and heart rate. Used to treat hypertension, angina, and arrhythmias. Used for chronic stable, unstable, and Prinzmetal's(variant) angina. Adverse - Cardiac conduction abnormalities, such as: bradycardia, AV block, heart failure. Anorexia, nausea, peripheral edema, and hypotension. Contraindications: Bradycardia, conduction defects, heart failure.

Clonidine

Anti-Hypertensives Centrally Acting Adrenergic Drug - Partial alpha2-Agonist Not first-line therapy because of side effects associated with their actions within the brain. Actions - Reduces sympathetic outflow by acting on presynaptic alpha2 receptors, leading to a decrease in PVR and CO. Does not decrease renal blood flow or GFR. Used to treat chronic hypertension and hypertensive crises. Adverse - Rebound hypertension from abrupt cessation(avoid concomitant use with beta-blockers), drowsiness, dry mouth, dizziness, headache, and sexual dysfunction.

Labetalol

Anti-Hypertensives Drug for Hypertensive Emergencies Combined alpha and beta blocker. Does not cause reflex tachycardia. Used to treat hypertensive emergencies. Contraindications: asthma, COPD, patients with 2nd or 3rd degree AV block or bradycardia

Sodium Nitroprusside

Anti-Hypertensives Drug for Hypertensive Emergencies Drug of choice for hypertensive emergencies. Actions - dilates both arterial and venous vessels, resulting in reduced PVR, by activating guanylyl cyclase, increasing cGMP. Rapidly broken down to cyanide, which is converted to thiocyanate and excreted slowly in the urine. Aqueous solution is sensitive to light and must be made up directly before administration and covered with opaque foil. Used for management of hypertensive emergencies, heart failure, controlled hypotension(ie. to reduce bleeding during surgery). Adverse - hypotension, reflex tachycardia, goosebumps, abdominal cramping, nausea, vomiting, headache, muscle twitching, sweating, cyanide toxicity(rare, but can be treated with sodium thiosulfate infusion)

Nitroglycerin

Anti-Hypertensives Drug for Hypertensive Emergencies Drug of choice in patients with cardiac ischemia or angina, or after cardiac bypass surgery. Activates guanylyl cyclase which increases intracellular cGMP, leading to relaxation via arterial and venous vasodilation. Used to manage hypertensive emergencies, treat acute decompensated heart failure, and for controlled hypotension. Adverse - hypotension, reflex tachycardia, methemoglobinemia, tolerance.

Hydralazine

Anti-Hypertensives Drug for Hypertensive Emergencies Drug of choice in treating hypertensive emergencies in pregnancies related to eclampsia.

Phentolamine

Anti-Hypertensives Drug for Hypertensive Emergencies Non-selective alpha antagonist. Used to manage hypertensive emergencies, for patients with catecholamine-related emergencies(eg. pheochromocytoma) Adverse - hypotension, reflex tachycardia, chest pain, nasal congestion, arrhythmia.

Nicardipine

Anti-Hypertensives Drug for Hypertensive Emergencies Reasonable alternative to sodium nitroprusside for treatment of hypertensive emergencies. Calcium channel blocker Used to manage hypertension and hypertensive emergencies. Adverse - hypotension, reflex tachycardia, dizziness, headache

Fenoldopam

Anti-Hypertensives Drug for Hypertensive Emergencies Reasonable alternative to sodium nitroprusside for treatment of hypertensive emergencies. Particularly useful for patients with renal failure. Selective postsynaptic D1 agonist. Actions - produces hypotensive effect by decreasing PVR with increased renal blood flow, diuresis, and natriuesis Used to manage hypertensive emergencies. Adverse - hypotension, reflex tachycardia, increased intraocular pressure, dizziness, headache, GI disturbances. Contraindications: glaucoma

Esmolol

Anti-Hypertensives Drug for Hypertensive Emergencies Used particularly for aortic dissection or postoperative hypertension. Completely blocks beta1 receptors. Used to manage of hypertensive emergencies. Adverse - hypotension, nausea, thrombophlebitis, painful extravasation.

Bosentan

Anti-Hypertensives Drug for Pulmonary Hypertension Nonselective receptor blocker of endothelin receptors on vascular endothelium and smooth muscle. Metabolized via CYP2C9 and 3A4, which it also is a strong inducer for. Actions - Inhibits endothelin synthesis. Blocks both initial transient depressor(ETa) and the prolonged pressor(ETb) responses to IV endothelin, causing vasodilation. Used to treat pulmonary hypertension. Adverse - edema, headache, spermatogenesis inhibition, respiratory tract infection. Contraindications: FDA pregnancy category X drug.

Epoprostenol

Anti-Hypertensives Drug for Pulmonary Hypertension Synthetic prostacyclin (PGI2). Actions - strong vasodilator of all vascular beds, and potent endogenous inhibitor of platelet aggregation. Capable of decreasing thrombogenesis and platelet clumping in the lungs. Used - to treat pulmonary hypertension. Adverse - tachycardia, flushing, hypotension, headache, anxiety, nausea, vomiting, arthralgia, jaw pain. Contraindications: hypersensitivity, chronic use in patients with heart failure due to severe left ventricular systolic dysfunction; and in patients who develop edema during dose initiation.

Ethacrynic Acid

Anti-Hypertensives Loop Diuretic Infrequently used for treatment of mild-moderate hypertension and is usually prescribed to patients who do not respond well to thiazide diuretics. However, they are preferable to thiazides in certain situations, such as severe hypertension, or hypertension in patients with advanced chronic kidney disease. Lowers blood pressure by causing diuresis. Has relatively short duration of action and are much more efficacious diuretics, so it is less useful for chronic dosage. Used for severe hypertension. Adverse - hypokalemia

Furosemide

Anti-Hypertensives Loop Diuretic Infrequently used for treatment of mild-moderate hypertension and is usually prescribed to patients who do not respond well to thiazide diuretics. However, they are preferable to thiazides in certain situations, such as severe hypertension, or hypertension in patients with advanced chronic kidney disease. Lowers blood pressure by causing diuresis. Has relatively short duration of action and are much more efficacious diuretics, so it is less useful for chronic dosage. Used for severe hypertension. Adverse - hypokalemia

Torsemide

Anti-Hypertensives Loop Diuretic Infrequently used for treatment of mild-moderate hypertension and is usually prescribed to patients who do not respond well to thiazide diuretics. However, they are preferable to thiazides in certain situations, such as severe hypertension, or hypertension in patients with advanced chronic kidney disease. Lowers blood pressure by causing diuresis. Has relatively short duration of action and are much more efficacious diuretics, so it is less useful for chronic dosage. Used for severe hypertension. Adverse - hypokalemia

Labetalol

Anti-Hypertensives Mixed alpha & beta Antagonists An alternative for the treatment of hypertensive emergencies in patients without second- or third-degree AV block, bronchospastic disease or bradycardia. Actions - Substantially more potent as a beta-antagonist than an alpha-antagonist. Reduces PVR(alpha blockade) without significant alteration in heart rate(reflex tachycardia) or CO(beta receptors are also blocked). Used in hypertension management. Safe to use during pregnancy. Also used to treat hypertensive emergencies. Adverse - Orthostatic hypotension

Eplerenone

Anti-Hypertensives Potassium Sparing Diuretic - Aldosterone Antagonist More potent antihypertensive than ENaC inhibiting K+ sparing diuretics. Less efficacious than thiazide and loop diuretics, and used primarily in combination with other diuretics to attenuate drug-induced K+ excretion and the resultant hypokalemia. Lowers blood pressure by causing diuresis. Has long duration of action and is especially useful in treating chronic hypertension. Also useful in treatment of secondary hypertension caused by hyperaldosteronism. Used to correct hypokalemia in other diuretics and treat hypertension. Adverse - hyperkalemia

Spironolactone

Anti-Hypertensives Potassium Sparing Diuretic - Aldosterone Antagonist More potent antihypertensive than ENaC inhibiting K+ sparing diuretics. Less efficacious than thiazide and loop diuretics, and used primarily in combination with other diuretics to attenuate drug-induced K+ excretion and the resultant hypokalemia. Lowers blood pressure by causing diuresis. Has long duration of action and is especially useful in treating chronic hypertension. Also useful in treatment of secondary hypertension caused by hyperaldosteronism. Used to correct hypokalemia in other diuretics and treat hypertension. Adverse - hyperkalemia

Amiloride

Anti-Hypertensives Potassium Sparing Diuretic - ENaC Inhibitor Less efficacious than thiazide and loop diuretics, and used primarily in combination with other diuretics to attenuate drug-induced K+ excretion and the resultant hypokalemia. Lowers blood pressure by causing diuresis. Has long duration of action and is especially useful in treating chronic hypertension. Used to correct hypokalemia in other diuretics and treat hypertension. Adverse - hyperkalemia

Triamterene

Anti-Hypertensives Potassium Sparing Diuretic - ENaC Inhibitor Less efficacious than thiazide and loop diuretics, and used primarily in combination with other diuretics to attenuate drug-induced K+ excretion and the resultant hypokalemia. Lowers blood pressure by causing diuresis. Has long duration of action and is especially useful in treating chronic hypertension. Used to correct hypokalemia in other diuretics and treat hypertension. Adverse - hyperkalemia

Aliskiren

Anti-Hypertensives Renin Inhibitors Approved for monotherapy and in combination with other drugs. Should only be used as an alternative therapy because of the lack of long-term studies evaluating CV event reduction. Blocks the RAS at its point of activation, which results in a decrease in blood pressure. Used for treatment of hypertension. Adverse - hypotension, hyperkalemia, acute renal failure, angioedema, GI disturbances. Contraindicated in pregnancy, bilateral renal artery stenosis, and hyperkalemia.

Chlorthalidone

Anti-Hypertensives Thiazide Diuretic Preferred type of diuretic for treating mild-moderate hypertension in patients with normal renal and cardiac function. Lowers blood pressure by causing diuresis by mobilizing sodium and water from arteriolar walls. Has long duration of action (~24hrs) and is especially useful in treatment of chronic hypertension. Used treating mild-moderate hypertension. Adverse - hypokalemia

Hydrochlorothiazide

Anti-Hypertensives Thiazide Diuretic Preferred type of diuretic for treating mild-moderate hypertension in patients with normal renal and cardiac function. Lowers blood pressure by causing diuresis by mobilizing sodium and water from arteriolar walls. Has long duration of action (~24hrs) and is especially useful in treatment of chronic hypertension. Used treating mild-moderate hypertension. Adverse - hypokalemia

Metolazone

Anti-Hypertensives Thiazide Diuretic Preferred type of diuretic for treating mild-moderate hypertension in patients with normal renal and cardiac function. Lowers blood pressure by causing diuresis by mobilizing sodium and water from arteriolar walls. Has long duration of action (~24hrs) and is especially useful in treatment of chronic hypertension. Used treating mild-moderate hypertension. Adverse - hypokalemia

Minoxidil

Anti-Hypertensives Vasodilator Not first-line agent. Direct acting smooth muscle relaxant. Arterial vasodilator. K+ channel opener that hyperpolarizes vascular smooth muscle cells. Used to manage severe hypertension and also for the treatment of alopecia androgenetica in males and females. Adverse - hypotension, reflex tachycardia, renin release, Na+ retention effects more dramatic than hydralazine. Reversible trichosis. Note: All patients taking this should first receive beta-blocker and diuretic to attenuate effects of reflex tachycardia and sodium retention.

Hydralazine

Anti-Hypertensives Vasodilator Not first-line therapy for hypertension, as it has short half-life, which necessitates frequent dosing and precipitates strong reflex tachycardia. Arterial vasodilator. Less potent that minoxidil. Used to treat moderate-severe hypertension. Also used in treating acute hypertensive emergencies, secondary hypertension caused by pre-eclampsia, and pulmonary hypertension. Has role in management of heart failure because it can enhance SV and ejection fraction, and is given along with a diuretic and often with a nitrodilator. Adverse - hypotension, reflex tachycardia and Na+ and water retention, reversible lupus-like syndrome, dermatitis, drug fever, peripheral neuropathy, hepatitis, vascular headaches, nausea, flushing. Note: All patients taking this should first receive beta-blocker and diuretic to attenuate effects of reflex tachycardia and sodium retention.

Heparin

Antiarrhythmics Anticoagulants Given IV in unstable patients who require immediate cardioversion. Also for patients with atrial fibrillation less than 48 hours in duration given at presentation, prior to cardioversion. Used to prevent thromboembolic events in patients with atrial fibrillation.

Warfarin

Antiarrhythmics Anticoagulants Given orally in stable patients. Cardioversion should be delayed for 3-4 weeks until adequate anticoagulation has been achieved. Control of ventricular rate should be undertaken whilst patient is waiting for cardioversion. Usually continued for at least 4 weeks after procedure. Used to prevent thromboembolic events in patients with atrial fibrillation.

Quinidine

Antiarrhythmics Class IA - Na+ Channel Antagonist Class IA has intermediate kinetics. May or may not affect conduction at normal heart rates. Has moderate anticholiergic effects. Forms active metabolites from breakdown with CYP 3A4. Also an inhibitor of CYP 2D6, 3A4, and the P-glycoprotein pump. Class IA has largely been replaced by safer antiarrhythmics. Actions - bind and block fast Na+ channels responsible for phase 0 depolarization, decreasing automaticity, decreasing the slope of phase 4 depolarization, raising the threshold for action potential firing, and slowing the rate of depolarization. Because nodal tissue action potentials do not rely on fast Na+ channels, Class I drugs do not have any direct effect. Also blocks K+ channels(phase 3) resulting in prolongation of the refractory period. Used to treat atrial fibrillation, supraventricular and ventricular tachyarrhythmias. Adverse - tachycardia, dry mouth, urinary retention, blurred vision, and constipation. Increases refractory period and can precipitate arrhythmias such as torsades de pointes. Can enhance digoxin toxicity by decreasing renal clearance. Cinchonism(blurred vision, tinnitus, headache, psychosis), nausea, vomiting, diarrhea, abdominal cramps, thrombocytopenia purpura, and hemolytic anemia. Contraindications: Patients with complete heart block. Advised caution in patients with: prolonged QT interval, history of torsades de pointes, incomplete heart block, uncompensated heart failure, myocarditis, and severe myocardial damage.

Disopyramide

Antiarrhythmics Class IA - Na+ Channel Antagonist Class IA has intermediate kinetics. May or may not affect conduction at normal heart rates. Has strong anticholiergic effects. Class IA has largely been replaced by safer antiarrhythmics. Actions - bind and block fast Na+ channels responsible for phase 0 depolarization, decreasing automaticity, decreasing the slope of phase 4 depolarization, raising the threshold for action potential firing, and slowing the rate of depolarization. Because nodal tissue action potentials do not rely on fast Na+ channels, Class I drugs do not have any direct effect. Also blocks K+ channels(phase 3) resulting in prolongation of the refractory period. Used to treat atrial fibrillation, supraventricular and ventricular tachyarrhythmias. Adverse - tachycardia, dry mouth, urinary retention, blurred vision, and constipation. Pronounced negative inotropic effects and may induce hypotension and cardiac failure without pre-existing myocardial dysfunction. Also associated with severe antimuscarinic effects. Contraindications: Patients with uncompensated heart failure due to its negative inotropic actions.

10⁸ cells 10⁹ cells 10¹² cells The log-kill hypothesis is a theory in which each cycle of chemotherapy kills ~99% of the cancer cells. This means that when the cancer is 10⁸ cells large, a round of chemotherapy will not longer make it visible on X-ray, but there are still 10⁶ cancer cells present and subsequent rounds of chemotherapy need to be continued in order to ensure that the entire neoplastic growth has been eliminated.

Approximately how many cells are required for a cancer to first be visible on X-ray? First palpable? To result in the death of the patient? What is the log-kill hypothesis and how do these numbers relate to treatment of cancer with chemotherapy?

1. NK1 receptor blocker in the CNS 2. Effective in decreasing both the early and delayed emesis associated with cancer chemotherapy

Aprepitant 1. Mechanism of action 2. Use

Atypical antipsychotics

Are classical of atypical antipsychotic drugs more likely to cause weight gain?

Atypical because of their beneficial effect on negative symptoms, diminished risk of EPRs and tardive dyskinesia, and because of a reduced increase in prolactin levels (when compared to classical antipsychotics). Risperidone Because of the risk of agranulocytosis with this drug

Are classical or atypical antipsychotic drugs preferred in the treatment of psychotic disorders and why? What is the most prescribed antipsychotic in the US? Clozapine is an atypical antipsychotic with a very low risk of developing EPRs (much lower than risperidone). Why then is its use reserved for refractory patients?

Vancomycin, Daptomycin, and Bacitracin are effective against gram-positives only. Fosomycin is effective against gram-positive and gram-negative organisms.

Are the Non-β-lactam inhibitor of cell wall synthesis (vancomycin, daptomycin, bacitracin, & fosomycin) effective against gram-positive, gram-negative, or both?

Suppressive They are phosphorylated by cellular enzymes to an active form. HBV and HIV

Are the actions of the nucleoside/nucleotide analogs suppressive or curative? How do they act selectively against virally infected cells? What are they used to treat?

Ester-linked local anesthetics No, administered amine-linked anesthetics Very rarely, as they are not metabolized to ρ-aminobenzoic acid Diphenhydramine Subcutaneous epinephrine

Are the ester-linked or amine-linked local anesthetics more likely to cause allergic reactions through metabolism to ρ-aminobenzoic acid derivatives? If a patient has had an allergic reaction to one ester-linked local anesthetic, can we give them a different ester-linked anesthetic? Are amine-linked local anesthetics associated with allergic reactions? How should mild cutaneous reaction be treated? How should more serious reactions be treated?

1. TCA 2. MAOI 3. SSRI 4. SSRI 5. TCA

Are the following MAO inhibitors, TCAs, SSRIs, or SNRIs? 1. Amitriptyline 2. Isocarboxazid 3. Citalopram 4. Paroxetine 5. Nortriptyline

1. TCA 2. SSRI 3. MAOI 4. SNRI 5. TCA

Are the following MAO inhibitors, TCAs, SSRIs, or SNRIs? 1. Amoxapine 2. Escitalopram 3. Phenelzine 4. Venlafaxine 5. Clomipramine

1. TCA 2. SNRI 3. TCA 4. SSRI 5. MAOI

Are the following MAO inhibitors, TCAs, SSRIs, or SNRIs? 1. Desipramine 2. Duloxetine 3. Maprotiline 4. Fluoxetine 5. Tranylcypromine

1. MAOI 2. SSRI 3. TCA 4. SSRI

Are the following MAO inhibitors, TCAs, SSRIs, or SNRIs? 1. Selegiline 2. Fluvoxamine 3. Imipramine 4. Sertraline

1. Purine antagonist 2. Pyrimidine antagonist 3. Pyrimidine antagonist 4. Folate antagonist 5. Pyrimidine antagonist 6. Purine antagonist 7. Pyrimidine antagonist S phase Myelosuppression

Are the following antimetabolite anti-cancer drugs folate antagonists, purine antagonists, or pyrimidine antagonists? 1. 6-mercaptopurine 2. Cytarabine 3. 5-flurouracil 4. Methotrexate 5. Capecitabine 6. 6-thioguanine 7. Gemcitabine Most of these drugs are cell cycle specific. What part of the cell cycle do they act in? What adverse effect do all of these drugs share?

1. HSV 1-4 2. CMV (ganciclovir-resistant strains) 3. CMV 4. HSV 1 -32 skin infections (topical treatment) 5. HSV 1 & 2 6. HSV 1-4 7. CMV 8. All (used to treat drug resistant strains of the viruses)

Are the following antiviral drugs used to treat HSV 1, HSV 2 , VZV, EBV, or CMV? 1. Acyclovir 2. Cidofovir 3. Ganciclovir 4. Penciclovir 5. Trifluridine 6. Valacylcovir 7. Valganciclovir 8. Foscarnet

1. Reversible (steroidal) 2. Reversible (non-steroidal) 3. Irreversible 4. Irreversible 5. Reversible (non-steroidal) Steroidal

Are the following aromatase inhibitors reversible or irreversible inhibitors of the aromatase enzyme? (if they are reversible state whether they are steroidal or non steroidal)...low yield 1. Aminogluthethimide 2. Letrozole 3. Exemestane 4. Formestane 5. Anastrozole Are the irreversible inhibitors steroidal or non-steroidal?

1. Chronic 2. Acute Chronic Normocytic or microcytic hypochromic anemia as a result of impaired heme production as a result of inhibition of δ=aminolevulinate dehydratase and ferrochelatase.

Are the following associated with acute or chronic lead poisoning? 1. Peripheral neuropathy, tremor, anemia, anorexia, weight loss, and GI symptoms 2. Abdominal colic and CNS changes Which is more common? What type of anemia occurs in patients with chronic lead poisoning and how does it occur?

1. Time-dependent 2. Concentration-dependent 3. Time-dependent

Are the following classes of drugs concentration dependent killing drugs or time dependent killing drugs? 1. Penicillins 2. Aminoglycosides 3. Cephalosporins

1. Psychostimulant 2. Psychedelic agent 3. Inhalant 4. CNS depressant 5. Psychostimulant

Are the following drugs CNS depressants, psychostimulants, opioids, psychedelic agents, or inhalants? 1. Amphetamine 2. Psilocybin 3. Nitrous oxide 4. Benzodiazepines 5. Theobromine

1. CNS depressant 2. Psychostimulant 3. Psychedelic agent 4. Psychostimulant 5. Inhalant

Are the following drugs CNS depressants, psychostimulants, opioids, psychedelic agents, or inhalants? 1. Barbiturates 2. Cocaine 3. Mescaline 4. Theophylline 5. Volatile organic solvents

1. Psychostimulant 2. CNS depressant 3. Psychostimulant 4. Psychedelic agent 5. Inhalant

Are the following drugs CNS depressants, psychostimulants, opioids, psychedelic agents, or inhalants? 1. Methamphetamine 2. Ethanol 3. Caffiene 4. MDMA 5. Organic nitrates

1. Bactericidal 2. Bacteriostatic 3. Bacteriostatic 4. Bactericidal 5. Bactericidal

Are the following drugs bactericidal or bacteriostatic? 1. Aminoglycosides 2. Sulfonamides 3. Clindamycin 4. Vancomycin 5. Fluoroquinolones Why would this be important in choosing a drug to treat our patients?

1. Bactericidal 2. Bactericidal 3. Bacteriostatic 4. Bacteriostatic 5. Bactericidal 6. Bacteriostatic

Are the following drugs bactericidal or bacteriostatic? 1. β-lactams 2. Metronidazole 3. Macrolides 4. Tetracyclines 5. Streptogramins 6. Trimethoprim

1. First line 2. Second line 3. First line 4. First line 5. Second line 6. Second line 7. First line 8. First line 9. Second line Rifabutin, because it has less of an effect on CYP450 enzymes

Are the following drugs considered first line drugs or second line drugs for the treatment of tuberculosis? 1. Isoniazid 2. Streptomycin 3. Rifampin 4. Rifabutin 5. Ethionamide 6. Levofloxacin 7. Ethambutol 8. Pyrazinamide 9. Amikacin Which of the drugs listed above is used specifically as a first line treatment for TB in HIV + patients and why?

1. HCV (in combination with ribavirin), HBV 2. Influenza type A 3. HBV and HIV 4. HCV 5. Influenza type A & B 6. Lamivudine-resistant strains of HBV and HIV 7. RSV, HCV (variety of DNA & RNA viruses) 8. Herpes viral infections

Are the following drugs used to treat influenza (type A and B), RSV, hepatitis (A-E), or herpes? 1. Interferon α 2. Ion channel blockers 3. Lamivudine 4. Protease inhibitors 5. Neuroaminidase inhibitors 6. Entecavir 7. Ribavirin 8. Nucleoside/nucleotide analogs

1. HIV-1 2. HIV-1 and HIV-2 3. HIV-1 and HIV-2 4.

Are the following drugs useful in the treatment of HIV-1, HIV-2, or both? 1. NNRTIs (non-nucleoside reverse transcriptase inhibitors) 2. Protease inhibitors 3. NRTIs (nucleoside-analog reverse transcriptase inhibitors) 4.

1. Estrogen 2. Progestin 3. Progestin 4. Progestin 5. Estrogen (prodrug of ethinyl estradiol)

Are the following estrogens or progestrins? 1. Ethinyl estradiol 2. Drospirenone 3. Norgesterel 4. Progesterone 5. Mestranol

1. Progestin 2. Progestin 3. Estrogen 4. Progestin 5. Estrogen

Are the following estrogens or progestrins? 1. Medroxyprogesterone 2. Norelgestromin 3. Estrone 4. Etonogestrel 5. Estriol

1. Progestin 2. Estrogen 3. Progestin 4. Estrogen 5. Progestin

Are the following estrogens or progestrins? 1. Norethindrone 2. Conjugated estrogen 3. Norgestimate 4. Quinestrol 5. Desogestrel

1. Mixed 2. Agonist 3. Agonist 4. Mixed 5. Antagonist If it begins with M, F, or C (Might Facilitate Coma) then it is an agonist, all the others are mixed except for naloxone and naltrexone.

Are the following opioid drugs agonists, mixed agonist-antagonists, or antagonists? 1. Buprenorphine 2. Fentanyl 3. Mepiridine 4. Nalbuphine 5. Naltrexone How can you remember which drugs are which?

1. Agonist 2. Mixed 3. Agonist 4. Antagonist 5. Agonist 6. Mixed

Are the following opioid drugs agonists, mixed agonist-antagonists, or antagonists? 1. Codeine 2. Butorphanol 3. Methadone 4. Naloxone 5. Morphine 6. Pentazocine

It is a partial agonist at D2 and 5-HT1A receptors and an antagonist of 5-HT2A receptors It has a high clinical potency with only a small risk of EPR, no sedation, and a tiny risk of hypotension development Clozapine and quetiapine No

Aripiprazole has unique mechanism of action from the other atypical antipsychotics. What is this MOA? How does this affect its clinical potency, EPR risk, sedation, and hypotension risk? Which atypical antipsychoitics are the least likely to induce extrapyramidal reactions? Do antipsychotic drugs interfere with the metabolism of other drugs, and if so, how?

1. Unknown (also called artesunate) 2. Used to treat severe falciparum malaria (not used widely yet) 3. Remarkable safe but because it has only started to be used more evidence is needed.

Artemisinins 1. Mechanism of actin 2. Use 3. Adverse effects

1. Given IV to induce general anesthesia 2. Used in the long-term management of tonic-clonic seizures, status epileptics, and eclampsia Because phenobarbital induces enzymes it can be used to treat hyperbilirubinemia and kernicterus in neonates (usually given as N-phenylbarbital because it lacks depressant effects of phenobarbital) In patients with porphyria because they increase porphyrin synthesis

Although the barbiturate drugs have largely been replaced by the benzodiazepines they still have some therapeutic uses. What are the uses of the following barbiturate drugs? 1. Thiopental 2. Phenobarbital What is a possible use of phenobarbital in neonates? The barbiturates should not be used in patients with what condition and why?

1. Gastric antacid 2. Used to raise gastric pH 3. Constipation and hypophosphatemia

Aluminum hydroxide 1. MOA 2. Use 3. Adverse effects

1. Opioid receptor antagonist 2. Used to block GI µ receptors to treat opioid induced constipation

Alvimopan 1. Mechanism of action 2. GI Use

1. An anti-viral drug that is used to increase the synthesis, release, and/or reuptake of dopamine from the surviving neurons 2. Used to to treat Parkinson's disease 3. Peripheral edema and livedo reticularis (a red spotty rash)

Amantadine 1. Mechanism of action 2. Use 3. Adverse effects

1. Blocks the viral membrane protein which is required for fusion of the viral cell membrane to the endosome which is required for uncoating of the virus. 2. Used for prophylaxis and treatment of influenza type A (not currently recommended as the first line treatment). 3. CNS complications 4. Pregnancy and nursing It is not extensively metabolized before urinary excretion (unlike Rimantadine) Category C

Amantadine 1. Mechanism of action 2. Use 3. Adverse effects 4. Contraindications Is this drug metabolized prior to urinary excretion? Pregnancy category?

1. Aminoglycoside drug that irreversibly binds to the 30S ribosomal subunit prior to ribosome formation 2. Commonly used as an initial treatment of an unknown infection for a short period of time and is discontinued after the offending organism is identified

Amikacin 1. Mechanism of action 2. Use

1. Aminoglycoside 2. Used to treat streptomycin or MDR stains of TB 3. Similar to streptomycin No, it is teratogenic

Amikacin 1. Mechanism of action 2. Use in TB treatment 3. Adverse effects Use in pregnancy?

1. Blocks the conversion of cholesterol to prenenolone which reduces the synthesis of all the steroids 2. Used to treat adrenal cancer

Aminoglutethimide 1. Mechanism of action 2. Use

Infective endocarditis Neomycin In the urine Ototoxicity and nephrotoxicity Category D

Aminoglycocides are used as empiric therapy in combination with either a penicillin or, more commonly, vancomycin to treat what condition? All are administered via parenteral administration except which drug(s)? How are they excreted? What are two adverse effects to be aware of? What is the pregnancy drug class of these antibiotics?

Can inhibit the conversion of T4 to T3 and lead to hypothyroidism like effects

Amiodarone Affect on the thyroid gland?

1. Tricyclic antidepressant that inhibits the reuptake of serotonin and norepinephrine 2. Used as an adjuvant for pain management.

Amitriptyline 1. Mechanism of action 2. Use

1. β-lactam inhibitor of cell wall synthesis (penicillin) 2. Used for the treatment of acute otitis media, streptococcal pharyngitis, pneumonia, skin infections, and UTI (as it is effective against gram-negative bacteria like E. coli) Also, widely used to treat upper respiratory tract infections caused by H. influenza and S. pneumoniae infections

Amoxicillin 1. Mechanism of action 2. Use

The risk of nephrotoxicity is reduced when this drug is given in lipid formulations.

Amphoteracin B is commonly given via a lipid formulation. Why?

1. Binds to ergosterol and forms pores in the cell membrane which causes leakage of intracellular ions and macromolecules which leads to cell death 2. Broad spectrum anti-fungal drug useful for nearly all-life threatening fungal infections treating both systemic and superficial mycoses 3. Infusion related toxicity (which can be managed by slow infusion) and possible renal toxicity causing renal impairment and anemia from reduce EPO production. It is typically used as part of the initial treatment regimen to rapidly reduce fungal burden but, because of this drugs adverse effects, patients should be switched to azoles with a better adverse effect profile.

Amphotericin B 1. Mechanism of action 2. Use 3. Adverse effects How should this drug be used?

1. β-lactam inhibitor of cell wall synthesis (penicillin) 2. Used for the treatment of acute otitis media, streptococcal pharyngitis, pneumonia, skin infections, and UTI (as it is effective against gram-negative bacteria like E. coli) Also, widely used to treat upper respiratory tract infections caused by H. influenza and S. pneumoniae infections. Enterococci and Listerial infections

Ampicillin 1. Mechanism of action 2. Use This drug is used in combination with amino glycoside to treat what?

Above the diaphragm - Clindamycin Below the diaphragm - Metronidizole

Anaerobic infections occur in many different areas. What drug should be used for anaerobic infections above and below the diaphragm?

1. IL-1 receptor blocker 2. Used to treat RA

Anakinra 1. Mechanism of action 2. Use

1. Reversible aromatase inhibitor 2. Used in the second line treatment of breast cancer after tamoxifen.

Anastrozole 1. Mechanism of action 2. Use

Interleukin-11

Anemia Hematopoietic Growth Factor Actions - Stimulates growth of primitive megakaryocytic progenitors and increases the number of peripheral platelets. Used for treatment of patients who have had a prior episode of thrombocytopenia after a cycle of cancer chemotherapy. In such patients it reduces the need for platelet transfusions.

Filgrastim

Anemia Hematopoietic Growth Factor Granulocyte colony-stimulating factor(G-CSF) stimulates the production and function of neutrophils. Used to accelerate recovery of neutrophils after cancer chemotherapy, and to treat other forms of secondary and primary neutropenia. Adverse - Toxicity is minimal. Sometimes causes bone pain.

Sargramostim

Anemia Hematopoietic Growth Factor Granulocyte-macrophage colony-stimulating factor(GM-CSF) stimulates the production and function of neutrophils and other myeloid and megakaryocyte progenitors. Used to accelerate recovery of neutrophils after cancer chemotherapy, and to treat other forms of secondary and primary neutropenia. Adverse - Can cause fever, arthralgias, and capillary damage with edema. Allergic reactions are rare.

1. Non-selective irreversible COX inhibitor 2. Antipyretic, analgesic, anti-inflammatory, and anti-platelet aggregation. Colon cancer

Aspirin 1. Mechanism of action 2. Use The use of aspirin is associated with a 50% decrease in the risk of which neoplasm?

In children and young adults <20 years old with a fever associated with a viral illness. Because of the risk of the development of Reye's syndrome. Acetominophen or ibuprofin. Pregnant women, especially close to term.

Aspirin and other salicylates are contraindicated in which patients to treat fever? Why? What is the drug of choice for fever in children and teens? What is a relative contraindication for NSAIDs?

1g, at this point zero-order kinetics is reached.

Aspirin follows first order kinetics until a dose of what amount is reached?

Usually initiated when CD4 counts fall below 500 cells/mm³ because the side effects can make the patients feel worse. Pregnant patients, patients with a history of an AIDS defining illness, patients with HIV-associated nephropathy, and in patients with and HIV/HBV co-infection.

At what stage is therapy usually initiated for HIV+ patients and why? Regardless of CD4 count, initiation of therapy is strongly recommended for which individuals?

1. Protease inhibitor - They are reversible inhibitors of HIV aspartyl protease which is responsible for cleavage of the viral polyprotein into reverse transcriptase, protease, and integrase. This prevents virus maturation and results in production of non-infections visions. 2. Combined with ritonavir it is the only once-daily preferred protease inhibitor It has less incidence of side effects than the other protease inhibitors

Atazanavir 1. Mechanism of action 2. Use How do the adverse effects of this drug compare to the adverse effects of other protease inhibitors?

1. Oxytocin antagonist 2. Used for the treatment of preterm labor but not used in the US

Atosiban 1. Mechanism of action 2. Use

1. Unknown (also called artesunate) 2. Used to treat severe falciparum malaria (not used widely yet) 3. Remarkable safe but because it has only started to be used more evidence is needed.

Atovaquone 1. Mechanism of actin 2. Use

No effect May cause hypotension and seizures It forms much less of the metabolite and as a result it has largely replaced atracurium. No, it does not cause histamine release

Atracurium is metabolized by plasma esterase's through a spontaneous reaction. How does this effect the half life in patients with renal failure? It is metabolized to laudanosine. If this metabolite accumulates what could occur? What is the difference in the amount of laudanosine formed by cisatracurium? Atracurium also causes a slight release of histamine which can lead to hypotension. Does cisatracurium share this complication?

1. Forms gold salts that are taken up by macrophages and suppress phagocytosis and lysosomal enzyme activity which inhibits progression of bone and articular destruction 2. Used to treat RA Orally Because of their toxicity

Auranofin 1. Mechanism of action 2. Use How is this drug administered? Why are gold compounds used infrequently today?

1. Pro-drug that is converted to 6-mercaptopurine (6-MP) which causes immune suppression 2. Used as an immunosuppresant in renal transplantation and autoimmune diseases

Azathioprine 1. Mechanism of action 2. Use

1. Anticancer drug that acts as a purine antimetabolite. It is converted to 6-mercaptopurine and other metabolites which inhibit purine synthesis. This leads to suppression of B and T-cell function. 2. Used to treat patients with refractory rheumatoid arthritis 3. Bone marrow suppression, GI disturbances, infections, and malignancies. Azathioprine is metabolized by xanthine oxidase. This enzyme is inhibited by allopurinol (a drug used to treat gout). Patients taking allopurinol should have their azathioprine dose reduced to avoid toxicities from occurring.

Azathioprine 1. Mechanism of action 2. Use 3. Adverse effects What drug interaction should be remembered for this drug and how should treatment be modified?

1. Macrolide drug that reversibly binds to the 50S ribosomal subunit and inhibits translocation 2. Used in empiric therapy of community-acquired pneumonia and to treat upper respiratory tract and soft-tissue infections (ex. Staph, H. influenza, S. pneumonia, and enterococci)

Azithromycin 1. Mechanism of action 2. Use

1. β-lactam inhibitor of cell wall synthesis (Monobactam) 2. Useful for treating aerobic gram-negative rods only (including Pseudomonas) Resistant

Aztreonam 1. Mechanism of action 2. Use Is this drug resistant or susceptible to β-lactamases?

1. Muscarinic agonist 2. Used to treat post-op and postpartum urinary and fecal retention.

Bethanechol 1. Mechanism of action 2. GI/GU use

1. Androgen receptor antagonist 2. Used to treat prostate cancer by inhibition testosterones prostatic hyper plastic activity.

Bicalutamide 1. Mechanism of action 2. Use

Orthostatic hypotension and impaired ejaculation.

Blockade of α1 receptors by antipsychotic drugs can cause what condition?

1. Non-β-lactam inhibitor of cell wall synthesis that interferes in late stages of cell wall synthesis 2. Used for topical treatments of gram positive infections Gram-positive organisms

Bacitracin 1. Mechanism of action 2. Use Is this drug affective against gram-negative, gram-positive, or both?

1. GABA agonist at GABAb receptors in the CNS 2. Used to treat patients with chronic spasms

Baclofen 1. Mechanism of action 2. Use

1. Releases 5-ASA in the large intestines which blocks the pro-inflammatory mediators IL1 and TNFα 2. Used to treat ulcerative colitis

Balsalazide 1. Mechanism of action 2. Use

1. Monoclonal antibody that acts asa IL-2 receptor antagonist 2. Used as an immunosuppressant preoperatively during transplantation They have the same mechanism of action but Daclizumab is a humanized antibody and Basiliximab is a chimeric antibody

Basiliximab 1. Mechanism of action 2. Use What is the difference between this drug and Daclizumab?

If the patient has depression along with suicidal thoughts/ideations they should be monitored closely because an overdose with these drugs could occur and lead to fatal cardiac arrhythmias. Sodium bicarbonate will reverse the conduction block

Because TCAs have a narrow therapeutic index, how should patients being treated for depression with these drugs be monitored? What is the treatment for an overdose of these drugs?

Ergosterol is found in the cell membranes of fungal cells but not in human cells (which contain cholesterol). As a result most of the therapy is targeted at ergosterol or its synthesis. Binds to ergosterol and forms pores in the cell membrane which causes leakage of intracellular ions and macromolecules which leads to cell death. Inhibit 14-α-demethylase, they last enzyme in ergosterol synthesis from lanosterol. -onazole except for clotrimAZOLE

Because fungi are eukaryotic it is difficult to develop anti fungal agents that are selective for fungi but don't damage human cells. What is an appropriate target? What is the mechanism of action of the polyene anti-fungal drugs? What is the mechanism of action of the azole anti-fungal drugs? What do all the azole anti-fungal drugs end in?

Antimuscarinic agents They are used as adjuvant therapy (not as primary therapy) and may improve tremor and rigidity but have no effect on bradykinesia (slowing of movement)

Benzotropine and trihexyphenidyl are both what types of drugs? How are they used to treat Parkinson's disease?

Extrapyramidal reactions Parkinson's syndrome, akathisia, and dystonic reactions. No, these patient should never be treated with levodopa because it can lead to activation or exacerbation of psychotic features.

Benztropine or trihexyphenidyl with diphenhydramine or amantadine can be used to treat what condition? What are EPRs? Can we treat this condition with levodopa (a drug used for parkinsonism)?

They can block glutamate and sodium channels which is likely to explain their ability to induce full surgical anesthesia and their increased CNS depressant effects when compared to the benzodiazepine drugs.

Besides increasing the duration of the GABA-gated chloride channel opening, what other effects do the barbiturate drugs have?

1. Neuropathic pain and bipolar disorder 2. Neuropathic pain 3. Bipolar disorder 4. Neuropathic pain 5. Migraine 6. Bipolar disorder and migraine

Besides treating seizure disorders, what other uses do the following anti seizure medications have? 1. Carbamazepine 2. Gabapentin 3. Lamotrigine 4. Pregabalin 5. Topiramate 6. Valproate

1. Bind reversibly to non-structural protein 3 (NS3) serene protease and inhibit replication of its target virus 2. Used in the treatment of HCV in adults who have been previously untreated or failed treatment with interferon α and ribavirin (can also be administered in combination with interferon α and ribavirin)

Boceprevir 1. Mechanism of action 2. Use

Depresses oxygen uptake and carbohydrate metabolism and intercalates into the DNA which disrupts the parasites replication and transcription. Qiunine is used as oral treatment of chloroquine-resistant P. falciparum malaria whereas quinidine is used as parenteral treatment for severefalciparum malaria infections

Both Quinine and Quinidine are used for falciparum malarial treatment. What is their mechanism of action? What is the difference between the drugs?

Inhibition of calcineurin Tacrolimus It is also an immunosuppressant but it inhibits the action of IL-2 instead of inhibiting its production.

Both cyclosporine and tacrolimus have a mechanism of action that ends in what? Which is more potent? How is sirolimus different than these drugs?

Progestins They can be used to treat endometrial cancer and as palliative care in terminally ill cancer patients in order to improve appetite. Androgens like fluoxymesterone and testosterone

Both hydroxyprogesterone and megestrol are what types of drugs? How can they be used in cancer therapy? What other steroidal drug can be administered for the same use?

Both passively diffuse across membranes and are actively transported in to the bacterial cell but aminoglycosides only passively diffuse across gram-negative membranes and require an oxygen dependent active transport across the membrane. As a result, aminoglycosides are effective against aerobic gram-negative bacteria (not anaerobic or gram-positive bacteria) but tetracyclines are effective against aerobic and anaerobic bacteria that are both gram-positive and gram-negative. Note: Aminoglycocides are bactericidal because they bind irreversibly and tetracyclines are bacteriostatic because they bind reversibly.

Both tetracyclines and aminoglycosides bind to the 30S subunit of the bacteria ribosome. How are they different and how does that change the bacteria they are effective in treating?

Epipodophyllotoxins (etoposide and tenoposide) inhibit topoisomerase II whereas the camptothecin drugs (topotecan and irinotecan) inhibit topoisomerase I. Both lead to poor ability of cancer cells to undergo replication properly which leads to cell death. Myelosuppression

Both the epipodophyllotoxin and the camptothecin drugs are natural products used for cancer therapy. What is the difference in their mechanism of action? What adverse side effects do these drugs share?

1. Blocks the release of acetylcholine from the presynaptic neuron 2. Used to treat chronic spastic conditions

Botulinum toxin 1. Mechanism of action 2. Use

1. Bulk-forming laxative that increases water retention. Leads to distention of the bowel and increased peristaltic stimulation of the gut. 2. Used to stimulate the peristaltic movement of the gut

Bran 1. Mechanism of action 2. Use

1. D2 receptor agonist 2. Used in the treatment of Parkinson's disease as well as to treat acromegly

Bromocriptine 1. Mechanism of action 2. Use

1. Dopamin agonists 2. Used to treat prolactinomas that still retain inhibition to dopamine 3. Nausea and psychiatric manifestations Parkinsons disease

Bromocriptine 1. Mechanism of action 2. Use 3. Adverse effects What other condition are the dopamine agonists used to treat?

1. Corticosteroid which inhibit TNFα, IL-1, and IL-8 2. Used to treat Crohn's disease and UC

Budesonide 1. Mechanism of action 2. GI Use

1. Partial µ agonist and κ antagonist 2. Used for the management of opioids addiction

Buprenorphine 1. Mechanism of action 2. Use

1. Inhibits norepinephrine and dopamine uptake and increases their release 2. Used as a secondary drug to treat depression It is not associated with the sexual dysfunction seen in SSRIs because of the lack of serotonergic activity. Seizures To help with smoking cessation

Bupropion 1. Mechanism of action 2. Use What is the benefit of this drug over the SSRIs? Overdose with this drug can cause what? What is a common use of this drug not associated with depression?

1. Patrial 5-HT1A receptor agonist 2. Can be used as a second-line agent for generalized anxiety disorder but sufficient data regarding its efficacy is not yet available

Busiprone 1. Mechanism of action 2. What anxiety condition can this drug be used for?

1. Partial 5-HT1A agonist 2. Used to manage anxiety disorders 2-3 weeks (same as its activity as an antidepressant) It has less psychomotor impairment than the benzodiazepines, has no interactions with alcohol, benzos, or other sedative-hypnotics, no dependence, and no rebound anxiety or withdrawal symptoms if stopped abruptly.

Buspirone 1. Mechanism of action 2. Use What is the onset of this drug? What are some of the advantages of this drug in treating anxiety?

1. κ agonist and µ antagonist or partial agonist 2. Useful in treating mild to moderate pain while keeping the risk of addiction low

Butorphanol 1. Mechanism of action 2. Use

The kidney and brain. Endothelial COX-2

COX-2 is constitutive in what organs of the body? The primary source of vascular prostacyclin comes from where?

1. Dopamin agonists 2. Used to treat prolactinomas that still retain inhibition to dopamine 3. Nausea and psychiatric manifestations This drug is preferred as it has a longer half life but it is also more expensive

Cabergoline 1. Mechanism of action 2. Use Is this drug or Bromocritpine preferred and why?

Osteoporosis It has a longer half life and greater potency than regular calcitonin. Estrogen

Calcitonin is approved for the treatment of what condition? What advantages are there to using Salmon Calcitonin? What hormone replacement can also be used to treat osteoporosis?

Secondary hyperparathyroidism as a result of chronic renal and/or liver disease Psoriasis Osteoporosis, chronic renal failure, nutritional rickets (due to a poor dietary intake), and chronic liver disease. Hypercalcemia and hyperphosphatemia

Calcitrol is approved for the treatment of what condition? Calcipotriol is approved to treat what condition? What other conditions are vitamin D supplements used to treat? Chronic overdose with vitamin D leads to what conditions?

1. Gastric antacid 2. Used to raise gastric pH 3. Hypercalcemia, nephrolithiasis, and constipation

Calcium carbonate 1. MOA 2. Use 3. Adverse effects

1. To treat hypocalcemic tetany 2. To counteract an overdose of magnesium sulfate used to treat eclampsia IM injection could result in necrosis and abscess formation and IV administration could cause thrombophlebitis.

Calcium preparations like calcium carbonate, calcium citrate, and calcium lactate are administered for two reasons. What are they? What adverse effect may occur?

No When several drugs are used in combination to produce the desired anesthetic state

Can any single drug achieve all of the desired goals of anesthesia (analgesia, amnesia, LOC, suppression of reflexes, and skeletal muscle relaxation)? What is balanced anesthesia?

Yes, but minor penicillin allergic patients can often be treated with a cephalosporin successfully with no reaction occurring. C. difficile pseudomembranous colitis

Can cross sensitivity between penicillin and cephalosporins occur? All the cephalosporins have a risk of developing what adverse side effect?

Carbamazepine

Can increase its own metabolism by both inducing CYP3A4 and being metabolized by CYP3A4

1. Like the sulfonamides it inhibits folate synthesis by inhibiting dihydropteroate synthetase which inhibits bacterial nucleic acid synthesis 2. Used as combination therapy to treat leprosy and to treat P. jiroveci pneumonia in HIV+ patients 3. Hemolysis (especially in patients with G6PD deficiency), erythema nodosum leprosum, and inhibition of CYP P450.

Dapsone 1. Mechanism of action 2. Use 3. Adverse effects

1. Non-β-lactam inhibitor of cell wall synthesis. It works by binding to the cell membrane via calcium-dependent insertion of the lipid tail and depolarization of the cell membrane through K+ efflux leading to cell death. 2. Recommended for treatment of severe infections caused by MRSA or VRE and for treatment of complicated skin/structure infections caused by susceptible S. aureus Effective against resistant gram-positive organisms including MRSA, VRE, & VRSA. Not effective against gram-negatives. Pneumonia

Daptomycin 1. Mechanism of action 2. Use Is this drug affective against gram-negative, gram-positive, or both? What condition will this drug not treat?

1. Protease inhibitor - They are reversible inhibitors of HIV aspartyl protease which is responsible for cleavage of the viral polyprotein into reverse transcriptase, protease, and integrase. This prevents virus maturation and results in production of non-infections visions. 2. Used to inhibit HIV proteases that are resistant to other protease inhibitor drugs Not specified but I assume it is

Darunavir 1. Mechanism of action 2. Use Is this drug given with ritonavir?

Start treatment with IV lorazepam. If the seizure continues the patient should be given phenytoin or fosphenytoin (prodrug of phenytoin) via IV. If the seizure still continues they should be given phenobarbital IV and if the seizure still continues they should be given general anesthesia with IV midazolam, proposal, or barbiturates.

Describe the algorithm for the treatment of status epilepticus.

APCs present antigen to CD4 positive T-cells which increases calcium levels. This lead to the activation of calcineurin to an active form. The active form of calcineurin dephosphorylates NFAT to an active form which moves to the nucleus and increases the production of IL-2.

Describe the cellular mechanism of the immune response involving the production of IL-2 by T-cells.

1. Pain associated with a progressive disease like cancer or AIDS 2. Pain associated with a life-threatening disease that lasts longer than 6 months beyond the healing period.

Describe the following: 1. Chronic malignant pain 2. Chronic non-malignant pain

Sunlight stimulates the conversion of 7-dehydrocholesterol to cholecalciferol. The liver enzyme, 25-hydroxylase, converts it to 25-hydroxycholecalciferol and then the kidney enzyme, 1-hydroxylase, converts it to 1,25-dihydroxycholecalciferol/calcitrol (active vitamin D).

Describe the process by which 7-dehydrocholesterol is converted to active vitamin D.

Tyrosine enters the presynaptic neuron through a sodium independent manner and is converted to DOPA by tyrosine hydroxylase (this is the rate limiting step). DOPA is almost immediately converted to dopamine by DOPA decarboxylase. Vitamin B6 By increasing the amount of exogenous substrate (levodopa)

Describe the process of dopamine synthesis in the presynaptic neuron. What is the cofactor for dopamine hydroxylase? Because the production of DOPA is the rate limiting step, how can dopamine formation be enhanced?

Iodine is moved into the follicular cell through a secondary active transport mechanism and the iodine is covalently bound to tyrosine residues on thyroglobulin forming MIT and DIT. This is completed by peroxidase enzymes. MIT and DIT are combined to form T3 and T4 which is stored in the colloid.

Describe the process that leads to the formation of thyroid hormone.

Calcineurin acts as a phosphatase which dephosphorylates NFAT leading to its activation. Activated NFAT enters the nucleus and stimulates the production genes which produce IL-2. Cyclosporine: It binds to cyclophilin which forms a complex with calcineurin which inhibits it. This inhibition leads to its inability to dephosphorylate NFAT which leads to an inability of the T-cell to secrete IL-2.

Describe the progression of IL-2 release from activated T-cells. What drug leads to the inhibition of this pathway and how does it work?

1. Long acting synthetic analog of vasopressin agonist 2. Drug of choice for diabetes insipidus and used for coagulopathy treatment in hemophilia A and von Willebrand's disease V2 receptor

Desmopressin 1. Mechanism of action 2. Use Does this drug act primary at the V1 or V2 receptor?

1. Corticosteroid 2. Used in combination with 5-HT3 receptor blockers to treat nausea and vomiting due to chemotherapy treatment

Dexamethasone 1. Mechanism of action 2. Use

1. Glucocorticoid 2. Used in advanced illness associated with pain for acute nerve compression, increased ICP, bone pain, visceral pain, anorexia, nausea, and depressed mood.

Dexamethasone 1. Mechanism of action 2. Use What types of pain are glucocorticoids

Glucocorticoids They bind to intra-cytoplasmic receptors and move to the nucleus where ether modulation protein expression. Immunosuppression, mood swings, osteoporosis, poor wound healing, hyperglycemia, and other Cushings-like symptoms Used for WBC tumors like ALL, Hodgkins lymphoma, non-hodgkins lymphoma, multiple myeloma, etc. They can be used as palliative care in order to improve feelings of well being.

Dexamethasone, hydrocortisone, prednisone, and prednisolone are all what types of drugs? What is the mechanism of action of the glucocorticoids in anti-cancer treatment? What are some long term, adverse effects of glucocorticoids? What types of tumors are glucocorticoids used for? What is the use of glucocorticoids in cancer treatment?

1. Mild to moderate µ receptor agonist 2. Commonly used in combination with acetaminophen as an antitussive It is a weaker analgesic than codeine and therefore lacks the sedation that can be seen with codeine so it has less chance of being abused.

Dextromethorphan 1. Mechanism of action 2. Use What is the advantage of this drug over codeine to treat cough?

1. Inhibits the conversion of T4 to T3 and may inhibit the release of hormone form the thyroid gland 2. Used to treat patients with thyrotoxicosis

Diatrizoate 1. Mechanism of action 2. Use

1. Non-selecive reversible COX inhibitor 2. Antipyretic, analgesic, and anti-inflammatory.

Diclofenac 1. Mechanism of action 2. Use

1. β-lactamase resistant inhibitor of cell wall synthesis (penicillin) 2. Used as first-line treatment for Staphylococcal endocarditis in patients without artificial heart valves

Dicloxacillin 1. Mechanism of action 2. Use

1. Muscarinic (cholinergic) agonists 2. Used to treat IBS.

Dicyclomine 1. Mechanism of action 2. Use

1. Nucleoside analog that lacks a 3' OH group which leads to termination of DNA elongation and competitive inhibitor of reverse transcriptase 2. Used to treat HIV 3. Pancreatitis, especially in alcoholics and patients with hypertriglyceridemia (should not be given to these patients)

Didanosine 1. Mechanism of action 2. Use 3. Adverse effects

1. Immobilizes microfilariae and renders the parasite susceptible to host defense mechanisms 2. Drug of choice for the treatment of lymphatic filariasis, loiasis, and tropical eosinophilia

Diethylcarbamazine 1. Mechanism of action 2. Use

Estrogens They are steroids that bind to cytoplasmic receptors and modulate protein expression in the nucleus. Prostate cancer To patients with endometrial or breast cancer.

Diethylstilbesterol and ethinylestradiol are both what types of drugs? What is the mechanism of action of these in cancer therapy? What type of cancer is this used for? What types of conditions would you not want to give these in?

It has been found to lead to infertility and vaginal cancer in a female child as a result of persistence of columnar epithelium in the upper 1/3 of the vagina instead of the normal squamous epithelium replacement.

Diethylstilbestrol (DES) is a non-steroidal estrogen agonist that used to be used in pregnancy. Why is it no longer used?

Captopril

Congestive Heart Failure ACE Inhibitor Reduces peripheral resistance, thus reducing afterload. Also reduces Na+ and water rentention, decreasing preload. Also shown to reduce sympathetic activity and long-term heart and vessel remodeling. Used to improve symptoms, decrease incidence of hospitalization and MI, and prolong survival in patients with HF and reduced LVEF(Stage C). Also should be used to prevent development in at-risk patients(Stages A & B). Also used to treat primary hypertension and hypertension caused by unilateral renal artery stenosis. Adverse - dry cough, hypotension, hyperkalemia(rarely clinically important, but can be serious in patients with chronic kidney disease), angioedema, acute renal failure(in patients with bilateral renal artery stenosis. Contraindications: Pregnancy, hyperkalemia, and bilateral renal artery stenosis.

1. Not specified 2. Used as the sole agent for the treatment of asymptomatic amebiasis and the luminal amebicide of choice

Diloxanide Furoate 1. Mechanism of action 2. Use

1. H1 receptor blocker (antihistamine) 2. Can be used to treat motion sickness and chemotherapy induced nausea.

Diphenhydramine 1. Mechanism of action 2. Use

They can be used to treat mild types of insomnia

Diphenhydramine and doxylamine are non-prescription antihistamines with sedating properties. How can they be used as a sedative-hypnotic?

Enalapril

Congestive Heart Failure ACE Inhibitor Reduces peripheral resistance, thus reducing afterload. Also reduces Na+ and water rentention, decreasing preload. Also shown to reduce sympathetic activity and long-term heart and vessel remodeling. Used to improve symptoms, decrease incidence of hospitalization and MI, and prolong survival in patients with HF and reduced LVEF(Stage C). Also should be used to prevent development in at-risk patients(Stages A & B). Also used to treat primary hypertension and hypertension caused by unilateral renal artery stenosis. Adverse - dry cough, hypotension, hyperkalemia(rarely clinically important, but can be serious in patients with chronic kidney disease), angioedema, acute renal failure(in patients with bilateral renal artery stenosis. Contraindications: Pregnancy, hyperkalemia, and bilateral renal artery stenosis.

1. Act through µ and δ receptors on enteric nerve, epithelial cells, and muscles 2. Used to treat diarrhea It acts as an anti-motility agent at low doses without causing analgesic effects

Diphenoxylate 1. Mechanism of action 2. Use How is this drug useful at low doses?

Warfarin

Disorders of Coagulation Anticoagulant - Coumarin Anticoagulant "Oral anticoagulant" because, unlike heparin, administered orally. Antagonizes the cofactor function of vitamin K. Initially used as a rodenticide. Coagulation factors involved have half-lives ranging from 6-60 hours, thus several hours are required before an effect is seen. Anticoagulant effect is apparent within 24 hours of administration. Has no direct effect on established thrombus, and does not reverse ischemic tissue damage. Has narrow therapeutic index and has many drug-drug interactions, therefore must be monitored with prothrombin time(PT). PT tests extrinsic and common pathway integrity. PT is standardized and expressed as the International Normalized Ratio(INR). Actions - Inhibits vitamin K epoxide reductase, inhibiting reduction and activation of vitamin K, preventing gamma-carboxylation activation of factors II, VII, IX, and X. Used to to prevent progression or recurrence of acute DVT or pulmonary embolism following an initial course of heparin. Also effective in preventing venous thromboembolism in patients undergoing orthopedic or gynecological surgery, recurrent coronary ischemia in patients with acute myocardial infarction, and systemic embolization in patients with prosthetic heart valves or chronic atrial fibrillation. For treatment of acute venous thromboembolism, heparin, LMWH, or fondaparinux is usually continued for at least 5 days after warfarin has begun and until INR is in therapeutic range. Adverse - Hemorrhage, hence why it is important to frequently monitor and adjust anticoagulant effect(effects can be overcome by vitamin K), cutaneous necrosis(due to reduced activity of protein C). Contraindications: Pregnancy(pregnancy category X. Never administer during pregnancy). Interactions - Inhibit warfarin metabolism: Cimetidine, Chloramphenicol, Disulfiram, Fluconazole, Metronidazole, Phenylbutazone, Sulfinpyrazone, Trimethoprim-Sulfamethoxazole. Stimulate warfarin metabolism: Barbituates, Carbamazepine, Phenytoin, Rifampin.

Lepirudin

Disorders of Coagulation Anticoagulant - Direct Thrombin Inhibitor (DTI) A reombinant form of hirudin, which is a specific thrombin inhibitor from leeches. Given parenterally. Monitored by the aPTT. No antidote exists. Actions - Independent from antithrombin III, therefore can inactivate fibrin-bound, or free, thrombin in thrombi. Binds directly to active site of thrombin. Used in patients with HIT to prevent further thromboembolic complications.

Argatroban

Disorders of Coagulation Anticoagulant - Direct Thrombin Inhibitor (DTI) Small molecule thrombin inhibitor. Given IV. Monitored by aPTT. Used for prophylaxis or treatment of thrombosis in patients with HIT. Also indicated in patients with or at risk for HIT undergoing percutaneous coronary intervention(PCI).

Bivalirudin

Disorders of Coagulation Anticoagulant - Direct Thrombin Inhibitor (DTI) Synthetic congener of naturally occuring hirudin. Bivalent inhibitor of thrombin. Given IV. Monitored by aPTT Actions - Binds to and directly inhibits thrombin. Also inhibits platelet activation. Used in patients undergoing percutaneous coronary intervention(PCI).

Vitamin K

Disorders of Coagulation Drugs used to treat bleeding Deficiency can result from inadequate intake, absorption, or utilization of the vitamin, or as a consequence of the action of an antagonist, such as warfarin. Available and best with IV or oral administration, because bioavailability after SC is erratic. Used therapeutically to correct the bleeding tendency or hemorrhage associated with its deficiency. Also used to raise the concentration of clotting factors to normal and control bleeding tendencies for newborn infants in neonates with hemorrhagic disease. If mothers are receiving anticonvulsants, can give oral Vit K prior to delivery.

Aminocaproic acid

Disorders of Coagulation Drugs used to treat bleeding EACA. Synthetic inhibitor of fibrinolysis. Competitive inhibitor of plasminogen activation. Can be given orally or IV Used as adjunctive therapy in hemophilia, therapy for bleeding from fibrinolytic therapy, prophylaxis for rebleeding from intracranial aneurysms, postsurgical GI bleeding, postprostatectomy bleeding, bladder hemorrhage secondary to radiation- and drug-induced cystitis. Adverse - intravascular thrombosis, hypotension, myopathy, abdominal discomfort, diarrhea, nasal stuffiness. Contraindications: DIC, genitourinary bleeding of upper tract.

Protamine sulfate

Disorders of Coagulation Drugs used to treat bleeding Low molecular weight protein. Given IV. Most active against UFH and partially against LMWHs. Inactive against fondaparinux. Actions - Chemical antagonist of heparin. Positively charged protein interacts with negatively charged heparin to form stable complex with no anticoagulant activity. Can interfere with coagulation in absence of heparin. Used to reverse the effects of heparin in situations of life-threatening hemorrhage or great heparin excess. Adverse - hypersensitivity, dyspnea, flushing, bradycardia, hypotension.

Lisinopril

Congestive Heart Failure ACE Inhibitor Reduces peripheral resistance, thus reducing afterload. Also reduces Na+ and water rentention, decreasing preload. Also shown to reduce sympathetic activity and long-term heart and vessel remodeling. Used to improve symptoms, decrease incidence of hospitalization and MI, and prolong survival in patients with HF and reduced LVEF(Stage C). Also should be used to prevent development in at-risk patients(Stages A & B). Also used to treat primary hypertension and hypertension caused by unilateral renal artery stenosis. Adverse - dry cough, hypotension, hyperkalemia(rarely clinically important, but can be serious in patients with chronic kidney disease), angioedema, acute renal failure(in patients with bilateral renal artery stenosis. Contraindications: Pregnancy, hyperkalemia, and bilateral renal artery stenosis.

Mefloquine

Currently, what is the only medication recommended for chemoprophylaxis in pregnant women in chloroquine-resistant malarial areas?

1. Anticonvulsant 2. Drug of choice for treatment of trigeminal neuralgia

Carbamazepine 1. Mechanism of action 2. Use

1. Block voltage gated sodium channels which leads to a decrease in the transmission of excitatory glutamatergic neuronal signaling. 2. Used in the treatment generalized tonic-clonic seizures, simple and complex partial seizures, and secondarily generalized tonic-clonic seizures. 3. 3. Induction of CYP P450 enzymes, aplastic anemia, agranulocytosis, thrombocytopenia, and a skin rash

Carbamazepine 1. Mechanism of action 2. Use 3. Adverse effects

Carbapenem-resistant Enterobacteriaceae and carbapenem-resistant Klebsilla. These bacteria make a carbapenemase which break the drug. 1. Yes 2. No 3. Yes 4. Yes 5. Yes

Carbapenems have a very broad spectrum of activity. Which bacteria are they not active against and why? Are they active against the following? 1. Penicillinase-producing gram positive bacteria 2. MRSA 3. Penicillinase-producing gram negative bacteria 4. Aerobes 5. Anaerobes

1. β-lactam inhibitor of cell wall synthesis (penicillin) 2. Used to treat P. aeruginosas infections and other susceptible gram-negative infections

Carbenicillin 1. Mechanism of action 2. Use

COX-2 selective NSAIDs. It is the result of the inhibition of endothelial COX-2. This leads to decreased production of PGI2 from the endothelial cells without inhibition of platelet COX-1 which leads to continued release of TXA2 (prothrombotic) from platelets with a decreased release of PGI2 (anticoagulant) from the endothelial cells. This leads to vasoconstriction, platelet aggregation, and thrombosis.

Cardiovascular risks are associated with which types of NSAIDs? How does this risk develop?

1. Large cyclic peptides linked to a long-chain fatty acid that inhibits the synthesis of β(1-3)-D-glucans in the fungal cell wall 2. Active against candida and aspergillus but not cryptococcus neoformans

Caspofungin 1. Mechanism of action 2. Use

1. Stimulant laxative. 2. Prokinetic

Castor oil 1. Mechanism of action 2. Use

2nd Generation

Cefaclor Generation?

2nd Generation

Cefamandole Generation?

1st Generation

Cefazoline Generation?

4th Generation

Cefipime Generation?

3rd Generation

Cefixime Generation?

3rd Generation

Cefoperazone Generation?

3rd Generation

Cefotaxime Generation?

2nd Generation

Cefotetan Generation?

Prophylaxis and therapy of abdominal and pelvic cavity infections

Cefotetan and Cefoxitin are used for what?

2nd Generation

Cefoxitin Generation?

5th Generation

Ceftaroline Generation?

3rd Generation

Ceftazidime Generation?

3rd Generation

Ceftriaxone Generation?

1. Partial selective COX-2 inhibitor 2. 3. Sulfonamide that may cause hypersensitivity reactions such as rashes They have fewer GI side effects because they do not inhibitor COX-1 but they have an increased risk of developing cardiovascular events.

Celecoxib 1. Mechanism of action 2. Use 3. Adverse effects What is the benefit and risk of the coxib drugs?

1st Generation

Cephalexin Generation?

1. GnRH receptor antagonist 2. Used to suppress gonadotropin production and prevent the LH surge during controlled ovarian hyperstimulaiton

Cetrorelix 1. Mechanism of action 2. Use

1. Binds to the 50S ribosomal subunit and inhibits protein synthesis 2. Toxicity limits its use to the treatment of life-threatening infections without other alternatives, ie. serious infections resistant to less toxic drugs (never given for minor infections) 3. Aplastic anemia and Gray Baby Syndrome (cyanosis) Its strong affinity for mitrochondrial ribosomes leading to bone marrow toxicity It is broad spectrum (used against aerobic and anaerobic gram-positive and gram-negative organisms) It inhibits them, especially CYP3A4 and CYP2C9

Chloramphenicol 1. Mechanism of action 2. Use 3. Adverse effects This drugs toxicity is a result of what? This drug is useful against what types of bacteria? What is this drugs effect on CYP450 enzymes?

1. Inhibits the parasites ability to convert heme to hemozoin which leads to accumulation of heme (produced by the parasites digestion of the host cells hemoglobin) which causes lysis of both the parasite and the host RBC 2. The drug of choice in the treatment of non-falciparum and sensitive uncomplicated falciparum malaria as well as the preferred chemoprophylactic agent for treatment in areas without resistant falciparum malaria Highly effective against blood form but not against the liver stage of the parasite.

Chloroquine 1. Mechanism of actin 2. Use Is this drug effective against the blood and liver or just blood stage of the parasites?

1. First generation sulfonylurea drug 2. Used to treat type II diabetes and is effective at reducing fasting plasma glucose and HbA1c levels 3. Elderly patients as hypoglycemia is common

Chlorpropamide 1. Mechanism of action 2. Use 3. Contraindications

1. Bile salt binding resins 2. Used to prevent diarrhea associated with IBS and IBD by blocking the osmotic and irritating actions of bile salts. To treat gallstones

Cholestyramine, colestipol, and colesevalam 1. Mechanism of action 2. GI Use What other use besides treating diarrhea associated IBS and IBD and for hyperlipidemia do these drugs have?

Carbachol

Cholinergic Agonist - Direct Choline ester - Quaternary ammonium compound Ester of carbamic acid. Not hydrolyzed by AChE, but by other esterases. Both muscarinic and nicotinic agonist. Used to obtain miosis during surgery, and to reduce intraocular pressure after cataract surgery.

Bethanechol

Cholinergic Agonist - Direct Choline ester - Quaternary ammonium compound Ester of carbamic acid. Not hydrolyzed by AChE, but by other esterases. Little or no nicotinic actions. Strong muscarinic activity. Used to treat non-obstructive urinary retention and for neurogenic atony of the urinary bladder with retention. Adverse - Causes generalized cholinergic stimulation: sweating, salivation, flushing, hypotension, nausea, abdominal pain, diarrhea, bronchospasm.

Methacholine

Cholinergic Agonist - Direct Choline ester - Quaternary ammonium compound Hydrolyzed by AChE at considerably slower rate than ACh, and almost totally resistant to hydrolysis by nonspecific cholinesterase or butyrylcholinesterase. Predominantly muscarinic agonist. Slight nicotinic actions. Used to diagnose bronchial airway hyperreactivity in subjects without clinically apparent asthma.

Acetylcholine

Cholinergic Agonist - Direct Choline ester - Quaternary ammonium compound (ACh) Virtually no systemic therapeutic applications. Rapidly hydrolyzed by acetylcholinesterase and plasma butyrylcholinesterase. Used to obtain rapid miosis in anterior segment eye surgeries.

Nicotine

Cholinergic Agonist - Direct Natural Alkaloid - Ganglion stimulant Tertiary amine. Affects NMJ in concentrations only slightly greater than those that affect ganglia. Action is same on both sympathetic and parasympathetic ganglia. At low dose, response resembles simultaneous discharge of both sympathetic/parasympathetics by depolarization. At high dose, a prolonged depolarization causes ganglionic blockade. In CVS, effects are sympathomimetic, and increase heart rate and blood pressure. In GIT and UT, effects are parasympathomimetic, causing nausea, vomiting, diarrhea, and voiding of urine, as well as salivary and bronchial secretions. Used for smoking cessation therapy. Adverse - Can cause poisoning. Hypotension, weak pulse. Paralysis of respiratory muscles

Muscarine

Cholinergic Agonist - Direct Natural alkaloid Acts almost exclusively at muscarinic receptor sites

Arecoline

Cholinergic Agonist - Direct Natural alkaloid Acts at muscarinic and nicotinic receptor sites

Pilocarpine

Cholinergic Agonist - Direct Natural alkaloid Tertiary amine. Stable to hydrolysis by AChE. Partial muscarinic agonist. Used as second line agent for open angle glaucoma. Also, for management of acute angle-closure glaucoma. Adverse - Can enter brain and cause CNS disturbances. Stimulates sweating and salivation.

Donepezil

Cholinergic Agonist - Indirect Anti-ChE Oral. Used to treat symptoms of Alzheimer's disease.

Galantamine

Cholinergic Agonist - Indirect Anti-ChE Oral. Used to treat symptoms of Alzheimer's disease.

Rivastigmine

Cholinergic Agonist - Indirect Anti-ChE Oral. Used to treat symptoms of Alzheimer's disease.

Tacrine

Cholinergic Agonist - Indirect Anti-ChE Oral. Used to treat symptoms of Alzheimer's disease.

Pyridostigmine

Cholinergic Agonist - Indirect Anti-ChE Quaternary ammonium. Carbamate. Forms covalent bond with AChE. Used to treat myasthenia gravis (most commonly used Anti-ChE for this indication).

Neostigmine

Cholinergic Agonist - Indirect Anti-ChE Quaternary ammonium. Does not enter CNS. Carbamate. Forms covalent bond with AChE. Used to stimulate bladder and GIT. Antidote for competitive, non-depolarizing NMJ blockers. Symptomatic treatment of myasthenia gravis. Adverse - Salivation, flushing, low blood pressure, nausea, abdominal pain, diarrhea, bronchospasm.

Edrophonium

Cholinergic Agonist - Indirect Anti-ChE Simple alcohol bearing quaternary ammonium. Binds reversibly to active site of AChE and does not form covalent bond, therefore is short-lived(2-10 minutes). Used to diagnose myasthenia gravis. IV dose leads to rapid increase in muscle strength. Also, to reverse neuromuscular block produced by non-depolarizing muscular blockers.

Malathion

Cholinergic Agonist - Indirect Anti-ChE Synthetic organophosphate. Forms covalent bond with AChE and is extremely stable and hydrolyzes very slowly. Liposoluble. Must be activated in the body. Used as insecticide.

Parathion

Cholinergic Agonist - Indirect Anti-ChE Synthetic organophosphate. Forms covalent bond with AChE and is extremely stable and hydrolyzes very slowly. Liposoluble. Must be activated in the body. Not detoxified effectively in vertebrates, therefore considered more dangerous than malathion. Used as insecticide.

Sarin

Cholinergic Agonist - Indirect Anti-ChE Synthetic organophosphate. Forms covalent bond with AChE and is extremely stable and hydrolyzes very slowly. Liposoluble. Nerve agent. Among most potent synthetic toxic agents known.

Soman

Cholinergic Agonist - Indirect Anti-ChE Synthetic organophosphate. Forms covalent bond with AChE and is extremely stable and hydrolyzes very slowly. Liposoluble. Nerve agent. Among most potent synthetic toxic agents known.

Tabun

Cholinergic Agonist - Indirect Anti-ChE Synthetic organophosphate. Forms covalent bond with AChE and is extremely stable and hydrolyzes very slowly. Liposoluble. Nerve agent. Among most potent synthetic toxic agents known.

Echothiphate

Cholinergic Agonist - Indirect Anti-ChE Synthetic organophosphate. Forms covalent bond with AChE and is extremely stable and hydrolyzes very slowly. Not liposoluble. Used for glaucoma.

Physostigmine

Cholinergic Agonist - Indirect Anti-ChE Tertiary amine. Can enter and stimulate CNS. Carbamate. Forms covalent bond with AChE. Used to treat overdoses of anticholinergic drugs. Note: Should not be given to pt. with suspected TCA overdose because it can aggravate depression of cardiac conduction. Adverse - May lead to convulsions if dosage high. Bradycardia may occur. Inhibition of AChEs at NMJ causes accumulation of ACh and results in skeletal muscle paralysis.

Pralidoxime

Cholinergic Agonist - Reactivator of AChE If given before ageing has occurred, splits phosphorous-enzyme covalent bond. Used to regenerate/reactivate inhibited cholinesterase for organophosphate insecticide poisoning, such as malathion and parathion.Should be given empirically.

Scopolamine

Cholinergic Antagonist Muscarinic Antagonist Belladonna alkaloid. Similar peripheral effects as atropine, but greater actions on CNS with longer duration. Actions - highly effective anti-motion sickness drug. Blocks short-term memory. Produces sedation(at high doses, excitement). Used for mydriasis and cyclopegia in diagnostic procedures or pre-/postoperative states, and prevention of nausea and vomiting associated with motion sickness. Contraindications for antimuscarinics: angle-closure glaucoma, prostatic hypertrophy, elderly(especially those with cognitive impairment)

Atropine

Cholinergic Antagonist Muscarinic Antagonist Belladonna alkaloid. Tertiary amine. Binds competitively to muscarinic receptors both centrally and peripherally. Actions - mydriasis, unresponsiveness to light, cycloplegia, elevated intraocular pressure, reduce GI motility, decrease bladder hypermotility, tachycardia(initial bradycardia if low dose), sometimes cutaneous vasodilation "atropine flush", and blocked salivary, sweat, and lacrimal gland secretions. Used to counteract excessive muscarinic effects with a blockade(ie. antisialogogue prior to surgery, increase heart rate/decrease AV-block). Antidote for cholinergic drug overdose, or Amanita muscaria poisoning. Alleviates muscarinic side effects of anticholinesterase drugs. Adverse - dry mouth, blurred vision, sandy eyes, tachycardia, constipation, restlessness, confusion, hallucinations, delirium to depression, collapse of circulatory/respiratory systems, death. Too risky for use on elderly for mydriasis or cycloplegia. Contraindications for antimuscarinics: angle-closure glaucoma, prostatic hypertrophy, elderly(especially those with cognitive impairment)

Ipratropium

Cholinergic Antagonist Muscarinic Antagonist Quaternary ammonium derivative of atropine. Inhalant. Used for asthma and chronic obstructive pulmonary disease in patients unable to take adrenergic agonists. Contraindications for antimuscarinics: angle-closure glaucoma, prostatic hypertrophy, elderly(especially those with cognitive impairment)

Glycopyrrolate

Cholinergic Antagonist Muscarinic Antagonist Quaternary ammonium. Oral. Used to inhibit GI motility. Also parenterally to prevent bradycardia during surgical procedures. Contraindications for antimuscarinics: angle-closure glaucoma, prostatic hypertrophy, elderly(especially those with cognitive impairment)

Tiotropium

Cholinergic Antagonist Muscarinic Antagonist Quaternary ammonium. Superior to ipratropium as bronchodilator. Used for chronic obstructive pulmonary disease. Not FDA-approved for asthma. Contraindications for antimuscarinics: angle-closure glaucoma, prostatic hypertrophy, elderly(especially those with cognitive impairment)

Tolterodine

Cholinergic Antagonist Muscarinic Antagonist Tertiary amine. Used for overactive bladder. Contraindications for antimuscarinics: angle-closure glaucoma, prostatic hypertrophy, elderly(especially those with cognitive impairment)

Benztropine

Cholinergic Antagonist Muscarinic Antagonist Tertiary amine. Gain access to CNS. Used to treat parkinsonism and the extrapyramidal effects of antipsychotic drugs. Contraindications for antimuscarinics: angle-closure glaucoma, prostatic hypertrophy, elderly(especially those with cognitive impairment)

Trihexyphenidyl

Cholinergic Antagonist Muscarinic Antagonist Tertiary amine. Gain access to CNS. Used to treat parkinsonism and the extrapyramidal effects of antipsychotic drugs. Contraindications for antimuscarinics: angle-closure glaucoma, prostatic hypertrophy, elderly(especially those with cognitive impairment)

Cyclopentolate

Cholinergic Antagonist Muscarinic Antagonist Tertiary amine. Preferred to atropine because of short duration. Used in ophthalmology to produce mydriasis with cycloplegia. Contraindications for antimuscarinics: angle-closure glaucoma, prostatic hypertrophy, elderly(especially those with cognitive impairment)

Homatropine

Cholinergic Antagonist Muscarinic Antagonist Tertiary amine. Preferred to atropine because of short duration. Used in ophthalmology to produce mydriasis with cycloplegia. Contraindications for antimuscarinics: angle-closure glaucoma, prostatic hypertrophy, elderly(especially those with cognitive impairment)

Tropicamide

Cholinergic Antagonist Muscarinic Antagonist Tertiary amine. Preferred to atropine because of short duration. Used in ophthalmology to produce mydriasis with cycloplegia. Contraindications for antimuscarinics: angle-closure glaucoma, prostatic hypertrophy, elderly(especially those with cognitive impairment)

Hexamethonium

Cholinergic Antagonist Nicotinic Antagonist - Ganglion blocker Originally used to treat hypertension, but replaced by antihypertensive agents. Effects can be predicted by knowledge of which division of ANS exercises dominant control over target organ.

Mecamylamine

Cholinergic Antagonist Nicotinic Antagonist - Ganglion blocker Originally used to treat hypertension, but replaced by antihypertensive agents. Effects can be predicted by knowledge of which division of ANS exercises dominant control over target organ.

Trimethaphan

Cholinergic Antagonist Nicotinic Antagonist - Ganglion blocker Originally used to treat hypertension, but replaced by antihypertensive agents. Effects can be predicted by knowledge of which division of ANS exercises dominant control over target organ.

Tubocurarine

Cholinergic Antagonist Nicotinic Antagonist - Neuromuscular junction blocker Competitive antagonist(non-depolarizing). Prototype. Given IV(oral absorption is minimal). Used as an adjuvant drug to produce complete muscle relaxation during surgery. Can be overcome by increasing concentration of acetylcholine with cholinesterase inhibitors such as neostigmine or edrophonium. Adverse - some agents are moderate muscarinic blockers. May also cause histamine release.

Botulinum Toxin

Cholinergic Antagonist Nicotinic Antagonist - Presynaptic drug Inhibitor of acetylcholine release. Potent neurotoxin preventing synaptic vesicle fusion with axon terminal membrane. Used in treatment of several diseases associated with increased muscle tone, such as torticollis, achalasia, strabismus, blepharospasm, and other focal dystonias. Also approved for cosmetic treatment of facial wrinkles, and increasingly used to treat various headache and pain syndromes.

Vesamicol

Cholinergic Antagonist Nicotinic Antagonist - Presynaptic drug Inhibitor of acetylcholine storage, blocking VAChT ACh-H+ antiporter. Used only as research tool.

Hemicholinium

Cholinergic Antagonist Nicotinic Antagonist - Presynaptic drug Inhibitor of acetylcholine synthesis, blocking CHT1 transporter for choline. Used only as research tool.

Succinylcholine

Cholinergic Antagonist (clinically) Nicotinic Agonist - Neuromuscular junction blocker Not metabolized effectively at the synapse, desensitizing the receptor, causing flaccid paralysis. Given IV by continuous infusion, rapidly hydrolyzed by plasma cholinesterase. Brief duration(5-10 min.) and rapid onset(1-1.5 min.). Used when rapid endotracheal intubation is needed. Also used during ECT. Adverse - Malignant hyperthermia, usually arising from the combination with a halogenated anesthetic. One of the main causes of anesthesia related death. Treated with dantrolene.

1. Nucleoside/nucleotide analog that is requires activation by host cell kinases but is not phosphorylated by viral kinases and causes DNA chain termination and DNA polymerase inhibition 2. Used in the treatment of CMV-induced retinitis in patients with HIV/AIDS To block renal tubular excretion of the drug to increase bioavailability.

Cidofovir 1. Mechanism of action 2. Use Probenecid must be co-administered with this drug. Why?

1. Metabolic enzyme inhibitor (dihydropeptidase inhibitor) 2. Co-administered with Imipenem to prevent high levels of a potentially nephrotoxic metabolite from building up.

Cilastatin 1. Mechanism of action 2. Use

1. Activates calcium-sensing receptors in the parathyroid cells which leads to decreased PTH synthesis and release 2. Used to treat secondary hyperparathyroidism in chronic renal disease and hyperparathyroidism in patient with a responsive parathyroid carcinoma 3. Nausea and hypocalcemia

Cinecalcet 1. Mechanism of action 2. Use 3. Adverse effects

1. Fluoroquinolone drug that inhibits bacterial DNA replication by interfering with topoisomerase II (DNA gyrase) and topoisomerase IV 2. Used to treat travelers diarrhea, P. aeruginosa, sand used as an alternative to deftriaxone and rifampin as a meningitis prophylaxis 2nd

Ciprofloxacin 1. Mechanism of action 2. Use Generation?

1. 5-HT4 agonist 2. Prokinetic used to treat gastroparesis, GERD, and constipation.

Cisapride 1. Mechanism of action 2. Use 3. Adverse effects

1. Monoclonal antibody against EFGR 2. Used for colorectal cancer treatment

Cituximab 1. Mechanism of action 2. Use

1. Macrolide drug that reversibly binds to the 50S ribosomal subunit and inhibits translocation 2. Used in empiric therapy of community-acquired pneumonia and to treat upper respiratory tract and soft-tissue infections (ex. Staph, H. influenza, S. pneumonia, and enterococci).

Clarithromycin 1. Mechanism of action 2. Use

1. β-lactamase inhibitor which binds to and inactivates most β-lactamases. 2. Co-administered in fixed combinations with penicillins

Clavulanic Acid 1. Mechanism of action 2. Use

1. Binds to 50S ribosome 2. Can be used as an alternative to doxycycline to finish up treatment of severe malaria after treatment with quinidine or artesunate

Clindamycin 1. Mechanism of actin 2. Use

1. Binds to the 50S ribosomal subunit and inhibits protein synthesis 2. Used to treat anaerobic infections such as abscesses and abdominal infections. 3. C. difficule caused pseudomembranouse colitis Pneumocystis carinii pneumonia Toxoplasmosis of the brain Primarily used against gram-positive anaerobic bacteria (most gram-negative aerobes and enterococci are intrinsically resistant)

Clindamycin 1. Mechanism of action 2. Use 3. Adverse effects This drug can be used in combination with primaquine to treat what condition? It can also be used in combination with pyrimethamine as an alternative treatment for what condition? This drug is useful against what types of bacteria?

1. Binds to DNA and inhibitrs replication 2. Used as combination treatment to treat leprosy 3. Red-brown discoloration of the skin No, because it also has anti-inflammatory actions.

Clofazimine 1. Mechanism of action 2. Use 3. Adverse effects Does erythema nodosum develop with the use of this drug?

1. Estrogen antagonist in the hypothalamus and anterior pituitary which prevents feedback inhibition of GnRH release, causing continued release of GnRH from the hypothalamus and elevated LH and FSH release from the pituitary leading to ovulation 2. Used to treat patients with infertility

Clomiphene 1. Mechanism of action 2. Use 3. Adverse effects

1. α2-agonist which acts on the presynaptic neurons to decrease sympathetic outflow 2. Used to treat the adrenergic mediated opioid withdrawal symptoms

Clonidine 1. Mechanism of action 2. Use in drug abuse

1. Inhibit 14-α-demethylase, they last enzyme in ergosterol synthesis from lanosterol 2. Most commonly used to topically treat superficial mycoses

Clotrimazole 1. Mechanism of action 2. Use 3. Adverse effects Imidazole or Triazole? Inhibits what CYP P450 enzymes?

Can cause agranulocytosis in 1-2% of patients Regular blood cell counts are required for patients taking this drug

Clozapine has what adverse reaction? As a result, how should these patients be monitored?

...

Co-trimoxazole 1. Mechanism of action 2. Use 3. Adverse effects

1. Mild to moderate µ receptor agonist 2. Used as an antitussive and to treat pain It is less efficacious than morphine CYP2D6. The metabolites of these drugs are much more potent opioid receptor agonists than the drugs themselves so for these drugs to be effective the patient has to have normal CYP2D6 activity. Ex. Codeine is metabolized to morphine. The antitussive properties may be due to the direction of codeine on distinct receptors.

Codeine 1. Mechanism of action 2. Use How does this drug efficacy in treating pain compare to that of morphine? Codeine, oxycodone, and hydrocodone are metabolized in the liver by what cytochrome? Why is this important for these drugs?

1. Binds to tubulin which inhibits it polymerization preventing the formation of microtubules. This disrupts the motility of granulocytes and decreases their migration into effected areas and blocks cell division. It also inhibits the release of leukotrienes 2. Used in the treatment of attacks of acute gouty arthritis 3. May cause myopathy neutropenia, aplastic anemia, and alopecia. No Patients with hepatic, renal, or cardiovascular disease. No, because of its troublesome diarrheal AE it has been replaced by NSAIDs

Colchicine 1. Mechanism of action 2. Use 3. Adverse effects Is this drug safe to use in pregnancy? In which patients should it be used with caution? Is this drug used much anymore?

1. Bile acid sequestrant whose MOA is unclear in DM treatment 2. Used for the treatment of type 2 DM

Colesevelam 1. Mechanism of action 2. Use

Increases the risk of hepatotoxicity Neutropenia and infections

Combination therapy for RA with Methotrexate and Leflunomide increases the risk of what? The combination of different biological agents increases the risk of what conditions?

Typically includes weekly methotrexate to which other agents are added (usually one of the following): Methotrexate + Hydroxychloroquine Methotrexate + Sulfasalazine Methotrexate + Hydroxychloroquine + Sulfasalazine Methotrexate + Cyclosporine Methotrexate + Leflunomide Methotrexate + Gold (not popularly used) Methotrexate + TNF inhibitor

Combination therapy with DMARDs usually includes what?

D1: Gs D2: Gi Stimulation of the D2 receptor although D1 stimulation may also be required for maximal benefit

D1 and D2 receptors are abundant in the striatum and are the most important receptor sites with regards to the causes and treatment of Parkinson's disease. What type of receptors are they? The benefits of dopaminergic antiparkinsonism drugs depends mostly on which receptor?

1. Monoclonal antibody that acts asa IL-2 receptor antagonist 2. Used as an immunosuppressant preoperatively during transplantation They have the same mechanism of action but Daclizumab is a humanized antibody and Basiliximab is a chimeric antibody.

Daclizumab 1. Mechanism of action 2. Use What is the difference between this drug and Basiliximab?

1. Inhibit 14-α-demethylase, they last enzyme in ergosterol synthesis from lanosterol 2. Many uses; DOC for candidiasis, candidemia, coccidioidomycosis, for secondary treatment of cryptococcal meningitis after amphoteracin B and for initial and secondary prophylaxis against cryptococcal meningitis. 3. Low AE profile It has a high CSF penetration which makes it very useful in treating fungal meningitis Aspergillus and other filamentous fungi CYP2C9 and a moderate inhibitor of CYP3A4

Fluconazole 1. Mechanism of action 2. Use 3. Adverse effects What is a major benefit of fluconazole? What fungi is this drug not affective against? Imidazole or Triazole? Inhibits what CYP P450 enzymes?

Mucormycosis and Fusariosis

For what fungal infections is the primary therapy only Amphoteracin B?

1. Analog of anion pyrophosphate that selectively inhibits the pyrophosphate binding site on viral DNA polymerases 2. Used to treat CMV retinitis in immunocompromised patients, acyclovir-resistant HSV & CMV retinitis, and ganciclovir-resistant CMV & VZV 3. Nephrotoxicity and electrolyte disturbances It does not require phosphorylation for its activity which is what makes it as useful as it is in the treatment of multi-drug resistant herpes viruses

Foscarnet 1. Mechanism of action 2. Use 3. Adverse effects What is unique about this herpes virus treating drug?

1. Non-β-lactam inhibitor of cell wall synthesis that interferes in early stages of cell wall synthesis 2. Used for treatment of uncomplicated lower UTIs Both

Fosfomycin 1. Mechanism of action 2. Use Is this drug affective against gram-negative, gram-positive, or both?

1. Estrogen receptor antagonist in all tissues 2. Use to treat tamoxifen resistant breast cancer

Fulvestrant 1. Mechanism of action 2. Use

1. Anticonvulsant. 2. Useful in the management of neuropathic pain

Gabapentin 1. Mechanism of action 2. Use

1. Increases GABA release in the CNS 2. Used to treat patients with chronic spasms

Gabapentin 1. Mechanism of action 2. Use

1. Increases the release of GABA from presynaptic neurons and decreases glutamate release by blocking presynaptic voltage gated calcium channels 2. Used as an adjunct to treat seizures as well as being used to treat neuropathic pain

Gabapentin 1. Mechanism of action 2. Use

1. Nucleoside/nucleotide analog that is phosphorylated by viral (different kinase than the one used by acyclovir) and cell kinases to an active form whose incorporation leads to DNA chain termination and DNA polymerase inhibition 2. Drug of choice for CMV retinitis and CMV prophylaxis in immunocompromised patients It is effective against HSV & ganciclovir resistant HSV

Ganciclovir 1. Mechanism of action 2. Use What is useful about this drug?

1. GnRH receptor antagonist 2. Used to suppress gonadotropin production and prevent the LH surge during controlled ovarian hyperstimulaiton.

Ganirelix 1. Mechanism of action 2. Use

1. Inhibits epidermal growth factor receptor signal transduction 2. Used to treat non-small cell lung cancer

Gefitinib 1. Mechanism of action 2. Use

1. Fluoroquinolone drug that inhibits bacterial DNA replication by interfering with topoisomerase II (DNA gyrase) and topoisomerase IV 2. Used to treat community acquired pneumonia. 4th

Gemifloxacin 1. Mechanism of action 2. Use Generation?

They are relatively non-toxic and the most common adverse effect is minor GI upset. Imidazoles: (MCK) Miconazole, Clotrimazole Triazoles: Itracoonazole, Fluconazole, Voriconazole, and Posaconazole The triazoles are more specific for fungal CYP P450 enzymes than the imidazoles CYP 3A4

Generally, what are the adverse effects of the azoles? Which azoles are imidazole and which are triazoles? What is the difference between the imidazoles and triazoles? Most azoles are inhibitors of what CYP P450 enzyme?

Methotrexate Moderate to severe RA.

Generally, what is the first DMARD prescribed for patients with rheumatoid arthritis? What severity of RA are biologic DMARDs reserved for?

1. Aminoglycoside drug that irreversibly binds to the 30S ribosomal subunit prior to ribosome formation 2. Commonly used as an initial treatment of an unknown infection for a short period of time and is discontinued after the offending organism is identified.

Gentamicin 1. Mechanism of action 2. Use

1. Second generation sulfonylurea drug 2. Used to treat type II diabetes and is effective at reducing fasting plasma glucose and HbA1c levels 3. Hypoglycemia and weight gain.

Glimepiride 1. Mechanism of action 2. Use 3. Adverse effects

1. Second generation sulfonylurea drug 2. Used to treat type II diabetes and is effective at reducing fasting plasma glucose and HbA1c levels. 3. Hypoglycemia and weight gain

Glipizide 1. Mechanism of action 2. Use 3. Adverse effects

1. Analog of glucagon 2. Used to reverse a serious insulin induced hypoglycemic state when IV glucose administration is not available

Glucagon 1. Mechanism of action 2. Use

1. GnRH analog 2. To treat male infertility and rarely female infertility. Can also be used to diagnose a patients LH responsiveness to GnRH. Also used to treat of endometriosis by removing exposure to cyclical changes in estrogen and progesterone during the menstrual cycle, to reduce the size of fibroids, and to treat prostate cancer. Inhibition of FSH and LH release leading to hypogonadism

Goserelin 1. Mechanism of action 2. Use What can occur if this drug is administered in a non-pulsitile manner?

High levels of uric acid in the blood which leads to deposition of sodium irate crystals in tissues and joints. No, but gout is always preceded by hyperuricemia. Management of the acute attacks of gouty arthritis and long-term management of chronic gout.

Gout is a metabolic disorder characterized by what? Does hyperuricemia always lead to gout? What are the two main strategies for the treatment of gout?

1. 5-HT3 receptor blockers 2. Used to treat chemotherapy and post-operative induced nausea and vomiting (antiemetic) Corticosteroids Corticosteroids + Ondansetron + aprepitant.

Granisetron & Ondansetron 1. Mechanism of action 2. Use What can be combined with these drugs to provide a greater anti-emetic effect? What is an effective combination for treatment of chemotherapy induced nausea and vomiting?

1. Disrupts the mitotic spindle and inhibits mitosis 2. Used for the treatment of severe dermatophytoses of the skin, hair, and nails (but is largely replaced by newer drugs like terbinafine and itraconazole) Yes, it inhibits them.

Griseofulvin 1. Mechanism of action 2. Use Does this drug affect CYP P450 enzymes?

Warfarin

Has a very narrow therapeutic index. Highly bound to albumin, with only a small fraction free. Slight displacement by sulfonamide will cause rapid, significant plasma concentration increase, which may lead to bleeding.

Streptokinase

Disorders of Coagulation Thrombolytic Protein produced by beta-hemolytic streptococci. Originally used to treat DVT, serious pulmonary embolism, acute MI, and peripheral arterial thrombosis, but now used less frequently. Actions - convert inactive zymogen plasminogen to active protease plasmin. Also catalyzes degradation of fibrinogen as well as clotting factors V and VII. Used to lyse blood clots and thereby restore the patency of an obstructed vessel before distal tissue necrosis occurs. Approved for use in acute MI, acute pulmonary embolism, arterial thrombosis, and occluded access shunts. Adverse - Also has potential to dissolve not only pathologic, but physiologically appropriate thrombi. Contraindications: healing wounds, pregnancy, history of cerebrovascular accident or metastatic cancer.

Alteplase

Disorders of Coagulation Thrombolytic Recombinant tPA. Tissue plasminogen activator(tPA) activates plasminogen bound to fibrin in a thrombus or hemostatic plug. Said to be "fibrin selective". The higher the tPA concentration, the more activation, leading to hemorrhage. Actions - convert inactive zymogen plasminogen to active protease plasmin. Used to manage acute MI and acute ischemic stroke. Given within 4.5 hours after onset of stroke symptoms. Adverse - Also has potential to dissolve not only pathologic, but physiologically appropriate thrombi. Contraindications: healing wounds, pregnancy, history of cerebrovascular accident or metastatic cancer.

1. Aldehyde dehydrogenase inhibitor 2. Used to create an aversion to drinking in alcoholic patients by causing unpleasant side effects associated with drinking alcohol including flushing and vomiting. 1. Orally available μ-receptor opioid antagonists 2. Used to treat alcoholics by reducing the craving for alcohol. Also used to after opioid detoxification to attempt to help a patient remain opioid free. 1. NMDA receptor antagonist 2. Used to prevent relapse in alcoholic patients who have undergone treatment and are currently not drinking alcohol

Disulfiram 1. Mechanism of action 2. Use Naltrexone 1. Mechanism of action 2. Use Acamprosate 1. Mechanism of action 2. Use

Conivaptan

Diuretic ADH Antagonist Acts on Collecting Duct(CD). ADH antagonist to V1 and V2 receptors in the CD, diluting urine. Must be given IV. It is metabolized by and is a potent inhibitor of CYP3A4. Actions - in absence of ADH, dilutes urine. Used to treat euvolemic and hypervolemic hyponatremia, SIADH, and heart failure(only when benefits outweigh risks since safety is not established). Adverse - infusion site reactions, thirst, a-fib, GI & electrolyte disturbances, and nephrogenic diabetes insipidus. Contraindicated in patients with hypovolemic hyponatremia or renal failure.

Acetazolamide

Diuretic Carbonic Anhydrase Inhibitor Acts on Proximal Convoluted Tubule(PCT). Potently inhibits both extracellular and intracellular forms of carbonic anhydrase, resulting in the reduction of HCO3- reabsorption in the proximal convoluted tubule. The diuretic efficacy decreases significantly with use over several days. Excreted unchanged, therefore dosing must be reduced in renal insufficiency. Actions - increases urinary pH. Urinary excretion: increase Na+, K+, HCO3-, and urine volume. Used to treat glaucoma, mountain sickness, metabolic alkalosis, and epilepsy. Adverse - metabolic acidosis, hyponatremia, hypokalemia, renal stones, malaise, fatigue, depression, drowsiness, paresthesias, and hypersensitivity.

1. Stool softner 2. Used to treat constipation Senna

Docusate 1. Mechanism of action 2. Use This drug is commonly used in combination with what other drug to treat cases of opioid-induced constipation?

Bradycardia as a result of activation of muscarinic receptors in the heart. With the use of muscarinic antagonists like atropine.

Does succinylcholine typically cause brady- or tachycardia and why? How can this be prevented?

They inhibit topoisomerase II which causes DNA breaks, form oxygen free radicals which damage DNA and cell membranes, and alter membrane fluidity and ion transport. Etoposide and tenoposide both inhibit topoisomerase II. Bleomycin forms free radicals which damage DNA. Cardiotoxicity It is the formation of free radicals that lead sot the cardiotoxicity because the heart has a limited capacity to neutralize free radicals. Administration of dexrazoxane, an iron chelating agent, can reduce the free radical damage.

Doxorubicin and Daunorubicin both have what mechanism of action? What other anti-cancer drugs have this same mechanism of action? What adverse effect should you be aware of in patients being treated with either of these drugs? How can this adverse effect be avoided?

1. Tetracycline drug that reversibly binds to the 30S ribosomal subunit which prevents binding of aminoacyl tRNA 2. Good choice of drug for STD's and prostatitis 3. Discoloration and hypoplasia of teeth and stunting of growth (because of brining to calcium ions) Mainly in the bile

Doxycycline 1. Mechanism of action 2. Use 3. Adverse effects Where is this drug excreted from?

1. Tetracycline inhibitor of of 30S ribosome 2. Used to complete treatment course after severe malaria is treated with quinidine or artesunate or alongside quinine as a treatment for severe falciparum malaria

Doxycylcine 1. Mechanism of actin 2. Use

1. Synthetic marijuana 2. Anti-emetic

Dronabinol 1. Mechanism of action 2. Use

1. Therapeutic version of THC 2. Used to treat anorexia and weight loss in patients with AIDS and to treat the nausea and vomiting associated with cancer chemotherapy

Dronabinol 1. Mechanism of action 2. Use

1. Non-competitive inhibitors of HIV-1 reverse transcriptase and cause inhibition of RNA and DNA dependent DNA polymerase 2. Use to treat HIV (currently part of the recommended regimen for the treatment of HIV) 3. Mostly CNS problems that typically resolve after a few weeks as well as a risk for hypersensitivity rashes and can cause increases in triglycerides, HDL, and total cholesterol. It has a long half life so it can be given through once a day dosing. Potent inducer of CYP P450 enzymes Class D

Efavirenz 1. Mechanism of action 2. Use 3. Adverse effects 4. What is important about this drugs pharmacokinetics? Is this an inducer or inhibitor of CYP3A4? Pregnancy Class?

Carboprost tromethamine

Eicosanoid (15-methyl-PGF2alpha) Used as an abortifacient in the second trimester of pregnancy.

Misoprostol

Eicosanoid (PGE1 derivative) Used in combination with progesterone antagonist mifepristone or methotrexate as an abortifacient combination. Also used to prevent peptic ulcers in patients who must take high doses of NSAIDs for arthritis and have a history of ulcer associated with this use.

Alprostadil

Eicosanoid (PGE1) Used as an infusion to maintain patency of the ductus arteriosus in infants with transposition of the great vessels until surgical correction can be undertaken. Also used in the treatment of impotence, injected into the penis or inserted into the urethra.

Dinoprostone

Eicosanoid (PGE2) Used to ripen the cervix at term before induction of labor with oxytocin. Also can be used as an abortifacient in the second trimester of pregnancy.

Latanoprost

Eicosanoid (PGF2alpha derivative) Used to treat glaucoma. Increases outflow of aqueous humor, thus reducing intraocular pressure.

Prostacyclin

Eicosanoid (PGI2) Used to lower peripheral, pulmonary, and coronary resistance.

Zileuton

Eicosanoid Antagonist Action - interrupts the leukotriene pathway. Inhibits 5-lipoxygenase, thereby preventing leukotriene synthesis. Used to treat moderate to severe asthma in patients who are poorly controlled by conventional therapy or experience adverse effects with corticoids.

Montelukast

Eicosanoid Antagonist Action - interrupts the leukotriene pathway. Inhibits the binding of LTD4 to its receptor in target tissues, thereby preventing its action, such as bronchoconstriction and mucus hypersecretion. Used to treat moderate to severe asthma in patients who are poorly controlled by conventional therapy or experience adverse effects with corticoids.

Zafirlukast

Eicosanoid Antagonist Action - interrupts the leukotriene pathway. Inhibits the binding of LTD4 to its receptor in target tissues, thereby preventing its action, such as bronchoconstriction and mucus hypersecretion. Used to treat moderate to severe asthma in patients who are poorly controlled by conventional therapy or experience adverse effects with corticoids.

1. Nucleoside analog that lacks a 3' OH group which leads to termination of DNA elongation and competitive inhibitor of reverse transcriptase 2. Use to treat HIV (currently part of the recommended regimen for the treatment of HIV) 3. Hyperpigmentation of plasm and soles (not harmful) It can be administered as a once a day dose.

Emtricitabine 1. Mechanism of action 2. Use 3. Adverse effects What is important about this drugs pharmacokinetics?

1. HIV fusion inhibitor with a similar structure to gp41 which binds to the gp41 subunit of the viral envelope glycoprotein and prevents the ability of the virion to fuse with the cell membrane 2. Approved for treatment of HIV in treatment experienced adults with evidence of HIV replication HIV-1, not HIV-2

Enfurvitide 1. Mechanism of action 2. Use Does this drug have activity against HIV-1, HIV-2, or both?

1. COMT inhibitor which decreases levodopa metabolism, reduces 3-ο-methyl dopa plasma levels which increases levodopa uptake into the CNS, and leads to higher dopamine levels in the brain 2. Used as an adjunct to levodopa/carbidopa therapy in patients with Parkinson's disease.

Entacapone 1. Mechanism of action 2. Use

1. The phosphorylated form competes with natural substrates for the viral polymerase and binding inhibits the reverse transcriptase activity 2. Used in the treatment of lamivudine-resistant strains of HBV and HIV Renal function must be assessed and drugs that can cause renal toxicity should be avoided and should continue to be monitored after discontinuation in case there is an exacerbation of severe hepatitis.

Entecavir 1. Mechanism of action 2. Use What needs to be followed in patients being treated with this drug?

1. Longer acting agonist of the BZ1 benzodiazepine receptor 2. Used for the short-term treatment of insomnia in patient that require drugs in order to maintain sleep

Eszopiclone 1. Mechanism of action 2. Use

1. Recombinant fusion protein which combines two TNF receptor and binds TNFα molecules and facilitates their inactivation and excretion. 2. Used to treat RA

Etanercept 1. Mechanism of action 2. Use

1. Causes inhibition of arabinosyl transferases 2. First line agent for the treatment of all susceptible forms of TB 3. Can lead to a dose-dependent visual disturbance like red/green color blindness. Children who are too young to receive sight tests as they would be unable to tell you if they are developing the adverse effect of red/green color blindness. Yes

Ethambutol 1. Mechanism of action 2. Use 3. Adverse effects Who should this drug not be given to? Is this drug safe in pregnancy?

Because it causes suppression of inhibitory systems initially which leads to these effects A wide variety of receptors including GABA receptors, adenosine reuptake, glycine receptors, NMDA receptors, 5-HT3 receptors, and Kir3/GIRK channels.

Ethanol is classed as a depressant but its effects are often perceived as stimulation. Why? What receptors does ethanol act on?

1. Not specified 2. Used as a second line drug in the treatment of TB 3. Severe GI irritation and adverse neurological effects No, it is teratogenic

Ethionamide 1. Mechanism of action 2. Use 3. Adverse effects Use in pregnancy?

1. Blocks T-type calcium channels 2. Used in the treatment of absence seizures

Ethosuximide 1. Mechanism of action 2. Use

1. They inhibit osteoclastic activity by decreasing farnesyl pyrophosphate synthesis by disrupting the mevalonate pathway leading to decreased osteoclast H+ ATPase function leading to reduced resorption and formation of hydroxyapatite 2. Used to treat osteoporosis, malignancy associated with hypercalcemia, and Paget's disease of the bone May cause bone malformation and decreased osteoblastic activity

Etidronate 1. Mechanism of action 2. Use Chronic use of this drug could lead to what condition?

They inhibit topoisomerase II and p Late S phase and early G2 phase Leukemia As part of the BEP regimen for testicular cancer.

Etoposide and Tenoposide are both epipodophyllotoxins. What is their mechanism of action? What part of the cell cycle do they act on? There is a definitive association between etoposide and what condition seen in cancer survivors treated with this drug? Etoposide is used as part of what drug combination?

1. Non-competitive inhibitors of HIV-1 reverse transcriptase and cause inhibition of RNA and DNA dependent DNA polymerase 2. Used to treat HIV in treatment-experienced patients 3. Risk of hypersensitivity rash and may cause elevations of tranaminase enzymes in patients co-infected with hepatitis Inducer CYP3A4 It is an inhibitor of CYP2C9 and CYP2C19 which makes its drug-drug interactions difficult to predict

Etravirine 1. Mechanism of action 2. Use 3. Adverse effects Is this an inducer or inhibitor of CYP3A4? What about other CYP P450 enzymes?

1. Reversible aromatase inhibitor 2. Used in the second line treatment of breast cancer after tamoxifen 3. Ovarian hyper-stimulation, ovarian enlargement, multiple pregnancies, and visual disturbances.

Exemestane 1. Mechanism of action 2. Use 3. Adverse effects

1. Analog of glucagon-like-polypeptide 1 (GLP-1) which acts like incretins to increase the level of insulin secretion in response to glucose stimulation 2. New agent used to improve glycemic control in adults with type 2 DM 3. Acute pancreatitis, nausea, and vomiting

Exenatide 1. Mechanism of action 2. Use 3. Adverse effects

1. Strong µ receptor agonist 2. Used to treat short term pain CYP3A4 100 times more potent Very short

Fentanyl 1. Mechanism of action 2. Use What cytochrome is responsible for the metabolism of this drug? How potent is this drug compared to morphine? Is the half life of the drug long or short?

1. Inhibits bacterial protein synthesis by binding to RNA polymerase 2. Used in the treatment of C. difficile infections Because of its high cost it is used to treat C. difficile infections after first trying metronidizole and vancomycin. Patients 18 years of age or older.

Fidoxamicin 1. Mechanism of action 2. Use When would this drug be used? This drug is only approved for what patients?

1. 5-α reductase inhibitor which inhibits the conversion of testosterone to DHT 2. Used to treat BPH and topically to cause hair growth (propecia) 3. Gynecomastia and impotence

Finasteride 1. Mechanism of action 2. Use 3. Adverse effects

Histamine

Histamine Agonist Most is bound in granules in mast cells or basophils. ALso functions as a neurotransmitter.Important site of storage/release is the enterochromaffin-like cell of the stomach fundus, which releases it to activate parietal cells. Released from mast cells and basophils, acts as a mediator in immediate (type I) allergic reactions (requires energy). Certain amines (ie. morphine, tubocurarine) displace it in cells and release it without requiring energy or mast cell injury/degranulation. Actions - Vasodilation(H1 &H2), increases both contractility and pacemaker rate of the heart(H2), and induces edema. Also responsible for the urticaria(hives) with pain and itching(H1). Contracts intestinal smooth muscle(H1), causes bronchoconstriction(H1), stimulates gastric acid secretion(H2). Used as an aerosol to test nonspecific bronchial hyperactivity. Adverse - Systemic mast cell degranulation can cause anaphylactic shock, and should not be given to asthmatics or patients with active ulcer disease or GI bleeding.

Chlorpheniramine

Histamine Antagonist H1 Receptor Antagonist - First Generation Has sedative effects and is more likely to block autonomic receptors. Historically considered to be H1-receptor antagonists, but recently shown to be inverse agonists. Histamine-induced bronchoconstriction and GI muscle contraction can be completely blocked. Have additional effects unrelated to H1 antagonism, probably reflecting binding to cholinergic, alpha-adrenergic, serotonin, and local anesthetic receptor sites. Used to treat allergies caused by antigens acting on IgE-antibody sensitized mast cells. Ineffective in treating bronchial asthma because histamine is not the only mediator. Adverse - Sedation, dry mouth. Although the margin of safety is high, acute poisoning is common, especially in children.

Hydroxyzine

Histamine Antagonist H1 Receptor Antagonist - First Generation Has sedative effects and is more likely to block autonomic receptors. Historically considered to be H1-receptor antagonists, but recently shown to be inverse agonists. Histamine-induced bronchoconstriction and GI muscle contraction can be completely blocked. Have additional effects unrelated to H1 antagonism, probably reflecting binding to cholinergic, alpha-adrenergic, serotonin, and local anesthetic receptor sites. Used to treat allergies caused by antigens acting on IgE-antibody sensitized mast cells. Ineffective in treating bronchial asthma because histamine is not the only mediator. Adverse - Sedation, dry mouth. Although the margin of safety is high, acute poisoning is common, especially in children.

Diphenhydramine

Histamine Antagonist H1 Receptor Antagonist - First Generation Has sedative effects and is more likely to block autonomic receptors. Historically considered to be H1-receptor antagonists, but recently shown to be inverse agonists. Histamine-induced bronchoconstriction and GI muscle contraction can be completely blocked. Have additional effects unrelated to H1 antagonism, probably reflecting binding to cholinergic, alpha-adrenergic, serotonin, and local anesthetic receptor sites. Used to treat allergies caused by antigens acting on IgE-antibody sensitized mast cells. Ineffective in treating bronchial asthma because histamine is not the only mediator. Also used to prevent symptoms of motion sickness, and to treat insomnia. Adverse - Sedation, dry mouth. Although the margin of safety is high, acute poisoning is common, especially in children.

Dimenhydrinate

Histamine Antagonist H1 Receptor Antagonist - First Generation Has sedative effects and is more likely to block autonomic receptors. Historically considered to be H1-receptor antagonists, but recently shown to be inverse agonists. Histamine-induced bronchoconstriction and GI muscle contraction can be completely blocked. Have additional effects unrelated to H1 antagonism, probably reflecting binding to cholinergic, alpha-adrenergic, serotonin, and local anesthetic receptor sites. Used to treat allergies caused by antigens acting on IgE-antibody sensitized mast cells. Ineffective in treating bronchial asthma because histamine is not the only mediator. Also used to prevent symptoms of motion sickness. Adverse - Sedation, dry mouth. Although the margin of safety is high, acute poisoning is common, especially in children.

Cetirizine

Histamine Antagonist H1 Receptor Antagonist - Second Generation Has sedative effects and is more likely to block autonomic receptors. Historically considered to be H1-receptor antagonists, but recently shown to be inverse agonists. Histamine-induced bronchoconstriction and GI muscle contraction can be completely blocked. Have additional effects unrelated to H1 antagonism, probably reflecting binding to cholinergic, alpha-adrenergic, serotonin, and local anesthetic receptor sites. Used to treat allergies caused by antigens acting on IgE-antibody sensitized mast cells. Ineffective in treating bronchial asthma because histamine is not the only mediator. Adverse - Sedation, dry mouth. Although the margin of safety is high, acute poisoning is common, especially in children.

Fexofenadine

Histamine Antagonist H1 Receptor Antagonist - Second Generation Has sedative effects and is more likely to block autonomic receptors. Historically considered to be H1-receptor antagonists, but recently shown to be inverse agonists. Histamine-induced bronchoconstriction and GI muscle contraction can be completely blocked. Have additional effects unrelated to H1 antagonism, probably reflecting binding to cholinergic, alpha-adrenergic, serotonin, and local anesthetic receptor sites. Used to treat allergies caused by antigens acting on IgE-antibody sensitized mast cells. Ineffective in treating bronchial asthma because histamine is not the only mediator. Adverse - Sedation, dry mouth. Although the margin of safety is high, acute poisoning is common, especially in children.

Loratadine

Histamine Antagonist H1 Receptor Antagonist - Second Generation Has sedative effects and is more likely to block autonomic receptors. Historically considered to be H1-receptor antagonists, but recently shown to be inverse agonists. Histamine-induced bronchoconstriction and GI muscle contraction can be completely blocked. Have additional effects unrelated to H1 antagonism, probably reflecting binding to cholinergic, alpha-adrenergic, serotonin, and local anesthetic receptor sites. Used to treat allergies caused by antigens acting on IgE-antibody sensitized mast cells. Ineffective in treating bronchial asthma because histamine is not the only mediator. Adverse - Sedation, dry mouth. Although the margin of safety is high, acute poisoning is common, especially in children.

1. To reduce anxiety, cause sedation, and for its general analgesic properties 2. As an adduct to other anesthetics and as a primary component of the anesthetic regimen. 3. Given via intraspinal administration to cause regional analgesia

How are opioids used in the following surgical situations? 1. Pre-surgery 2. Intraoperatively 3. Regional analgesia

They are used to enhance erection

How are the organic nitrate inhalants, amyl nitrite and butyl nitrite, used?

They act on post-synaptic neurons and enhance GABAergic neurotransmission and lead to Cl- influx.

How can benzodiazepines, barbiturates, and topiramate be used to treat seizures?

Because GH acts in opposition to insulin its continued use may cause increased insulin production which eventually wears out the beta cells of the pancreas and causes diabetic syndrome. Otitis media Peripheral edema, myalgias, and arthralgias as well as carpal tunnel syndrome.

How can chronic use of recombinant GH in children can lead to diabetic syndrome? Children being treated with growth hormone who have Turners syndrome are at an increased risk of developing what adverse effect? What are some adverse effects in adults?

They are the most commonly used drugs in the management of akathisia (EPRs)

How can clonazepam or propanolol be used in patients with schizophrenia?

Can be used as an alternative agent in the treatment of anxiety disorder Can be used as an alternative agent in the treatment of anxiety disorder

How can hydroxyzine be used to treat anxiety? How can pregabalin be used to treat anxiety?

1. MESNA 2. Good hydration and administration of amifostine 3. Dexrazoxane 4. Filgrastim (GM-CSF) 5. Leucovorin (tetrahydrofolic acid)

How can we prevent or minimize the following anti-cancer drug induced adverse reaction? 1. Hemorrhagic cystitis associated with cyclophosphamide and ifosfamide 2. Cisplatin induced nephrotoxicity 3. Dilated cardiomyopathy caused by doxorubicin and daunorubicin 4. Bone marrow suppression by a variety of drugs 5. Methotrexate induced bone marrow suppression

1. PEcK (Proteus mirabilis, E. coli, and Klebsiella pneumoniae) and gram-positive cocci 2. HEN PEcKS (H. influenzae, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, and Serratia marcescens 3. Serious gram negative infections Ceftriaxone for meningitis and gonhorrhea Ceftazidime for Pseudomonoas 4. Activity against Pseudomonas and gram-positive organisms 5. MRSA, gram-negatives, and gram positives

How can we remember what each of the following generations of cephalosporins are used to treat? 1. 1st generation 2. 2nd generation 3. 3rd generation 4. 4th generation 5. 5th generation

Some end in -citalopram (Citalopram & escitalopram) and some end in -oxetine. (Note: Duloxetine, an SNRI also ends in this). If it begins with Flu or P (which looks like an F) then it is in this class (Fluoxetine, Fluvoxamine, & Paroxetine) and the last drug looks kind of like serotonin (SERtraline) They selectively inhibit the reuptake of serotonin only with little effect on muscarinic, α-adrenergic, and histamine receptors (when compared to TCAs). As a result, many of the side effects seen with the TCAs are not seen with the SSRIs.

How can you remember the SSRI drugs? What is the mechanism of action of these drugs? As a result of their mechanism of action, how does the side effect profile of SSRIs differ from the TCAs?

Take the first or first and second letter after the cef(vowel). If not vowel is there then take the tr. 1 Z-Line (cefaZoline & cephaLexin) 2 Cats, Tets, Mice, and Oxen (cefaClor, cefoTETan, cefaMandole, cefOXitin) 3 T-pex (cefTriaxone, cefoTaxime, cefTazidime, cefoPErazone, cefiXime) 4 Pies (cefiPIme) 5 Tarts (cefTARoline)

How can you remember the cephalosporins in each generation?

Can Treat Pseudomonas Carbenicillin Ticarcillin Piperacillin They are effective against many gram-negative bacilli 1. β-lactamase inhibitors

How can you remember the drugs that are considered antipseudomonal penicillin drugs? What other types of bacteria are these drugs effective in treating besides P. aeruginosa infections? What are these drugs commonly combined with?

Staph is a DeMON in patients with acute endocarditis It is used as a first line treatment for patients with staphylococcal endocarditis. Dicloxacillin Methicillin (no longer used) Oxacillin Nafcillin (not really used clinically or in the lab anymore)

How can you remember the penicillin drugs that are resistant to β-lactamase and the bacteria that it is used as a first line treatment against?

Celecoxib AIDs IN PAIN Lowest risk: Celecoxib Low risk: Aspirin, Ibuprofen, & Diclofenac Medium risk: Indomethacin & Naproxen High risk: Piroxicam

How can you remember the relative risk of GI adverse effects between the following NSAIDs? Ibuprofen, Aspirin, Naproxen, Indomethacin, Celecoxib, Piroxicam, Diclofenac

VETTT CAP Vitamin D, Estrogen, Testosterone, T3/T4, Cortisol, Aldosterone, Progesterone

How can you remember the types of hormones that act via steroid receptors?

GOAT HAG GnRH, Oxytocin, ADH (V1 receptor), TRH, Histamine (H1 receptor), Angiotensin II, Gastrin

How can you remember the types of receptors that act via GPCR (Gq)?

FLAT ChAMP FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2 receptor), MSH, PTH

How can you remember the types of receptors that act via GPCR (Gs)?

Mary jane CRAVes PoT Short-acting: Mivacurium Intermediate: Cisatracurium, rocuronium, atracurium, & vecuronium Long-acting: Pancuronium & tubocurarine The drugs that are excreted by the kidneys typically have a longer half-life (ie. longer duration of action) and those eliminated by the liver tend to have shorter half-lives (ie. shorter duration of action)

How can you remember which non-depolarizing neuromuscular blockers are short-acting, intermediate-acting, and long-acting? (Tubocurarine, atracurium, cisatracurium, mivacurium, rocuronium, pancuronium, vecuronium) How does the mechanism of metabolism relate to the duration of action of these drugs?

1. Inhibition of COX diminishes synthesis of prostaglandins and thus modulates those aspects of inflammation in which prostaglandins act as mediators 2. PGE2 sensitizes nerve endings to the action of chemical mediators released by the inflammatory process and COX inhibitors repress pain by inhibiting the formation of PGE2. 3. Inhibit fever by blocking PGE2 synthesis COX-2

How do NSAIDs act to cause the following actions? 1. Anti-inflammatory actions 2. Analgesic actions 3. Antipyretic actions Which COX isoform is the main source of prostaglandins that mediate rise in temperature?

1. Part of the action of ACE-inhibitors is to prevent the breakdown of kinins which stimulate prostaglandin production. NSAIDs may diminish this effect 2. NSAIDs increase the frequency or severity of GI ulceration when combined with corticosteroids 3. NSAIDs may increase the risk of bleeding in patients being co-administered warfarin

How do NSAIDs interact with the following drugs? 1. ACE-inhibitors 2. Corticosteroids 3. Warfarin

Serotonin and norepinephrine mediate inhibition of pain through the inhibitory pathways. TCAs cause analgesia by inhibiting norepinephrine and serotonin reuptake which causes increased inhibition of ascending pain signaling. Their anticholinergic activity as they tend to increase adrenergic signaling. The side effects therefore include constipation, dry mouth, blurry vision, tachycardia, urinary retention, orthostatic hypotension, falls, weight gain, and sedation. Angle-closure glaucoma, BPH, urinary retention, constipation, CV disease, and impaired liver function.

How do TCA's act as an adjuvant to other analgesic drugs? The adverse effects of TCA's are associated with what? TCAs should be administered cautiously in patients with what sort of conditions?

They suppress the hypoxic and chemoreceptor response to CO2 which leads to respiratory depression and, possibly, death. They induce P450 enzymes (think phenobarbital)

How do barbiturates cause respiratory depression? Do barbiturates have an effects on CYP P450 enzymes?

It inhibits it through carbamoylation of the active sites Shorter Atropine No, because the inhibition is spontaneously reversible and short-lived they would not be treated with this drug.

How do carbamate insecticides affect acetylcholinesterease? Are the effects of these insecticides short or longer than those of organophosphates? What is the antidote for these drugs? Would you give patients with carbamate insecticide intoxication pralidoxime and why?

Increased pulmonary blood flow slows the rate of the rise in arterial tension which leads to slowing of the onset of an inhaled anesthetic. The more an anesthetic is taken up by other tissues besides the brain (ex. adipose tissue) the slower the onset.

How do changes in pulmonary blood flow affect the rate of rise in arterial tension and, therefore, the onset of an inhaled anesthetic? How does uptake by the tissues affect the onset of an anesthetic?

They relieve pain by inhibition/modifying the inflammatory response by inhibiting phospholipase A2, through induction of MAPK phosphatase 1, and by reducing expression of COX-2.

How do glucocorticoids act as analgesics?

They combine with functional groups that are essential for normal physiological functions such as -OH, -SH, and -NH2. Chelating agents which have two or more electronegative groups that can form complexes with heavy metals. Lead, arsenic, and mercury.

How do heavy metals exert their toxic effects? What is the general therapy for heavy metal intoxication and how do they work? What are the heavy metals?

A moderate decline in magnesium levels enhances the secretion of PTH but a severe decrease in magnesium levels decreases PTH secretion. Chronic diarrhea, diuretics and alcohol abuse and chronic PPI and aminoglycoside use.

How do magnesium levels affect the secretion of PTH? Name some conditions that cause a decrease in magnesium levels.

They have antiemetic effects as a result of their blockade of D2 receptors of the chemoreceptor trigger zone in the medulla Aripiprazole (atypical) and thiridazine (classical)

How do most neuroleptics effect nausea/vomiting? Which do not have this activity?

1. The proposed mechanism includes reducing anxiety and reducing the preload and afteload on the heart by causing vasodilation and inhibition of the baroreceptor reflex 2. They depress the cough reflex through a direct effect on the cough center in the medulla 3. They lead to inhibition of GI peristaltic activity Dextrometorphan and codeine Meperidine by acting on α₂ adrenoceptors

How do opioid drugs act to perform the following function? 1. Treat acute pulmonary edema 2. Treat cough 3. Diarrhea Which opioid drugs are commonly used as antitussives? Although all opioid agonists may reduce shivering, which has the most pronounced anti-shivering effects and how does it cause this activity?

Promethazine

Histamine Antagonist H1 Receptor Antagonist - First Generation Has sedative effects and is more likely to block autonomic receptors. Historically considered to be H1-receptor antagonists, but recently shown to be inverse agonists. Histamine-induced bronchoconstriction and GI muscle contraction can be completely blocked. Have additional effects unrelated to H1 antagonism, probably reflecting binding to cholinergic, alpha-adrenergic, serotonin, and local anesthetic receptor sites. Used to treat allergies caused by antigens acting on IgE-antibody sensitized mast cells. Ineffective in treating bronchial asthma because histamine is not the only mediator. Also used to prevent symptoms of motion sickness. Adverse - Sedation, dry mouth. Although the margin of safety is high, acute poisoning is common, especially in children.

They reduce the responsiveness of the brainstem respiratory centers to CO2 levels. No, it is generally not a serious clinical problem and is seen more commonly in patients who are opioid abusers. They depress the cough reflex through a direct effect on the cough center in the medulla. They excite parasympathetics for the nerves innervating the pupil. This is why opioid overdose/toxicity presents with pinpoint pupils. Seen in patients with severe respiratory depression and asphyxia as a result of opioid toxicity.

How do opioid drugs lead to respiratory depression? Is this typically a problem that you should worry about when treating patients with opioid drugs? How do opioids affect cough? How do they cause miosis? Under what opioid toxicity conditions do you see patients with mydriasis?

They activate receptors (µ, δ, κ) located in the brain and spinal cord involved in transmission and modulation of pain. They close voltage-gated calcium channels on presynaptic neurons and open K+ channels on post-synaptic neurons both of which prevent the transmission of pain through reduced neurotransmitter release Gi receptors

How do opioids produce analgesia? They have two main mechanisms of action that inhibit ascending pain transmission. What are they? The three receptors that opioids act on are GPCRs. What type of receptors are they?

They directly inhibit insulin secretion They deplete serum K+ levels which inhibits insulin secretion directly (because insulin secretion would lead to an exacerbation of hypokalemia).

How do phenytoin, clonidine, and calcium channel blockers lead to hyperglycemia? How do some diuretics lead to hyperglycemia?

They suppress the release of FSH and LH which inhibits ovulation. Patients with a history of thromboembolism, breast & endometrial cancer, liver disease, and in patients who are pregnant.

How do preparations of estrogen and progesterone act as oral contraceptives? What are the absolute contraindications of estrogen use?

They bind to and interfere with ribosomes They target the whole or part of the 70S ribosome found in bacteria and do not target the 80S ribosomes found in mammalian cells. The mitochondrial ribosomes are 70S which can lead to some adverse effects. Mostly bacteriostatic

How do protein synthesis inhibitor drugs work? How can these drugs be used to selectively target bacteria as opposed to human cells? What part of the mammalian cell could still be at risk? Are most of these drugs bactericidal or bacteriostatic?

They act as agonists on the 5-HT2 receptors in the CNS. Mydriasis, hypertension, tachycardia, increased body temperature, flushing, sweating, tremors, and piloerection. If they are suffering from a bad trip and/or severe agitation Diazepam

How do the LSD-like group of drugs, LSD, mescaline, and psilocybin, have what sort of mechanism of action? What are the symptoms that are associated with LSD, and the LSD-like group of drugs? When do patients taking LSD require medical attention? What is the treatment?

They are analogs of native ribosides but lack a 3' OH group which leads to termination of DNA elongation and competitive inhibitor of reverse transcriptase. Most have activity of against both HIV-1 and HIV-2 It occurs between agents of the same analog class. Mainly due to inhibition of mitochondria DNA polymerase leading to peripheral neuropathy, myopathy, lipoatrophy, and lactic acidosis. Liver toxicity that is rare but can be fatal.

How do the antiretroviral nucleoside/nucleotide reverse transcriptase inhibitors work? What strains of the HIV virus are most of these drugs effective against? When does cross-resistance between agents occur? What causes the majority of adverse effects with these drugs? What other adverse effect should be considered with these drugs?

1. Increases the neuromuscular blockade 2. Prolongs the blockade, likely as a result of decreased drug clearance 3. Resistant to non-depolarizing muscle relaxants but the use of succinylcholine is contraindicated because of the risk of the development of hyperkalemia in these patients 4. Resistant to non-depolarizing muscle relaxants Rocuronium

How do the following conditions affect the neuromuscular blockade by neuromuscular blocking drugs? 1. Patients with myasthenia gravis 2. Advanced age 3. Patient with severe burns 4. Patients with upper motor neuron disease What is the recommended drug for neuromuscular blockade in patients with severe burns?

They compete with irate for a transporter in the kidneys and inhibit the reabsorption of uric acid. NSAIDs or colchicine

How do uricosuric agents act to treat chronic gout? What must be given along with these drugs to avoid causing an attack of gout?

Perform a caffeine-halothane muscle contracture test on a muscle sample, removed from the thigh, and if an abnormal muscle contraction deviation occurs it can be determined that the patient would develop this condition if they were administered a halogenated anesthetic with succinylcholine.

How do we test for malignant hyperthermia?

It acts on osteoblasts through a Gs receptor and stimulates them to release RANKL (RANK ligand) which binds to the RANK receptor on osteoclasts and stimulates the resorption of bone and the release of calcium into the plasma. Continuous high doses cause subperiosteal bone resorption whereas intermittent low doses increase new bone formation.

How does PTH cause the reabsorption of bone? What is the different in the effect on bone if high levels of PTH are present continuously versus low doses intermittently?

Because inhaled anesthetics are not rapid the initial anesthesia is usually initiated using IV agents. If the anesthesia is going to be short it can likely be maintained with these IV agents but if the anesthesia will be prolonged it can then be maintained with inhaled agents Neuromuscular blockers

How does anesthesia typically take place? What agents are used to provide paralysis that is adequate for surgical access?

It causes constriction of blood vessels by potentiating the action of norepinephrine thereby preventing its own absorption. A vasoconstrictor (usually epinephrine) They reduce systemic absorption by causing vasoconstriction which allows for enhanced neuronal uptake of the drug and reduced systemic toxic effects.

How does cocaine prevent its own absorption and have a longer duration of action as a local anesthetic? As a result, in clinical practice, preparations of local anesthetics commonly contain what? How do these additions help the administration of these drugs?

It is a steroid hormone that enters the cell and binds to an intranuclear receptor. The cortisol-receptor complex then regulates the transcription of proteins that lead to the desired change. Glucagon requires the presence of cortisol in order to increase gluconeogenesis and glycogen synthesis in the liver during fasting. It also stimulates lipolysis and stimulates protein catabolism in conduction with glucagon.

How does cortisol act on its target cell? This hormone is required for what important met metabolic process?

It inhibits phospholipase A2, reduces COX-2 synthesis, and induces MAPK phosphatase I which normally activates pro inflammatory signaling pathways. ACTH, GH, TSH, and LH. It can induce the development of fetal lungs in premature infants and stimulate surfactant production.

How does cortisol and other glucocorticoids cause anti-inflammatory effects? Chronic use of glucocorticoids can lead to suppression of the release of what hormones? How can these drugs be used for premature neonates?

Although levodopa is rapidly absorbed by the small intestines the absorption is delayed by food in the SI including certain amino acids that compete with the drug for absorption from the gut and for transport from the blood to the brain.

How does food affect the absorption of levodopa?

It is directly dependent on the rate and depth of ventilation, i.e. increased rate and depth of ventilation increases the rate at which the arterial tension rises which increases the rate of onset of a drug. A drug with a low blood solubility (like nitrous oxide) will only see a small rise in time of onset whereas an agent that has a moderate or high blood solubility will show a significant increase in arterial tension and onset.

How does respiratory system affect the rate of rise in tension in the arterial blood of a inhaled anesthetic? How does the blood solubility of the agent affect the change in onset?

It can last months to years. Multiple drugs must be taken for sufficiently long periods of time. Typically starts with a 3-4 drug combination regimen. DOT (directly observed therapy)

How long does therapy for mycobacterial infections typically last? The goal of therapy, especially for TB, is kill the tubercle bacilli, prevent emergence of resistance, and eliminate bacilli from the host's tissues to prevent relapse. To accomplish these goals, how is treatment undergone? What type of therapy is recommended in noncompliant patients or in patients with resistant strains?

With proton pump inhibitors. They can inhibit nearly 100% of gastric acid secretions. Very few side effects that include nausea and diarrhea. Omeprazole inhibits CYP450 enzymes which can lead to the inhibition of metabolism of drugs like warfarin, phenytoin, diazepam, and cyclosporine.

How should NSAID-induced ulcers be treated? How effective are these types of drugs? What sort of side effects are associated with these drugs? What drug interactions should a physician be aware of?

The oral treatment should be discontinued and the patient should be placed on insulin therapy throughout their acute illness.

How should a diabetic hospitalized patient be managed if they are currently on oral anti diabetic treatment?

The patient should be instructed to drink orange juice, take glucose by mouth or have a sugar containing beverage or food. IV glucose infusion Glucagon via subcutaneous injection or IM administration

How should a mild hypoglycemic state in a conscious patient be managed? How should a severe hypoglycemic states with an unconscious or stuporous patient be managed? If IV therapy is not available how should the patient be treated?

In the initial stages it should be given by the clock (ie. at fixed I'm intervals) with doses gradually decreased until the patient is comfortable. As the pain subsides it can by given on an as-needed basis. A typical rescue dose is 5-15% of the basal daily requirement of opioid. If you need to give more then it is likely that the patients is under-medicated. Fentanyl

How should analgesic dosing be administered? Rescue doses are given for breakthrough pain that occurs. What is a typical rescue dose? What drug can be given for this breakthrough pain?

They should be administered naloxone if necessary.

How should patients suffering from respiratory depression as a result of opioid use be managed?

Start treatment with glucocorticoids and if they are ineffective move on to treatment with anti-cancer agents and other drugs. Crohn's disease and ulcerative colitis.

How should the inflammatory bowel diseases be treated? What are the classic IBDs?

Through a slow IV infusion of 60-90 minutes duration. "Red-man" or "red-neck" syndrome where flushing over the face and upper torso occurs. Ototoxicity and nephrotoxicity

How should vancomycin be administered? If this administration technique is not undertaken what can occur? What are two other severe complications that should be monitored for in patients receiving vancomycin?

To achieve anesthesia, as part of balanced anesthesia, and to sedate patient in ICUs that need to be mechanically ventilated for long periods of time. Barbiturates, ketamine, etomidate, and propofol.

IV anesthetics are used alone or with other drugs for what purpose? Name 4 IV anesthetics.

1. Non-selecive reversible COX inhibitor 2. Antipyretic, analgesic, and anti-inflammatory.

Ibuprofen 1. Mechanism of action 2. Use

1. May involve the inhibition of gluatmatergic transmission in the CNS 2. New drug used to treat ALS

Idrocilamide 1. Mechanism of action 2. Use

It is a monoclonal antibody It is a chimeric molecule It is a fully human molecule

If a ends in -mab what does it mean? If it has a xi in it, what does that mean? If it has a zu in it, what does that mean?

A tetracycline Chlamydia, mycoplasma penumoniae, lyme disease, cholera, anthrax prophylaxis and rickettsial infections. H. pylori eradication malaria prophylaxis and treatment, and for the treatment of plague, tularemia, and brucellosis.

If a patient is allergic to penicillin but they have been diagnosed with syphilis, what type of drug can they be given? This is the drug of choice for what conditions? This drug is used as part of combination therapy for what sort of conditions?

Initially they can cause CNS stimulation causing restlessness and tremor that can lead to seizures and then progress to CNS depression resulting in respiratory failure. Benzodiazepines

If systemic levels of local anesthetics become too high, how can they affect the CNS? If a large dose of a local anesthetic is required, what can patients be pre-treated with to avoid the risk of seizures?

1. It inhibits the BCR tyrosine kinase that is over-expressed in t(9;22) CML 2. Used to treat CML Gleevec

Imatinib 1. Mechanism of action 2. Use What is the other name that this drug goes by?

1. β-lactam inhibitor of cell wall synthesis (carbapenem) 2. Used for serious infections that require broad spectrum antibiotics 3. Forms a potentially nephrotoxic metabolite. Cilastatin is administered with Imipenem which inhibitors the metabolic enzymes and prevents toxicity and increases the availability of the drug.

Imipenem 1. Mechanism of action 2. Use 3. Adverse effects How can this adverse effect be managed?

1. Tricyclic antidepressant that inhibits the reuptake of serotonin and norepinephrine 2. Used as an adjuvant for pain management

Imipramine 1. Mechanism of action 2. Use

Antipyretic, analgesic, and anti-inflammatory. They inhibit COX (cyclooxygenase) which leads to a decreased production of prostaglandins and thromboxanes.

NSAIDs are what types of drugs? What is the mechanism of action of NSAIDs?

Very little effect They have no immediate analgesic effects but can control symptoms and delay and possibly stop progression of the disease.

NSAIDs can offer symptomatic relief for patients suffering from rheumatoid arthritis. What affect does it have on the progression of bone and cartilage destruction? What is the function of DMARDs?

1. If a patient already has compromised renal blood flow they kidneys make PGE2 & PGI2 to prevent vasoconstriction and maintain renal perfusion but NSAIDs decrease this effect 2. Type I hypersensitivity reaction that leads to acute renal failure 3. Chronic interstitial nephritis caused by excessive consumption of analgesics, especially when combined with different agents. Decreased PGE2: Increase sodium and water retention Decreased PGI2: Can lead to hyperkalemia and acute renal failure

NSAIDs have 3 types of renal adverse effects. How does it cause each of the following? 1. Decreased renal blood flow 2. Acute interstitial nephritis 3. Analgesic nephropathy Decreases in PGE2 and PGI2 lead to decreased renal blood flow. What effect does the decrease of each have?

1. GnRH analog 2. Used to treat prostatic cancer It should be given by a pulsatile dose as a continuous dose of this drug can lead to reversible medical castration

Nafarelin 1. Mechanism of action 2. Use How should this drug be administered and why?

1. GnRH analog 2. To treat male infertility and rarely female infertility. Can also be used to diagnose a patients LH responsiveness to GnRH. Also used to control ovarian hyper stimulation and used for the treatment of endometriosis by removing exposure to cyclical changes in estrogen and progesterone during the menstrual cycle Inhibition of FSH and LH release leading to hypogonadism

Nafarelin 1. Mechanism of action 2. Use What can occur if this drug is administered in a non-pulsitile manner?

1. β-lactamase resistant inhibitor of cell wall synthesis (penicillin) 2. Used as first-line treatment for Staphylococcal endocarditis in patients without artificial heart valves No, it has erratic oral absorption.

Nafcillin 1. Mechanism of action 2. Use Can this drug be administered orally?

1. κ agonist and µ antagonist or partial agonist. 2. Useful in treating mild to moderate pain while keeping the risk of addiction low.

Nalbuphine 1. Mechanism of action 2. Use

1. Fluoroquinolone drug that inhibits bacterial DNA replication by interfering with topoisomerase II (DNA gyrase) and topoisomerase IV 2. Used to treat uncomplicated UTIs 1st

Nalidixic acid 1. Mechanism of action 2. Use Generation?

1. µ, δ, and κ receptor antagonist 2. Used in the treatment of acute opioid overdose

Naloxone 1. Mechanism of action 2. Use

1. µ, δ, and κ 2. Used to treat opioid addiction and decrease cravings for alcohol in chronic alcoholics

Naltrexone 1. Mechanism of action 2. Use

1. Patients with psychiatric conditions as it may induce/exacerbate their psychosis 2. In patients with high vitamin B6 levels as this can lead to increased peripheral metabolism of levodopa 3. Should not be given with patients taking MAO inhibitors as it can cause a hypertensive crisis 4. Patients with angle closure glaucoma 5. Cardiac patients should be carefully monitored as it may cause arrhythmias

Name five contraindications for the use of levodopa.

Glucose (the most important stimulus for insulin secretion), amino acids, and gastrointestinal hormones. Incretins. They increase the plasma insulin secretion during oral administration of glucose (as a result of the enteric stimulation leading to its release). When IV glucose is administered the insulin levels do not rise as much as a result of the lack of incretin secretion which would stimulate additional insulin secretion.

Name three things that stimulate glucose release from pancreatic beta cells. What gastrointestinal hormones are responsible for the increased release of insulin after the ingestion of food and how do these levels vary with oral and IV administration of glucose?

Inhaled anesthetics, aminoglycosides, and tetracyclines.

Name three types of drugs that enhance the neuromuscular blockade by neuromuscular blockers.

1. Non-selecive reversible COX inhibitor 2. Antipyretic, analgesic, and anti-inflammatory.

Naproxen 1. Mechanism of action 2. Use

1. Blocker of leukocyte integrins 2. Used to treat IBD 3. Multifocal leukoencephalopathy

Natalizumab 1. Mechanism of action 2. Use 3. Adverse effects

An ACE inhibitor or ARBs. Opioids, TCAs, SNRIs, and GABAnergic drugs (amitriptyline, pregabalin, gabapentin, duloxetine, venlafaxine, valproate)

In diabetic patients with signs of nephropathy, such as albuminuria, what drug can be started? If neuropathic pain begins what sort of drugs can be used to treat this condition?

Overactivity of the mesolimbic pathway Hypoactivity of the mesocortical pathway The receptors are the same for both pathways so there is a difficult balance between reducing the overactivity of the mesolimbic pathway without under stimulating the mesocortical pathway.

In patients with schizophrenia the positive symptoms are believed to be linked to what? The negative symptoms may be linked to what? How does this make the treatment of this condition difficult?

8.5% It should typically be started at a low dose with a single injection of basal insulin (NPH, glargine, or detemir). Glargine or detemir are preferred. Prandial insulin therapy with rapid acting insulins prior to meals.

In type 2 diabetic patients, the decision to transition to insulin should be favored when the HbA1c level is greater than how much? How should this be started? If significant postprandial glucose excursions occur the patient will require the addition of what?

Patients with PUD, osteoporosis, psychoses, heart disease or HTN with heart failure, TB or varicella zoster infections, diabetes, and glaucoma.

In which patients are corticosteroids contraindicated?

1. Blocks the ATP-sensitive K+ channel in the beta cell membrane which leads to increased secretion of insulin 2. Used to treat type II diabetes and to reduce fasting plasma glucose and HbA1c levels 3. Hypoglycemia and weight gain. No

Nateglinide 1. Mechanism of action 2. Use 3. Adverse effects Does this drug contain sulfur?

1. The 5HT-2 antagonists/reuptake inhibitors (SARI) 2. Previously prescribed for depression 3. No longer prescribed because of the risk of hepatotoxicity

Nefazodone 1. Mechanism of action 2. Use 3. Adverse effects

1. Protease inhibitor - They are reversible inhibitors of HIV aspartyl protease which is responsible for cleavage of the viral polyprotein into reverse transcriptase, protease, and integrase. This prevents virus maturation and results in production of non-infections visions. 2. Used for treatment of HIV Yes

Indinavir 1. Mechanism of action 2. Use Is this drug given with ritonavir?

1. Non-selecive reversible COX inhibitor 2. Drug of choice for treating acute gouty arthritis and used to promote closure of the ductus arteriosus. Antipyretic, analgesic, and anti-inflammatory.

Indomethacin 1. Mechanism of action 2. Use

1. NSAID 2. Most popular drug in the treatment of pain for patients suffering from an acute gouty arthritis attack

Indomethacin 1. Mechanism of action 2. Use in gout

Mycoses Dermatophytoses and candidiasis Systemic mycoses Candidiasis, crytococcosis, and aspergillosis

Infections caused by fungi are called what? What are the main superficial mycoses? What are the most serious fungal infections? What are the three most common systemic fungal infections in humans?

1. IgG1 anti-TNF monoclonal antibody which binds to TNFα and prevents its interaction with TNF receptors which down regulates macrophages and T-cell function. 2. Used to treat RA Chimeric: mix between human Ab with a mouse derived variant chain

Infliximab 1. Mechanism of action 2. Use Is this Ab human or chimeric? If chimeric what is it mixed with?

1. Monoclonal antibody that targets TNFα which is a principle mediator in Crohn's disease 2. Used to treat flare-ups of IBD, particularly in Crohn's related fistulas. 3. Reactivation of latent TB

Infliximab 1. Mechanism of action 2. Use 3. Adverse effects

1. Protease inhibitor - They are reversible inhibitors of HIV aspartyl protease which is responsible for cleavage of the viral polyprotein into reverse transcriptase, protease, and integrase. This prevents virus maturation and results in production of non-infections visions. 2. Used to treat HIV No, this drugs effect cannot be boosted by co-administration of ritonavir

Nelfinavir 1. Mechanism of action 2. Use Is this drug given with ritonavir?

1. Aminoglycoside drug that irreversibly binds to the 30S ribosomal subunit prior to ribosome formation 2. Used as an oral treatment for hepatic encephalopathy Lactulose: it is a non-absorbable disaccharide that is degraded by intestinal bacteria to lactic acid and other organic acids. This acidifies the gut lumen and favors formation of NH4+, trapping it in the colon and reducing plasma ammonia concentrations.

Neomycin 1. Mechanism of action 2. Use This is used as an adjunct in the treatment of what condition? What is the drug of choice for this condition and how does it work?

1. Acetylcholinesterase inhibitor 2. Used to treat colonic pseudo-obstruction in hospitalized patients by its pro-kinetic activity

Neostigmine 1. Mechanism of action 2. GI use

1. Rapid acting insulin 2. Used to simulate the prandial release of insulin in the treatment of type I diabetes mellitus In the beta chain a proline is exchanged for aspartate

Insulin aspart 1. Mechanism of action 2. Use Where does this drug name come from?

1. Long acting insulin 2. Used for the daily treatment of type I diabetes mellitus

Insulin detemir 1. Mechanism of action 2. Use

1. Long acting insulin 2. Used for the daily treatment of type I diabetes mellitus It is injected with in acidic solution with causes precipitation of the drug in the subcutaneous tissue which lead to slow dissolution of free glargine hexamers form the precipitated glargine leading to a long duration of activity of the drug.

Insulin glargine 1. Mechanism of action 2. Use How does this drug act as a long acting release?

1. Rapid acting insulin 2. Used to simulate the prandial release of insulin in the treatment of type I diabetes mellitus In the beta chain a glutamate and lysine are exchanged for two different amino acids

Insulin glulisine 1. Mechanism of action 2. Use Where does this drug name come from?

1. Rapid acting insulin 2. Used to simulate the prandial release of insulin in the treatment of type I diabetes mellitus In the beta chain of this insulin the lysine and proline at one position were changed.

Insulin lispro 1. Mechanism of action 2. Use Where does this drug name come from?

May provoke autoimmune or destructive inflammatory thyroiditis leading to hypothyroidism

Interferon Affect on the thyroid gland?

1. Naturally occurring cytokine that inhibits RNA & DNA synthesis by activating/inducing protein expression that inhibits virus infection 2. Used to treat HCV (in combination with ribavirin), HBV, condyloma acuminata, hairy-cell leukemia, and Kaposi's sarcoma 3. Flu-like symptoms, fatigue, and mental depression No

Interferon α 1. Mechanism of action 2. Use 3. Adverse effects Does this drug target viral gene products directly?

May provoke autoimmune or destructive inflammatory thyroiditis leading to hypothyroidism.

Interleukin-2 Affect on the thyroid gland?

1. At high levels they inhibit thyroid hormone synthesis by decreasing organification and release of thyroid hormones. 2. Used prior to thyroid surgery in patients with hyperthyroidism After approximately 10-14 days the iodide effect ends.

Iodide 1. Mechanism of action 2. Use What is the Wolff-Chaikoff effect?

1. Inhibits the conversion of T4 to T3 and may inhibit the release of hormone form the thyroid gland 2. Used to treat patients with thyrotoxicosis.

Iohexol 1. Mechanism of action 2. Use

Physical dependence can commonly develop but addiction is not commonly associated with therapeutic opioid use.

Is physical dependence and/or addiction common when opioids are used for therapeutic purposes?

1. Glucocorticoid 2. Glucocorticoid 3. Mineralocorticoid 4. Glucocorticoid

Is the following a synthetic glucocorticoid or mineralocorticoid? 1. Beclomethasone 2. Dexamethasone 3. Aldosterone 4. Hydrocortisone

1. Mineralocorticoid 2. Glucocorticoid 3. Prodrug of prednisolone, a glucocorticoid 4. Glucocorticoid

Is the following a synthetic glucocorticoid or mineralocorticoid? 1. Fludrocortisone 2. Methylprednisolone 3. Prednisone 4. Triamcinolone

1. µ, δ, κ (mainly µ) 2. µ 3. µ, δ, κ 4. µ 5. µ, δ 6. µ, κ

Is the following action mainly mediated by a µ, δ, or κ receptor? 1. Supra-spinal analgesia 2. Respiratory depression 3. Spinal analgesia 4. Physiological dependence 5. Reduction in GI motility 6. Sedation

Slightly broader (but they are most active against gram-positive bacteria). They are a common substitute for treating patients who have a penicillin allergy. QT prolongation. It is very unlikely and usually only seen in patients who are predisposed.

Is the macrolide spectrum broader or less broad than penicillin drugs? As a result, how can these drugs also be used? What is a unique adverse effect of the macrolide antibiotics and how common is it?

Yes Partial Partial

Is there cross-resistance between eh macrolide drugs? Between the macrolide drugs and clindamycin? Between the macrolide drugs and the streptogramin drugs?

1. Pro-drug that is activated by the mycobacterial catalase peroxidase - KatG which targets enzymes involved in my colic acid synthesis 2. Used as part of combination therapy to treat TB or alone to treat latent TB infection 3. Peripheral neuritis, hepatotoxicity (more common in pregnant women), lupus-like syndrome, and inhibition of CYP450 enzymes First line No

Isoniazid 1. Mechanism of action 2. Use 3. Adverse effects Is this a first line or second line drug? Does cross resistance between this drug and other anti-tuberculosis drugs occur?

8 weeks Isoniazid and Rifampin are continued. Whether Pyrazinamide was used of the initial phase of treatment determines the duration of treatment with Isoniazid and Rifampin. If Pyrazinamide was used the continued duration of treatment should be 18 weeks but if it was not used then it these drugs should be given for 31 weeks.

Isoniazid, Rifampin, and Ethambutol are used as the drugs of choice for the initial phase of treatment for pulmonary TB. How long are these drugs used initially? Which drugs are continued after this period and for how long?

1. Inhibit 14-α-demethylase, they last enzyme in ergosterol synthesis from lanosterol 2. Preferred azole for mycoses due to Blastomyces, Sporothrix, and Histoplasmosis and used for dermatophytoses and onychomycosis. 3. May cause fatal arrhythmias if given with cisapride or quinidine Triazole CYP3A4

Itraconazole 1. Mechanism of action 2. Use 3. Adverse effects Imidazole or Triazole? Inhibits what CYP P450 enzymes?

1. GABA agonist that causes chlorine influx leading to hyperpolariation of parasitic nerves/muscles causing paralysis and death of the parasite 2. Drug of choice for the treatment of onchocerciasis, cutaneous larva migrans, and strongyloides. This reaction occurs when the parasite is dying and gives us a good indication that our treatment is working No

Ivermectin 1. Mechanism of action 2. Use This drug causes a Mazotti-like reaction with symptoms that include fever, dizziness, somnolence, and hypotension. What does this tell us? Can this drug be given in pregnancy?

1. Inhibitor of adrenal and gonadal steroid synthesis 2. Used to treat Cushings syndrome and prostate cancer

Ketoconazole 1. Mechanism of action 2. Use

1. Steroid synthesis inhibotr 2. Used to treat advanced prostate cancer that is resistant to first line drugs as well as treating Cushing's disease 3. CYP P450 enzyme inhibition

Ketoconazole 1. Mechanism of action 2. Use 3. Adverse effects

1. Inhibit 14-α-demethylase, they last enzyme in ergosterol synthesis from lanosterol 2. Due to narrow spectrum and adverse effects it is only used for superficial mycoses 3. Large amount of adverse effects when used to treat systemic infections so it is only used for superficial mycoses Imidazole CYP3A4

Ketoconazole 1. Mechanism of action 2. Use 3. Adverse effects Imidazole or Triazole? Inhibits what CYP P450 enzymes?

1. Non-selecive reversible COX inhibitor 2. Antipyretic, analgesic, and anti-inflammatory.

Ketorolac 1. Mechanism of action 2. Use

1. Reduces plasma ammonia concentrations by acidifying the gut lumen and conversion of NH3 to NH4+ 2. Drug of choice for treatment of hepatic encephalopathy

Lactulose 1. Mechanism of action 2. Use

1. Non-digestible sugar that acts as an osmotic agent in the gut 2. Used to treat simple constipation and as a bowel preparation for endoscopic procedures

Lactulose and Sorbitol 1. Mechanism of action 2. Use

1. Nucleoside/nucleotide analog. Monophosphate form is incorporated into DNA by HBV polymerase resulting in chain termination and the triphosphate form inhibits HBV and HIV reverse transcriptase 2. Used to treat HBV and as a combination drug in the treatment of HIV

Lamivudine 1. Mechanism of action 2. Use

1. Nucleoside analog that lacks a 3' OH group which leads to termination of DNA elongation and competitive inhibitor of reverse transcriptase 2. Used to treat HIV 3. Few significant AE It does not affect mitochondrial DNA synthesis or bone marrow precursor cells so the adverse effect profile is low

Lamivudine 1. Mechanism of action 2. Use 3. Adverse effects What is unique about the adverse effects of this drug?

1. Block voltage gated sodium channels which leads to a decrease in the transmission of excitatory glutamatergic neuronal signaling. 2. Used in the treatment generalized tonic-clonic seizures, simple and complex partial seizures, and secondarily generalized tonic-clonic seizures

Lamotrigine 1. Mechanism of action 2. Use

They do not enter the cells or cross the BBB. Always given IV or IM

Neuromuscular blockers contain quaternary ammonium group which make them highly polar and poorly soluble lipids. How does this affect their ability to enter cells or cross the BBB? How are these drugs administered?

1. Converted to an active metabolite which inhibits dihydroorotate dehydrogenase which leads to lower levels of UMP which arrests cells in the G1 phase. This inhibits autoimmune T-cell proliferation and production of autoantibodies by B-cells 2. Used to treat RA 3. Myelosuppresion and increased aminotransferase activity. CBC and liver function tests should be monitored. Activated lymphocytes require the de novo synthesis of pyrimidine because of their increases need but other cells can use the salvage pathway to fulfill their pyrimidine needs. Contraindicated in pregnancy

Leflunomide 1. Mechanism of action 2. Use 3. Adverse effects How should patients taking this drug be monitored? This drug affects T-cells and B-cells. Why are other cells not affected? Pregnancy safe?

Caused by Mycobacterium leprae and Mycobacterium lepromatis It is primarily a granulomatous disease of peripheral nerves and mucosa of the upper respiratory tract. Dapsone, Clofazimine, and Rifampin.

Leprosy is a disease caused by what bacteria? Where does it affect? The WHO recommends three drugs be used in combination to treat this condition. What are they?

1. Reversible aromatase inhibitor. 2. Used in the second line treatment of breast cancer after tamoxifen

Letrozole 1. Mechanism of action 2. Use

1. GnRH analog 2. Used to treat prostatic cancer It should be given by a pulsatile dose as a continuous dose of this drug can lead to reversible medical castration

Leuprolide 1. Mechanism of action 2. Use How should this drug be administered and why?

1. GnRH analog 2. To treat male infertility and rarely female infertility. Can also be used to diagnose a patients LH responsiveness to GnRH. Also used to control ovarian hyper stimulation and used for the treatment of endometriosis by removing exposure to cyclical changes in estrogen and progesterone during the menstrual cycle, to reduce the size of fibroids, and to treat prostate cancer. Inhibition of FSH and LH release leading to hypogonadism

Leuprolide 1. Mechanism of action 2. Use What can occur if this drug is administered in a non-pulsitile manner?

Only neurons with active receptors are affected.

Lithiums inhibition of inositol polyphosphatase and monophosphatase is uncompetitive. What does this mean for which neurons are affected by this drug?

At a physiological pH of ~7.4 more of the drug will be in the charged (cationic) form than the uncharged form. The cationic form The uncharged form is required for penetration of the neuronal membrane.

Local anesthetics are weak bases (pK = ~8-9). What does this mean for their charge at physiological pH? Is the cationic or uncharged form more active? What is important about the uncharged form?

1. α2-agonist which acts on the presynaptic neurons to decrease sympathetic outflow 2. Used to treat the adrenergic mediated opioid withdrawal symptoms.

Lofexidine 1. Mechanism of action 2. Use in drug abuse

1. Acts on GI µ-opiod receptors leading to inhibition of ACh release and decreased peristalsis 2. Used to treat diarrhea associated IBS/diarrhea (Imodium)

Loperamide 1. Mechanism of action 2. Use

1. Act through µ and δ receptors on enteric nerve, epithelial cells, and muscles 2. Used to treat diarrhea It acts as an anti-motility agent at low doses without causing analgesic effects.

Loperamide 1. Mechanism of action 2. Use How is this drug useful at low doses?

1. Protease inhibitor - They are reversible inhibitors of HIV aspartyl protease which is responsible for cleavage of the viral polyprotein into reverse transcriptase, protease, and integrase. This prevents virus maturation and results in production of non-infections visions. 2. One of the preferred protease inhibitors for the treatment of HIV 3. Should not be given with enzyme inducers like St. Johns Wort. Oral solution contains alcohol so this drug should be avoided in patients taking disulfiram, metronidizole, and some cephalosporins with disulfiram-like effects. Yes

Lopinavir 1. Mechanism of action 2. Use 3. Contraindications Is this drug given with ritonavir?

Benzodiazepines Their antiemetic potency is low but it can reduce anticipatory vomiting due to anxiety.

Lorazepam, Alprozalam and Diazepam are all what type of drug? What GI use do they serve?

1. Chloride channel activator 2. Used to treat constipation associated IBS

Lubiprostone 1. Mechanism of action 2. Use

It is the concentration that results in the immobility of 50% of patients when exposed to a noxious stimulus such as a surgical incision expressed as the percent of alveolar gas mixture of the inhaled anesthetic agent. Low It means that a physician can use two or more agents at varying MAC levels in order to achieve anesthesia in patients (ex. 0.7 MAC of isoflurane and 0.3 MAC of nitrous oxide yields 1 MAC and sedation in 100% of patients)

MAC (minimum alveolar concentration) is a standard method of comparing the potency of inhaled general anesthetics. What is MAC? Is MAC low or high for potent anesthetics? MAC values are additive. What does this mean for a physician who is using a combination of inhaled anesthetics?

Serotonin syndrome: It occurs when MAO inhibitors are combined with serotinergic agents like SSRIs, SNRIs, TCAs, or meperidine. It elevates serotonin to elevated levels which overstimulates the 5-HT1A & 5-HT2 receptors leading to hyperthermia, muscle rigidity, and myoclonus. Wine/Cheese reaction: Tyramine, contained in aged cheeses, red wines, etc. can cause the release of catecholamines. It is normally metabolized by MAO but, in patients taking MAOIs they cannot degrade tyramine as efficiently which can lead to tachycardia, HTN, arrhythmias, seizures, and possibly, stroke.

MAO inhibitors are involved in two classes of serious drug interactions. What are they?

Gram-positive infections Bacteriostatic but can be bactericidal at high concentrations. Should not be used in patients who are taking statin drugs as they inhibit CYP450 enzymes (except for azithromycin) Telithromycin

Macrolide antibiotics are mainly used to treat what types of infections? Are these drugs bacteriostatic or bactericidal? What are the contraindications of these drugs? If we have a patient who presents with hepatotoxicity, exacerbations of myasthenia gravis, or visual disturbances, what macrolide antibiotic would you first suspect?

1. Saline cathartic that acts as an osmotic agent in the gut 2. Used to treat simple constipation and as a bowel preparation for endoscopic procedures

Magnesium citrate 1. Mechanism of action 2. Use

1. Gastric antacid 2. Used to raise gastric pH and to stimulate GI motility 3. Diarrhea

Magnesium hydroxide 1. MOA 2. Use 3. Adverse effects

1. Bladder (hemorrhagic cystitis) 2. Bone marrow (suppression) 3. Kidney (nephrotoxicity) and hearing (ototoxicity) 4. Heart (dilated cardiomyopathy) 5. Bone marrow (suppression) 6. Pancreas (pancreatitis and bleeding)

Many anti-cancer drugs affect a variety of organ systems. What organ system do the following drugs affect? 1. Cyclophophamide 2. Vinblastine 3. Cisplatin 4. Doxorubicin 5. Methotrexate 6. L-Asparaginase

1. Bladder (hemorrhagic cystitis) 2. Heart (dilated cardiomyopathy) 3. Bone marrow (suppression) 4. Lung (pulmonary fibrosis) 5. Neurons (Peripheral neuropathy) 6. Bone marrow (suppression)

Many anti-cancer drugs affect a variety of organ systems. What organ system do the following drugs affect? 1. Ifofamide 2. Daunorubicin 3. Etoposide 4. Bleomycin 5. Vincristine 6. Dacarbazine

1. β-lactamase producing gram-positive bacteria 2. β-lactamase producing gram-positive & gram-negative bacteria 3. β-lactamase producing gram-negative bacteria 4. MRSA and enterococci 5. MRSA, enterococci, and VRE 6. MDR gram-positive and some gram-negative bacteria 7. MRSA and VRE 8. MRSA and VRE

Many drugs can be used to treat multi-drug resistant infections. What types of MDR infections would the following drugs treat? 1. Anti-staphylococcal penicillins 2. Carbepenems 3. Aztreonam 4. Vancomycin 5. Daptomycin 6. Tigecycline 7. Streptogramins 8. Linezolid

1. HIV entry inhibitor which binds to the CCR5 receptor which blocks HIV entry into cells 2. Used to treat HIVp Metabolized by CYP3A4 The dose of this drug that is given to patients taking protease inhibitors (strong cytochrome inhibitors) needs to be reduced to account for the inhibition of the cytochrome enzymes)

Maraviroc 1. Mechanism of action 2. Use This drug is metabolized by what cytochrome? How does this affect its co-administration with other drugs?

1. Active form of the drugs sulfasalazine and malsalazide (5-ASA) which blocks the pro-inflammatory mediators IL1 and TNFα 2. Used to treat Crohn's disease and UC

Masalamine 1. Mechanism of action 2. Use

1. Inhibits microtubule synthesis and glucose uptake which inhibits ATP production and leads to worm immobization and death 2. Drug of choice for whipworm, pinworm, hookworm, and roundworm. No, it is contraindicated in pregnancy

Mebendazole 1. Mechanism of action 2. Use Can this drug be given to pregnant women?

1. IGF-1 (insulin like growth factor 1) analog 2. Used in patients with an IGF-1 deficiency 3. Hypoglycemia (so patients should eat 20 minutes before or after administration) Either a genetic mutation in the GH receptor or development of neutralizing antibodies to GH.

Mecasermin 1. Mechanism of action 2. Use 3. Adverse effects What can lead to the deficiency that this drug is used to treat?

1. H1 receptor blocker (antihistamine) 2. Can be used to treat motion sickness and chemotherapy induced nausea

Meclizine 1. Mechanism of action 2. Use

1. Destroy the asexual blood forms of malarial pathogens by an unknown mechanism 2. Used to treat many chloroquine-resistant strains of malaria and the only medication recommended for chemoprophyaxis in pregnant women in chloroquine-resistant areas 3. Serious neuropsychiatric toxicities No

Mefloquine 1. Mechanism of actin 2. Use 3. Adverse effects Is this drug appropriate for treating severe complicated malaria?

1. Reduces glucose levels by inhibiting gluconeogenesis through inhibition of gluconeogenic enzymes and it increases insulin mediated glucose utilization by muscle and liver cells. 2. Used to treat type II diabetes and is effective at reducing fasting plasma glucose and HbA1c levels Through the activation of AMP activated protein kinase. No They are equivalent

Metformin 1. Mechanism of action 2. Use Through what mechanism are the actions mediated? Generally, does this drug cause hypoglycemia? How does this drug compare to the sulfonylurea drugs in reducing fasting plasma glucose levels and HbA1c levels?

1. Strong µ receptor agonist, NMDA receptor antagonist, and a serotonin and norepinephrine reuptake inhibitor 2. Used in the treatment of opioid addiction 3. QT prolongation, torsades de pointes, and death have been reported It has a longer duration of action but it produces less euphoria

Methadone 1. Mechanism of action 2. Use 3. Adverse effects Why is this drug as useful as it is in treating opioid addiction?

1. β-lactamase resistant inhibitor of cell wall synthesis (penicillin) 2. No longer used clinically or in the lab but it was previously used as first-line treatment for Staphylococcal infection

Methicillin 1. Mechanism of action 2. Use

1. Block iodination of thyroglobulin and inhibit the coupling reaction of DIT with MIT and DIT with DIT reducing the formation of T3/T4

Methimazole 1. Mechanism of action 2. Use

1. Ultra-short acting barbiturate 2. Used for induction of anesthesia and for short surgical procedures. Decreases ICP Does not produce analgesia and may even cause hyperalgesia

Methohexital 1. Mechanism of action 2. Use How does this drug affect intracranial pressure? What analgesic affect does this drug have?

1. Acts as an immunosuppressant at low doses by inhibiting aminoimidazolecarboxamide ribonucleotide transformylase and thymidylate synthase. 2. Used in the treatment of rheumatoid arthritis 3. Bone marrow suppression

Methotrexate 1. Mechanism of action 2. Immunosuppresion use 3. Adverse effects

1. Blocks dihydrofolate reductase which causes immune suppression 2. Used to treat moderate to severe Crohn's disease and UC

Methotrexate 1. Mechanism of action 2. Use

1. Inhibits AICAR transformylase and dihydrofolate reductase which inhibits the final steps of de novo purine synthesis resulting in accumulation and release of adenosine which is a potent anti-inflammatory mediator 2. First drug of choice to treat rheumatoid arthritis 3. Nausea and mucosal ulcers By coadministration with leucovorin or folic acid. The dose is much lower than the dose given for cancer chemotherapy Pregnancy

Methotrexate 1. Mechanism of action 2. Use 3. Adverse effects How can the adverse effects be reduced? What dose is given when compared to the dose given for cancer treatment? Contraindication?

1. Muscarinic (cholinergic) agonists. 2. Used to treat IBS.

Methscopolamine 1. Mechanism of action 2. Use

1. Bulk-forming laxative that increases water retention. Leads to distention of the bowel and increased peristaltic stimulation of the gut 2. Used to stimulate the peristaltic movement of the gut

Methylcellulose 1. Mechanism of action 2. Use

1. Opioid receptor antagonist 2. Used to block GI µ receptors to treat opioid induced constipation.

Methylnaltrexone 1. Mechanism of action 2. Use

1. Corticosteroid 2. Used in combination with 5-HT3 receptor blockers to treat nausea and vomiting due to chemotherapy treatment.

Methylprednisolone 1. Mechanism of action 2. Use

1. 5-HT3 and D2 receptor blocker that acts as an anti-emetic and 5-HT4 receptor agonist that acts as a pro kinetic 2. To treat post-operative gastroparesis and used as an anti-emetic 3. Due to dopamine block it can cause Parkinsonion effects

Metoclopramide 1. Mechanism of action 2. Use 3. Adverse effects

1. Undergoes reductive bioactivation under anaerobic conditions and forms a cytotoxic product that interferes with nucleic acid synthesis (just remember it is an inhibitor of nucleic acid synthesis) 2. Used to treat C. difficile infections, anaerobic infections below the diaphragm, vaginitis (trichomoas and bacterial vaginosis), brain abscesses, and used as part of a combination to eradicate H. pylori infections Bactericidal Has activity against anaerobic bacteria including bactericides and Clostridium. It is an antimicrobial, amebicide, and antiprotozoal. Hepatic elimination

Metronidazole 1. Mechanism of action 2. Use Is this drug bacteriostatic or bactericidal? What type of bacteria does this drug work against? What types of organisms does this drug work against? How is this drug eliminated?

1. The reduction of metronidizole produces cytotoxic compounds that bind to proteins and DNA causing cell death 2. GET GAPs

Metronidizole 1. Mechanism of action 2. Use

1. Inhibitor of steroid 11-hydroxylation which interferes with cortisol and corticosterone synthesis 2. Used to test adrenal function and to treat Cushing's in pregnant women 3. Salt and water retention, hirsutism, transient dizziness, and GI disturbances

Metyrapone 1. Mechanism of action 2. Use 3. Adverse effects

1. Inhibit 14-α-demethylase, they last enzyme in ergosterol synthesis from lanosterol 2. Most commonly used to topically treat superficial mycoses.

Miconazole 1. Mechanism of action 2. Use 3. Adverse effects Imidazole or Triazole? Inhibits what CYP P450 enzymes?

1. Competitive inhibitor of progesterone and glucocorticoid receptors 2. Can be used as an agent to cause abortion or can be given with PGE or PGF to increase myometrial contractions and induce labor

Mifepristone 1. Mechanism of action 2. Use

1. Antagonist of glucocorticoid and progesterone receptors 2. Used to treat patients with inoperable ectopic ACTH syndrome or adrenal carcinoma Glucocorticoid antagonist

Mifepristone 1. Mechanism of action 2. Use Is this a glucocorticoid or mineralocorticoid antagonist?

1. Competitive inhibitor of α-glucosidases which are required for breaking down starch and disaccharides 2. Used in the treatment of type 2 DM and cause modest reductions in fasting plasma glucose levels and HbA1c

Miglitol 1. Mechanism of action 2. Use

1. Stool softener 2. Used to treat constipation

Mineral oil 1. Mechanism of action 2. Use

1. Tetracycline drug that reversibly binds to the 30S ribosomal subunit which prevents binding of aminoacyl tRNA 2. Reaches high concentrations in secretions so is useful for eradication of meningococcal carrier state 3. Discoloration and hypoplasia of teeth and stunting of growth (because of brining to calcium ions) Mainly in the urine

Minocycline 1. Mechanism of action 2. Use 3. Adverse effects Where is this drug excreted from?

1. Noradrenergic and specific serotonergic antidepressant. It acts as an antagonist of central presynaptic α2 receptors and enhances the release of norepinephrine and serotonin while antagonizing 5HT-2 & 5HT-3 receptors. 2. Can be useful in the treatment of depression if insomnia and agitation are prominent

Mirtazapine 1. Mechanism of action 2. Use

1. PGE1 analogue which inhibits the parietal cell H+/K+ exchanger 2. Prevention of gastric ulcers induced by NSAIDs 3. Diarrhea, abortions, and exacerbations of IBD

Misoprostol 1. Mechanism of action 2. Use 3. Adverse effects

Butyrylcholinesterase Succinylcholine Some patients have abnormal variants of butyrylcholinesterase which can prolong the neuromuscular blockade in patients receiving these drugs leading to these patients requiring mechanical ventilation until muscle function returns. Rocuronium As an alternative to succinylchloline for rapid sequence intubation

Mivacurium has a short duration of action with metabolism not dependent on the liver and kidney. What is responsible for its metabolism? What other neuromuscular blocker is also metabolized by this enzyme? How can this be a problem in some patients? Which non-depolarizing blocker has the most rapid onset? As a result, how is this drug commonly used?

They have a ceiling effect in which increased doses will not cause an increased effect so their use in treating pain is limited. Pentazocine, butorphanol, and nalbuphine may fuse psychotomimetic effects. Psychotomimetic effects are uncommon with buprenorphine because of its κ antagonist effects

Mixed agonists are not recommended as routine analgesics. Why? Of the following four mixed agonist-antagonist opioid drugs, which are associated with psychotomimetic effects? Pentazocine, butorphanol, nalbuphine, and buprenorphine. Why are some of the drugs not associated with these effects?

Excessive dopaminergic activity. Drugs that cause increased dopaminergic activity are likely to produce or increase positive psychotic symptoms and this that decrease dopaminergic activity can be used to decrease or stop positive symptoms.

Most evidence suggests that schizophrenia is the result of what? How do drugs that either increase dopaminergic activity or decrease dopaminergic activity affect patients with this condition?

-triptyline (Amitriptyline & Nortriptyline) or -ipramine (Clomipramine, desipramine, & imipramine) They also block α-adrenergic, muscarinic, histamine, and 5-HT receptors. The blockade of these other receptors

Most of the TCAs end in what? Besides blocking the reuptake of norepinephrine and serotonin, what other receptors do these drugs act on? What causes the adverse effects associated with the TCA drugs?

Cephalexin, cefaclor, and cefixime.

Most of the cephalosporins are administered parenterally. What are the exceptions?

1. Fluoroquinolone drug that inhibits bacterial DNA replication by interfering with topoisomerase II (DNA gyrase) and topoisomerase IV 2. Used to treat community acquired pneumonia 4th

Moxifloxacin 1. Mechanism of action 2. Use Generation?

1. Binds to the bacterial isoleukyl transfer-RNA synthetase causing inhibition of protein synthesis 2. Used intranasally to treat colonizations of MRSA and used topically to treat impetigo or secondary infected traumatic skin lesions due to S. aureus or S. pyogenes. It is the only topical/intranasal agent with activity against MRSA.

Mupirocin 1. Mechanism of action 2. Use What is unique about this drug?

1. Anti-C3 antibody which kills T lymphocytes which suppresses cell mediated immunity 2. Used to treat acute graft rejections

Muromonab 1. Mechanism of action 2. Use

1. Inhibits inosine monophosphate dehydrogenase, an enzyme that is necessary for guanosine synthesis which leads to suppression of both T-cell and B-cell activation (as their activation and proliferation requires de novo nucleic acid synthesis) 2. Immunosuppression

Mycophenolate mofetil 1. Mechanism of action 2. Use

1. Intermediate acting insulin 2. Used for basal control of type I diabetes It has a cloudy appearance Protamine

NPH insulin 1. Mechanism of action 2. Use What does this preparation look like? This drug has an added protein. What is it?

1. Inhibition of COX 2. First-line drug for the treatment of acute gouty arthritis Aspirin: it competes with uric acid for excretion from the proximal tubules of the kidneys which can lead to increased levels of urate in the blood.

NSAIDs 1. Mechanism of action 2. Use in gout What NSAID is contraindicated in patients with gout and why?

1. Binds to ergosterol and forms pores in the cell membrane which causes leakage of intracellular ions and macromolecules which leads to cell death 2. Used only to treat candidiasis infections (cutaneous, vaginal, or oral administration) It is too toxic for IV administration

Nystatin 1. Mechanism of action 2. Use Why is this drug only used to topically

1. Long-acting somatostatin analog 2. Used to treat patients with carcinoid tumors, VIPomas, acute vatical bleeding, and acromegaly (as a result of somatostatin inhibiting GH release)

Octreotide 1. Mechanism of action 2. Use

1. Somatostatin analogue 2. Used to suppress secretion of GH in patients with GH excess, used to treat hormone secreting tumors such as seen in carcinoid syndrome, gastrinoma, glucagonoma, etc, and used for acute control of bleeding from esophageal varices 3. Biliary sludge and gallstones, sinus bradycardia, and vitamin B12 deficiency with long term use.

Octreotide 1. Mechanism of action 2. Use 3. Adverse effects

Citalopram, escitalopram, & sertraline MAO inhibitors because they may cause serotonin syndrome. It can cause seizures but the likelihood of fatalities from overdoses with SSRIs is extremely low (especially when compared to TCAs).

Of the SSRIs, which have a low cytochrome inhibition and, as a result, should be used in patients taking other drugs (citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, & sertraline)? What other drug, also used to treat depression, should these drugs not be given with and why? If patients overdose on these drugs, what may occur?

High potency: Fluphenazine and Haloperidol - more likely to produce EPRs Low potency: Chlorpromazine and Thioridazine - less likely to produce EPRs but more likely to produce sedation and postural hypotension Risperidone Haloperidol

Of the drugs listed as classical antipsychotics (chlorpromazine, fluphenazine, thioridazine, haloperidol), which have a high potency and which have a lower potency and how does this relate to their likelihood of producing extrapyramidal reactions? Which of the atypical antipsychotic drugs is most likely to cause EPRs (although rare at therapeutic levels)? Which classical antipsychotic drug is most likely to cause EPRs?

1. Not 2. β-lactam 3. β-lactam 4. Not 5. Not 6. β-lactam 7. β-lactam 8. Not

Of the following inhibitors of cell wall synthesis, which are β-lactams and which are not? 1. Vancomycin 2. Penicillins 3. Cephalosporins 4. Daptomycin 5. Bacitracin 6. Carbapenems 7. Monobactams 8. Fosfomycin

1. Intermediate 2. Long 3. Short 4. Long 5. Short 6. Intermediate 7. Intermediate 8. Long

Of the following local anesthetics, which are short acting, intermediate acting, and long-acting? 1. Mepivacaine 2. Bupivacaine 3. Chloroprocaine 4. Etidocaine 5. Procaine 6. Lidocaine 7. Prilocaine 8. Tetracaine

Glimepiride is the best because it has the lowest chance of causing hypoglycemia and it can be given by a once daily administration.

Of the second generation sulfonylureas (glyburide, glimepiride, and glipizide) which is the best and why?

Entacapone is preferred because tolcapone is associated with the development of fulminating hepatic necrosis, not seen in patients being treated with entacapone.

Of the two COMT inhibitors, tolcapone & entacapone, which is preferred and why?

Developed to try to avoid the respiratory depression seen with µ agonists. High affinity for µ receptors with a lower to no affinity for δ and κ receptors. It is effect seen with mixed agonist-antagonists in which, at a certain dose, no increase in dose will provide a larger effect. To either treat opioid overdose or physiological dependence. All of them (ie. µ, δ, & κ)

Opioid analgesics can be either pure agonists, mixed agonist-antagonists, or antagonists. What is the purpose of the mixed agonist-antagonists? What sort of affinity do most of the pure agonists have for each opioid receptor? What is the analgesic ceiling effect and which type of opioid analgesics have this effect? What is the function of the antagonists? What opioid receptors do the antagonists block?

1. (Neuroaminidase inhibitor) Inhibits the ability of neuroaminidase mediated cleavage of receptors which normally releases the virion release. This in turn leads to an inability for the virion to release from the cell 2. Used as prophylaxis prior to exposure to influenza type A and type B or within 24-48 hours Orally Gi discomfort and nausea which can be alleviated when taken with food. In infants >2 weeks old

Oseltamivir 1. Mechanism of action 2. Use How is this drug administered? How does this method of administration effect its adverse effect profile? What age group can be given this drug?

1. β-lactamase resistant inhibitor of cell wall synthesis (penicillin). 2. Used as first-line treatment for Staphylococcal endocarditis in patients without artificial heart valves

Oxacillin 1. Mechanism of action 2. Use

1. Mild to moderate opioid receptor agonist 2. Used as an antitussive and to treat pain. It is less efficacious than morphine

Oxycodone 1. Mechanism of action 2. Use How does this drug efficacy in treating pain compare to that of morphine?

1. Strong opioid receptor agonist 2. Useful in treating severe pain. High affinity for µ receptor and a lower affinity for the δ and κ receptors.

Oxymorphone 1. Mechanism of action 2. Use What is the affinity of this drug for the µ, δ, and κ opioid receptors?

1. Acts on GPCRs and stimulates the release of prostaglandins and leukotrienes that augment uterine contraction 2. IV infusion used to initiate and augment labor and given IM to control postpartum bleeding 3. Can cause fetal distress, placental abruption, and uterine rupture. Because a bolus injection can cause hypotension

Oxytocin 1. Mechanism of action 2. Use 3. Adverse effects Why should this drug be given IV as a dilute solution at a controlled rate?

1. They inhibit osteoclastic activity by decreasing farnesyl pyrophosphate synthesis by disrupting the mevalonate pathway leading to decreased osteoclast H+ ATPase function leading to reduced resorption and formation of hydroxyapatite. 2. Used to treat osteoporosis, malignancy associated with hypercalcemia, and Paget's disease of the bone

Pamidronate 1. Mechanism of action 2. Use

1. Replacement pancreatic enzyme 2. Used to improve the digestion of dietary fat, proteins, carbs, and fat solubles vitamins A, D, E, and K in patients with chronic pancreatitis, pancreatectomy, steatorrhea, and CF.

Pancrelipase 1. Mechanism of action 2. Use

Diazepam rectal gel

Patients being treated for seizures may still have breakthrough seizures. What drug is approved to treat breakthrough seizures?

An ACE inhibitor or an ARB. A statin drug Those with overt CVD or patients without CVD who are greater than 40 years old and have one or more other CVD risk such as a family history of CVD, HTN, smoking, dyslipidemia, or albuminuria.

Patients with diabetes and HTN should be started on what drugs in order to avoid developing cardiovascular disease? If they have dyslipidemia what should they be given? What diabetic patients with dyslipidemia should be placed on statins?

The flushing is mediated by the release of PGD2 which can be inhibited by co-administration of aspirin with niacin.

Patients with hyperlipidemia are sometimes treated with niacin which can cause intense cutaneous flushing. What drug can be given to decrease the likelihood of this condition and how does it work?

1. GH receptor antagonist which prevents dimerization of the GH receptors 2. Used to treat patient with excessive GH secretion

Pegvisomant 1. Mechanism of action 2. Use

1. Nucleoside/nucleotide analog that is monophosphorylated by viral thymidine kinase and then di- and triphosphorylated by host cell kinases which and is inserted into DNA which causes DNA chain termination and inhibition of DNA polymerase 2. Used for the topical treatment of HSV cold sores (active against HSV 1-3)

Penciclovir 1. Mechanism of action 2. Use

1. β-lactam inhibitor of cell wall synthesis (penicillin) 2. Drug of choice for syphilis (especially in patients who may not follow up or take all doses) and prophylaxis for rheumatic fever It has a very long have life (much longer than Penicillin G) of about 3-4 weeks so it can be given as a single dose via IM injection to patients who may not follow up or continue to take medication for a syphilis infection.

Pencillin G Benzathine 1. Mechanism of action 2. Use Why was this drug developed?

1. β-lactam inhibitor of cell wall synthesis (penicillin) 2. Drug of choice for the treatment of syphilis, streptococcal infections, and susceptible pneumococci 1. Effective against most gram-positive cocci 2. Affective against some such as Listeria and C. perfringens 3. Mainly affective against Neissseria spp. 4. Affective against most anaerobes except Bacteroides Staphylococci because it makes β-lactamase.

Penicillin G 1. Mechanism of action 2. Use/Drug of choice for How does this drug affect the following? 1. Gram-positive cocci 2. Gram-positive rods 3. Gram-negative cocci 4. Anaerobes What gram-positive cocci is this drug not effective against and why?

1. β-lactam inhibitor of cell wall synthesis (penicillin) 2. Seldom used anymore because of increased resistance Because it has a longer duration of action than Pencillin G.

Penicillin G Procaine 1. Mechanism of action 2. Use Why was this drug developed?

1. β-lactam inhibitor of cell wall synthesis (penicillin) 2. Drug of choice for treating Strep throat orally but can be used for other mild to moderate infections caused by streptococcal bacteria. It is the oral version of Penicillin as it is more acid stable than Penicillin G.

Penicillin V 1. Mechanism of action 2. Use How is this drug administered and how does that compare to Penicillin G?

Penicillins facilitate movement of amino glycosides through the cell well. Infective endocarditis No, they should never be placed in the same infusion fluid because it will cause them to form an inactive complex.

Penicillin and aminoglycoside drugs are commonly used synergistically. How do they act synergistically? They are used as effective empiric treatment of what condition? Can we place them in the same infusion fluid?

Pencillin requires more time in contact with bacteria so it requires dosing more often (~2-3 times a day) but aminoglycosides, when combined with their post-antibiotic effect ability just require a high concentration to be effective, and as a result, can be given once a day.

Penicillin is a time dependent drug but aminoglycosides are concentration dependent. What does this mean about the dosing of each drug?

1. κ agonist and µ antagonist or partial agonist 2. Useful in treating mild to moderate pain while keeping the risk of addiction low.

Pentazocine 1. Mechanism of action 2. Use

1. Reduce intraglandular iodide concentration by blocking transportation into the follicular cell 2. Used to treat hyperthyroidism 3. Aplasic anemia

Perchlorate 1. Mechanism of action 2. Use 3. Adverse effects

1. Non-competitive inhibitors of HIV-1 reverse transcriptase and cause inhibition of RNA and DNA dependent DNA polymerase 2. Used to treat HIV 3. Potential severe heptatoxicity and risk of hypersensitivity rash Inducer of CYP3A4

Nevirapine 1. Mechanism of action 2. Use 3. Adverse effects Is this an inducer or inhibitor of CYP3A4?

Projects from the substantia nigra to the basal ganglia Motor movements Blockade can lead to the development of extrapyramidal reactions

Nigrostriatal pathway Where does this pathway travel in the brain? This pathway is believed to play an important role in what behaviors? Blocking of D2 receptors in this pathway could result in what?

1. Androgen receptor antagonist. 2. Used to treat prostate cancer by inhibition testosterones prostatic hyper plastic activity

Nilutamide 1. Mechanism of action 2. Use

1. The drug is reduced by bacteria in the urine which leads to the formation of reactive intermediates that damage bacterial DNA 2. Used as a urinary antiseptic to treat UTIs 3. Renal insufficiency can cause drug accumulation, shouldn't be used after 38 weeks of pregnancy, and should not be used in infants <1 month as it has a risk of hemolytic anemia Depending on the bacteria it can be bacteriostatic or bactericidal Active against many gram-positives and gram-negatives

Nitrofurantoin 1. Mechanism of action 2. Use 3. Contraindications Is this drug bacteriostatic or bactericidal? What bacteria does this drug have activity against?

1. Inhibit 14-α-demethylase, they last enzyme in ergosterol synthesis from lanosterol 2. Similar spectrum as Itraconazole (Blastomyces, Sporothrix, and Histoplasmosis and used for dermatophytoses and onychomycosis). Can be used to treat Mucor. Triazole Inhibits CYP3A4

Posaconazole 1. Mechanism of action 2. Use 3. Adverse effects Imidazole or Triazole? Inhibits what CYP P450 enzymes?

1. Reduce intraglandular iodide concentration by blocking transportation into the follicular cell 2. Used to treat hyperthyroidism. 3. Aplasic anemia

Pertechnetate 1. Mechanism of action 2. Use 3. Adverse effects

Primaquine

Pharmacogenomics Idiosyncratic Anti-malarial drug. Causes oxidative stress on red blood cells. Oxidative injury is prevented by glutathione, which is replenished by NADPH, which is replenished with the help of the enzyme glucose 6-phosphate dehydrogenase(G6PD). Patients who are G6PD deficient(ie. G6PD A-, which causes a 90-95% reduction in enzyme function) and exposed to this drug may develop hemolytic anemia. Used for treatment of malaria. Other drugs that can cause oxidative stress on red blood cells include: sulfonamides, other antimalarials, and chloramphenicol.

Gefitinib

Pharmacogenomics Pharmacodynamics Inhibitor of tyrosine kinase of epidermal growth factor receptor(EGFR). EGFR often overexpressed in non-small cell lung carcinoma. Used for approved treatment of non-small cell lung carcinoma. Patients with mutation in ATP-binding site of tyrosine kinase domain of EGFR respond better.

Succinylcholine

Pharmacogenomics Pharmacokinetics Depolarizing nicotinic neuromuscular blocker. Onset is very rapid: within 1 minute. Duration is usually 5-10 minutes because of rapid hydrolysis by plasta butyrylcholinesterase(BChE). Typically rare genetic variant. Actions - Genetic variations in BChE have a decrease rate of succinylcholine metabolism, causing prolonged paralysis, treated with continued mechanical ventilation until muscle function returns to normal. Caused by BCHE defects, transmitted as an autosomal recessive trait. Used during surgery to paralyze skeletal muscle.

(Sulfonamides)

Pharmacogenomics Pharmacokinetics Metabolized by N-acetyltransferase 2(NAT2). Genetic variation results in either slow acetylators(metabolizing drugs slowly, leading to high plasma levels), or fast acetylators(metabolizing drugs fast, leading to low plasma levels). Slow acetylators may have hypersensitivity reactions, hemolytic anemia.

Procainamide

Pharmacogenomics Pharmacokinetics Metabolized by N-acetyltransferase 2(NAT2). Genetic variation results in either slow acetylators(metabolizing drugs slowly, leading to high plasma levels), or fast acetylators(metabolizing drugs fast, leading to low plasma levels). Used as a Class IA anti-arryhthmic. Slow acetylators may have systemic lupus erythematosus.

Hydralazine

Pharmacogenomics Pharmacokinetics Metabolized by N-acetyltransferase 2(NAT2). Genetic variation results in either slow acetylators(metabolizing drugs slowly, leading to high plasma levels), or fast acetylators(metabolizing drugs fast, leading to low plasma levels). Used as a direct vasodilator for HF and hypertension. Slow acetylators may have systemic lupus erythematosus.

Isoniazid

Pharmacogenomics Pharmacokinetics Metabolized by N-acetyltransferase 2(NAT2). Genetic variation results in either slow acetylators(metabolizing drugs slowly, leading to high plasma levels), or fast acetylators(metabolizing drugs fast, leading to low plasma levels). Used as an anti-mycobacterial. Slow acetylators may have neuropathy and hepatotoxicity.

Codeine

Pharmacogenomics Pharmacokinetics Opioid. Requires CYP2D6 to catalyze and convert to active morphine. Actions - Poor CYP2D6 metabolizers do not catalyze enough, and result in low, ineffective levels of morphine. Ultrarapid metabolizers can overdose, suffering respiratory depression or even respiratory arrest in response to standard doses. Used as an analgesic. Note: CYP2D6 also metabolizes many other drugs, such as: metoprolol(beta-blocker), haloperidol(neuroleptic), dextromethrophan(opioid analgesic), fluoxetine, imipramine, and desipramine(antidepressants).

6-mercaptopurine

Pharmacogenomics Pharmacokinetics Thiopurine. Has narrow therapeutic window, and some patients suffer from life-threatening myelosuppression. Inactivated by methylation via Thiopurine S-methyltransferase(TPMT). Used to treat cancer. Approximately 1/300 individuals are homozygous for polymorphism leading to low TPMT activity, increasing risk for myelosuppression when treated with standard dose. Must then be treated with 1/10 standard dose.

Azathioprine

Pharmacogenomics Pharmacokinetics Thiopurine. Has narrow therapeutic window, and some patients suffer from life-threatening myelosuppression. Inactivated by methylation via Thiopurine S-methyltransferase(TPMT). Used to treat cancer. Approximately 1/300 individuals are homozygous for polymorphism leading to low TPMT activity, increasing risk for myelosuppression when treated with standard dose. Must then be treated with 1/10 standard dose.

1. They are agonists of the peroxisome proliferator-activated receptor-γ (PPAR-γ) which causes decreased insulin resistance in muscles, fat, and liver cells and promotes the uptake of glucose. 2. Used in the treatment of type 2 DM This drug has a more favorable lipid effect than rosiglitazone because it increases HDLs and decreases TAGs whereas rosiglitazone increases HDLs, has no effect on TAGs, and increases LDLs.

Pioglitazone 1. Mechanism of action 2. Use This drug can be favored over rosiglitazone because of what?

1. β-lactam inhibitor of cell wall synthesis (penicillin). 2. Used to treat P. aeruginosas infections and other susceptible gram-negative infections

Piperacillin 1. Mechanism of action 2. Use

1. Non-selecive reversible COX inhibitor 2. Antipyretic, analgesic, and anti-inflammatory.

Piroxicam 1. Mechanism of action 2. Use

HIV-infected patients CO-trimoxazole (SMZ-TMP): this drug is also used for prevention of PCP in immunocompromised patients

Pneumocystis jirovecii pneumonia does not respond to antifungals like most other mycoses. It is the most common opportunistic infection in which population? What is the drug of choice for treatment of this condition?

1. Used as a bowel prepartation for endoscopic and radiological procedures

Polyetheylene glycol 1. Use

1. Blocks transcription by binding to the beta subunit of bacterial DNA-dependent RNA polymerase which causes inhibition of RNA synthesis 2. Used to treat TB, leprosy, as a prophylaxis for individuals exposed to meningitis, and to treat MRSA with vancomycin. 3. Strong inducer of CYP P450 enzymes and the development of orange/red color to bodily fluids. Yes, it is safe in pregnancy Treats M. tuberculosis, M kansasii, gram-positive, and gram-negative organisms including MRSA.

Rifampin 1. Mechanism of action 2. Use 3. Adverse effects Can this drug be used in pregnancy? What bacterial spectrum does this drug cover?

Used as an alternative treatment for hepatic encephalopathy

Rifaximin Use?

1. May involve the inhibition of gluatmatergic transmission in the CNS 2. New drug used to treat ALS.

Riluzole 1. Mechanism of action 2. Use

1. Blocks the viral membrane protein which is required for fusion of the viral cell membrane to the endosome which is required for uncoating of the virus. 2. Used for prophylaxis and treatment of influenza type A (not currently recommended as the first line treatment) 3. Pregnancy and nursing Yes Because it is more expensive Category C

Rimantadine 1. Mechanism of action 2. Use 3. Contraindications Is this drug metabolized prior to urinary excretion? This drug has fewer adverse effects than its sister drug Amantadine. Why is it no the primary drug given? Pregnancy category?

1. They inhibit osteoclastic activity by decreasing farnesyl pyrophosphate synthesis by disrupting the mevalonate pathway leading to decreased osteoclast H+ ATPase function leading to reduced resorption and formation of hydroxyapatite 2. Used to treat osteoporosis, malignancy associated with hypercalcemia, and Paget's disease of the bone

Risedronate 1. Mechanism of action 2. Use

1. Mild to moderate opioid receptor agonist 2. No longer used in the US due to cardiotoxicity

Propoxyphene 1. Mechanism of action 2. Use

1. Non-selective beta blocker 2. Used to treat the symptoms and feelings associated with performance anxiety Clonidine

Propranolol 1. Mechanism of action 2. Sedative-hypnotic use What other autonomic drug can be used to treat this condition?

1. Prevents the conversion of T4 to T3 2. Used to treat hyperthyroidism

Propranolol 1. Mechanism of action 2. Use

1. Block iodination of thyroglobulin and inhibit the coupling reaction of DIT with MIT and DIT with DIT reducing the formation of T3/T4. This drug also inhibits 5-deiodinase which results in a decreased conversion of T4 to T4. 2. Used to treat hyperthyroidism Because it doesn't inhibit the preformed T4/T3 from being secreted, it just reduces their formation.

Propylthiouracil 1. Mechanism of action 2. Use Why does this drug have a slow onset of action?

PTU also inhibits the conversion of T4 to T3 by inhibiting 5-deiodinase which Methimazole does not. Also, methimazole can be given by a once daily dose as opposed to propylthiouracil which requires dosing three times a day. PTU is preferred because it inhibits the 5-deiodinase. It is typically reserved for this condition or for patients who cannot tolerate methimazole. PTU

Propylthiouracil and Methimazole have the same effect in the thyroid. What are two important differences? Which drug is preferred in a thyroid storm? Which has worse side effects?

1. Bulk-forming laxative that increases water retention. Leads to distention of the bowel and increased peristaltic stimulation of the gut 2. Used to stimulate the peristaltic movement of the gut.

Psyllium 1. Mechanism of action 2. Use

The ceiling of the non-opioid drug. Yes, and as a result they are poor choices for management of severe pain.

Pure opioid analgesics do not have a ceiling effect but NSAIDs do. When using a combination of an opioid with a non-opioid what is the dose-limiting factor? Do mixed agonist-antagonists have a ceiling effect?

1. Enzymatically hydrolyzed to an active form (MOA beyond this is not specified) 2. First line agent for the treatment of all susceptible forms of TB 3. Nongouty polyarthralgia occurs in ~40% of patients being treated with this drug

Pyrazinamide 1. Mechanism of action 2. Use 3. Adverse effects

1. Inhibitor of folate synthesis by inhibiting dihydrofolate reductase 2. Used in combination with sulfadoxine for chemoprophyaxis and treatment of chloroquine-resistant falciparum malaria (not used for severe malarial infection)

Pyrimethamine 1. Mechanism of actin 2. Use

1. Depresses oxygen uptake and carbohydrate metabolism and intercalates into the DNA which disrupts the parasites replication and transcription 2. Parenteral treatment of severe falciparum malaria

Quinidine 1. Mechanism of actin 2. Use

1. Depresses oxygen uptake and carbohydrate metabolism and intercalates into the DNA which disrupts the parasites replication and transcription 2. Oral treatment of falciparum malaria (as an alternative to treatment in chloroquine-resistant areas)

Quinine 1. Mechanism of actin 2. Use

1. Estrogen receptor antagonist on breast tissue and endometrium and agonistic on bone 2. Used to treat breast cancer It does not have an increased risk of endometrial cancer development

Raloxifene 1. Mechanism of action 2. Use How is this drug different than tamoxifen?

1. Binds to integrase and causes inhibition of the final step of integration of the viral DNA into the host cell DNA 2. Approved for treatment of HIV in both treatment-naive and treatment-experienced patients Both It has very few drug interactions as a result

Raltegravir 1. Mechanism of action 2. Use Is this drug used to treat HIV-1, HIV-2, or both? This drugs metabolism is via UGT1A1-mediated glucuronidation. How does this affect its potential drug interactions?

1. MT1 & MT2 melatonin receptor agonists 2. Used to treat insomnia in patients with difficulty initiating sleep

Ramelteon 1. Mechanism of action 2. Use

1. MAO-B inhibitor which reduces the metabolism of dopamine and enhances the effects of levodopa 2. Used as an adjunct to levodopa in patients with Parkinson's disease 3. Metabolized to methamphetamine and amphetamine so it can cause insomnia if taken too late in the day.

Rasagiline 1. Mechanism of action 2. Use 3. Adverse effects

1. Animal derived enzyme that oxidizes uric acid to allantoin, a soluble compound that is easily excreted from the kidneys 2. Used to prevent renal injury caused by rapid lysis of tumor cells and release of free nucleotides (which increases plasma urate levels) in patients receiving chemotherapy. Aspergillus

Rasburicase 1. Mechanism of action 2. Use In the US, where is this drug obtained from?

1. Dopamine receptor agonist 2. Increasingly used as initial treatment for Parkinson's disease instead of as an adjunct to levodopa Pramipexole

Pramipexole 1. Mechanism of action 2. Use Does this drug or bromocriptine have a better adverse effect profile?

1. Amylin analog which inhibits food intake, gastric emptying, and glucagon secretion 2. Used as an injectable adjunct to insulin therapy in patients with type 1 & 2 DM

Pramlintide 1. Mechanism of action 2. Use

1. Strong µ receptor agonist 2. Used to treat short term pain

Remifentanil 1. Mechanism of action 2. Use

1. Blocks the ATP-sensitive K+ channel in the beta cell membrane which leads to increased secretion of insulin 2. Used to treat type II diabetes and to reduce fasting plasma glucose and HbA1c levels 3. Hypoglycemia and weight gain. Repaglinide No

Repaglinide 1. Mechanism of action 2. Use 3. Adverse effects The meglitinide drugs may cause hypoglycemia and weight gain. Does this drug or Nateglinide pose a greater risk of hypoglycemia? Does this drug contain sulfur?

Metaproterenol

Respirator Short-acting beta2-Agonist AKA Alupent. Drug of choice for acute relief of bronchospasm. Inhalation minimizes side effects, because poorly absorbed into circulation via lungs. Actions - Increases intracellular cAMP concentration, resulting in relaxation of bronchial smooth muscle, causing bronchodilation. Used to treat asthma and acute relief of bronchospasm. Adverse - tremors, bradycardia, arrhythmias, and tolerance with excessive use.

Terbutaline

Respirator Short-acting beta2-Agonist AKA Brethaire. Drug of choice for acute relief of bronchospasm. Inhalation minimizes side effects, because poorly absorbed into circulation via lungs. Actions - Increases intracellular cAMP concentration, resulting in relaxation of bronchial smooth muscle, causing bronchodilation. Used to treat asthma and acute relief of bronchospasm. Adverse - tremors, bradycardia, arrhythmias, and tolerance with excessive use.

Albuterol

Respirator Short-acting beta2-Agonist AKA Proventil. Drug of choice for acute relief of bronchospasm. Inhalation minimizes side effects, because poorly absorbed into circulation via lungs. Actions - Increases intracellular cAMP concentration, resulting in relaxation of bronchial smooth muscle, causing bronchodilation. Used to treat asthma and acute relief of bronchospasm. Adverse - tremors, bradycardia, arrhythmias, and tolerance with excessive use.

Omalizumab

Respiratory Antibody Given parenterally and expensive. Actions - Binds to IgE on sensitized mast cells, preventing activation, preventing release of Lets(?) and other mediators. Used for prophylactic management in asthmatic patients. Adverse - As an antibody drug, causes anaphylaxis in 1-2/1000 patients.

Dexamethasone

Respiratory Corticosteroids (Assuming systemic corticosteroid?) Actions - Inhibits synthesis of arachidonic acid by phospholipase A2, inhibiting leukotrienes, cytokines, and prostaglandins. Binds to intracellular receptors and activates glucocoricoid response elements(GRE) in the nucleus, synthesizing substances that inhibit expression of inflammation and allergy. Used as for bronchial asthma. Adverse - abnormalities in glucose metabolism, increased appetite, weight gain, hypertension, adrenal suppression. Can be minimized by limiting systemic therapy to few days.

Flunisolide

Respiratory Corticosteroids - Inhaled AKA Aerobid. Actions - Inhibits synthesis of arachidonic acid by phospholipase A2, inhibiting leukotrienes, cytokines, and prostaglandins. Binds to intracellular receptors and activates glucocoricoid response elements(GRE) in the nucleus, synthesizing substances that inhibit expression of inflammation and allergy. Used for both acute(systemic steroids when severe) and maintenance(low dose inhalational) asthma management. If compliant and still symptomatic, add LABA. For uncontrolled asthma, add Omalizumab. Adverse - Much more limited than systemic steroids. Cough, oral thrush, dysphonia.

Fluticasone

Respiratory Corticosteroids - Inhaled AKA Flovent. Actions - Inhibits synthesis of arachidonic acid by phospholipase A2, inhibiting leukotrienes, cytokines, and prostaglandins. Binds to intracellular receptors and activates glucocoricoid response elements(GRE) in the nucleus, synthesizing substances that inhibit expression of inflammation and allergy. Used for both acute(systemic steroids when severe) and maintenance(low dose inhalational) asthma management. If compliant and still symptomatic, add LABA. For uncontrolled asthma, add Omalizumab. Adverse - Much more limited than systemic steroids. Cough, oral thrush, dysphonia.

Budesonide

Respiratory Corticosteroids - Inhaled AKA Pulmicort. Actions - Inhibits synthesis of arachidonic acid by phospholipase A2, inhibiting leukotrienes, cytokines, and prostaglandins. Binds to intracellular receptors and activates glucocoricoid response elements(GRE) in the nucleus, synthesizing substances that inhibit expression of inflammation and allergy. Used for both acute(systemic steroids when severe) and maintenance(low dose inhalational) asthma management. If compliant and still symptomatic, add LABA. For uncontrolled asthma, add Omalizumab. Adverse - Much more limited than systemic steroids. Cough, oral thrush, dysphonia.

Beclomethasone

Respiratory Corticosteroids - Inhaled AKA Vanceril. Actions - Inhibits synthesis of arachidonic acid by phospholipase A2, inhibiting leukotrienes, cytokines, and prostaglandins. Binds to intracellular receptors and activates glucocoricoid response elements(GRE) in the nucleus, synthesizing substances that inhibit expression of inflammation and allergy. Used for both acute(systemic steroids when severe) and maintenance(low dose inhalational) asthma management. If compliant and still symptomatic, add LABA. For uncontrolled asthma, add Omalizumab. Adverse - Much more limited than systemic steroids. Cough, oral thrush, dysphonia.

Hydrocortisone

Respiratory Corticosteroids - Systemic Actions - Inhibits synthesis of arachidonic acid by phospholipase A2, inhibiting leukotrienes, cytokines, and prostaglandins. Binds to intracellular receptors and activates glucocoricoid response elements(GRE) in the nucleus, synthesizing substances that inhibit expression of inflammation and allergy. Used as a life-saving steroid in status asthmaticus. Adverse - abnormalities in glucose metabolism, increased appetite, weight gain, hypertension, adrenal suppression. Can be minimized by limiting systemic therapy to few days.

Prednisolone

Respiratory Corticosteroids - Systemic Actions - Inhibits synthesis of arachidonic acid by phospholipase A2, inhibiting leukotrienes, cytokines, and prostaglandins. Binds to intracellular receptors and activates glucocoricoid response elements(GRE) in the nucleus, synthesizing substances that inhibit expression of inflammation and allergy. Used as a life-saving steroid in status asthmaticus. Adverse - abnormalities in glucose metabolism, increased appetite, weight gain, hypertension, adrenal suppression. Can be minimized by limiting systemic therapy to few days.

Zafirlukast

Respiratory Leukotriene antagnoist AKA Accolate. Given Orally. Actions - Block LTD4 receptor. Used in exercise, antigen, and aspirin induced asthma. Used for chronic maintenance of mild asthma. Not beneficial in acute bronchospasm. Adverse - Overall safe. Rarely develop vasculitis and systemic eosinophilia resembling Churg-Strauss syndrome.

Montelukast

Respiratory Leukotriene antagnoist AKA Singulair. Given Orally. Actions - Block LTD4 receptor. Used in exercise, antigen, and aspirin induced asthma. Used for chronic maintenance of mild asthma. Not beneficial in acute bronchospasm. Adverse - Overall safe. Rarely develop vasculitis and systemic eosinophilia resembling Churg-Strauss syndrome.

Zileuton

Respiratory Leukotriene antagnoist AKA Zyflo. Given orally. Actions - Inhibits LOX-5, which catalyzes formation of leukotrienes from arachidonic acid. Used in exercise, antigen, and aspirin induced asthma. Used for chronic maintenance of mild asthma. Not beneficial in acute bronchospasm. Adverse - Overall safe. Some cases of elevated liver enzymes.

Salmeterol

Respiratory Long-acting beta2-Agonist AKA Serevent. Long-acting. Inhalation minimizes side effects, because poorly absorbed into circulation via lungs. Actions - Increases intracellular cAMP concentration, resulting in relaxation of bronchial smooth muscle, causing bronchodilation. Used mainly for prophylaxis of symptoms. Adverse - tremors, bradycardia, arrhythmias, and tolerance with excessive use.

Formoterol

Respiratory Long-acting beta2-Agonist Long-acting. Inhalation minimizes side effects, because poorly absorbed into circulation via lungs. Actions - Increases intracellular cAMP concentration, resulting in relaxation of bronchial smooth muscle, causing bronchodilation. Used mainly for prophylaxis of symptoms. Adverse - tremors, bradycardia, arrhythmias, and tolerance with excessive use.

Aminophylline

Respiratory Methylxanthine (No information. Assuming similar to Theophylline?) Actions - Inhibits PDE, increasing cAMP levels, resulting in bronchodilation. No significant anti-inflammatory effects. Blocks adenosine receptors. Used to treat asthma. Adverse - Overdosing causes tremors, insomnia, GI distress, and nausea. Most dangerous is seizures and arrhythmias.

Theophylline

Respiratory Methylxanthine Very small therapeutic window. Actions - Inhibits PDE, increasing cAMP levels, resulting in bronchodilation. No significant anti-inflammatory effects. Blocks adenosine receptors. Used to treat asthma. Adverse - Overdosing causes tremors, insomnia, GI distress, and nausea. Most dangerous is seizures and arrhythmias. Interactions - Cimetidine, erythromycin, and quinolones(cipro) increase plasma levels. Phenytoin decreases plasma levels.

Ipratropium

Respiratory Muscarinic Antagonist Inhaled anticholinergic. AKA Atrovent. Actions - Blocks parasympathetic bronchoconstriction and mucus secretion, maintaining bronchial dilation of airways. Used to prevent vagal mediated bronchoconstriction, and for treatment of asthma and COPD. Adverse - Dry mouth, sedation.

Tiotropium

Respiratory Muscarinic Antagonist Long-acting anticholinergic. (According to earlier lectures, superior to Ipratropium as bronchodilator.) Actions - Blocks parasympathetic bronchoconstriction and mucus secretion, maintaining bronchial dilation of airways. Used to prevent vagal mediated bronchoconstriction, and for treatment of asthma and COPD. Adverse - Dry mouth, sedation.

1. Increases the permeability of the cell membrane to calcium with causes contracture and paralysis of the worms musculature which results in the detachment of the worms suckers form the blood vessel walls 2. Drug of choice for all forms of schistosomiasis, most trematodes (not fasciola hepatica) and most cestode infections.

Praziquantel 1. Mechanism of action 2. Use

1. Corticosteroid which inhibit TNFα, IL-1, and IL-8 2. Used to treat Crohn's disease and UC.

Prednisolone 1. Mechanism of action 2. GI Use

1. Corticosteroid which inhibit TNFα, IL-1, and IL-8. 2. Used to treat Crohn's disease and UC.

Prednisone 1. Mechanism of action 2. GI Use

1. Anticonvulsant 2. Useful in the management of neuropathic pain

Pregabalin 1. Mechanism of action 2. Use

1. Increases the release of GABA from presynaptic neurons and decreases glutamate release by blocking presynaptic voltage gated calcium channels 2. Used as an adjunct to treat seizures as well as being used to treat neuropathic pain.

Pregabalin 1. Mechanism of action 2. Use

1. Not well understood 2. Drug of choice for the eradication of dormant liver forms of P. vivax and P. ovale (it is the only available agent active against the dormant liver forms) No, because it crosses the placenta and the fetus is relatively G6PD deficient so it can cause hemolysis in the fetus

Primaquine 1. Mechanism of actin 2. Use Can this drug be given to pregnant women? Why or why not?

Cromolyn

Respiratory Release Inhibitor AKA Intal. Available orally, as aerosol, and as drops. Actions - Stabilize membranes of mast cells and prevent release of inflammatory mediators. Used as effective prophylactic agents. Not used for treating acute asthma attacks. Pre-treatment blocks allergen- and exercise-induced bronchoconstriction. Also used to prevent food allergies and hay fever. Adverse - Potential toxicity causing infrequent laryngeal edema, cough, and wheezing.

Nedocromil

Respiratory Release Inhibitor AKA Tilade. Available orally, as aerosol, and as drops. Actions - Stabilize membranes of mast cells and prevent release of inflammatory mediators. Used as effective prophylactic agents. Not used for treating acute asthma attacks. Pre-treatment blocks allergen- and exercise-induced bronchoconstriction. Also used to prevent food allergies and hay fever. Adverse - Potential toxicity causing unpleasant taste.

1. Uricosuric agent which inhibits uric acid reabsorption in the kidneys 2. Used to treat chronic gout 3. Hypersensitivity reactions In patients with nephrolithiasis as it may form kidney stones. Drink lots of water to minimize the risk of developing kidney stones.

Probenecid 1. Mechanism of action 2. Use 3. Adverse effects In what patients should this drug not be used? Patients taking this drug should be recommended to do what?

1. D2 receptor antagonist 2. Anti-emetic

Proclorperazine 1. Mechanism of action 2. Use

1. GABAa & GABAb agonist in the CNS 2. Used to treat patients with chronic spasms

Progabide 1. Mechanism of action 2. Use

1. Inhibitor of folate synthesis by inhibiting dihydrofolate reductase 2. Used in combination with sulfadoxine for chemoprophyaxis and treatment of chloroquine-resistant falciparum malaria (not used for severe malarial infection)

Proguanil 1. Mechanism of actin 2. Use

Vitamin B12, digoxin, and ketoconazole because acid is required for their absorption. Proton pump inhibitors +/- H2 blockers

Prolonged therapeutic use of PPIs & H2 blocker may decrease the bioavailability of what and why? What drug(s) are used to treat GERD?

1. Acts as a synthetic guanosine analog which prevents viral mRNA viral capping and inhibits RNA-dependent RNA polymerase which causes inhibition of viral protein synthesis. 2. Useful in the treatment against a broad spectrum of RNA and DNA viruses including RSV, and HCV (commonly in combination with interferon α 3. Dose-dependent transient anemia (because it binds to RBC's for 16-40 days) 4. Need to ensure patient being treated is not pregnant and is not in contact with someone who is pregnant. Should also ensure that the patient does not get pregnant for a period of time after stopping administration of the drug to ensure there is not residual drug in the patients system Category X

Ribavirin 1. Mechanism of action 2. Use 3. Adverse effects 4. Contraindications Pregnancy category

1. Not specified 2. It is the #1 drug used with isoniazid to treat TB and is the preferred drug of choice for use in HIV+ patients because it has less of an effect on CYP enzymes There is insufficient data to recommend use in pregnancy

Rifabutin 1. Mechanism of action 2. Use Can this drug be used in pregnancy?

Rifampin is a strong inducer of CYP P450 enzyme but Rifabutin has less of an effect on these enzymes making it the preferred drug for the treatment of TB in HIV+ patients or those taking lots of drugs that require CYP enzymes for metabolism.

Rifabutin and Rifampin are both Rifamycins. What is an important difference

1. Selectively binds to necrotic tissue and acts as a barrier to acid in the stomach. Also stimulates endogenous prostaglandin synthesis. 2. Used to treat peptic ulcer disease H2 receptor blockers or PPIs. It requires an acidic pH to be activated so if it is administered with either of these drugs it will not be useful.

Sucralfate 1. Mechanism of action 2. Use What drugs should this not be administered with any why?

1. Strong µ receptor agonist 2. Used to treat short term pain because of the short action of the drug 1000 times more potent then morphine

Sufentanil 1. Mechanism of action 2. Use How potent is this drug compared to morphine?

1. β-lactamase inhibitor which binds to and inactivates most β-lactamases 2. Co-administered in fixed combinations with penicillins

Sulbactam 1. Mechanism of action 2. Use

1. Sulfonamide drug that acts as a structural analog of PABA and inhibits bacterial folic acid synthesis 2. Can be used as a topical agent for burn infections or ocular infections or as oral agents for simple UTIs (although not commonly used for this anymore).

Sulfadiazine 1. Mechanism of action 2. Use

1. Inhibitor of folate synthesis by inhibiting dihydropteroate synthase 2. Used in combination with pyrimethamine for chemoprophyaxis and treatment of chloroquine-resistant falciparum malaria (not used for severe malarial infection)

Sulfadoxine 1. Mechanism of actin 2. Use

1. Sulfonamide drug that acts as a structural analog of PABA and inhibits bacterial folic acid synthesis 2. Can be used as a topical agent for burn infections or ocular infections or as oral agents for simple UTIs (although not commonly used for this anymore)

Sulfamethoxazole 1. Mechanism of action 2. Use

1. Sulfonamide drug that acts as a structural analog of PABA and inhibits bacterial folic acid synthesis 2. Used to treat ulcerative colitis, enteritis, and IBD

Sulfasalazine 1. Mechanism of action 2. Use

1. 5-ASA moiety 2. Could be used to treat RA but it is more commonly used to treat ulcerative colitis 3. Hemolysis in patients with a G6PD deficiency, lupus-like syndrome. Probably safe in pregnancy

Sulfasalazine 1. Mechanism of action 2. Use 3. Adverse effects Pregnancy safe?

1. Inhibits the pro-inflammatory mediators IL1 and TNFα 2. Used to treat mild to moderate Crohn's disease or UC 3. Hypersensitivity and reversible oligospermia. It is a sulfa drug so it should not be used in patients with a sulfa allergy or a G6PD deficiency

Sulfasalazine 1. Mechanism of action 2. Use 3. Adverse effects What patients should this drug be avoided in?

1. Uricosuric agent which inhibits uric acid reabsorption in the kidneys 2. Used to treat chronic gout 3. Hypersensitivity reactions and depression of hematopoesis Because of the possibility of depressing hematopoesis this drug should not be used in patients with underlying blood dyscrasias. Drink lots of water to minimize the risk of developing kidney stones. It can inhibit the metabolism of warfarin.

Sulfinpyrazone 1. Mechanism of action 2. Use 3. Adverse effects In what patients should this drug not be used? Patients taking this drug should be recommended to do what?f What drug interaction should be remembered for this drug?

N-acetylcysteine

Supplies cysteine as a precursor for increased glutathione production to act as an antidote for acetaminophen poisoning. Also directly detoxifies NAPQI.

Second or third degree heart block, arrhythmias, prolonged QT interval, severe liver disease, and recent acute MI. This is the result of the drugs 1A anti-arrhythmic-like effects.

TCAs should be avoided in patients with what conditions?

1. A potent inhibitor of CYP3A4 which increases the levels of other protease inhibitors 2. Used to boost the levels of other protease inhibitors. Combined with atazanavir as the only once-daily preferred protease inhibitors

Ritonavir 1. Mechanism of action 2. Use

1. Monoclonal antibody against CD20 antigen 2. Used in the treatment of non-hodgkins lymphoma and rheumatoid arthritis

Rituximab 1. Mechanism of action 2. Use

1. Dopamine receptor agonist 2. Increasingly used as initial treatment for Parkinson's disease instead of as an adjunct to levodopa Ropinirole

Ropinirole 1. Mechanism of action 2. Use Does this drug or bromocriptine have a better adverse effect profile?

1. They are agonists of the peroxisome proliferator-activated receptor-γ (PPAR-γ) which causes decreased insulin resistance in muscles, fat, and liver cells and promotes the uptake of glucose 2. Used in the treatment of type 2 DM Because it can exacerbate CHF in some patients.

Rosiglitazone 1. Mechanism of action 2. Use In 2010 the FDA restricted the use of this drug. Why?

1. Transdermal dopamine receptor agonist 2. Used as a once daily treatment for Parkinson's disease

Rotigotine 1. Mechanism of action 2. Use

1. Muscarinic antagonist 2. Used to treat motion sickness

Scopolamine 1. Mechanism of action 2. Use

1. MAO-B inhibitor which reduces the metabolism of dopamine and enhances the effects of levodopa 2. Used as an adjunct to levodopa in patients with Parkinson's disease 3. Metabolized to methamphetamine and amphetamine so it can cause insomnia if taken too late in the day

Selegiline 1. Mechanism of action 2. Use 3. Adverse effects

1. Stimulant laxative 2. Prokinetic Docusate

Senna 1. Mechanism of action 2. Use This drug is commonly used in combination with what other drug to treat cases of opioid-induced constipation?

1. Macrolide antibiotic that is 100 time more potent than cyclosporine which binds to the FK-506 binding protein and inhibits calciineurin. 2. Used as an immunosuppressant

Tacrolimus 1. Mechanism of action 2. Use

1. Estrogen receptor antagonist on breast tissue and agonist at liver, endometrium, and bone 2. Used to treat breast cancer 3. Increased risk of developing endometrial cancer

Tamoxifen 1. Mechanism of action 2. Use 3. Adverse effects

Selective estrogen receptor modulators Both are typically used in the treatment of breast cancer but they have a beneficial effect on bone through their agonistic effect on the bone estrogen receptors. An important difference between the two drugs is that tamoxifen use has an increased risk of endometrial cancer development whereas raloxifen does not have this potential risk.

Tamoxifen and Raloxifen are what types of drugs? What is the difference between the two and what effect do they have on the bone?

1. β-lactamase inhibitor which binds to and inactivates most β-lactamases 2. Co-administered in fixed combinations with penicillins.

Tazobactam 1. Mechanism of action 2. Use

1. Bind reversibly to non-structural protein 3 (NS3) serene protease and inhibit replication of its target virus 2. Used in the treatment of HCV in adults who have been previously untreated or failed treatment with interferon α and ribavirin (can also be administered in combination with interferon α and ribavirin).

Telaprevir 1. Mechanism of action 2. Use

1. Macrolide drug that reversibly binds to the 50S ribosomal subunit and inhibits translocation. 2. Used in empiric therapy of community-acquired pneumonia and to treat upper respiratory tract and soft-tissue infections (ex. Staph, H. influenza, S. pneumonia, and enterococci)

Telithromycin 1. Mechanism of action 2. Use

1. Nucleoside analog that lacks a 3' OH group which leads to termination of DNA elongation and competitive inhibitor of reverse transcriptase 2. Use to treat HIV (currently part of the recommended regimen for the treatment of HIV) 3. GI effects It has a long half-life so can be administered as a once a day dose. Emtricitabine (NRTI) and efavirenz (NNRTI)

Tenofovir 1. Mechanism of action 2. Use 3. Adverse effects What is important about this drugs pharmacokinetics? This drug can be found in fixed dose cominationsions with what other drugs?

1. Inhibits squalene epoxidase which prevents the synthesis of ergosterol. This also leads to toxic accumulation of squalene in the cell both of which lead to cell death. 2. Effective in treating onychomycosis 3. Very minimal Does not affect P450 enzymes so has no drug interactions

Terbinafine 1. Mechanism of action 2. Use 3. Adverse effects Does this drug affect CYP P450 enzymes?

1. Recombinant PTH given via pulsitile doses to stimulate bone formation 2. Used in the treatment of osteoporosis to restore normal bone loss 3. Hypercalcemia and hypercalciuria

Teriparatide 1. Mechanism of action 2. Use 3. Adverse effects

1. Tetracycline drug that reversibly binds to the 30S ribosomal subunit which prevents binding of aminoacyl tRNA 2. Drug of choice for chlamydia, mycoplasma pneumoniae, Lyme disease, cholera, anthrax prophylaxis, and rickettsial infections 3. Discoloration and hypoplasia of teeth and stunting of growth (because of brining to calcium ions) Mainly in the urine

Tetracycline 1. Mechanism of action 2. Use 3. Adverse effects Where is this drug excreted from?

1. Decreases TNF-α production and enhances cell mediated immunity 2. Multiple myeloma 3. It has an anti-angiogenic effect which can cause phocomelia (sealed limb deformities if given to pregnant women)

Thalidomide 1. Mechanism of action 2. First line drug for what? 3. Adverse effects

-azodone Stimulation of the 5HT-1A receptors in the rap he nuclei may help depression but stimulation of the 5HT-2 receptors in the forebrain can cause agitation or anxiety and sexual dysfunction is overstimulated in the spinal cord. These drugs block these adverse effects of SSRIs by 5HT-2 receptors but still causing serotonin reuptake and stimulating the 5HT-1A receptors

The 5HT-2 antagonists/reuptake inhibitors (SARIs) end in what? How are these drugs effective in treating depression?

-capone (Tolcapone & entacapone) Tolcapone inhibits COMT in both the periphery and the CNS whereas entacapone only inhibits COMT in the periphery. When levodopa and carbidopa are given simultaneously the inhibition of peripheral dopa decarboxylase leads to an increased breakdown of levodopa to 3-ο-methyl dopa which competes for transporters with levodopa to cross the BBB. By inhibiting COMT there is a reduction in the metabolism of levodopa which keeps levodopa levels higher (and allows lower doses to be given) as well as allowing more levodopa to enter the CNS.

The COMT inhibitors end in what? Both inhibit COMT which breaks down dopamine. How are they different? How do these drugs help treat patients with Parkinson's disease?

-giline (Selegiline and rasagiline) They irreversibly inhibit MAO-B (a selective metabolizer of dopamine) which leased to a decreased dopamine breakdown and enhances the effects of levodopa. They are metabolized to methamphetamine and amphetamine which may cause insomnia if taken too late in the day

The MAO inhibitors used for Parkinsons disease all end in what? What is their mechanism of action? What is a particularly interesting adverse effect of these drugs?

1. For pain you should initially try a non-opioid drug with or without an adjuvant. 2. If the pain persists or increases an opioid of dmild to moderate pain should be tried with or without a non-opioid analgesic drug and adjuvant 3. If pain persists or increases an opioid for moderate to severe pain should be tried with or without a non-opioid analgesic drug and adjuvant. 1. Step 1 2. Step 2 3. Step 3

The WHO developed a 3-step model to guide the management of pain. Describe the steps. What step should the following severity of pain be started at? 1. Mild pain (1-3/10) 2. Moderate pain (4-6/10) 3. Severe pain (7-10/10)

1. To control pain 2. To achieve normal concentrations of plasma urate

The aims of therapy for gout are different for each strategy. What is the aim of therapy for the following strategies? 1. Management of the acute attacks of gouty arthritis 2. Management of chronic gout

-utamide Used to treat prostate cancer by inhibition testosterones prostatic hyper plastic activity.

The androgen receptor antagonists end in what? What is their function?

COX-2 COX-1 Selective COX-2 inhibitors Misoprostol, proton pump inhibitors, and H2 receptor blockers.

The anti-inflammatory action of the NSAIDs is mainly related to their inhibition of which COX isoform? Gastric damage is due to inhibition of which COX isoform? To avoid gastric damage what kind of drugs can be used? What drugs can be co-administered with non-selective COX inhibitors to reduce the risk of gastric ulcers?

-previr They bind reversibly to non-structural protein 3 (NS3) serene protease and inhibit replication of its target virus Used in the treatment of HCV in adults who have been previously untreated or failed treatment with interferon α and ribavirin (can also be administered in combination with interferon α and ribavirin).

The antiviral (not antiretroviral) protease inhibitors all end in what? What is the mechanism of action of these drugs? What are they used to treat?

-mantadine They block a viral membrane protein which is required for fusion of the viral cell membrane to the endosome which is required for uncoating of the virus. Type A only Can be equally effective when used for both treatment and prophylaxis but since 2006 it has not been recommended as first-line treatments due to resistance development.

The antiviral ion channel blocker drugs end in what? What is their mechanism of action? Are they effective against influenza type A, type B, or RSV? When should they be administered to have an optimal effect?

When an anesthetic has a low solubility in blood and it diffuses from the lung into the arterial blood the arterial tension of the anesthetic quickly rises. There is an inverse relationship between the blood solubility of an anesthetic agent and the onset. So an agent with a high blood:gas partition coefficient has a slow onset. High potency correlates with slow onset Anesthetics with large oil:gas have a low blood:gas partition coefficient Fastest onset: Nitrous oxide Slowest onset: Methoxyflurane

The blood:gas partition coefficient is a good index of an inhaled anesthetics solubility in the blood. How does this relate to the time required for the onset of a particular agent? How does the potency and onset of the inhaled anesthetic compare? How does the oil:gas and blood:gas partition coefficient of an inhaled anesthetic compare? Which inhaled anesthetic has the fastest onset and which has the slowest onset (nitrous oxide, desflurane, sevoflurane, methoxyflurane, halothane, enflurane, isoflurane)?

A decrease in inhibitory synaptic activity or an increase in excitatory activity could lead to the triggering of a seizure. Inhibitory: GABA Excitatory: Glutamate GABA antagonists and glutamate agonists can trigger seizures and GABA agonists and glutamate antagonists are likely to inhibit seizure activity.

The brain has excitatory and inhibitory activity on different areas at different times. What about this is likely to cause a seizure? What are the main inhibitory and excitatory neurotransmitters in the brain? So which sort of drugs are likely to trigger seizures and which are likely to inhibit seizures?

-otecan (Topotecan and Irinotecan) They inhibit topoisomerase I which inhibits replication of cancer cells. Gilbert's syndrome because the metabolism of this drug requires UDP-glucuronidase which has decreased function in this condition.

The camptothecins end in what? What is their mechanism of action? Irinotocans used in patients with what condition should be used with caution? Why?

IV

The entry and fusion inhibitors, maraviroc and enfuvirtide respectively, are both administered in what manner?

-floxacin (except for nalidixic acid) Noone Can Learn Multiple Generations 1st Generation: Nalidixic acid 2nd Genration: Ciprofloxacin 3rd Generation: Levoflaxacin 4th Generation: Moxifloxacin and Gemifloxacin Lower generations have excellent gram-negative activity and higher generations have gram-negative activity and improved gram-positive and atypical organism activity.

The fluoroquinolones all end in what suffix? They come in four generations. How can you remember the generations? How does the spectrum of activity change with each generation?

1. Neutralize gastric acid 2. Reduce gastric acid secretion 3. Reduce gastric acid secretion 4. Augment mucosal surface defense 5. Eradicate H. pylori infection They chelate tetracycline which reduces its ability to be absorbed from the GI tract.

The following are therapeutic choices for dealing with GI disorders. How do they work? 1. Antacids 2. H₂ receptor blockers 3. Proton pump inhibitors 4. Mucosal protective agents 5. Antimicrobials The antacids either contain magnesium, aluminum, or calcium. What affect do they have on tetracycline absorption?

1. Ethanol leads to an imbalance in the NADH/NAD+ ratio which leads to inhibition of gluconeogenesis 2. They block the effects of catecholamines on gluconeogenesis and glycogenolysis. 3. They enhance pancreatic beta cell sensitivity to glucose and increase insulin secretion. They can mask the sympathetically mediated symptoms of hypoglycemia such as tremor and palpatations

The following drugs can cause hypoglycemia. How does this occur? 1. Ethanol 2. Beta blockers 3. Salicylates What is an additional danger of beta blockers in diabetic patients?

Serotonin

Serotonin Agonist AKA 5-hydroxytryptamine,5-HT. Widely distributed in nature, formed from L-tryptophan, and is stored or rapidly inactivated, usually by oxidation by MAO. Over 90% in body is found in enterochromaffin cells in GIT. Also found in platelets, in the pineal gland as a precursor of melatonin, and in the raphe nuclei. Actions - increases GI motility(5-HT2), increased ACh release in GIT(5-HT4), constricts large arteries and veins(5-HT2), platelet aggregation(5-HT2A), stimulate vomiting reflex(5-HT3), stimulate pain and itch(5-HT3) No clinical applications.

Cisapride

Serotonin Agonist Activates 5-HT4 receptors. It was one of the most commonly used prokinetic agents, particularly for GERD and gastroparesis, but was found to cause serious cardiac adverse effects. It extends the action potential and the QT interval, and is no longer generally available in the US. It is only available on a limited basis.

Metoclopramide

Serotonin Agonist Prokinetic agent, meaning administration results in coordinated contractions that enhance transit. Actions - facilitates ACh release from enteric neurons, and has both central and peripheral antidopaminergic actions. Used to increase GIT motility. Adverse - somnolence, nervousness, and dystonic reactions. Extrapyramidal effects and tardive dyskinesia, although rare, may occur. Also, infrequently, galactorrhea

Sumatriptan

Serotonin Agonist Selective for the 5-HT1B and 5-HT1D receptors subtypes. Reduces both sensory activation in the periphery and nociceptive transmission in the brainstem trigeminal nucleus. Also cause vasoconstriction. Used almost exclusively in migraine headaches(Substance P and neurokinin A may also be involved). Currently first-line therapy for acute severe migraine attacks. Adverse - Should not be used in patients at risk for CHD Note: Although effective in ameliorating acute symptoms of migraines, other drugs are used for migraine prophylaxis, such as beta-blockers, amitriptyline, valproic acid, topiramate, and calcium channel blockers.

Cyproheptadine

Serotonin Antagonist 5-HT2 Receptor Antagonist Resembles phenothiazine antihistaminic agents in chemical structure and has potent H1 blocking actions. Prevents smooth muscle effects of both serotonin and histamine, but has no effect on gastric seecretion stimulated by histamine. Has significant antimuscarinic effects and causes sedation. Used for perennial and seasonal allergic rhinitis, vasomotor rhinitis, allergic conjunctivitis, cold urticaria, and dermatographism. Also, used to treat serotonin syndrome, from a result of overstimulation of 5-HT1A and 5-HT2 receptors. It may be fatal.

Granisetron

Serotonin Antagonist 5-HT3 Receptor Antagonist (Similar action and use to Ondansetron) Used as anti-emetic drug, particularly for controlling the severe nausea and vomiting that occurs with many forms of cancer chemotherapy.

Ondansetron

Serotonin Antagonist 5-HT3 Receptor Antagonist Used as anti-emetic drug, particularly for controlling the severe nausea and vomiting that occurs with many forms of cancer chemotherapy.

Ergonovine

Serotonin Antagonist Ergot Alkaloid Produced by Claviceps purpurea, a fungus that infects grain. Acts on several receptor types. Has a large powerful stimulant effect on uterus, seemingly due to agonist or partial agonist effects at 5-HT2 receptors. Used as a diagnostic agent to provoke coronary artery spasm. Also used to control postpartum hemorrhage if Oxytocin is ineffective. Should be used only for control of late uterine bleeding and should never be given before delivery.

Dihydroergotamine

Serotonin Antagonist Ergot Alkaloid Produced by Claviceps purpurea, a fungus that infects grain. Acts on several receptor types. Has a large powerful stimulant effect on uterus, seemingly due to agonist or partial agonist effects at 5-HT2 receptors. Used for migraine pain, especially when given during the prodrome of an attack.

Ergotamine

Serotonin Antagonist Ergot Alkaloid Produced by Claviceps purpurea, a fungus that infects grain. Acts on several receptor types. Has a large powerful stimulant effect on uterus, seemingly due to agonist or partial agonist effects at 5-HT2 receptors. Used for migraine pain, especially when given during the prodrome of an attack.

Methylergonovine

Serotonin Antagonist Ergot Alkaloid Produced by Claviceps purpurea, a fungus that infects grain. Acts on several receptor types. Has a large powerful stimulant effect on uterus, seemingly due to agonist or partial agonist effects at 5-HT2 receptors. Used to control postpartum hemorrhage if Oxytocin is ineffective. Should be used only for control of late uterine bleeding and should never be given before delivery.

Bromocriptine

Serotonin Antagonist Ergot Alkaloid Produced by Claviceps purpurea, a fungus that infects grain. Acts on several receptor types. Has a large powerful stimulant effect on uterus, seemingly due to agonist or partial agonist effects at 5-HT2 receptors. Used to reduce the high levels of prolactin that result from pituitary tumors and has been associated with regression of the tumor in some cases.

Cabergoline

Serotonin Antagonist Ergot Alkaloid Produced by Claviceps purpurea, a fungus that infects grain. Acts on several receptor types. Has a large powerful stimulant effect on uterus, seemingly due to agonist or partial agonist effects at 5-HT2 receptors. Used to reduce the high levels of prolactin that result from pituitary tumors and has been associated with regression of the tumor in some cases. More potent than Bromocriptine.

OCD and for acute and long-term treatment of PTSD

Sertraline is approved to treat what conditions listed in this lecture?

1. Phosphate binding drug that binds to dietary phosphate and prevents its absorption from the GI tract 2. Used to prevent hyperphosphatemia in patients with chronic renal failure

Sevelamer 1. Mechanism of action 2. Use

Regular insulin This drug needs to be given about 30 minutes before a meal and rapid acting insulin can be given 15 minutes before a meal. It is given via IV during hyperglycemic emergencies.

Short acting insulin is what? How does the administration of this drug differ from the administration of rapid acting insulin? When is this drug used?

1. Selective inhibitor of DPP-IV which leads to a lack of incretin breakdown. 2. Used to improve glycemic control in adults with type 2 DM 3. Pancreatitis

Sitagliptin 1. Mechanism of action 2. Use 3. Adverse effects

1. GH analog 2. Used in patients with a deficiency of GH 3. In patients with known malignancies as it can lead to accelerated growth of the tumor

Somatrem 1. Mechanism of action 2. Use 3. Contraindications

1. Recombinant growth hormone 2. Used in patients with a deficiency of GH 3. In patients with known malignancies as it can lead to accelerated growth of the tumor 1. Can be used to increase lean body mass, weight, and physical endurance 2. Can be used to improve GI function in patients who are receiving specialized nutritional support

Somatropin 1. Mechanism of action 2. Use 3. Contraindications How can this drug be used for patents with the following conditions? 1. HIV+ patients 2. Patients with short bowel syndrome

The release of histamine and ganglionic blockade Tubocurarine, and mivacurium and atracurium to a lesser extent Slight risk of this in patient given succinylcholine They can be pretreated with antihistamines to avoid this problem Tubocurarine

Some benzylisoquinolines can cause hypotension due to what? Which drugs are most prone to cause this problem as a result of histamine release Does succinylcholine have this adverse effect? How can these patients be treated? Which drug is most likely to cause a block of nicotinic receptors of the autonomic ganglia and the adrenal medulla leading to hypotension and tachycardia?

1. Normal subject 2. Type 2 diabetes 3. Type 1 diabetes Elevated blood glucose and ketone bodies. Type 2 Because type 2 diabetics still secrete insulin and it is enough to restrain ketogenesis

The following photo shows the response to infusion with glucose of a normal subject, a patient with type I diabetes, and a patient with type II diabetes. Which line does each represent? What are the hallmarks of untreated diabetes mellitus type 1? Which is more common, type 1 or type 2 diabetes? Although there is hyperglycemia in both type 1 and type 2 diabetes, type 2 diabetes does not present with ketoacidosis. Why?

Halogenated hydrocarbons -flurane (except halothane) They act on ligand gated ion channels and cause positive modulation of GABAa and glycine receptors and inhibition of nicotinic receptors

The inhaled anesthetics, besides nitrous oxide (N₂O) are also referred to as what? They all end in what? What is their mechanism of action?

The receptor is a tyrosine kinase receptor and the alpha subunit is the recognition site for insulin and the beta subunit is spans the cellular membrane. Stimulation of the receptor leads to expression of the Glut-4 receptor on the surface of target cells. Muscle and adipose tissue

The insulin receptor contains both alpha and beta subunits. Describe them and detail what occurs when they are stimulated by insulin binding. Glut-4 receptors are important for what cells?

Aimed at restoring the dopamine in the basal ganglia and antagonizing the excitatory effect of cholinergic neurons. Both of these methods are aimed at restoring the balance between dopamine and ACh acting on the GABAergic neurons in the striatum.

The medicinal therapy for Parkinson's disease are aimed at what two pharmacological goals?

1. Moderate to severe pain 2. Mild to moderate pain 3. Moderate to severe pain 4. Moderate to severe pain 5. Mild to moderate pain 6. Moderate to severe pain Meperidine has a short half life of 3 hours but its metabolite normeperidine has a longer half life of 15-20 hours and can cause tremulousness, dysphoria, myoclonus, and seizures if toxic levels build up. The dosing of meperidine for moderate to severe pain would lead to toxic levels of normeperidine developing and increase the risk of seizures occurring.

Some opioid drugs are used to treat mild to moderate pain and some are used to treat moderate to severe pain. Which are the following drugs used to treat? 1. Morphine 2. Oxycodone 3. Levorphanol 4. Fentanyl 5. Meperidine 6. Hydromorphone Why is meperidine not used to treat moderate to severe pain?

1. Mild to moderate pain 2. Moderate to severe pain 3. Moderate to severe pain 4. Mild to moderate pain 5. Mild to moderate pain 6. Moderate to severe pain

Some opioid drugs are used to treat mild-moderate pain and some are used to treat moderate-severe pain. Which are the following drugs used to treat? 1. Codeine 2. Oxymorphone 3. Sufentanil 4. Tramadol 5. Hydrocodone 6. Methadone

1. Competitive aldosterone receptor antagonist 2. Used to treat primary hyperaldosteronism (Conn's syndrome), hirsutism in women (by acting as an androgen antagonist), and can be used as a potassium sparing diuretic. Mineralocorticoid antagonist

Spironolactone 1. Mechanism of action 2. Use Is this a glucocorticoid or mineralocorticoid antagonist?

1. Nucleoside analog that inhibits β and γ DNA polymerases 2. Used to treat HIV 3. Peripheral neuropathy and lactic acidosis as a result of its high affinity for mitochondrial DNA polymerase)

Stavudine 1. Mechanism of action 2. Use 3. Adverse effects

1. Treated with H1 blockers like hydroxyzine or diphenhydramine because it is the result of histamine release from mast cells. 2. Can be managed by giving a stimulant laxative. 3. Disappears as tolerance develops but can be treated with anti-emetic H1 blockers like hydroxyzine and metoclopramide. 4. Can be managed by administration of methylphenidate or modafinil but it typically disappears over a few days as tolerance develops Because they require substantial fluid intake

The most common adverse effects of opioids are nausea, vomiting, sedation, itching, and constipation. How can the following AE be managed? 1. Urticaria and pruritis 2. Constipation 3. Nausea and vomiting 4. Sedation Why are bulk-forming agents not recommended for treatment of opioid induced constipation?

Hypoglycemia Rapid-acting insulin analogs Long-acting insulin analogs

The most serious and common adverse reaction to an overdose of insulin is what? Is the risk of hypoglycemia less with rapid-acting insulin analogs or regular insulin? Is the risk of hypoglycemia less with NPH insulin or long acting insulin analogs?

Called the Z-drugs because they start with Z (for the most part) They bind only the BZ1 receptors and act to activate the opening of these Cl- channels (unlike benzodiazepines which bind to both BZ1 & BZ2 receptors). Act more as hypnotics Used of the treatment of insomnia in patients with sleep onset issues

The non-benzodiazepine benzodiazepine receptor agonists are called what drugs? What is their mechanism of action? Do these drugs act as sedatives or hypnotics? In general, what are they used to treat?

Amoxicillin The prostate, eye, and CSF (except in patients with meningitis as the condition make the BBB leaky. Nafcillin Oxacillin and dicloxacillin

The oral absorption of the penicillins is impaired by food except for which drug? Which area is penicillin not well distributed into? Most penicillins are excreted primarily via the kidney. Which is excreted primarily in the bile? Which undergo both renal and biliary excretion?

1. Inhibits the reuptake of GABA from presynaptic neurons 2. Used to treat seizures

Tiagabine 1. Mechanism of action 2. Use

1. β-lactam inhibitor of cell wall synthesis (penicillin) 2. Used to treat P. aeruginosas infections and other susceptible gram-negative infections.

Ticarcillin 1. Mechanism of action 2. Use

1. Broad spectrum antibiotic with a similar MOA as the tetracycline drugs 2. Used to treat complicated skin, soft tissue, and intra-abdominal infections (especially when there is a potential for mixed infections) Primarily in the bile/feces It is effective against multi-drug resistant gram-positive, some gram-negative, and anaerobic organisms but there is an increased risk of mortality seen with this drug compared to other antibiotics with the same activity.

Tigecycline 1. Mechanism of action 2. Use Where is this drug excreted from? This drug is only used to treat serious infections. Why?

1. Similar action as metronidazole 2. A better tolerated drug than metronidizole with a short treatment course and same adverse effects

Tinidazole 1. Mechanism of action 2. Use

1. Protease inhibitor - They are reversible inhibitors of HIV aspartyl protease which is responsible for cleavage of the viral polyprotein into reverse transcriptase, protease, and integrase. This prevents virus maturation and results in production of non-infections visions. 2. Used to inhibit HIV proteases that are resistant to other protease inhibitor drugs Yes, and it is given twice daily, not once.

Tipranavir 1. Mechanism of action 2. Use Is this drug given with ritonavir?

1. α2-adrendoceptor agonist in the CNS 2. Used to treat patients with chronic spasms

Tizanidine 1. Mechanism of action 2. Use

1. Aminoglycoside drug that irreversibly binds to the 30S ribosomal subunit prior to ribosome formation 2. Commonly used as an initial treatment of an unknown infection for a short period of time and is discontinued after the offending organism is identified

Tobramycin 1. Mechanism of action 2. Use

1. First generation sulfonylurea drug 2. Used to treat type II diabetes and is effective at reducing fasting plasma glucose and HbA1c levels

Tolbutamide 1. Mechanism of action 2. Use

1. COMT inhibitor which decreases levodopa metabolism, reduces 3-ο-methyl dopa plasma levels which increases levodopa uptake into the CNS, and leads to higher dopamine levels in the brain 2. Used as an adjunct to levodopa/carbidopa therapy in patients with Parkinson's disease

Tolcapone 1. Mechanism of action 2. Use

1. Non-selecive reversible COX inhibitor 2. Antipyretic, analgesic, and anti-inflammatory.

Tolmetin 1. Mechanism of action 2. Use

Liposolubility The oil:gas partition coefficient Blood solubility Redistribution of the drug out of the brain (not as a result of metabolism) Increase brain perfusion, cause bronchodilation, and decrease minute ventilation.

The potency of the inhaled anesthetic agents increases as what increases? How is this measured? The rate of onset inversely correlates with what factor? What cause recovery from these agents? What affect do these agents have on the brain and respiratory system?

ABVD Adriamycin (Doxorubicin), Bleomycin, Vincristine, and Dacarbazine A: In the G₀ phase B: Acts in G₂ phase V: Acts in M phase D: Cycle cycle non-specific including G₀ phase

The principle treatment for Hodgkin's lymphoma is what? In which part of the cell cycle does each of these drugs act?

-ifene/iphene (tamoxifen is the exception which doesn't end with an e). Used to treat breast cancer Clomiphene is used to treat infertility. Hot flashes and risk of endometrial cancer Tamoxifen is an antagonist of breast tissues estrogen receptors but an agonist on the endometrium which can cause an increased risk of endometrial cancer. Raloxifene is an antagonists at both the breast and endometrium so it does not have an increased risk of endometrial cancer.

The selective estrogen receptor modulators end in what? Most are used to treat what condition? What is the exception? What are the possible adverse effects? What is the difference between tamoxifen and raloxifene?

-pristin (Dalfopristin/Quinupristin) They are given together through as a combination drug therapy. They bind to separate sites on the 50S ribosome to inhibit bacterial protein synthesis. Because they work in combination, resistance is uncommon. Infections with gram-positive cocci and infections with multi-drug resistant bacteria (because of its low incidence of resistance). As a result their use is restricted to the treatment of infections caused by drug-resistant Staph. or VRE. They inhibit them

The streptogramin drugs end in what? How are these drugs administered? What is their mechanism of action? What are they used to treat? How do these drugs affect CYP450 enzymes?

-taxel (Paclitaxel and docetaxel) They stabilize microtubules in a polymerized state which keeps them from being able to break down the mitotic spindle during mitosis. M phase Ovarian and breast cancer

The taxane drugs all end in what? What is their mechanism of action? What part of the cell cycle do they act on? what are these drugs used for?

It is a broad spectrum antibiotic which is active against aerobic and anaerobic gram-positive and gram-negative bacteria. They reversibly bind to the 30S subunit of the bacteria ribosome which prevents the binding of aminoacyl tRNA. They enter via passive diffusion and energy-dependent transport (which can account for one method of bacterial resistance occurring) Used for severe acne and rosacea.

The tetracycline drugs are useful for what sort of bacteria? What is the mechanism of action of these drugs? How do these drugs enter a bacterial cell? What is the most common use of this drug?

-glitazone They are agonists of the peroxisome proliferator-activated receptor-γ (PPAR-γ) which causes decreased insulin resistance in muscles, fat, and liver cells and promotes the uptake of glucose. Can take weeks to months

The thiazolidinediones end in what? What is their mechanism of action? The mechanism of action of these drugs involves gene regulation. As a result, how long do these drugs take to have an effect?

Vincristine: Peripheal neuropathy (NOTE: IT DOES NOT CAUSE MYELOSUPPRESSION) Vinblastine: Myelosuppression Vinorelbine: Granulocytopenia Because it does not cause myelosuppression it can be given to immunocompromised patients. It is part of the ABVD regimen for the treatment of Hodgkins lymphoma.

The vinca alkaloids (vincristine, vinblastine, and vinorelbine) have a variety of important to remember sid effects. What are they? Why is vincristine a very important drug in the vinca alkaloid class? What is vincristine used for?

Erythrocyte only: P. falciparum & P. malariae Erythrocyte and hepatic: P. vivax & P. ovale P. falciparum

There are 4 strains of malaria. Which ones only require erythrocytic parasite elimination and which ones require both erythrocytic and hepatic parasite elimination as the result of a dormant hepatic stage? Which is the most severe and the only likely to cause fatal disease if untreated?

1. Inflammatory pain 2. Neuropathic pain 3. Nociceptive pain 4.Functional pain Usually nociceptive but can also be neuropathic Can be nociceptive, inflammatory, neuropathic, or functional pain.

There are 4 types of pain, Nociceptive, inflammatory, neuropathic, and functional. Which is described? 1. When tissue damage occurs despite nociceptive defense systems 2. The result of damage to or dysfunction of the peripheral or central nervous system rather than stimulation of pain receptors 3. Pain in response to a noxious stimulus (can be either somatic or visceral) 4. Abnormal processing or function of the central nervous system in response to normal stimuli What type of pain is acute pain? What type of pain is chronic pain?

1. NNRTI & 2 NRTIs 2. A protease inhibitor (boosted with rionavir) & 2 NRTIs 3. INSTI (raltegravir) & 2 NRTIs Tenofovir and emtricitabine Ensure that the two agents given are not of the same nucleotide analog.

There are three current recommendations for HIV treatment in treatment-naive patients. What are they? Which two NRTIs are used in each of the 3 possible treatments in treatment-naïve patients? When selecting nucleotide analogs, what should you avoid?

They act on gram-positive And gram-negative bacteria. The A helps you remember that both of these begin with A: Ampicillin and Amoxicillin. Yes By co-adminstering them with a β-lactamase inhibitor UTIs

There are two extended-spectrum penicillins. What are they and how can you remember them? Are these drugs susceptible to β-lactamase? As a result, how can we enhance the activity of these drugs? Because these drugs act on both gram-positive and gram-negative bacteria, what is an important, and common, condition these will treat better than other penicillin drugs?

COX-1 is a constitutive enzyme involved in tissue homeostasis. COX-2 is the dominant isoform in gastric epithelial cells and a major source of cytoprotective prostaglandin formation as well as the major source of prostanoids that are released during inflammation and cancer. Growth factors, tumor promoters, and cytokines.

There are two types of COX, COX-1 and COX-2. What is the difference? What induces COX-2?

1. Benzylisoquinoline 2. Ammonio steroids 3. Ammonio steroids 4. Benzylisoquinoline 5. Benzylisoquinoline 6. Ammonio steroids 7. Benzylisoquinoline Benzylisoquinolines end in -curium and the ammonio steroids end in -curonium Succinylcholine

There are two types of non-depolarizing blockers, benzylisoquinolines and ammonio steroids. Which are the following? 1. Tubocurarine 2. Pancuronium 3. Rocuronium 4. Atracurium 5. Cisatracurium 6. Vecuronium 7. Mivacurium How can you remember the difference? What is the name of the only depolarizing blocker?

1. Reduce intraglandular iodide concentration by blocking transportation into the follicular cell 2. Used to treat hyperthyroidism 3. Aplasic anemia.

Thiocyanate 1. Mechanism of action 2. Use 3. Adverse effects

1. Ultra-short acting barbiturate 2. Used for induction of anesthesia and for short surgical procedures Decreases ICP Does not produce analgesia and may even cause hyperalgesia

Thiopental 1. Mechanism of action 2. Use How does this drug affect intracranial pressure? What analgesic affect does this drug have?

Children: Cretinism - mental retardation and short stature with a protruding umbilicus, pot belly, pale and puffy face and protruded tongue. Adults: Myxedema Drugs that induce cytochrome enzymes like rifampin, phenobarbital, and phenytoin

Thyroid hormone preps are called levothyroxine (T4) and liothyronine (T3). What conditions do these treat in children and adults? Describe the presentation of the childhood condition. What can cause increased metabolism of thyroid hormones?

1. Block voltage gated sodium channels which leads to a decrease in the transmission of excitatory glutamatergic neuronal signaling, enhances GABAergic neurotransmission on the postsynaptic neuron, and blocks postsynaptic glutamate receptors 2. Used in the treatment generalized tonic-clonic seizures, secondarily in the treatment of simple and complex partial seizures, secondarily generalized tonic-clonic seizures, and absence seizures

Topiramate 1. Mechanism of action 2. Use

1. Estrogen receptor antagonist on selective receptors like breast tissue 2. Used in the treatment of metastatic breast cancer

Toremifene 1. Mechanism of action 2. Use

1. Weak µ receptor agonist and norepinephrine and serotonin reuptake inhibitor 2. Useful in treating neuropathic pain MAO inhibitors as a result of the risk of developing serotonin syndrome.

Tramadol 1. Mechanism of action 2. Use This drug should not be co-administered with what other drugs?

1. Inhibits epidermal growth factor receptor 2. Used to treat breast cancer in patients with a HER2 positive breast cancer 3. Cardiotoxicity including CHF Herceptin (HEARTceptin to remember it has cardiotoxicity)

Trastuzumab 1. Mechanism of action 2. Use 3. Adverse effects What is another rename for this drug?

1. The 5HT-2 antagonists/reuptake inhibitors (SARI) as well as blocking α-adrenergic and H1 receptors 2. Used as a hypnotic because of their excellent sedating and hypnotic effects

Trazodone 1. Mechanism of action 2. Use

1. Nucleoside/nucleotide analog who triphosphate form is inserted into viral DNA causing fragmentation 2. Drug of choice for HSV keratoconjunctivitis and recurrent epithelial keratitis 3. Because it is administered in the eye it can cause transient irritation of the eye and palpebral edema

Trifluridine 1. Mechanism of action 2. Use 3. Adverse effects

1. Have a similar structure to folic acid 2. Can be used to treat UTIs, bacterial prostatitis and bacterial vaginitis (but is not a DOC of any of these conditions) Because it reaches high concentrations in prostatic and vaginal fluids. Gram-positive and gram-negative organisms Can not be given to pregnant women as it reduces the utilization of folic acid and can lead to fetal complications.

Trimethroprim 1. Mechanism of action 2. Use Why is this drug useful in treating bacterial prostatitis and bacterial vaginitis? This drug is bacteriostatic against which types of bacteria? What is a contraindication of this drug and why?

Projects from the hypothalamus to the anterior pituitary Inhibits the release of prolactin Blocking this pathway leads to a rise in prolactin which can cause amenorrhea, galactorrhea, and infertility.

Tuberoinfundibular pathway Where does this pathway travel in the brain? This pathway is believed to play an important role in what? Blocking of D2 receptors in this pathway could result in what?

1. Purified human FSH extract (purified from urine) 2. Used to treat male and female infertility 3. Ovarian hyperstimulation syndrome, multiple pregnancies, and precocious puberty 4. Gynecomastia

Urofollitropin 1. Mechanism of action 2. Use 3. Adverse effects in women 4. Adverse effects in men

It is a diet where patients eat four parts aft to one part protein and carbs. The high fat, low carb diet produces ketosis which appears to have a direct anti seizure effect but the exact mechanism is unknown. A lead is hooked up to the vagus nerve with an implanted pacemaker device and the patient can activate the device when they sense a seizure is imminent. Resection of an the abnormal part of the brain from which a localized seizure occurs can markedly improve symptoms but can be associated with decline in function as a result of resection of any part of the brain.

What is the ketogenic diet and how can it be used by patients who suffer from seizures? Vagus nerve stimulation is also used for this condition. How does it work? What is another controversial, but effective way, of treating seizures without drugs?

Diloxanide furoate

What is the luminal agent of choice for amebiasis?

Carbon monoxide poisoning. It is a byproduct of incomplete combustion High flow oxygen treatment in a hyperbaric chamber.

What is the main cause of death due to poisoning in the US? How is it formed? What is the treatment of carbon monoxide poisoning?

They are safe in all patients (including pregnant women), have little toxicity, and are widely effective. They inhibit the last step in peptidoglycan synthesis through binding to PBPs (penicillin-binding proteins) which inhibits cell wall synthesis. They also activate autolysins to initiate cell death. Both of these activities lead to bacterial lysis and death. Because they do not contain a cell wall.

What is the major advantage of the penicillin group of antibiotics? How do they act? Why are the penicillin drugs not effective against mycoplasma, protozoa, fungi, or viruses?

Penicilloic acid can act as an antigen leading to this condition. We can treat with a different β-lactam in the hopes that there would be no cross-reaction. Treat with another drug if there is a history of a severe allergic reaction.

What is the major antigenic determinant of hypersensitivity reactions involving penicillin drugs? If a patient reports a minor penicillin allergy and their condition indicates use of penicillin what can we do? What about a severe allergy?

It is converted to deoxyribonucleotide which inhibits thymidylate synthase which leads to inhibition of DNA synthesis due to a thymidine deficiency as well as being incorporated into RNA in place of uracil and inhibiting protein synthesis. Leucovorin Myelosuppression and hand-foot syndrome in which skin exfoliation occurs on the palms and feet.

What is the mechanism of action of 5-flurouracil (5-FU)? What drug can be added to increase the cytotoxic effect of this drug? What are adverse effects of this drug that you should be aware of?

It is an alkylating agent that causes cross-linking of DNA. Pulmonary fibrosis which limits the use of this drug now.

What is the mechanism of action of Busulfan? What is the major side effect of this drug?

Alkylating agent that causing cross-linking of DNA. It is used as part of the ABVD treatment for Hodgkins lymphoma.

What is the mechanism of action of Dacarbazine? What is an important use of this drug?

Causes depletion of serum asparagine to aspartic acid and ammonia which reduces blood glutamine levels and lead to inhibition of protein synthesis. Because neoplastic cells require an external source of asparagine it leads to cancer cell death. ALL Pancreatitis

What is the mechanism of action of L-Asparaginase? What is it used to treat? What is an adverse effect to be aware of with the use of this drug? What other drug has this adverse side effect?

MDMA leads to a strong increase in the concentration of serotonin in the synaptic cleft which leads to feelings of empathy and intimacy without impairing intellectual capacity.

What is the mechanism of action of MDMA (ecstasy)?

It is a dissociative anesthetic that blocks the reuptake of norepinephrine and dopamine, causes cholinergic and anticholinergic effects, and has actions at nicotinic and opioid receptors. The non-competitive antagonism of the NMDA receptors (anti-glutaminergic action) They appear to be having a psychotic episode With benzodiazepines

What is the mechanism of action of PCP? The dissociative properties of PCP are believed to be due to what actions of this drug? What is the typical presentation of a patient with PCP intoxication? Some severe complications of PCP include extremely violent and psychotic behavior and seizures. How should these conditions be treated?

They are both selective estrogen receptor modulators but they exhibit different effects on different tissues. Tamoxifen: Acts as an antagonist on breast tissue but an agonist on endometrial and bone tissue. Raloxifene, on the other hand, is antagonistic at the breast and endometrium but an agonist on the bone. Tamoxifen has an increased risk of endometrial cancer when it is used for along period of time as a result of its agonistic activity on the endometrial tissue whereas Raloxifene does not have this increased risk. Primary therapy for metastatic breast cancer in both men and postmenopausal women.

What is the mechanism of action of Tamoxifen and Raloxifene in treating cancer? As a result, what is the risk difference between these drugs? What ar these drugs used for?

They increases the release of catecholamines, act as weak MAO inhibitors, and are also possible direct catecholaminergic agonists in the brain. Dopamine They cause increased activity through elevated NE release. Can be used to treat attention deficit disorder and narcolepsy

What is the mechanism of action of amphetamine drugs? The behavioral effects are due to the release of what neurotransmitter? What affect do these drugs have on the SNS? What are some therapeutic uses of amphetamine and methylphenidate?

It is a prodrug of 5-FU which has the same mechanism of action. It inhibits thymidylate synthase which leads to inhibition of DNA synthesis due to a thymidine deficiency as well as being incorporated into RNA in place of uracil and inhibiting protein synthesis. Capecitabine is converted to 5-FU inside the tumor cells so it is less toxic than 5-FU. Similar to 5-FU including myelosuppression and hand-foot syndrome.

What is the mechanism of action of capecitabine? What is the the difference between this drug and 5-FU? What are the adverse effects of this drug?

Inhibits the reuptake of dopamine, norepinephrine, and serotonin. The limbic system Peripherally, cocaine potentiates the action of norepinephrine which results in adrenergic stimulation leading to tachycardia, HTN, mydriasis, and diaphoresis.

What is the mechanism of action of cocaine? What brain system acted on by this drug produces the intense euphoria that cocaine initially causes? What are the peripheral actions of this drug?

It is a competitive inhibitor of DNA polymerase. Pyrimidine analog which can cause myelosuppression

What is the mechanism of action of cytarabine (ara-C)? What sort of drug is this and what adverse effect does it have?

It binds to DNA non-covalently which intercalates it. dACTinomycin: Kids ACT out. The drug is used for childhood tumors like Wilm's tumors, Ewing Sarcomas, Rhabdomyosarcomas, etc.

What is the mechanism of action of dactinomycin? What types of tumors is this used for and how can you remember?

Glucose enters the beta cell via a Glut-2 transporter and glycolysis leads to the production of ATP. Increased ATP levels leads to the closure of K+ channels which causes depolarization of the cell membrane which causes calcium channels to open. As a result of the calcium channels opening, calcium moves into the cell and stimulates the exocytosis of insulin and C-peptide containing vesicles.

What is the mechanism of action of insulin release?

It stimulates NK cells and increases the expression of HLA molecules on tumor cells which make them more susceptible to destruction by the hosts immune system. Flu-like symptoms like fever, myalgia, headache, etc.

What is the mechanism of action of interferon? What sort of adverse effects can administration of interferon cause?

It is a folic acid analog that inhibits dihydrofolate reductase. Choriocarcinoma, ALL, Burkitt's lymphoma, Osteosarcoma, and breast cancer. Rheumatoid arthritis Administration of leucovorin can help by providing a source of reduced folate which can overcome the blockade that is caused by methotrexate.

What is the mechanism of action of methotrexate? What cancers is this drug used to treat? When given at low doses for long periods of time, what is this drug used to treat commonly? If this drug is given in too high of a dose or in high-dose protocols it can lead to severe bone marrow suppression and immune suppression. How can this be prevented?

It is a full agonist of the nicotine receptor leading to ganglionic stimulation by depolarization at low doses and possible ganglionic blockade at high doses. The ventral tegmental area Dopamine

What is the mechanism of action of nicotine? The rewarding effect of nicotine requires the involvement of what area of the brain? When nicotine excites these neurons, what neurotransmitter is released?

Activates nicotinic receptors and depolarizes the neuromuscular junction. Initially this causes fasciculations but, because succinylcholine is not effectively metabolized by acetylcholinesterase the neuronal membrane remains depolarized leaving it unresponsive to additional impulses causing flaccid paralysis. Because it is rapidly hydrolyzed by plasma pseudocholinesterases its neuromuscular duration is about 5-10 minutes

What is the mechanism of action of succinylcholine? What is the duration of action of this drug and why?

It creates free radicals and reactive oxygen species which lead to DNA damage and breaks. It is the only drug that acts on G₂ phase. It is used as part of the ABVD regimen for treating Hodgkin's lymphoma and as part of the BEP regimen used for the treatment of testicular cancer. Pulmonary fibrosis It is bone marrow sparing so it can be administered to HIV patients or immunocompromised patients to treat kaposi sarcoma.

What is the mechanism of action of the Bleomycin? What part of the cell cycle does it act on? What is the clinical use of this drug? What adverse effect should you remember for this drug? What is an important bonus of using this drug and why is this important in treatment of certain patients?

They block voltage gated calcium channels which leads to a reduction of the release of calcium from neurons and a decrease release of glutamate, norepinephrine, and substance P. Dizziness, somnolence, and peripheral edema.

What is the mechanism of action of the anticonvulsants gabapentin and pregabalin? What are some adverse effects?

They are β-lactam inhibitors of cell wall synthesis

What is the mechanism of action of the cephalosporins?

They inhibit bacterial DNA replication by interfering with topoisomerase II (DNA gyrase) and topoisomerase IV. Broad spectrum, bactericidal drugs.

What is the mechanism of action of the fluoroquinolone drugs? Are these drugs narrow or broad spectrum? Bacteriostatic or bactericidal?

They bind to, and block, voltage gated sodium channels on the intracellular end of the neuron thereby abolishing action potentials. The smaller and more lipophilic the drug the faster the onset. The more lipophilic, the more potent.

What is the mechanism of action of the local anesthetics? How does size and lipophilicity of the anesthetic affect its onset? Potency?

They are alkylating agents cause alkylation at N7 position of guanine in DNA which leads to intrastrand linking and cross-linking of guanines. No Cyclophosphamide -phamide/-famide (Cylcophophosphamide and ifosfamide)

What is the mechanism of action of the nitrogen mustards? Are they cell cycle specific? What is the most commonly used agent? What do the important drugs in this class end in?

Alkylating agent that alkylates nucleic acids and proteins causing cross-linking of DNA. -mustine (Carmustine, Lomustine, and Semustine) Because they are highly lipophilic they cross the BBB so they are used to treat primary brain cancers and cancer metastasis to the brain.

What is the mechanism of action of the nitrosoureas? What suffix do they end in? What is the importance of these drugs?

They are non-competitive inhibitors of HIV-1 reverse transcriptase and cause inhibition of RNA and DNA dependent DNA polymerase. No Because the binding site is away from the active site a mutation in this site could result in resistance developing without the reverse transcriptase activity being affected Yes, because they all bind within the same pocket (but no cross-resistance with NRTIs)

What is the mechanism of action of the non-nucleoside reverse transcriptase inhibitors? Do these drugs require phosphorylation by cellular enzymes? Why is resistance a problem with these drugs? Is there cross resistance with these drugs?

The bind to the mineralocorticoid receptor and form a complex which enters the nucleus and alters gene transcription. It leads to an increased expression of Na+/K+ ATPase and increased expression of ENaC They promote Na+ reabsorption from the renal tubules and promote K+ and H+ excretion.

What is the mechanism of action of the synthetic mineralocorticoids? What is the effect of activating the aldosterone receptor? What are the major effects of mineralocorticoids?

Based on information about other effects of some commonly used drugs it was determined that depression may be due to lowered monoamine neurotransmitters at brain synapses. As a result, the treatment of depression may be achieved by restoring the monamine levels or action to normal levels. Norepinephrine and serotonin

What is the monoamine hypothesis? Which neurotransmitters fall under the category of monoamines?

∆⁹-THC CB1 receptors are found in the brain and mediate the psychological effects of THC CB2 receptors are present mainly in the immune system with unknown function

What is the most active ingredient in marijuana? There are two cannabinoid receptors found within the body, CB1 & CB2. What actions do they have?

Hypoglycemia IV glucose bolus can be given and IV octreotide can be given if glucose infusions do not maintain satisfactory glycemia. It is a long-acting somatostatin analog which antagonizes pancreatic insulin release.

What is the most common adverse side effect of sulfonylureas and meglitinides? How can this problem be treated? How does octreotide treat this condition?

21-hydroxylase deficiency The patient should initially be treated with parenteral hydrocortisone (as an acute adrenal crisis) to suppress ACTH release and once stabilized they can be treated with oral glucocorticoids (hydrocortisone or prednisone) and fludrocortisone.

What is the most common defect in adrenal hyperplasia? How should patients with congenital adrenal hyperplasia be treated?

Teriparatide It is expensive

What is the most effects drug in increasing bone mineral density of the lumbar spine? Why is it not more commonly used?

Clindamycin

What is the most likely drug to cause pseudomembranous colitis superinfection with C. difficile?

Propofol For induction and maintenance of anesthesia Produces no analgesia

What is the most popular IV anesthetic? What is this drug used for? What analgesic affect does this drug have?

Propranolol Blocks Na+ channels and, because they are lipophilic drugs, they can enter the CNS and cause seizures and coma. Bradycardia and hypotension Glucagon as it increases cAMP in the cardiac cells through stimulation of glucagon receptors.

What is the most toxic beta blocker? At high doses what does toxicity with beta blockers cause? What is the most common manifestation of toxicity? What is used as an antidote to beta blocker overdose and why?

Caffeine Theophylline and theobromine They block the presynaptic adenosine receptors. Noramlly the activation of adenosine receptors inhibits norepinephrine release, so inhibition of the adenosine receptors leads to increased norepinephrine release.

What is the most widely consumed stimulant? It is considered a methylxanthine. What are the other methylxanthines? What is their mechanism of action?

Ketamine Increases ICP Diazepam, midazolam, and propofol

What is the only IV anesthetic that has both analgesic properties and the ability to produce cardiovascular stimulation? What affect does it have on ICP? This drug can also cause perceptual illusions and vivid dreams. What drugs can be co-administered to avoid these effects?

To treat skin and soft tissue infections due to MRSA, particularly if there is gram-negative co-infection.

What is the only use of the 5th generation cephalosporins?

Dantrolene It blocks the calcium release form the sarcoplasmic reticulum

What is the pharmacological treatment of malignant hyperthermia? What is its mechanism of action?

Chloroquine

What is the preferred chemoprophylactic agent used for malaria in areas without resistant falciparum malaria?

Amphotericin B

What is the preferred treatment for deep fungal infections during pregnancy?

Stones, bones, groans, thrones, and psychiatric overtones. Furosemide with saline infusion, bisphosphonates, calcitonin, and parathyroidectomy if it is a result of a parathyroid imbalance

What is the presentation of a patient with hypercalcemia? What are some possible treatments for patients with hypercalcemia?

It is primarily used for IV anesthetic induction of patients that are at risk of hypotension as they cause minimal cardiovascular and respiratory depression.

What is the primary use of etomidate and why?

β-lactam antibiotics can have their β-lactam ring hydrolyzed by bacterial β-lactamases which makes them inactive. As a result, the bacteria that contain β-lactamase are resistant to β-lactam antibiotics. To combat this we can co-adminiter a β-lactam antibiotic with a β-lactamase inhibitor (like clavulanic acid) which will inhibit the bacterial β-lactamases and make them susceptible to these antibiotics.

What is the problem with β-lactam antibiotics and how can we overcome this problem?

Misoprostol

Uterine Agents Oxtocic PGE1 analogue. Given orrally or vaginally. Used as an effective agent for both cervical ripening and labor induction. Also widely used to treat postpartum hemorrhage. Note: Not FDA-approved for obstetric indications, only currently approved for reducing risk of NSAID-induced gastric ulcers in patients at high risk of complications from gastric ulcers.

Dinoprostone

Uterine Agents Oxtocic PGE2. More effective stimulant of uterine contraction through second trimester of pregnancy than oxytocin. Inhibition of endogenous PG synthesis with NSAID(aspirin or ibuprofen) can increase length of gestation, prolong spontaneous labor, or interrupt premature labor. Given as vaginal insert, vaginal suppository, or cervical gel. Used to induce abortion in second trimester of pregnancy, evacuate uterine contents in management of missed abortion, manage benign hydatidiform mole, ripen cervix for induction of labor in patients at/near term.

Carboprost tromethamine

Uterine Agents Oxtocic PGF2apha. More effective stimulant of uterine contraction through second trimester of pregnancy than oxytocin. Inhibition of endogenous PG synthesis with NSAID(aspirin or ibuprofen) can increase length of gestation, prolong spontaneous labor, or interrupt premature labor. Given IM. Used to induce abortion in second trimester of pregnancy and to control postpartum hemorrhage due to uterine atony which has not responded to oxytocin or ergonovine.

Ergonovine

Uterine Agents Oxtocic Partial agonist at alpha and some serotonin receptors. Sensitivity of uterus to ergot alkaloids increases dramatically during pregnancy. Drug of choice for obstetric applications. Actions - Perhaps exerts effects at increasingly dominant alpha1 receptors in early pregnancy. At very small doses, can evoke rhythmic contraction and relaxation. At higher concentrations, induces powerful and prolonged contracture. More selective than other ergot alkaloids. Used to control postpartum hemorrhage. Should only be used for control of late uterine bleeding and should never be given before delivery. Adverse - hypertension, headache, possible seizures, nausea, vomiting, chest pains, difficulties in breathing, leg cramps. Contraindications: angina pectoris, MI, pregnancy, Hx of CVA, TIA, or HTN, and should not be administered longer than necessary, since can be found in breast milk and can lead to ergot poisoning in nursing infant.

Methylergonovine

Uterine Agents Oxtocic Partial agonist at alpha and some serotonin receptors. Sensitivity of uterus to ergot alkaloids increases dramatically during pregnancy. Drug of choice for obstetric applications. Actions - Perhaps exerts effects at increasingly dominant alpha1 receptors in early pregnancy. At very small doses, can evoke rhythmic contraction and relaxation. At higher concentrations, induces powerful and prolonged contracture. More selective than other ergot alkaloids. Used to control postpartum hemorrhage. Should only be used for control of late uterine bleeding and should never be given before delivery. Adverse - hypertension, headache, possible seizures, nausea, vomiting, chest pains, difficulties in breathing, leg cramps. Contraindications: angina pectoris, MI, pregnancy, Hx of CVA, TIA, or HTN, and should not be administered longer than necessary, since can be found in breast milk and can lead to ergot poisoning in nursing infant.

Oxytocin

Uterine Agents Oxtocic Peptide hormone secreted by posterior pituitary. Uterus is particularly sensitive(increased receptor expression) during the second half of pregnancy. May be giv en by IV, IM, or as nasal spray. Actions - Binds to Gq receptor, increasing intracellular Ca2+, resulting in myometrial contraction. Also leads to activation of MAPK cascade and of cPLA2, resulting in increased prostaglandin synthesis, further stimulating uterine contractions. Used as drug of choice for labor induction. Effective when there is prolonged cervical dilation to augment dysfunctional labor. Used to help maintain uterine contractions and tone to prevent postpartum hemorrhage. The challenge test measures fetal HR response, and may indicate immediate cesarean delivery. In high doses, can be used to induce abortion. Adverse - Toxicity due either to excessive stimulation or inadvertent activation of vasopressin receptors, fetal distress, placental abruption, uterine rupture, excessive fluid retention, water intoxication(leading to hyponatremia, heart failure, seizures, and death), hypotension. Contraindications: fetal distress, prematurity, abnormal fetal presentation, cephalopelvic disproportion, and other predispositions for uterine rupture.

Nifedipine

Uterine Agents Tocolytic Calcium Channel Blocker. No tocolytic is first-line choice. Effective and safe alternative. Associated with more frequent successful prolongation of pregnancy. Actions - Impairs entry of Ca2+ into myometrial cells via voltage-dependent Ca2+ channels, thus inhibiting contractility. Used to manage preterm labor. Adverse - (Maternal) tachycardia, palpitations, flushing, headaches, dizziness, nausea. Continuous fetal heart rate monitoring is recommended. Contraindications: acute fetal distress(except during intrauterine resuscitation), chorioamnionitis, eclampsia, or severe preeclampsia, fetal demise(of singleton pregnancy), fetal maturity, and maternal hemodynamic instability.

Indomethacin

Uterine Agents Tocolytic NSAID. No tocolytic is first-line choice. Has similar efficacy to terbutaline and associated with infrequent maternal side effects. Actions - Inhibits prostaglandin synthesis. Also causes premature closure or constriction of ductus arteriosus(More common after 32 weeks' gestation). Used to delay preterm labor. Adverse - Can readily cross placenta and cause oligohydramnios due to decrease in fetal renal blood flow if used for >48 hours. Do not use after 32 weeks' gestation. Contraindications: acute fetal distress(except during intrauterine resuscitation), chorioamnionitis, eclampsia, or severe preeclampsia, fetal demise(of singleton pregnancy), fetal maturity, and maternal hemodynamic instability.

1. Vasopressin agonist 2. Drug of choice for diabetes insipidus and to treat esophageal variceal and colonic diverticular bleeding V1: Gq GPCR which is found in vascular smooth muscle whose activation causes vascular smooth muscle vasoconstriction V2: Gs GPCR which is found in the renal tubular cells which increases water permeability and water reabsorption

Vasopressin 1. Mechanism of action 2. Use This acts on both the V1 and V2 receptors. What type of receptors are they and what is their mechanism of action

1. Serotonin & norepinephrine reuptake inhibitor (potent 5-HT uptake inhibitor and, at higher doses, it inhibits norepinephrine uptake) 2. May be effective in treating depression in patients whose depression is not well controlled by SSRIs They do not block H1, muscarinic, and α-adrenergic receptors which gives them a lower adverse effect profile

Venlafaxine 1. Mechanism of action 2. Use How does this drug differ from TCAs?

1. SNRI (serotonin and norepinephrine reuptake inhibitor) 2. Used as an adjuvant for pain management 3. Nausea, sexual dysfunction, and somnolence They lack the antihistamine, α-adrenergic antagonist, and anticholinergic effects of TCAs

Venlafaxine 1. Mechanism of action 2. Use 3. Adverse effects Why are these drugs useful over the TCA drugs?

1. Inhibits the degradation of GABA by inhibiting GABA aminotransferase 2. Can be used to treat infantile seizures and possibly other seizure disorders 3. Long-term therapy associated with irreversible visual field defects in 1/3 of patients being treated

Vigabatrin 1. Mechanism of action 2. Use 3. Adverse effects

1. Inhibit 14-α-demethylase, they last enzyme in ergosterol synthesis from lanosterol 2. Drug of choice for invasive aspergillosis and similar spectrum as Itraconazole (Blastomyces, Sporothrix, and Histoplasmosis and used for dermatophytoses and onychomycosis) 3. Significant drug interactions because of cytochrome interactions limits its use Triazole Inhibits CYP2C19, CYP2C9, and CYP3A4

Voriconazole 1. Mechanism of action 2. Use 3. Adverse effects Imidazole or Triazole? Inhibits what CYP P450 enzymes?

None, as they do not cross the BBB

What adverse effects do the non-depolarizing and depolarizing neuromuscular blockers have?

It can decrease the activity of methionine synthetase activity leading to megaloblastic anemia.

What affect can prolonged exposure to nitrous oxide have?

They can block sodium channels in the heart (acting like class I anti-arrhythmics) leading to depressed cardiac pacemaker activity, excitability, and arrhythmias. Bupivacaine

What affect can toxic systemic levels of local anesthetics have on the cardiovascular system? What is the most cardiotoxic local anesthetic?

Depress contractility Decrease MAP SID (Sevoflurane, isoflurane, desflurane). The main cardiovascular effects of these drugs is the production of vasodilation with minimal effect on cardiac output whereas halothane and enflurane cause myocardial depression. Also, halothane sensitizes the myocardium to circulating catecholamines which can lead to arrhythmias.

What affect do most inhaled anesthetics have on cardiac contractility? How does this affect MAP (mean arterial pressure)? Which of the following inhaled anesthetics are the better choices for patients with impaired myocardial function and why (halothane, isoflurane, desflurane, enflurane, sevoflurane)?

The decrease the excretion of calcium by increasing calcium reabsorption Prevention of renal stone formation and can be used to treat osteoporosis in patients with HTN.

What affect do thiazide diuretics have on calcium homeostasis? As a result, what other conditions can they be useful in treating?

1. Causes increased phosphate and calcium reabsorption 2. Increases phosphate and calcium absorption 3. Promotes the actions of PTH on the bone

What affect does activated vitamin D have on phosphate and calcium levels in the: 1. Kidneys 2. Intestines 3. Bone

It acts on α2-adrenoceptors which inhibits the release of substance P (a mediator of pain). Can cause delayed wound healing, tissue edema, and necrosis.

What affect does epinephrine, administered along with a local anesthetic, have in spinal anesthesia? What negative affect can a vasoconstrictor have?

It increases Na+/K+ ATPase activity which increases respirations, temperature, and oxygen consumption. It potentiates the effects of catecholamines (especially on the beta effects) which leads to an increased cardiac output and heart rate. It promotes CNS development and is especially important in developing infants and children in order to reach their full IQ potential.

What affect does thyroxine have on BMR (basal metabolic rate)? What affect does it have on sympathetic activity? What affect does it have on the brain?

1. They inhibit the vasomotor center in the brainstem which can lead to hypotension and inhibition of a compensatory baroreceptor reflex 2. Constipation 3. Contract biliary smooth muscle which can lead to biliary colic 4. Decreased renal plasma flow leading to decreased renal function 5. Can prolong labor

What affects to opioids have on the following peripheral systems? 1. Vascular system 2. GI tract 3. Biliary tract 4. Genitourinary tract 5. Uterus

Cefazolin Ampicillin with sulbactam Vancomycin and clindamycin

What antimicrobial is used in the surgical antimicrobial prophylaxis for almost all surgical procedures? It is not used for colorectal surgery. What drug is used for prophylaxis in those surgeries? If a patient has a penicillin allergy what drugs are almost always given either individually or as part of a combination prophylaxis treatment?

They are drugs that are useful in the management of pain but are not primarily classified as analgesics. Antidepressants and anticonvulsants.

What are adjuvant analgesics? Some adjuvants are antidepressants, anticonvulsants, glucocorticoids, and others. Which adjuvants are a mainstay of treatment for several neuropathic pain syndromes?

They are immunoglobulin preparations from a pool of selected human donors or animals that provide passive immunity for patients with acute contact with things like tetanus, rabies, snake bites, and digoxin (digibind). Used to prevent hepatitis B in newborns.

What are hyperimmune globulins and how are they used to treat patients? How are hyperimmune globulins used for infants?

It can reduce the chance of developing resistance, can be used to treat mixed infections, can be used in emergencies, and can have synergistic and, therefore, increased efficacy. Some drugs can inhibit the activity of other drugs making them unable to work properly. Ex. Some agents only act on bacteria that are multiplying. If the patient is co-administered a drug that is bactericidal or bacteriostatic the cells won't multiply and the co-adminsitered drug won't work.

What are some advantages to combination antibiotic therapy? What is a disadvantage and give an example?

It is well tolerated by most patients but some patients can have a hypersensitivity reaction that can cause skin rashes and may lead to Steven-Johnson syndrome. The drugs use should be discontinued

What are some adverse effects of allopurinol? What should be done if a cutaneous reaction to allopurinol occurs?

Cytopenia, serious infections, and recurrence of latent TB infections. They should have CBCs performed regularly and screen for latent TB infection before and during treatment.

What are some adverse effects of the anti-TNFα drugs? How should these patients be monitored as a result?

Connective tissue problems, QT prolongation (with 3rd and 4th generation) and have a high risk of causing pseudomembranous colitis C. difficile infections. Pregnant women, nursing mothers, and children under 18. These drugs can enhance the toxicity of fluoroquinolones. 3rd and 4th generation fluoroquinolones

What are some adverse effects of the fluroquinolone drugs? Which groups should these drugs be avoided in? What is the drug-drug interaction between these drugs and theophylline, NSAIDs, and corticosteroids? Which of these drugs can cause increased serum levels of warfarin, caffeine, and cyclosporines?

Drowsiness and confusion are common as well as ataxia and cognitive impairment. Anxiety, irritability, hostility and rage, paranoia, and depression and suicidal ideation.

What are some common adverse effects associated with benzodiazepine drugs? What sort of psychological adverse effects, although rare, can occur?

Cushings-like appearance with redistribution of body fat, osteoporosis, adrenal insufficiency, peptic ulcers, CNS effects (euphoria, psychosis, and depression), myopaty, and growth retardation in children. Dexamethasone

What are some common adverse effects of glucocorticoids? Which glucocorticoid has the longest acting anti-inflammatory effects?

In low doses it improves attention, learning, problem solving, reaction time, and acts as an appetite suppressant. Irritability and sleeplessness. Bupropion

What are some positives about cigarette smoking? What are the symptoms of nicotine withdrawal? What drug, with an unclear mechanism of action, can be used to treat nicotine addiction?

1. Can be used alone or with estradiol for contraception 2. Can be used in combination with estrogen as HRT (hormone replacement therapy) 3. Decrease the incidence of endometrial hyperplasia and carcinoma 4. Can be used to cause ovarian suppression in the treatment of dysmenorrhea and endometriosis Can be given orally or IM

What are some therapeutic uses of progesterone? How is it administered?

Parathion, malathion, sarin, tabun, and soman. It phosphorylates the acetylcholinesterase enzyme and causes a loss of an alkoxy group in a process called ageing which further strengthens the phosphorus-enzyme bond DUMBELS Diarrhea Urinary frequency Miosis Bradycardia/Bronchoconstriction Emesis Lacrimation Salivation/Sweating Respiratory paralysis Before ageing: Pralidoxime After ageing: Atropine in large doses

What are some widely used cholinesterase inhibitors that can cause toxicity? How do organophosphate insecticides cause inhibition of acetylcholinesterase? What is the mnemonic for organophosphate insecticide poisoning and what do they stand for? What is the most common cause of death in these patients? What are two treatments of intoxication with these drugs, both before and after ageing has occurred?

They both reduce anxiety (sedative actions) and can induce sleep (hypnotic actions), act as anticonvulsants, relax muscles, and can be used to a lesser extent as part of the drug regimen for anesthesia TO ALerT FD Short acting: Triazolam & Oxazepam Intermediate acting: Alprazolam, lorazepam, & Temazepam Long acting: Flurazepam & Diazepam

What are the actions of the benzodiazepine drugs? The benzodiazepine drugs have various durations of action. How can you remember which drugs are short-acting, intermediate-acting, and long-acting (alprazolam, diazepam, lorazepam, oxazepam, triazolam, temazepam, flurazepam)?

They lack effects on the host blood-forming elements and lack cross resistance with NRTIs) They have cross-resistance with one another, are involved in drug interactions, and have a high incidence of hypersensitivity reactions. vir

What are the advantages of the NNRTIs (non-nucleotide reverse transcriptase inhibitors)? What are the disadvantages? All these drugs have what in the the middle of their name?

Crystalluria, hypersensitivity reactions (can lead to Steven Johnson syndrome), hematopoietic disturbances (in patients with a G6PD deficiency as these are sulfa drugs), and kernicterus in newborns and infants <2 months (because they compete with bilirubin for binding sites on albumin). Warfarin, phenytoin, and methotrexate.

What are the adverse effects of sulfonamide drugs? What drugs can lead to increased plasma levels of these drugs?

Tonic-clonic: Grand mal Absence: Petit mal Both are a type of generalized seizure that involves an immediate loss of consciousness. The grand mal seizures involves convulsions which are followed by a postictal state in which they appear catatonic and in a sleep state. Petit mal seizures involve a brief, abrupt LOC in which there are no convulsions but the patient stares and exhibits rapid eye-blinking. 3 Hz spike-and-wave pattern emerges abruptly and ceases after a few seconds.

What are the alternate names for tonic-clonic and absence seizures? How can you compare these two types of seizure activity? What does the EEG pattern show for patients having an absence seizure?

Resting tremor, muscular rigidity, bradykinesia, and gait impairment. Loss of the neurons in the substantia nigra which provide dopaminergic innervation to the striatum. There is a careful balance between excitatory cholinergic and inhibitory dopaminergic inputs on GABAergic output from the striatum and the reduction/loss of the inhibitory dopamine secretion results in loss of the control of muscle movement. At least 70%

What are the cardinal features of parkinson's disease? What change occurs in the brain that leads to the development of this condition? What percent of the substantia nigra neurons are typically destroyed before symptoms first appear?

Parathesias, nausea, vomiting, diarrhea, disturbances in lipid metabolism, and fat redistribution and accumulation causing a cushingoid appearance. Atazanavir

What are the common side effects of the protease inhibitors? Which of the protease inhibitors has less side effects when compared to the other protease inhibitors?

History of malignant HTN, history of skeletal muscle myopathies, major burns, multiple trauma, denervation of skeletal muscle, and upper motor neuron injury.

What are the contraindications for the use of succinylcholine?

Carbamazepine, oxcarbazepine, lamotrigine, or phenytoin. The same drugs Valproate and topiramate

What are the drugs of choice for simple and complex partial seizures? For secondarily generalized tonic-clonic seizures? What are two other drugs that can also be used?

Valproate. carbamazepine, and phenytoin Lamotrigine and topiramate

What are the drugs of choice for the treatment of generalized tonic-clonic seizures? What other drugs are also approved for treatment of this condition?

1. Acts on a Gs receptor which leads to activation of the H+/K+ exchanger 2. Acts on a Gi receptor which leads to inhibition of the H+/K+ exchanger 3. Increases Ca2+ levels which leads to activation of the H+/K+ exchanger 4. Increases Ca2+ levels which leads to activation of the H+/K+ exchanger Proton pump inhibitors -prazole

What are the effects of the following on gastric acid secretion? 1. Histamine 2. Prostaglandin E2 3. Gastrin 4. Acetylcholine What type of drugs are the most effective at inhibiting gastric acid secretion? What do all proton pump inhibitors end in?

Antidepressants Venlafaxine (SNRI) or SSRIs are preferred over TCAs because of improved safety and tolerability. 2-4 weeks

What are the first line agents in the treatment of GAD (generalized anxiety disorder)? Which antidepressants are usually preferred? How long does it typically take for patients with this condition to see the anti-anxiety effects of antidepressants?

1. Antimicrobial drug 2. Antibacterial drug 3. Antibiotic drug

What are the following definitions of? 1. Drugs that inhibits growth of micro-organisms 2. Drugs that inhibits growth of bacteria 3. Drugs that inhibits growth of micro-organisms, made my other microorganisms but can be extended to include synthetic drugs

1. Rarely the drug of choice for any infection 2. Used to treat sinusitis, otitis, and lower respiratory tract infections 3. Highly active against enterobacteriacae, Neisseria, and H. influenza 4. Treatment of serious infections with susceptible organisms 5. Used to treat MRSA infections

What are the following generations of cephalosporins used to treat? 1. 1st Generation 2. 2nd Generation 3. 3rd Generation 4. 4th Generation 5. 5th Generation

It reduces bone resorption and prevents bone loss and leads to the closure of the epiphyseal plates in long bones. Lead to the growth and development of the vagina, uterus, fallopian tube, and leads to breast enlargement. It is also responsible for the development of female secondary sexual characteristics.

What are the non-reproductive functions of estrogen? What are the reproductive functions?

Ritonavir and Atazanavir

What are the once daily preferred protease inhibitors for HIV patients?

Anti-pseudo penicillins, aztreonam, and 2nd generation cephalosporins. (all others are either extended spectrum or useful against gram-positives)

What are the only antimicrobials studied that are affective only against gram-negative bacteria?

Penicillin G/V and anti-staph pencillins, 1st generation cephalosporins, vancomycin, daptomycin, bacitracin, and streptogramins. (all others are either extended spectrum or useful against gram-negatives)

What are the only antimicrobials studied that are affective only against gram-negative bacteria?

It depresses myocardial function which leads to a reduction in MAP. It also sensitizes the myocardium to circulating catecholamines which an lead to arrhythmias.

What are the potential cardiac adverse effects associated with halothane use?

Rash, and rarely, agranulocytosis, aplastic anemia, hepatotoxicty,a dn vasculitis. It is a possible teratogen.

What are the potential side effects PTU? What about methimazole?

2 NRTIs 3 drug combination (NNRTI or protease inhibitor with 2 NRTIs) Treat for one month starting within 1-2 hours after the needle stick. Generally nothing but you can consider a 2 drug treatment regimen.

What are the recommended treatments for a less severe needle stick (solid needle & superficial injury) from an HIV+ patients? What are the recommended treatments for a more severe needle stick (large-bore hollow needle and/or deep puncture) from an HIV+ patients? How long should treatment continue? What are the recommendations for needle sticks in patients with an unknown HIV status?

Diarrheal, constipation, and alternating between the two. Symptomatic treatment

What are the three types of IBS? What is the treatment of these conditions aimed at?

1. Isoniazid, rifampin, and ethambutol 2. A 2 drug combination choosing from the following; rifampin, ethambutol, clarithromycin, minocycline, doxycycline, and sulfonamides 3. Clarithromycin and ethambutol with or without rifampin 4. Clarithromycin 5. Amikacin, cefoxitin, levofloxacin, sulfonamides, and imipenem

What are the treatment options for the treatment of the following atypical mycobacterial infections? (don't waste too much time on this) 1. M. kansaii 2. M. marinum 3. M. avium complex 4. M. chelonae 5. M. fortuitum

Oxandronlone and STanozolol To treat hypogonadism and to increase bone density and muscle mass. Feminization including gynecomastia, testicular shrinkage, and infertility as a result of feedback inhibition decreasing natural FSH and LH secretion and the exogenous conversion of testosterone into estrogen.

What are the two most commonly used synthetic androgens? Oxandronlone, Fluoxymesterone, Oxymetholone, Nandrolone, or Stanozolol What are the clinical uses of androgen substitution therapy in men? Excessive use of androgens in men can lead to what?

They are now only used in the treatment of depression in patients that are unresponsive to other antidepressants due to their toxicity and potential for lethal food and drug interactions.

What are the uses of MAO inhibitors?

Used to treat mild to moderate pain, especially pain associated with inflammation. Rheumatoid arthritis, osteoarthritis, and acute gouty arthritis. Note: Aspirin & tolmetin are contraindicated in treating acute gouty arthritis.

What are the uses of NSAIDs? Name 3 well known conditions that NSAIDs are approved to treat.

Surgical relaxation, to control ventilation, treatment of convulsions, and preventing trauma during ECT.

What are the uses of the neuromuscular blockers?

1. It allows for a variety of mechanisms of action to act on the tumor cells and cause cell death 2. It keeps the toxicity profile to a minimum by selecting a combination of drugs that each have toxicities in different organs 3. To prevent the development of tumor resistance to any one chemotherapeutic agent

What are three reasons that combination chemotherapy is usually initiated?

As a general rule, all addictive drugs activate the mesolimbic dopamine system.

What area of the brain is the prime target of addictive drugs that is the primary mechanism behind addiction?

Serotonin syndrome which causes overstimulation of 5-HT1A and 5-HT2 receptors causing confusion, hyperthermia, muscle rigidity, myoclonus, and hyperreflexia. This can be fatal. Cyproheptadine which acts as a 5-HT2 receptor antagonist. For seizures, rigidity, and agitation patients can be treated with benzodiazepines.

What can occur to patients taking an irreversible MAO inhibitor with a serotonergic agent? What is the treatment for this condition and how does it work?

Category C in the first and second trimester. Category Din the third trimester.

What category drug is aspirin in pregnancy?

As a result of COX inhibition there is a diversion of arachidonate to 5-LOX which leads to an increase in leukotrienes.

What causes aspirin hypersensitivity reactions?

It is the result of a genetic mutation, usually in the ryanodine receptor gene (RYR1) which causes altered control of Ca2+ release form the SR. Increased [Ca2+] causes sustained muscle contraction which generates heat (hyperthermia). Increased aerobic metabolism depletes oxygen and ATP and accumulates CO2 and anaerobic metabolism kicks in which produces lactate worsening acidosis. As muscle fibers die it causes hyperkalemia (also caused by acidosis) and myoglobinuria.

What causes malignant hyperthermia? How do the symptoms of this condition develop?

It is a potentially fatal genetic disorder of skeletal muscle that occurs in patients who are given volatile inhalation anesthetics (ex. halothane) and succinylcholine, a depolarizing skeletal muscle relaxant. Autosomal dominant Hyperthermia, hyperkalemia, tachycardia, HTN, severe muscle rigidity, and acidosis.

What causes malignant hyperthermia? How is this condition transmitted? What are the symptoms of the development of this condition?

GHRH stimulate the secretion of GH and somatostatin inhibits its secretion. Its secretion is moderately stimulated by TSH but it is inhibited by dopamine. In children it can cause dwarfism (short stature and adiposity) and in adults it can cause hypoglycemia as a result of unopposed insulin action (as GH opposes the actions of insulin).

What causes secretion and inhibition of GH? How is prolactin secretion regulated? What can occur in children and adults with a GH deficiency?

Finite episodes of brain dysfunction resulting from abnormal discharge of cerebral neurons. 1. Partial seizure 2. Generalized seizure 3. Partial seizure with secondarily generalized tonic-clonic seizure 4. Complex partial seizure

What causes seizures? What type of seizure are the following? 1. A single brain focus seizures with no loss of consciousness with abnormal activity of a single limb or muscle group 2. Seizure whose focus begins at the thalamus (no evidence of localized onset) that can be convulsive or non-convulsive and presents with an immediate loss of consciousness 3. A partial seizure whose single focus spreads to the thalamus and, as a result, evolves into a tonic-clonic seizure with loss of consciousness 4. A seizure in which there is loss of consciousness with motor dysfunction that may involve chewing movements, diarrhea, and/or urination

Bleomycin and Busulfan L-Asparaginase Cisplatin Vincristine

What chemotherapeutic drug can cause pulmonary fibrosis? Which can cause pancreatitis? Which can cause deafness and nephrotoxicity? Which can cause peripheral neuropathy?

Tachypnea, tachycardia, tinnitus, and hearing loss. Initially there is hyperventilation which leads to a respiratory alkalosis which is then followed by an increased anion gap acidosis. Supportive care and aggressive gut decontamination including gastric lavage and repeated doses of activated charcoal. To alkalinize urine and promote salicylate excretion.

What clinical manifestations can be seen in patients with aspirin poisoning? What occurs to ventilations and what acid base disorder occurs? How is aspirin poisoning treated? What is the purpose of IV sodium bicarbonate infusion in patients with a moderate poisoning?

GET GAP Giardia lamblia, Entamoeba histolytica, Trichomonas vaginalis, Gardnerella vaginalis (bacterial vaginosis), anaerobic bacterial infections (especially below the diaphragm), and as a combination therapy for H. Pylori infections Tinidazole

What conditions does Metronidizole treat and how can you remember them? What other drug can be given for this condition?

At high doses it can lead to acute psychosis, HTN, tachycardia, arrhythmias and can cause seizures and muscular hyperactivity which can cause hyperthermia and rhabdomyolysis. 1. Phentoamine or nitroprusside 2. Propranolol or esmolol 3. Benzodiazepines

What dangers are there in patients who overdose on amphetamines or other stimulants? What sort of treatment can be administered to patients suffering from the following toxicity complications? 1. HTN 2. Tachyarrhythmias 3. Seizures

-tidine Cimetidine, Famotidine, Ranitidine, and Nizatidine. 1. They block H2 receptors which normally lead to the activation of the H+/K+ exchanger. 2. To treat acute stress ulcers, GERD, and to promote healing of gastric and duodenal ulcers Cimitidine inhibits CYP450 enzymes and the newer drugs do not inhibit these enzymes and have fewer side effects.

What do all the H2 receptor blockers end in? Name them. 1. Mechanism of action 2. Use Why are newer drugs now used as opposed to Cimetidine?

-caine Esters have only one i in their name but amines have 2 i's in their name. Esters have a shorter duration of action because they are more prone to hydrolysis than amides.

What do all the local anesthetics end in? Local anesthetics consist of a lipophilic group (an aromatic ring) connected by an intermediate chain (ester or amide) to an ionizable group (usually a tertiary amine). How can you determine which are esters and which are amides? What is the difference in duration of action between the esters and amides and why?

They all start with Vin and end with -ine (vincristine, vinblastine, and vinorelbine) They bind to the β-tubulin and prevent formation of microtubules which inhibits mitotic spindle formation. M phase

What do all the vinca alkaloid drugs end in? What is their mechanism of action? What part of the cell cycle to they act on?

-azolam (think alprazolam) or -azepam (think lorazepam) They bind to a site located between the α & γ subunit of the BZ1 and BZ2 receptors (both GABAa receptors). These drugs enhance the GABA's effects which increases the frequency of opening these channels which leads to an influx of Cl- into the cell. It is an inhibitory neurotransmitter in the CNS. Yes, but they bind to an another portion of the GABAa receptor.

What do the benzodiazepine drugs end in? What is the mechanism of action of the benzodiazepine drugs? What is the function of GABA in the brain? Do barbiturates bind to the same receptor?

-curium/-curonium (besides tubocurarine) They are competitive antagonists of acetylcholine receptors in the neuromuscular junction. Acetylcholinesterase inhibitors like edrophonium and neostigmine

What do the non-depolarizing neuromuscular blockers end in? What is their mechanism of action? What drugs can be administered to overcome the action of these drugs?

Children: Rickets Adults: Osteomalacia Type I: Defect in the 1-α-hydroxylase enzyme which leads to a decreased amount of active vitamin D and decreased calcium and phosphate levels Type II: Defective vitamin D receptor calci

What does a deficiency of vitamin D cause in children and adults? What is vitamin D dependent rickets type I & II? All the derivatives of vitamin D have what in their name?

It is hydrolyzed to PABA which inhibits the actions of sulfonamides. As a result, large doses of this drug should not be administered to patients taking sulfonamides.

What drug interaction does procaine have?

Fluconazole

What drug is an alternative to amphotericin B for non-severe cryptococcal meningitis?

Malarone Treatment and prophylaxis of P. falciparum

What drug is the combination of atovaquone and proguanil? What is it used for?

Amoxicillin Think about the common diseases seen in infants and children like otitis media, streptococcal pharyngitis, skin infections, and upper respiratory tract infections caused by H. influenzae and S. pneumoniae

What drug is used as a standard regimen for endocarditis prophylaxis during dental or respiratory procedures in patients with damaged or prosthetic heart valves? When you think of the types of diseases that ampicillin and amoxicillin treat what should you think?

Terbinafine

What drug is used to treat tinea infections?

Aminoglycosides

What drugs are both effective against gram-negative drugs and can act as extended spectrum drugs?

Clindamycin and Linezolid

What drugs are both effective against gram-positive drugs and can act as extended spectrum drugs?

Interferon α and ribavirin (a protease inhibitor can also be administered in combination for treatment of this condition).

What drugs are commonly used in combination for the treatment of HCV?

Chloramphenicol, clindamycin, clarithromycin, erythromycin, and nafcillin. (most others are excreted through renal elimination or some combination of the two)

What drugs are eliminated via hepatic methods?

Acetaminophen and NSAIDs They have a maximum dose after which increasing the dose will not provide any further analgesic effects. Acetaminophen is often selected as an initial therapy for mild to moderate pain but it does not have an anti-inflammatory effect so in patients suffering from mild to moderate pain associated with inflammation they should be treated with NSAIDs.

What drugs are often effective for mild to moderate pain and do not cause physical dependence or tolerance? These drugs have an analgesic ceiling effect. What does this mean? What is the difference in the type of pain that acetaminophen and NSAIDs should be used for?

Tenofovir, emtircitabine, and efavirenz

What drugs are part of the preferred NRTIs in the currently recommended regimen for the treatment of HIV?

Rifampin, ciprofloxacin, and ceftriaxone Vancomycin and a 3rd generation cephalosporin

What drugs are used as prophylaxis against bacterial meningitis? What would be the empiric therapy for bacterial meningitis prior to identification of the causative organism?

Patient controlled administration in which patients self-administer parenteral analgesics by depressing a button. Morphine, hydromorphone, fentanyl, and methadone (all strong agonists).

What is considered the gold standard for management of acute postoperative pain? What drugs can be given in this manner?

Levodopa and carbidopa Dopamine receptor agonists

What is currently considered the best treatment for Parkinson's disease? What are the next most effective drugs?

It is an iron chelating drug that is administered with Doxorubicin and/or Daunorubicin to reduce free radical induced cardiotoxicity

What is dexrazoxane used for?

It is the development of red patches on the skin as a result of death of mycobacteria in the skin of leprosy patients. Dapsone Corticosteroids or thalidomide

What is erythema nodosum leprosum? What drug causes this condition? How is this condition treated?

Chemotherapy that is given to obtain a complete remission from a tumor Usually used for blood cancers Chemotherapy that is given to maintain remission from a cancer

What is induction chemotherapy? What kinds of cancer are these commonly given for? What is maintenance chemotherapy?

A rare, and life-threatening disorder, where patients present with rigidity, tremor, hyperthermia, AMS, etc. Dantrolene (a blocker of Ca2+ release) or bromocriptine (a dopamine agonist)

What is neuroleptic malignant syndrome? How is it treated?

TCA (tricyclic antidepressants) 1. Muscarinic receptor blockers 2. α-receptor blockers causing vasodilation They have quinidine-like depressant effects as they block the fast Na+ channels in the heart slowing conduction and depressing cardiac contractility. Norepinephrine to treat hypotension and sodium bicarbonate to increase extracellular sodium and overcome the sodium channel blockade which reverses the quinidine-like effects Physostigmine

What is one of the most common prescription drugs involved in life-threatening drug overdoses? How do they affect the following receptors? 1. Muscarinic receptors 2. α-receptors What sort of effects do TCA's have on the heart? What is the treatment for TCA overdose? What drug should not be given to these patients?

Warfarin Inhibits the hepatic synthesis of vitamin K dependent coagulation factors II, VII, IX, X, and protein C & S Vitamin K can help to restore clotting factors but to prevent active hemorrhage these patients should be given fresh-frozen plasma or fresh whole blood.

What is one of the most frequently used rodenticides? How does warfarin act? How do you treat patients with poisoning of this substance?

T4 is converted to T3 by deiodinase in the tissues because T3 is more potent. This process removes an iodine from T4. rT3 has a different iodine removed than T3 which has no activity on T3 receptors but does block the action of T3

What is reverse triiodothyronine (rT3)?

It is a drugs ability to injure or kill an invading microorganism without harming host cells It is a property of some antibiotics where the killing action continues once drug plasma levels are below measurable levels.

What is selective toxicity? What is postantibiotic effect?

It is a fixed combination drug that combined carbidopa and levodopa in a 1:10 or 1:4 proportion. Because the action of levodopa requires that the substantia nigra neurons still be present in order to make dopamine. As this disease progresses it leads to significant destruction of the neurons in this pathway until they are unable to keep up with dopamine production and the patient because refractory to the treatment.

What is sinemet? This preparation is an efficacious drug in the treatment of Parkinson's disease but there is commonly a decline in response during year 3-5 of therapy. Why does this likely occur?

It is a potentially irreversible adverse reaction associated with the use of choreoathetoid movements. Upregulation of dopamine receptors as a result of long term blockage of D2 receptors by antipsychotic medications Discontinue to the drug or reduce the dose and administer diazepam. Clozapine

What is tardive dyskinesia? What is the suspected mechanism behind the development of this condition? How do you treat this condition? What is the recommended drug for patients with tardive dyskinesia who require antipsychotics?

1. Inhibit the reuptake of serotonin and norepinephrine 2. Inhibitors of monoamine metabolism by MAO 3. Inhibit the reuptake of serotonin and norepinephrine 4. Inhibit the reuptake of serotonin only Their pharmacological actions are immediate but the clinical effects of the drugs take weeks to develop (~2-4 weeks to produce any improvements and 6-8 weeks to achieve substantial benefits)

What is the activity of the following types of drugs? 1. TCAs 2. MOA inhibitors 3. SNRIs 4. SSRIs What is the difference between eh pharmacological actions duration and the clinical effect duration with the TCAs and MAOIs?

Many patients with Parkinson's disease have significant reductions in the enzymes responsible for dopamine production, including dopa decarboxylase, the enzyme responsible for the conversion of levodopa to dopamine which limits levodopa's effectiveness in these patients. The dopamine receptor agonists do not require enzymatic conversion for their activity, and as a result can have a better effect in patients with significant reduction in nigrostriatal neurons.

What is the advantage of the dopamine receptor agonists over levodopa in treating Parkinson's disease?

They block nerve conduction of sensory impulses form the periphery to the CNS without producing unconsciousness.

What is the basic mechanism of action of the local anesthetic drugs?

It inactivates free radicals generated by this drug which, if amifostine is not given, can lead to nephrotoxicity, ototoxicity, neurotoxicity, and myelosuppression.

What is the benefit of administering amifostine to patients being treated with cisplatin?

They specifically act on tumor cells which means that they usually have less toxicity associations like bone marrow suppression, alopecia, mucositis, etc.

What is the benefit of using signal transduction inhibitors in treating cancers?

Severe hypertensive reactions Phentolamine or labetalol

What is the biggest complication associated with patients taking MAO inhibitors and eating or drinking tyramine containing foods or drugs such as phenylpropanolamine or ephedrine? What is the treatment?

BEP Bleomycin, Etoposide, and Platinum (Cisplatin) B: Acts in G₂ phase E: Late S phase and early G₂ phase P: Cell cycle non-specific including G₀ phase

What is the chemotherapeutic regimen for testicular cancer? In which part of the cell cycle does each of these drugs act?

Pinpoint pupils, respiratory depression, coma, and death. Naloxone or nalmefene

What is the clinical manifestation of opioid overdose? What is the treatment?

It is a test used in the diagnosis of Cushing's disease. The patient is given a low dose of dexamethasone which should inhibit the release of ACTH. If ACTH levels after administration are found to be low then the problem is in the adrenal glands but if they continue to be elevated then it is an extra renal problem. Patients are then given a high dose of dexamethasone. In patients with a pituitary ACTH-secreting adenoma this high dose of dexamethasone will lead to suppression of ACTH release but if the condition is the result of a paraneoplastic condition then the ACTH levels will remain elevated.

What is the dexamethasone suppression test?

Cushing's syndrome is the result of a hyperfunctioning of the adrenal gland and excess cortisol secretion. Cushing's disease is the result of an ACTH secreting pituitary adenoma which leads to bilateral adrenal hyperplasia. Surgical removal of the tumor, irradiation of a pituitary tumor, and possible resection of one or both adrenal glands. They require high doses of cortisol before and after surgery and then the dose should be slowly decreased to provent withdrawal.

What is the difference between Cushing's syndrome and Cushing's disease? How should this condition be treated? What pharmacotherapy should be given to these patients?

MIC is the lowest concentration of an antibiotic that prevents visible growth in a broth/tube or through disc sensitivity examination. MBC is the lowest concentration of antibiotic that results in a 99.9% decline in colony count after overnight broth dilution incubations. Serial dilutions are undergone initially to fine MIC which would be identified as the dilution at which the broth/tube shows no bacterial growth. These tubes are then plated and the MBC is the lowest concentration of antibiotic where there is no growth on plates.

What is the difference between MIC (minimum inhibitory concentration) and MBC (minimum bactericidal concentration)? How do you test for this?

Bacteriostatic drugs reversibly inhibit growth of bacteria and bactericidal drugs irreversibly inhibit growth of bacteria. In immunocompromised patients because bacteriostatic agents don't kill the bacteria but just inhibit their growth so the host immune system can take over.

What is the difference between bacteriostatic and bactericidal agents? What sort of patients would bacteriostatic drugs not be useful in and why?

Positive symptoms are the presentation of an excess of normal functions such as hallucinations, thought disorders, perceptual disturbances, etc. Negative symptoms are the loss of diminishment of normal functions such as blunted affect, poverty of speech, social withdrawal, and diminished motivation. Cognitive symptoms are deficits in memory and cognitive control of behavior.

What is the difference between positive symptoms, negative symptoms, and cognitive symptoms in patients with schizophrenia?

Mild infections can typically be treated with antibiotics through an oral route but severe infections requires IV antibiotic therapy. Patients suffering from co-morbidities like liver or renal disease/dysfunction will likely have a longer duration of action of antibiotics as a result of decreased metabolism and/or excretion so antibiotics should be administered with these in mind.

What is the difference between the likely route of administration for patients who have a mild infection versus patients with a serious infection? How can the route of elimination affect the dosing of antibiotics?

Ester-linked locals are metabolized by tissue and plasma esterase's (psuedocholinesterases) whereas amide-linked locals are generally decreased by liver cytochromes.

What is the difference between the metabolism and excretion of ester-linked and amide-linked local anesthetics?

Barbiturates show a linear dose-response curve where an increased dose, above that needed for hypnosis, could lead to a general state of anesthesia, coma, or death. Benzodiazepines have a non-linear dose-response curve which eventually reaches a ceiling right around the ability of the drugs to achieve anesthesia. The benzodiazepines are safer as a result of their dose-response curve plateau and as a result they have largely phased out the barbiturates in the treatment of anxiety

What is the difference in the dose-response curve between barbiturates and benzodiazepines? As a result, which are more commonly used to treat anxiety?

Uncomplicated malarial treatment can typically be treated with oral antimalarial drugs but complicated cases need to be treated aggressively with parenteral antimalarial drugs.

What is the difference in treatment method between uncomplicated malaria and complicated malaria?

Tenofovir increases didanosine levels so co-administration of these drugs requires reduction in the dose of didanosine. Tenofovir decreases concentrations of atazanavir but its levels can be boosted by co-adminstration with ritonavir. No

What is the drug interaction between didanosine and tenofovir? What is the drug interaction between atazanavir and tenofovir? Are the NRTIs generally metabolized by cytochrome enzymes?

Metronidizole It has disulfiram-like effects so patients taking this drug should avoid alcohol. Its use is generally not recommended in the 1st trimester.

What is the drug of choice for C. difficile infections? What is an important adverse effect of this drug? What is the recommendation for the use of this drug in pregnant women?

Cotrimoxazole

What is the drug of choice for Pneumocystis carinii pneumonia?

Cyclophosphamide Hemorrhagic cystitis as a result of acrolein formation which can be prevented by co-administration of MESNA.

What is the drug of choice for Wegener's granulomatosis? What is an important adverse effect of this drug to remember and how can we prevent this condition from occurring?

Fluconazole

What is the drug of choice for candidemia?

Fluconazole

What is the drug of choice for coccidioidomycosis?

Primaquine

What is the drug of choice for eradication of dormant liver forms of P. vivax and P. oval?

Bithionol

What is the drug of choice for fasciolosis (Fasciola hepatica)?

Mebendazole

What is the drug of choice for hookworm (Necator americanus and Ancylostoma duodenale)?

Fluconazole

What is the drug of choice for initial and secondary prophylaxis against cryptococcal meningitis?

Voriconazole

What is the drug of choice for invasive aspergillosis?

Praziquantel

What is the drug of choice for most cestode infections?

Praziquantel

What is the drug of choice for most trematode infections?

Tetracycline drugs or Macrolide antibiotics.

What is the drug of choice for mycoplasma pneumoniae?

Cotrimoxazole

What is the drug of choice for nocardiosis?

Mebendazole

What is the drug of choice for pinworm (Enterobius vermicularis)?

Mebendazole

What is the drug of choice for roundworm (Ascariasis lumbricoides)?

Praziquantel

What is the drug of choice for schistosomiasis?

Carbapenem drugs To avoid the development of resistance There is partial cross-reactivity

What is the drug of choice for serious infections that require board spectrum antibiotics? Why are they not used for other, more mild infections? Do these drugs have a cross reactivity allergic reactions with penicillin?

Quinidine Uterine contractions

What is the drug of choice for severe falciparum malaria in pregnancy? What is a dangerous complication of this drug in pregnant women?

Ivermectin

What is the drug of choice for strongyloides?

Indomethacin

What is the drug of choice for the closure of the ductus arteriosus?

Ivermectin

What is the drug of choice for the treatment of cutaneous larva migrans?

Diethylcarbamazine

What is the drug of choice for the treatment of loiasis?

Diethylcarbamazine

What is the drug of choice for the treatment of lymphatic filariasis?

Carbamazepine It blocks voltage gated sodium channels which lead to inhibition of transmission of neuropathic pain along sensory neurons. A carbamazepine-induced leukopenia and, although rare, aplastic anemia can also occur.

What is the drug of choice for the treatment of trigeminal neuralgia? What is the mechanism of action of this drug? What are some interesting adverse effects of this drug?

Albendazole

What is the drug of choice for toxocariasis?

Lithium The inositol depletion theory: Gq GPCR activate PLC which cleaves PIP2 to DAG and IP3. IP3 signaling is eventually terminated by conversion to IP2 which is then converted to IP1 by inositol polyphophatase and then to inositol by inositol monophosphate. Lithium inhibits inositol polyphosphatase and monophosphtase which blocks the regeneration of inositol wchih is essential for synthesis of PIP2. As a result, this drug blocks the phosphatidylinositol signaling cascade in the brain. Adrenergic, muscarnic, and serotonergic tranmission, although we are not currently sure which receptor is involved with causing this condition.

What is the drug of choice for treating bipolar disorder? What is the most widely accepted mechanism of action explanation for this drug? As a result of this mechanism of action, which neurotransmission is inhibited?

Metronidizole

What is the drug of choice for treating invasive amebiasis?

Chloroquine

What is the drug of choice for treatment of non-falciparum and sensitive uncomplicated falciparum malaria?

Ivermectin

What is the drug of choice for treatment of onchocerciasis (Onchocerca volvulus)?

Diethylcarbamazine

What is the drug of choice for tropical eosinophilia?

Cotrimoxazole

What is the drug of choice for uncomplicated UTIs?

Mebendazole

What is the drug of choice for whipworm (Trichuris trichiura)?

Fluconazole

What is the drug of choice in esophageal, oropharyngeal, vulvovaginal, or urinary candidiasis?

Valproate

What is the drug of choice to treat myoclonic seizures?

1. 6-9 months 2. 4 months

What is the duration of treatment of latent TB with the following drugs? 1. Isoniazid 2. Rifampin

They inhibit the production of TXA2 which induces platelet aggregation. Because platelets have no nuclei, the inhibition of the enzymes (especially the irreversible inhibition by aspirin) leads to a decrease in platelet aggregation and a prolonged bleeding time. These cells are nucleated and can make new COX.

What is the effect of NSAIDs on platelets? Why are the endothelial cells, which make PGI2, relatively unaffected?

Increases the reabsorption of calcium and decreases the reabsorption of phosphate Decreases the reabsorption of calcium AND phosphate

What is the effect of PTH on phosphate and calcium reabsorption/secretion from the kidneys? What is the effect of calcitonin?

It prevents the primary immune response to Rh antigen on fetal red blood cells in Rh negative mothers who have had an Rh positive child. Its administration prevents the development of hemolytic disease of the newborn in subsequent pregnancies. Within 72 hours of delivery or termination of a pregnancy.

What is the function of Rh₀GAM? When should this drug be administered to Rh negative mothers?

When administered with methotrexate it can provide a source of reduced folate which can overcome the blockade that is caused by methotrexate and limit the myelosuppression that occurs. When administered with 5-FU it increases the cytotoxic effects of 5-FU by increasing the incorporation of the drug into RNA (reason not understood).

What is the function of adding leucovorin to certain chemotherapeutic regimens?

Elevations signify ovulation, induces secretory changes in the endometirum, and it is required to maintain the pregnancy. (ie. pro-gestation = progesterone).

What is the function of progesterone?

It activates NK cells and causes increased HLA expression on the surface of cells to increase immune mediated destruction of infected cells and tumor cells. 1. α 2. β 3. α 4. α 5. γ γ is the 3rd letter of the greek alphabet and CGD has 3 letters and starts with C. MS (microsoft) needs beta testing All others discussed are α

What is the general action of interferon? Are the following conditions treated using Interferon α, β, or γ? 1. Hepatitis B & C 2. Multiple sclerosis 3. Malignant melanoma 4. Kaposi sarcoma 5. Chronic granulomatous disease (CGD) How can you remember this?

1. Used during surgical procedures and in ICUs to cause paralysis 2. Used to reduce spasticity in a variety of neurological conditions Non-depolarizing blockers (antagonists) and depolarizing blockers (agonists)

What is the general use of the following? 1. Neuromuscular blockers 2. Spasmolytics What are the two types of neuromuscular blockers?

Mercaptopurine and azothioprine are both metabolized by xanthine oxidase. If a patient starts taking allopurinol their dose of these drugs should be reduced in order to account for this change.

What is the interaction between allopurinol, mercaptopurine, and azathioprine?

Because estrogens lead to an increase in factor II, VII, IX, X and XII and a decrease in antithrombin III and protein C & S. They lead to an increase in HDLs and a decrease in LDLs They can lead to an increase in cholesterol levels in the bile which can lead to the formation of gall stones.

Why can oral contraceptives lead to thrombus formation? What effect does estrogen have on the lipid profile? What about their effect on the gallbladder?

Dopamine does not cross the BBB but levodopa does. As a result it can move into the neurons and be converted to dopamine by the surviving neuronal cells. Peripheral decarboxylation of levodopa to dopamine causing nausea, vomiting, cardiac arrhythmias, and hypotension. Carbidopa: This drug is a dopa decarboxylase inhibitor but does not cross the BBB so it helps to reduce the peripheral conversion of levodopa to dopamine without affecting the conversion of levodopa to dopamine in the neurons.

Why do we administered levodopa to patients with Parkinson's disease instead of directly administering dopamine? The side effects of levodopa are the result of what and what are the adverse effects? What drug is given to prevent these adverse effects and how does it work?

Because antidepressants have a better side effect profile, no risk of dependency, and are effective in the treatment of the other common comorbidities of this condition including depression, panic disorder, OCD, and social anxiety disorder. They can be used to manage acute anxiety attacks when short-term relief is needed (as an adjunct during the initiation of antidepressant therapy, or to improve sleep.

Why have these drugs replaced benzodiazepines for the chronic treatment of GAD? What use do benzodiazepines have in the treatment of this condition?

Low doses of aspirin compete with uric acid for secretion in the kidneys which leads to an increase in serum uric acid levels which leads to increases in symptoms and likelihood of attacks. Because they can cause hepatic injury when treated with high doses.

Why is aspirin not used to treat acute gouty arthritis? Why are salicylates contraindicated in patients with chronic liver disease?

It has a narrow therapeutic window Neurological effects which progress from confusion and motor impairment, coma, convulsions, and death if the plasma concentration reaches 3-5 mM. Category D (not for use in pregnant women or nursing mothers) Congenital cardiac anomalies

Why is lithium difficult to properly administer in proper doses. Why? What are some serious adverse effects of this drug? What pregnancy category is this drug? What are the risks associated with this drug and its use during pregnancy?

It can lead to the develop of withdrawal symptoms as the weak partial agonist competes for binding sites with the pure agonist. CO2 retention caused by respiratory depression can result in cerebral vasodilation and if a head injury exists it can cause increased ICP and lethal alterations in brain function. Because it can cause fetal dependence.

Why should a pure opioid agonists not be used with a weak partial agonist? Why should opioid drugs not be used in patients suffering from a head injury? Why should it not be used in pregnant women?

Because they can precipitate withdrawal in patients who have already been getting treated with pure opioid agonists. Opioid naive patients.

Why should mixed opioid agonist-antagonists not be used with pure opioid agonists? As a result, what patients should they be used in?

Patient is being treated with isoniazid and has developed an adverse effect. Patient is being treated with Rifampin and has developed a unique adverse effect to this drug. It is a harmless side effect of Clofazimine and will reverse once the drug is stopped. Metronidizole

You have a patient being treated for TB who develops signs of lupus. Antibody testing shows anti-histone antibodies. What should you suspect? You have a patient being treated for TB who develops orange/red color to bodily fluids (tears, urine, etc). What should you suspect? You have a patient being treated for leprosy and they develop a red-brown discoloration to their skin. What should you suspect? What antimicrobial drug makes the urine darker?

1. Short acting agonist of the BZ1 benzodiazepine receptor 2. Used for the short-term treatment of insomnia in patients with difficulties initiating sleep.

Zaleplon 1. Mechanism of action 2. Use

1. (Neuroaminidase inhibitor) Inhibits the ability of neuroaminidase mediated cleavage of receptors which normally releases the virion release. This in turn leads to an inability for the virion to release from the cell 2. Used as prophylaxis prior to exposure to influenza type A and type B or within 24-48 hours Inhaled or intranasally Airway irritation, so it should be avoided in patients with severe asthma and/or COPD In patients >7 years old

Zanamivir 1. Mechanism of action 2. Use How is this drug administered? How does this method of administration effect its adverse effect profile? What age group can be given this drug?

1. Nucleoside analog that lacks a 3' OH group which leads to termination of DNA elongation and competitive inhibitor of reverse transcriptase 2. Used to treat HIV 3. Bone marrow suppression

Zidovudine (AZT) 1. Mechanism of action 2. Use 3. Adverse effects

Elimination is through exhalation (not metabolism) and follows the same process as the uptake and onset of the agents. An agent with a high blood:gas partition coefficient (high blood solubility) has a slow onset and, as a result, take longer to be removed from the body (and longer duration of recovery) than the agents with a low blood:gas partition coefficient (low blood solubility) which have a more rapid removal from the body an rapid recovery from anesthesia. Those with a high solubility can accumulate within tissues and blood. Therefor the recovery is a function of the duration of anesthetic administration.

What is the process of elimination of the inhaled anesthetics and how does the blood:gas partition coefficient affect the elimination? How is the elimination of agents with a high blood and and tissue solubility different from those with a low solubility?

1. To reduce anxiety and for their ability to cause anterograde amnesia 2. To cause analgesia 3. To cause muscular relaxation (succinylcholine) 4. To prevent possible aspiration of stomach contents (ondansetron) 5. For its amnesic effects, to prevent salivation and bronchial secretions, and to protect the heart from bradycardia caused by inhalation agents and neuromuscular blockers (scopolamine)

What is the purpose of the following drugs as adjuncts in anesthesia? 1. Benzodiazepines 2. Opioids 3. Neuromuscular blockers (give one example) 4. Antiemetics (give one example) 5. Antimuscarinics (give one example)

They cause sedation and/or encourage sleep. Should reduce anxiety and exert a calming effect with little or no effect on motor or mental functions. They should produce drowsiness and encourage the onset and maintenance of a state of sleep that resembles the natural sleep state. Hypnotics

What is the purpose of the sedative-hypnotics? What are the properties of a good sedative? What are the properties of a good hypnotic? Which type of drug produces a more pronounced depression of the CNS?

Ritonavir boosted lopinavir (twice daily) and zidovudine/lamivudine Zidovudine started immediately after birth and administered for 6 weeks

What is the recommended HIV treatment for pregnant patients? What is the current recommendation for an infant born to an HIV infected mother?

Long acting benzodiazepines such as diazepam and chlordiazepoxide. Given to elderly patients or patients with liver failure/damage (alcoholic cirrhosis) as these drugs do not undergo hepatic metabolism.

What is the recommended treatment of alcohol withdrawal? Why would lorazepam and orazepam (both intermediate acting drugs) be given to patients suffering from alcohol withdrawal and why?

1. Block voltage gated sodium channels which leads to a decrease in the transmission of excitatory glutamatergic neuronal signaling. 2. Used as an adjunct to treat seizures

Zonisamide 1. Mechanism of action 2. Use

1. Short acting agonist of the BZ1 benzodiazepine receptor 2. Used for the short-term treatment of insomnia in patients with difficulties initiating sleep

Zopidem 1. Mechanism of action 2. Use

As the oil:gas partition coefficient increases the potency increases and the MAC decreases. Highest: Nitrous oxide Lowest: Methoxyflurane Lowest potency: Nitrous oxide Highest potency: Methoxyflurane

What is the relationship between an inhaled anesthetics potency, oil:gas partition coefficient, and MAC? Of the following inhaled anesthetics, which has the highest and lowest MAC (nitrous oxide, desflurane, sevoflurane, methoxyflurane, halothane, enflurane, isoflurane)? Which has the highest oil:gas partition coefficient and therefor, the highest potency?

They uncouple oxidative phosphorylation which leads to elevated CO2 and increased respiration. At higher doses it leads to hyperventilation and at toxic levels it leads to central respiratory paralysis and death.

What is the respiratory adverse effect of aspirin and other salicylates?

Isoniazid Resistance rapidly emerges Yes, but there is an increased risk of hepatitis but the risk can be reduced with pyridoxine supplementation

What is the sole drug used for the treatment of latent TB infection? If this drug is used alone to treat a current TB infection what can occur? Is this drug safe in pregnancy?

Subcutaneous injection Regular insulin given by IV infusion.

What is the standard mode of insulin therapy? During a diabetic emergency which insulin is given and how is it administered?

Mercury poisoning Oral or IV unithiol, IM dimercaprol, or oral succimer

What is the suspected toxicity in a patient presenting like the one seen in these photos? What is the treatment of this condition?

Rifampin and dapsone (6 month duration of treatment) Rifampin, clofazimine, and dapsone (12 month duration of treatment)

What is the the recommended drugs to treat leprosy that presents with 1-5 skin lesions (pauci-bacillary)? What is the recommended drugs to treat leprosy that presents with more than 5 skin lesions (multi-bacillary)?

Deferoxamine

What is the treatment for iron poisoning?

1. Diazepam 2. Mannitol and dexamethasone 3. Chelation therapy with edentate calcium disodium (condtinous IV infusion), dimercaprol (given IM), and succimer (given orally).

What is the treatment for the following problems associated with lead poisoning? 1. Seizures 2. Cerebral edema 3. Lead poisoning

Patients should be started on a long acting benzodiazepine like diazepam with the dose gradually being reduced

What is the treatment of benzodiazepine addiction and the management of withdrawal?

Acyclovir Ganciclovir Trifluridine

What is the treatment of choice of HSV encephalitis? What is the drug of choice for CMV retinitis & CMV prophylaxis in immunocompromised patients? What is the drug of choice for HSV keratoconjunctivitis and recurrent epithelial keratitis?

Strictly supportive treatment Diazepam given via IV or via a rectal solution

What is the treatment of febrile convulsions that last less than 15 minutes? What is the treatment of febrile convulsions that last more than 15 minutes?

Management of vital signs and prevention of aspiration. IV dextrose can be administered and electrolyte imbalances should be corrected. Thiamine

What is the treatment of patients with ethanol intoxication? What is the treatment of a patient with suspected Wernicke-Korsakoff syndrome?

It is a combination of a once daily shot of a long acting insulin analog (glargine or detemir) and the administration of a rapid acting analog (lispro, aspart, or glulisine) prior to meals. Yes, these preparations improve HbA1c levels and reduce hypoglycemia occurrence better than an NPH and regular insulin plan.

What is the typical medication treatment plan for a patient with type I diabetes? Is this better than using NPH and regular insulin?

They are metabolized mainly through phase 2 reactions by conjugation with glucuronic acid 1. Neuroexcitatory properties 2. Analgesic with a potency 4-6 times that of morphine Because they are polar compounds which do not readily cross the BBB.

What is the typical metabolism of opioid drugs? Morphine is metabolized through this pathway into two different metabolites. What is the effect of each? 1. Morphine-3-glucuronide (M3G) 2. Morphine-6-glucuronide (M6G) Why do these compounds not play a significant role in the CNS effects of morphine?

It can be used in the treatment of PML (pro-myelocytic leukemia) by causing differentiation of leukemic cells. All-trans-retinoic acid

What is the use of arsenic trioxide and how does it work? What is the preferred treatment for this condition?

FEVER (Fever, Encephalopathy, unstable Vitals, Elevated Enzyme, and muscle Rigidity) Antipsychotic agents Bromocriptine and dantrolene

What mnemonic can be used to remember the features of neuroleptic malignant syndrome? What types of drugs is it caused by? What is the treatment of this condition?

1. Cytosine 2. Thymidine 3. Adenosine 4. Adenosine 5. Guanosine 6. Cytosine 7. Thymidine

What nucleoside are the following NRTIs analogs of? 1. Emtricitabine 2. Stavudine 3. Didanosine 4. Tenofovir 5. Abacavir 6. Lamivudine 7. Zidovudine

Guanosine

What nucleoside is the following NRTI an analog of? Abacavir

Adenosine

What nucleoside is the following NRTI an analog of? Didanosine

Cytosine

What nucleoside is the following NRTI an analog of? Emtricitabine

Cytosine

What nucleoside is the following NRTI an analog of? Lamivudine

Thymidine

What nucleoside is the following NRTI an analog of? Stavudine

Adenosine

What nucleoside is the following NRTI an analog of? Tenofovir

Thymidine

What nucleoside is the following NRTI an analog of? Zidovudine

1. The cell prepares for DNA synthesis and replication by synthesizing substrates and enzymes necessary for this process 2. DNA replication 3. Proof reading of synthesized DNA, recognition of problems, and either fixing those problems or, if a problem can't be fixed, inducing apoptosis 4. Mitosis and formation of 2 daughter cells 5. Differentiation into a mature cell stable from the cell cycle

What occurs at each phase of the cell cycle? 1. G₁ 2. S 3. G₂ 4. M 5. G₀

Uncoupling of oxidative phosphorylation and inhibition of the krebs cycle leading to increased lactate production. 1. Impaired ability to generate ATP 2. Increased oxygen use 3. Increased carbon dioxide production 4. Increased heat production Increased glycolysis with increased peripheral glucose demand, increased glycogenolysis, gluconeogenesis, lipolysis, and fatty acid oxidation leading to increased ketone body formation.

What occurs during aspirin poisoning? How does this poisoning affect: 1. The ability to generate ATP 2. Oxygen use 3. Carbon dioxide production 4. Heat production What metabolic changes occur?

The growth of the tumor decreases as the rapidly dividing cells start to receive less nutrients due to their decreased blood supply.

What occurs to the growth of a tumor as it gets bigger and why?

Depression of sinus node automaticity, slowing of AV node condition, and reduction in cardiac output and blood pressure IV calcium infusion as well as glucagon and epinephrine, if needed, to increase BP and heart rate.

What occurs with calcium channel blocker toxicity? What is the antidote for calcium channel blocker toxicity?

Methanol is metabolized to formaldehyde and then formic acid. Formic acid toxicity leads to severe acidosis (increased anion gap), retinal damage, and blindness. Sudden cessation of respiration Ethanol infusion is given to saturate alcohol dehydrogenase and reduce the product of formic acid and fomepizole is used to inhibit alcohol dehydrogenase. Bicarbonate is also given to treat the metabolic acidosis and hemodialysis may be necessary. Ethylene glycol

What occurs with methanol ingestion? What is the cause of death in these patients? How do you treat this condition? The treatment of this condition is the same for what other toxin?

1. Deposits in the cornea and lens 2. Deposits in the retina

What ocular complications occur with the following antipsychotic drugs? 1. Chlorpromazine 2. Thioridazine

S phase M phase G₂ phase M phase Late S phase and early G₂ phase They inhibit topoisomerase II

What part of the cell cycle does methotrexate act in? What part of the cell cycle do taxanes (docetaxel and paclitaxel) act in? What cell cycle does bleomycin act in? What cell cycle do the vinca alkaloids (vincristine, vinblastine, and vinrelbine) act in? What part of the cell cycle do the epipodophyllotoxins (etoposide and teniposide) act in? What is the mechanism of action of the epipodophyllotoxins?

Clozapine is a category B drug and all the other drugs are category C.

What pregnancy class do the antipsychotic drugs fall into?

5-HT and α2 adrenergic receptors The descending noradrenergic and serotonergic inhibitory neurons release norepi and 5-HT, respectively which leads to inhibition of presynaptic calcium channels and reduced neurotransmitter release. GABAergic interneurons inhibit these descending inhibitory neurons which leads to lack of inhibition of pain. Opioids affect this system by inhibiting these GABAergic neurons which activates the pain-inhibitory descending neurons which results in enhanced inhibition of pain transmission.

What receptors are involved in the pain-inhibitory descending neuronal pathway. Describe the pathway.

5-HT2A and D2 receptors Classical antipsychotics Classical antipsychotics Classical antipsychotics Atypical antipsychotics

What receptors do all the atypical antipsychotic drugs block? Are classical of atypical antipsychotic drugs more likely to cause extrapyramidal reactions? Are classical of atypical antipsychotic drugs more likely to cause tardive dyskinesia? Are classical of atypical antipsychotic drugs more likely to cause increased prolactin levels? Are classical of atypical antipsychotic drugs better at treating negative symptoms?

There is an increased risk of congenital malformations in infants born to women taking these drugs with a particularly increased risk associated with valproate. These induced enzymes can also increase the degradation of vitamin K in the fetus can cause bleeding in the newborn. As a result, vitamin K supplementation is recommended for the mother in the final month of pregnancy.

What risks are associated with anti seizure drugs and pregnancy? How can the drugs that cause enzyme induction cause problems in a fetus?

They inhibit cardiac fast sodium channels and act like Class I antiarrhythmics. This inhibition can lead to arrhythmias and is the most common cause of death in patients with TCA intoxication. Sexual dysfunction

What serious adverse effect is associated with the TCA drugs? What side effect is particularly common in patients taking highly serotonergic agents such as clomipramine?

Amphoteracin B Fluconazole

What should be the initial treatment of a cryptococcal meningitis infection? What is the drug of choice for the consolidation and maintenance therapy for this condition?

It is no longer used because it has leukomogenic effects

What should you remember about Procarbazine?

A mixed respiratory alkalosis and metabolic acidosis. Respiratory failure.

What sort of acid-base profile do patients suffering from acute salicylate overdose present with? What is the usual cause of death in these patients?

Dissociative anesthesia characterized by catatonia, amnesia and analgesia. It can but does not necessarily. If necessary, another drug should be administered to ensure loss of consciousness occurs Likely, involves the blockade of NMDA receptors

What sort of anesthesia does ketamine cause? Does this drug cause LOC? What is the mechanism of action of this drug?

Arsine gas poisoning Chelating agents are not useful in treating this type of poisoning. No treatment listed

What sort of poisoning would you suspect in a patient presenting with massive hemolysis, hemoglobinuria, and signs of renal failure? How is this treated?

Acute inorganic arsenic poisoning The trivalent arsenicals react with -SH groups that inhibit enzymes and the pyruvate dehydrogenase complex is very sensitive to this activity. Uncouplling of oxidative phosphorylation.

What sort of poisoning would you suspect in a patient with severe vomiting, diarrhea "rice water" stools, and sweet, garlicky odor of the breath and stools? What is the mechanism of action of trivalent arsenic poisoning and what enzyme is very sensitive to this? What is the mechanism of action of pentavalent arsenic poisoning?

1. Both can cause CNS depression and respiratory depression so their combined effect can cause severe CNS/respiratory depression 2. Increase in sedation and variable effects on respiratory depression which accentuation of cardiovascular effects 3. The use of some opioids with MAO inhibitors has been associated with potentially life-threatening reactions as a result of increases in serotonin and norepinephrine. Meperidine and tramadol Serotonin syndrome which presents with delirium, hyperthermia, headache, hyper- or hypotension, rigidity, convulsions, coma, and death.

What sort of problems can occur when opioid drugs are mixed with the following types of drugs? 1. Sedative-hypnotics 2. Antipsychotics 3. MAO inhibitors What opioid drugs are particularly associated with potentially life-threatening reactions when combined with MAO inhibitors? What is this syndrome called and how does it present?

TRH Somatostatin (although it is more specifically for GH), T4, and T3

What stimulates the secretion of TSH from the anterior pituitary? What inhibits its release?

A high osmolar gap with a high anion gap metabolic acidosis.

What two criteria indicate methanol or ethylene glycol intoxication?

Methadone: Long-acting opioid receptor agonist Buprenorphine: Partial opioid receptor agonist Adrenergic agonists

What two drugs can be used to treat opioid withdrawal and what is their mechanism of action? What other types of drugs can be used to treat the adrenergic symptoms of opioid withdrawal?

1. Benzodiazepine 2. Benzodiazepine receptor antagonist 3. Benzodiazepine 4. Barbiturate 5. Non-benzodiazepine benzodiazepine receptor agonist 6. Benzodiazepine

What type of drug are the following? 1. Alprazolam 2. Flumazenil 3. Diazepam 4. Phenobarbital 5. Zolpiden 6. Temazepam

1. Benzodiazepine 2. Non-benzodiazepine benzodiazepine receptor agonist 3. Barbiturate 4. Benzodiazepine 5. Benzodiazepine

What type of drug are the following? 1. Clonazepam 2. Zalepion 3. Thiopental 4. Triazolam 5. Flurazepam

1. Non-benzodiazepine benzodiazepine receptor agonist 2. Benzodiazepine 3. Benzodiazepine 4. Barbiturate 5. Benzodiazepine

What type of drug are the following? 1. Eszopiclone 2. Oxazepam 3. Midazolam 4. Pentobarbital 5. Lorazepam

It is an anti-androgen drug It can lead to medical castration and decreased release of LH and FSH. Used to treat prostate cancer.

What type of drug is Goserelin? What can occur if this is given as a continuous dose instead of pulsitile? How is this drug used?

It is an anti-androgen drug It can lead to medical castration and decreased release of LH and FSH. Used to treat prostate cancer

What type of drug is Leuprolide? What can occur if this is given as a continuous dose instead of pulsitile? How is this drug used?

It is a reversible steroidal aromatase inhibitor It inhibits the extra-adrenal synthesis of estrone and estradiol by inhibiting the aromatase enzyme that converts androstenedione to estrone. To treat ER-positive metastatic breast cancer

What type of drug is aminogluthethimide? What is the mechanism of action of this drug? What is the use of this drug?

They are reversible non-steroidal aromatase inhibitors It inhibits the extra-adrenal synthesis of estrone and estradiol by inhibiting the aromatase enzyme that converts androstenedione to estrone. To treat advanced ER-positive breast cancer that is resistant to tamoxifen Menopausal-like symptoms that include hot flashes and headache.

What type of drug is anastrozole and letrozole? What is the mechanism of action of these drugs? What is the use of these drugs? What are the adverse effects of these drugs?

They are irreversible steroidal aromatase inhibitors It inhibits the extra-adrenal synthesis of estrone and estradiol by inhibiting the aromatase enzyme that converts androstenedione to estrone. To treat advanced ER-positive breast cancer that is resistant to tamoxifen

What type of drug is exemestane and formestane? What is the mechanism of action of these drugs? What is the use of these drugs?

It is a androgen receptor blocker used to treat prostate cancer. Gynecomastia

What type of drug is flutamide? What adverse effect should you be mindful of in patients receiving this drug or other anti-androgen drugs?

Strep. pneumoniae, HAV, HBV, and influenza. (inactive viruses) Live vaccines like MMR and varicella.

What type of prophylactic vaccines should be given to HIV + patients? What type of prophylactic vaccine should not be given to HIV + patients?

GPCR (Gs)

What type of receptor does the following hormone act on? ACTH

GPCR (Gq)

What type of receptor does the following hormone act on? ADH (V1 receptor)

GPCR (Gs)

What type of receptor does the following hormone act on? ADH (V2 receptor)

Intracellular/intranuclear steroid receptor

What type of receptor does the following hormone act on? Aldosterone

GPCR (Gq)

What type of receptor does the following hormone act on? Angiotensin II

GPCR (Gs)

What type of receptor does the following hormone act on? CRH

Intracellular/intranuclear steroid receptor

What type of receptor does the following hormone act on? Cortisol

Intracellular/intranuclear steroid receptor

What type of receptor does the following hormone act on? Estrogen

GPCR (Gs)

What type of receptor does the following hormone act on? FSH

JAK/STAT

What type of receptor does the following hormone act on? GH

GPCR (Gq)

What type of receptor does the following hormone act on? Gastrin

GPCR (Gq)

What type of receptor does the following hormone act on? GnRH

GPCR (Gq)

What type of receptor does the following hormone act on? Histamine

Tyrosine kinase receptor

What type of receptor does the following hormone act on? IGF-1

Tyrosine kinase receptor

What type of receptor does the following hormone act on? Insulin

GPCR (Gs)

What type of receptor does the following hormone act on? LH

GPCR (Gs)

What type of receptor does the following hormone act on? MSH

GPCR (Gq)

What type of receptor does the following hormone act on? Oxytocin

GPCR (Gs)

What type of receptor does the following hormone act on? PTH

Intracellular/intranuclear steroid receptor

What type of receptor does the following hormone act on? Progesterone

JAK/STAT

What type of receptor does the following hormone act on? Prolactin

Intracellular/intranuclear steroid receptor

What type of receptor does the following hormone act on? T3/T4

GPCR (Gq)

What type of receptor does the following hormone act on? TRH

GPCR (Gs)

What type of receptor does the following hormone act on? TSH

Intracellular/intranuclear steroid receptor

What type of receptor does the following hormone act on? Testosterone

Intracellular/intranuclear steroid receptor

What type of receptor does the following hormone act on? Vitamin D

GPCR (Gs)

What type of receptor does the following hormone act on? hCG

cGMP

What type of receptor/signaling molecule does the following hormone act on? ANP

cGMP

What type of receptor/signaling molecule does the following hormone act on? NO

1. JAK/STAT 2. GPCR (Gs) 3. GPCR (Gs) 4. GPCR (Gs) 5. JAK/STAT 6. GPCR (Gs)

What type of receptors do the following anterior pituitary hormones act on? 1. GH 2. TSH 3. ACTH 4. FSH 5. Prolactin 6. LH

Acetylcholinesterase inhibitors like neostigmine or edrophonium Atropine and glycopyrrolate Nothing, there is no antidote. The patient needs to receive supportive care until the drug wears off.

What types of drugs can be used in the treatment of non-depolarizing neuromuscular blockers? What drugs can be used to prevent bradycardia? What can be used to treat an overdose of succinylcholine?

By concurrent administration of 65% nitrous oxide in oxygen.

When a potent opioid analgesic, such as fentanyl, is combined with a neuroleptic such as droperidol, neurolept analgesia is established. How can we then convert neurolept analgesia to neurolept anesthesia?

If the patient is seizure free for 3-5 years then discontinuation is warranted but should be discontinued slowly. Benzodiazepines and barbiturates should be discontinued gradually to avoid withdrawal and, if the patient is on combination therapy, the drugs should be removed one at a time.

When can a patient safely discontinue anti epileptic therapy?

Cefaperazone and Ceftazidime

Which Cephalosporin has activity against P. aeruginosa?

Ceftriaxone

Which Cephalosporin is the drug of choice for Lyme disease that has spread to the CNS or joints?

Ceftriaxone

Which Cephalosporin is the drug of choice for gonorrhea?

Ceftriaxone

Which Cephalosporin is the drug of choice for meningitis due to ampicillin-resistant H. influenzae?

Ceftriaxone

Which Cephalosporin is used as prophylaxis for meningitis in exposed individuals?

Cefazolin Zoo-keeper prophylaxis

Which Cephalosporin is used for surgical prophylaxis?

1. All (but rare) 2. All 3. All 4. Leuprolide and nafarelin 5. Leuprolide, nafarelin, and goserelin 6. Leuprolide, nafarelin, and goserelin

Which GnRH/analogs are used for the following (Gonadorelin, Leuprolide, Nafarelin, Goserelin)? 1. Female infertility 2. Male infertility 3. Diagnosis of LH responsiveness 4. Control of ovarian hyper stimulation through suppression of gonadotropin release 5. Used to treat endometriosis by suppressing gonadotropin release 6. Used to treat leiomyomata by suppressing gonadotropin release

1. Leuprolide and goserelin 2. Leuprolide and nafarelin 3. All 4. All 5. All Pregnant and breastfeeding women

Which GnRH/analogs are used for the following (Gonadorelin, Leuprolide, Nafarelin, Goserelin)? 1. Used to treat prostate cancer by suppressing gonadotropin release 2. Suppressing precocious puberty 3. Used to treat advance breast and ovarian cancer 4. Treating amenorrhea and infertility in women with PCOD 5. Thinning of the endometrial lining These drugs are contraindicated in which patients?

Indomethacin

Which NSAID is commonly used to treat gout?

Amphotericin B, flucytosine, azoles, and echinocandins (caspofungin) Griseofulvin, terbinafine, ketoconazole, fluconazole, and itraconazole. Nystatin, Amphoteracin B, Clotrimazole, Miconazole, Ketoconazole, and Terbinafine. Clotrimazole and Miconazole

Which anti-fungal drugs are used for subcutaneous and systemic mycoses? Which systemic anti-fungal drugs can be used for superficial mycoses? What topical anti-fungal drugs can be used for superficial mycoses? What are the two most commonly used topical azoles?

Epipodophyllotoxins (etoposide and teniposide) Antimetabolites (Cytarabine, cepacitabine, 5-FU, 6-MP, 6-TG, gemcitabine, and methotrexate) Bleomycin Taxanes (docetaxel and paclitaxel) and vinca alkaloids (vincristine, vinblastine, and vinrelbine).

Which anticancer drugs are cell cycle specific for late S phase and early G₂ phase? S phase? G₂ phase? M phase?

TCAs and SNRIs because they enhance both the serotonergic and noradrenergic transmission. No, because they only enhance serotonergic transmission.

Which antidepressants have the greatest analgesic effects? Are SSRIs as effects as SNRIs and TCAs?

Clindamycin Ampicillin, amoxicillin, cephalosporins, and fluoroquinolones Start with metronidizole. If this is not effective you can use vancomycin and if this is still ineffective you move up to fidaxomicin.

Which antimicrobial is the most common cause of C. difficile colitis? What are the other frequent causes? What is the treatment of this condition?

Metro Clark; Transvestite Amy Clarithromycin, Amoxicillin, Metronidazole, and Tetracycline. Please Make Tummy Better Proton pump inhibitors Metronidazole Tetracycline Bismuth subsalicylate

Which antimicrobials are used to treat H. pylori infections and how can you remember them? How can you remember the rough guidelines for treating H. pylori?

Risperidone Schizophrenia, as an adjunct in the treatment of bipolar disorder, to suppress tics in Tourette's syndrome, as an adjunct antidepressant in treatment resistant MDD, and in combination with antidepressants for patients with psychotic depression.

Which antipsychotic is approved for treating irritability associated with autism? What conditions are antipsychotics used to treat?

Diazepam and oxazepam Short-acting: Triazolam Intermediate-acting: Temazepam Long-acting: Flurazepam

Which benzodiazepines are used to treat withdrawal from alcohol? Which short-acting, intermediate-acting, and long-acting benzodiazepines are used to treat sleep disorders?

Let him eat and drink. ThE PERson is a MAN (cefoTEtan, cefoPERazone, and cefaMANdole) Administer vitamin K The same drugs as seen above.

Which cephalosporins can cause hypoprothrombinemia as a result of inhibition of vitamin K? What can be done to prevent this complication? What cephalosporins can cause disulfiram-like reactions?

Anaerobic conditions

Which conditions are necessary for the optimal activity of Metronidazole?

Bromocriptine Uncontrollable somnolence that requires discontinuation of the medication. Patients with a history of psychotic illness or recent MI.

Which dopamine receptor agonist(s) have a unique adverse effect profile that includes pulmonary infiltrates, pleural and retroperitoneal fibrosis, and erythromelalgia? Pramipexole, ropinirole, and rotigotine can cause what unique adverse effect and what should be done if this adverse effect develops? Dopamine agonists are contraindicated in which patients?

Albendazole

Which drug can be used as an alternative to Mebendazole?

Fluoxetine Fluoxetine and sertraline TCAs

Which drug is approved for the treatment of bulimia? Which drugs have been approved for the treatment of PMDD? Which types of drugs have been found to be effective in treating enuresis (an inability to control urination)?

Duloxetine (SNRI) TCAs

Which drug is approved for the treatment of pain associated with diabetic neuropathy and fibromyalgia? What other type of drug is commonly used to treat neuropathic pain?

Clindamycin

Which drug is used as prophylaxis of endocarditis in valvular patients that are allergic to penicillin?

Diloxanide furoate

Which drug is used as the sole treatment of asymptomatic amebiasis?

1. Aminoglycosides 2. Chloramphenicol 3. Nitrofurantoin 4. Fluoroquinolones 5. Sulfonamides 6. Tetracyclines and Glycylcyclines (Tigecycline) 7. Trimethoprim and cotrimoxazole

Which drugs are involved in the following fetal and neonatal effects? 1. Possible damage to the eighth cranial nerve of the fetus 2. Gray baby syndrome 3. Hemolytic anemia 4. Tendon rupture/damage 5. Kernicterus (as the result of displacement of bilirubin from albumin) 6. Tooth enamel dysplasia and inhibition of bone growth 7. Folate deficiency

SSRIs are the drug of choice A TCA or MAO inhibitor may be effective

Which drugs are recommended for the treatment of panic disorder? If SSRIs are not effective what other drugs could be used?

Aztreonam (gram-negative) and aminoglycosides (gram-negative and extended spectrum)

Which drugs are specifically useful against aerobes?

Metronidazole

Which drugs are specifically useful against anaerobes?

SSRIs and sometimes TCAs Clomipramine Fluoxetine, fluvoxamine, paroxetine, and sertraline A benzodiazepine or an antipsychotic

Which drugs are the drugs of choice for OCD treatment? Which TCA is used for treatment of OCD? Which SSRIs? If these patients show a high level of anxiety what other drugs could be added to their drug regimen?

SSRIs 8-12 weeks

Which drugs are the drugs of choice for social anxiety disorder? How long after beginning treatment with these drugs could it take for a response to this therapy?

SSRIs Sertraline and paroxetine Sertraline

Which drugs are the first-line drugs in the treatment of PTSD? Which SSRIs are approved to acutely treat this condition? Which is approved for long-term treatment of PTSD?

β-blockers Propanolol and nadolol. Both are highly lipophilic and, as a result, cross the BBB The adverse effects of β-blockers such as hypotension

Which drugs are used to treat performance anxiety? Which specific drugs are used and why? The use of this drug is limited by what?

Fluoroquinolones

Which drugs are useful against aerobes and some anaerobes?

SNRIs

Which drugs have fewer CYP P450, and thus drug interactions, SNRIs or SSRIs?

1. Ciprofloxacin 2. Levofloxacin 3. Nalidixic acid 4. Ciprofloxacin 5. Levofloxacin 6. Levofloxacin, Moxifloxacin, and Gemifloxacin 7. Levofloxacin 8. Ciprofloxacin 9. Levofloxacin

Which fluoroquinolone drug is used to treat the following condition? 1. Travelers diarrhea (E. coli) 2. STDs (not syphilis) 3. Uncomplicated UTIs 4. Prophylaxis against meningitis 5. Prostatitis (E. coli) 6. Community acquired pneumonia 7. Skin infections 8. P. aeruginosa (CF patients) 9. Acute sinusitis, bronchitis, and TB

Levofloxacin (3rd generation), moxifloxacin (4th generation), and gemifloxacin (4th generation) Because they have excellent activity against S. pneumoniae, H. influenza, and M. catarhallis (all common causes of community acquired pneumonia). When first line agents have failed, if there are co-morbidities present, or if the patient is an inpatient.

Which fluoroquinolones are used to treat community acquired pneumonia? Why are they so useful in treating this condition? When are they used to treat this condition?

5th Generation Similar spectrum of activity to the 3rd generation cephalosporins

Which generation of Cephalosporins have activity against MRSA? What other bacteria do they have activity against?

1. All 2. Triamcinolone 3. Dexamethasone, Hydrocortisone, Methylprednisolone, and Prednisolone 4. Beclomethasone and Triamcinolone 5. Beclomethasone, Dexamethasone, Hydrocortisone, and Triamcinolone

Which glucocorticoids can be administered via the following routes? (Prednisolone, Hydrocortisone, Methylprednisolone, Dexamethasone, Beclomethasone, and Triamcinolone) 1. Oral 2. IM only 3. IM or IV 4. Aerosol 5. Topical

Halothane Methoxyflurane

Which inhaled anesthetic is associated with potentially sever and life-threatening hepatitis? Which inhaled anesthetic is associated with a nephrotoxic potential?

1. Aspart, Lispro, and Glulisine 2. Regular insulin 3. NPH 4. Glargine and Detemir

Which insulin analog drugs cause the following changes in insulin levels seen in the following graph? Glargine, Lispro, Glulisine, Regular insulin, NPH, Detemir, Aspart

NSAIDs

Which is more superior in handling pain due to inflammation, NSAIDs or opioids?

Halothane, sevoflurane, and nitrous oxide. Increase intracranial pressure

Which of the following inhaled anesthetics should be administered to patients with bronchospasms (Halothane, isoflurane, desflurane, sevoflurane, nitrous oxide)? How do the inhaled anesthetic affect intracranial pressures?

Azithromycin, clarithromycin, and telithromycin have a broader spectrum of activity than erythromycin (but erythromycin is cheaper). Clarithromycin, azithromycin, and telithromycin have improved oral absorption, a longer half life, and increased bioavailability. All but azithromycin Many HIV drugs require metabolism by CYP450 enzymes and those with HIV are commonly being treated with antibiotics to prevent and treat opportunistic infections.

Which of the following macrolide antibiotics have a wider spectrum? Azithromycin, erythromycin, clarithromycin, and telithromycin. Which have a higher bioavailability? Which are inhibitors of CYP450 enzymes? Why could this be important?

Most are targeting the viral enzymes, specifically viral integrase, reverse transcriptase, and protease. With combination therapy, HAART (highly active antriretroviral therapy)

Which parts of the HIV virus are most drugs that treat this condition targeting? How is HIV treated?

1. Ampicillin 2. Ampicillin & Amoxicillin 3. Methicillin (one of the reasons it is no longer used) 4. Ticarcillin 5. Nafcillin 6. Oxcillin

Which penicillin drugs are the following adverse effects commonly caused by? 1. Pseudomembranous colitis 2. Maculopapular rash 3. Interstitial nephritis 4. Hematologic toxicities 5. Neutropenia 6. Hepatitis

Amoxicillin Babies are treated for infections with amoxicillin and it is administered using a dropper. Children and pregnant women

Which penicillin has the highest oral bioavailability? How can you remember this? As a result of this drugs high oral bioavailability it is a common antibiotic prescribed for what subgroup(s)?

1. Taken up and sequestered by the thyroid gland which causes intracellular damage and permanent reduction in thyroid tissue 2. Used to treat patients with Grave's disease and hyperthyroidism that is refractory to other treatments. 3. Can lead to too much of a reduction in thyroid tissue and permanent hypothyroidism 4. Pregnant and nursing women

¹³¹I (radioactive iodine) 1. Mechanism of action 2. Use 3. Adverse effects 4. Contraindications

1. Stimulator of FSH and LH receptors 2. Used to treat male and female infertility 3. Ovarian hyperstimulation syndrome, multiple pregnancies, and precocious puberty 4. Gynecomastia

hCG 1. Mechanism of action 2. Use 3. Adverse effects in women 4. Adverse effects in men

1. Dopamine receptor agonist 2. Used as rescue therapy for treatment of off episodes of akinesia in patients on dopaminergic therapy

Apomorphine 1. Mechanism of action 2. Use

Aspirin

Anti-Anginals Antiplatelet Agent - Cyclooxygenase Inhibitor Should be administered (as well as aggressive cardiovascular risk reduction) to all patients with stable angina. Anti-thrombotic, thus increasing oxygen supply to myocardium. Displays zero-order kinetics at high doses.

Pulmonary fibrosis due to Bleomycin or Busulfan Hodgkin's lymphoma, testicular cancer, or kaposis sarcoma.

A patient presents to the ER complaining of difficulty breathing. He has been undergoing chemotherapy but can't remember the drugs he is currently being given. A chest X-ray shows the following presentation. What is seen here and what drugs could cause this condition as an adverse side effect? You are able to get the patients doctor on the phone and he informs you that he is taking Bleomycin. What neoplastic conditions would this drug likely be administered for?

Chronic inorganic arsenic poisoning Raindrop pattern of hyper pigmentation and hyperkeratosis. Chelation Acute: Chelation therapy with unithiol IV or dimercaprol IM Chronic: Chelation with dimercaprol

A patient presents with the following skin changes, hair loss, bone marrow depression, and anemia. What poisoning do you suspect? What is this sign referred to as? How is acute and chronic arsenic poisoning treated?

Chronic Addison's disease (primary adrenocortical insufficiency) With daily hydrocortisone (with increased doses during stress) and gludrocortisone. Long acting glucocorticoids With large amounts of parenteral hydrocortisone and correction of fluid and electrolyte imbalances. Later, salt-retaining hormones can be administered (after hydrocortisone levels are reduced)

A patient presents with weakness, fatigue, weight loss, hypotension, hyper pigmentation, and an inability to maintain blood glucose levels during fasting. What condition do you suspect? How should this patient be treated? What type of glucocorticoids should not be administered to these patients? If a patient presents with the acute symptoms of adrenocortical insufficiency, how should they be treated?

Epinephrine

Adrenergic Agonist - Direct Endogenous Catecholamine Sythesized from tyrosine in the adrenal medulla. Interacts with both alpha and beta receptors. Effects depend on concentration as well as present receptor type. beta effects predominate at low doses, alpha effects predominate at high doses. Rapid onset. Brief duration. Given IV in emergency situations. Also given SC, ET tube, inhalation, and topically to eye. Oral is ineffective. Actions - Potent vasopressor, strengthens myocardial contractility, increases myocardial contraction rate, increase blood pressure(with large dose), decrease blood pressure(with low dose), bronchodilation, relaxes GI smooth muscle, relaxes detrusor, contracts trigone and sphincter, causes hyperglycemia and stimulates lipolysis. Used to treat Type 1 hypersensitivity anaphylactic shock, treat asthmatic attacks, restore cardiac rhythm to patients with cardiac arrest, in local anesthetics to increase anesthetic duration, for glaucoma(not common today). Adverse - CNS disturbances(ie. anxiety, fear, tension, tremor), hemorrhage, cardiac arrhythmias, pulmonary edema. Interactions - enhanced CV actions in patients with hyperthyroidism or taking cocaine. beta-blockers prevent epinephrine's activation, leaving alpha receptor activation unopposed.

Phenylephrine

Adrenergic Agonist - Direct alpha1-Agonist Vasconstrictor. Given orally or topically. Induces reflex bradycardia when given IV. Used as nasal decongestant, mydriatic, or to increase blood pressure and terminate episodes of supraventricular tachycardia.

Methyldopa

Adrenergic Agonist - Direct alpha2-Agonist Activates central alpha2-adrenoceptors and decreases blood pressure. Used to treat hypertension during pregnancy.

Clonidine

Adrenergic Agonist - Direct alpha2-Agonist Partial alpha2 agonist. Activates central receptors. reduces sympathetic outflow. Used to reduce blood pressure

Brimonidine

Adrenergic Agonist - Direct alpha2-Agonist Reduces aqueous humor production and increases outflow. Given ocularly. Used to lower intraocular pressure in glaucoma.

Isoproterenol

Adrenergic Agonist - Direct beta-Agonist - Non-selective Stimulates beta1 and beta2 adrenergic receptors. alpha receptor action is insignificant. Increases heart rate and force of contraction(beta1). Dilates skeletal muscle arterioles and decreases TPR(beta2). Bronchodilates(beta2). Used to stimulate heart in emergency situations. Rarely used as bronchodilate in asthma.

Dobutamine

Adrenergic Agonist - Direct beta1-Agonist (-)-isomer is alpha1 agonist and weak beta1 agonist. (+)-isomer is an alpha1 antagonist and potent beta1 agonist. Resulting selective beta1 agonist. Used for acute management of CHF by increasing CO with little change in heart rate and not significantly elevating O2 demands of myocardium.

Albuterol

Adrenergic Agonist - Direct beta2-Agonist AKA Salbutamol. Used for Asthma.

Salmeterol

Adrenergic Agonist - Direct beta2-Agonist Long-acting. Prolonged duration of action: 12 hours. Slow onset of action, therefore not suitable for prompt relief of breakthrough attacks of bronchospasm. Better for asthma maintenance/attack prevention.

Formoterol

Adrenergic Agonist - Direct beta2-Agonist Long-acting. Similar to salmeterol. Used for asthma attack prevention

Terbutaline

Adrenergic Agonist - Direct beta2-Agonist Used for Asthma.

Amphetamine

Adrenergic Agonist - Indirect Releasing agent Cause norepinephrine release from presynaptic terminals, potentiating effects. Central stimulatory action. Used to increase blood pressure on both vasculature and heart.

Tyramine

Adrenergic Agonist - Indirect Releasing agent Cause norepinephrine release from presynaptic terminals, potentiating effects. Found in fermented food, such as ripe cheese and Chianti. Oxidized by MAO. Adverse - If patient taking MAOI, can precipitate serious vasopressor episodes.

Methylphenidate

Adrenergic Agonist - Indirect Releasing agent Cause norepinephrine release from presynaptic terminals, potentiating effects. Structural analogue of amphetamine. Used to treat ADHD in children.

Cocaine

Adrenergic Agonist - Indirect Uptake inhibitor Blocks monoamine reuptake(DAT, SERT, and NET), accumulating in synapse, resulting in potentiation and prolongation of central and peripheral actions. Actions - In CNS, inhibition of dopamine reuptake in limbic system pleasure centers, causing intense euphoria. tachycardia, hypertension, pupillary dilation, peripheral vasoconstriction. Used as local anesthetic by blockin voltage-activated sodium channels. Only therapeutic indication.

Atomoxetine

Adrenergic Agonist - Indirect Uptake inhibitor Selective inhibitor of norepinephrine reuptake transporter, NET1. Used for treatment of ADHD.

Pseudoephedrine

Adrenergic Agonist - Mixed-action Induce release of NE. Activates adrenergic receptors. One of four ephedrine enantiomers. Available OTC as component of many decongestant mixtures, usually found with H1-histamine antagonist.

Ephedrine

Adrenergic Agonist - Mixed-action Induce release of NE. Activates adrenergic receptors. Stimulates alpha and beta receptors. Not a catecholamine, which means longer duration since poor substrate of MAO/COMT. Excellent absorption orally and penetrates CNS. Actions - increases systolic and diastolic BPs, bronchodilation, prophylactic chronic asthma Tx, mild CNS stimulation, athletic performance improvement. Used to treat asthma, as a nasal decongestant, and to raise BP. Use is declining due to better agents with fewer side effects.

Guanethidine

Adrenergic Antagonist Inhibitor of Norepinephrine release Displaces NE from vesicles, leading to depletion. Inhibits release of NE. Causes gradual decrease in BP and heart rate. Used as major antihypertensive in early 1970s

Reserpine

Adrenergic Antagonist Inhibitor of Norepinephrine storage Irreversibly damages VMAT. Vesicles cannot store NE or Dopamine. Depletes NE, since MAO degrades NE in cytoplasm. Gradual decrease in bp and slowing of cardiac rate. Used in past to treat hypertension.

alpha-Methyltyrosine

Adrenergic Antagonist Inhibitor of Norepinephrine synthesis AKA Metyrosine. Competitive inhibitor of tyrosine hydroxylase. Used for management of malignant pheochromocytoma. Also, preoperatively in preparation of patients for resection of pheochromocytoma.

Propranolol

Adrenergic Antagonist beta-Antagonist - Non-selective Blocks beta1 and beta2 receptors. Actions - slows heart rate and decreases myocardial contractility, especially when sympathetic nervous system is active. Also increases peripheral resistance due to blockade of vascular beta2 receptors(also causing compensatory sympathetic reflexes activating vascular alpha receptors). Hypertensive patients show gradual reduction of both systolic and diastolic pressures. Can cause contraction of bronchiolar smooth muscle, and is thus contraindicated in patients with asthma. Decreased glycoenolysis and glucagon secretion, so monitor insulin-dependent diabetics, since pronounced hypoglycemia may occur after insulin injection. Used to treat hypertension, hyperthyroidism, angina pectoris, atrial fibrillation, myocardial infarction, performance anxiety, and essential tremors. Adverse - bronchoconstrictions(lethal in asthmatics), hypoglycemia in insulin-dependant diabetics, and CNS effects. Should not be withdrawn abruptly.

Nadolol

Adrenergic Antagonist beta-Antagonist - Non-selective Similar properties to Propranolol. Long duration of action. Used for long-term management of patients with angina pectoris. Also used for management of hypertension.

Timolol

Adrenergic Antagonist beta-Antagonist - Non-selective Similar properties to Propranolol. Used for treatment of hypertension, prophylaxis of migraine headaches, and treatment of open-angle glaucoma.

Esmolol

Adrenergic Antagonist beta1-Antagonist Ultra-short acting. RBCs rapidly metabolize ester bond in drug, resulting in half-life of about 10 minutes. Given IV, and steady state concentrations are achieved quickly. Used in critically ill patients to control supraventricular arrhythmias, arrhythmias associated with thyrotoxicosis, perioperative hypertension, and myocardial ischemia.

Atenolol

Adrenergic Antagonist beta1-Antagonist Useful in hypertensive patients with impaired pulmonary function, and diabetic hypertensive patients receiving insulin. Used for management of hypertension, long-term management of patients with angina pectoris, and management of patients with acute myocardial infarction to reduce cardiovascular mortality. Adverse - blockade of beta2-receptors in bronchial smooth muscle(should be avoided, if at all possible, in asthmatic patients).

Metoprolol

Adrenergic Antagonist beta1-Antagonist Useful in hypertensive patients with impaired pulmonary function, and diabetic hypertensive patients receiving insulin. Used for management of hypertension, long-term management of patients with angina pectoris, and management of patients with acute myocardial infarction to reduce cardiovascular mortality. Adverse - blockade of beta2-receptors in bronchial smooth muscle(should be avoided, if at all possible, in asthmatic patients).

Pindolol

Adrenergic Antagonist (clinically) beta-Partial Agonist Said to possess intrinsic sympathomimetic activity(ISA). Used for management of hypertension.

-micin or -mycin except for amikacin. Aminoglycosides are used AGaiNST infections before they are identified. (Amikacin, Gentamicin, Neomycin, Streptomycin, and Tobramycin) Macrolide antibiotics also have -mycin at the end but all of them end in -thromycin. They are associated with serious toxicities which limits their use to ~5 days and, as a result, are largely replaced by safer antibiotics. They are usually started initially before a specific offending organism is identified but once the organism is identified it is discontinued and a less toxic and more specific drug is started. Bactericidal (unique because most inhibitors of protein synthesis are bacteriostatic).

All the aminoglycocides end in what? Other drugs end in this suffix. How can you remember these drugs? What other drugs end in this suffix and how can you differentiate? These drugs are only recommended for short courses. Why? As a result, how are they commonly used? Are aminoglycocides bactericidal or bacteriostatic?

-navir (note: antiviral protease inhibitors end in -previr and most of the antiviral nucleoside/nucleotide analogs end in -vir) They are reversible inhibitors of HIV aspartyl protease which is responsible for cleavage of the viral polyprotein into reverse transcriptase, protease, and integrase. This prevents virus maturation and results in production of non-infections virions. No

All the antiretroviral protease inhibitors end in what? What is the mechanism of action of the protease inhibitors? Do these drugs require intracellular activation?

-ovir (except for trifluridine and foscarnet) They cause DNA chain termination (during viral replication) and inhibit DNA polymerase both of which inhibit viral replication Herpes virus infections Yes

All the antiviral (not antiretroviral) purine/pyrimidine analogs end with what? What mechanism of action do all these drugs share? What viral infections are these drugs used for? Does cross resistance occur between the -cyclovir drugs?

-zapine (think clozapine) or -idone (think risperidone) Aripiprazole They have blocking effects on the D2 receptors (like classical antipsychotics) but have higher affinities for other receptors other than the D2 receptors.

All the atypical antipsychotics, besides one, end in what? What atypical antipsychotic drug does not end in -zapine/-idone? What is the mechanism of action of these drugs and why are they considered atypical?

-dronate (etidronate, alendronate, pamidronate, and risedronate) They inhibit osteoclastic activity by decreasing farnesyl pyrophosphate synthesis by disrupting the mevalonate pathway leading to decreased osteoclast H+ ATPase function leading to reduced resorption and formation of hydroxyapatite Etidronate because it may cause osteomalacia Erosive esophagitis as a result of direct irritation that can be prevented by taking the medication in the upright position and by increasing fluid intake during administration.

All the bisphosphonate drugs end in what? What is their mechanism of action? Of all of the drugs in this class (etidronate, alendronate, pamidronate, and risedronate), which are not approved for long term use? What adverse effect should be monitored for in patients taking this medication and how can the risk be minimized?

-azine (chlorpromazine, fluphenazine, thioridazine) Haloperidol They block D2 receptors in the mesolimbic pathway thereby reducing the positive symptoms of schizophrenia

All the classical antipsychotic drugs, besides one, end in what? What classical antipsychotic drug does not end in -azine? What is the mechanism of action of these drugs?

They enhance GABAergic neurotransmission from presynaptic neurons by either inhibiting reuptake, inhibiting GABA degradation, or increasing GABA release.

All the drugs with gaba in their name have what general same mechanism of action?

-glinide The same as the sulfonylurea drugs, they blocks the ATP-sensitive K+ channel in the beta cell membrane which leads to increased secretion of insulin Sulfonylureas These drugs have a rapid onset and short duration of action. They do not contain sulfur so they can be given instead of sulfonylurea drugs to patients with a sulfa allergy.

All the meglitidines end in what? What is their mechanism of action? Are these drugs or the sulfonylurea drugs more effective at reducing fasting plasma glucose and HbA1c levels? What is the difference in duration of action? What is the advantage of these drugs?

-amivir They inhibit the ability of neuroaminidase mediated cleavage of receptors which normally releases the virion release. This in turn leads to an inability for the virion to release from the cell. Influenza type A and B Should be administered prior to exposure as prophylaxis (best outcome) or within 24-48 hours after infection (moderate effect on symptoms)

All the neuroaminidase inhibitors end in what? What is their mechanism of action? Are they effective against influenza type A, type B, or RSV? When should they be administered to have an optimal effect?

-prazole They are converted to an active form once they are transported into the parietal cell. There they form a stable covalent bond with the cysteine residue of the H+/K+-ATPase leading to irreversible inactivation of the pump. To treat GERD, duodenal and gastric ulcers, and MEN-1/Zollinger-Ellison Syndrome. They contribute to the eradication of H. pylori.

All the proton pump inhibitors end with what? What is their mechanism of action? What are the uses of proton pump inhibitors? What function do they serve when combined with antibiotics?

They all start with sulfa. They are a structural analog of PABA which inhibits the enzyme (dihydropteroate synthase) required for bacterial folic acid synthesis. Can be used as a topical agent for burn infections or ocular infections or as oral agents for simple UTIs (although not commonly used for this anymore). Oral Sulfasalazine

All the sulfonamides have what in their name? What is their mechanism of action? Because of the high resistance that has developed to these drugs they are rarely used as single agents. What is their general clinical application? Which can be used to treat UC, enteritis, and IBD?

-cycline Tigecycline ends in -cycline but it is glycylcyline drug which binds to the same ribosomal subunit as tetracyclines (30S subunit) To remember, it is the only -cycline (besides tetracycline) that starts with a T. Tigecycline can be used against multi-drug resistant bacteria but it is not commonly used because of its mortality risk. Pregnant women and children under 8. Class D

All the tetracycline drugs end in what? What non-tetracycline drug ends in this same suffix and how can you differentiate? Neither of these drugs should be used in what groups? What pregnancy class of drug are the tetracyclines?

Darbepoetin

Anemia Hematopoietic Growth Factor Long-acting version of erythropoietin that differes by addition of two carbohydrate chains, which improves biologic activity. Therefore has decreased clearance and has half-life ~3x longer. Member of JAK/STAT superfamily of cytokine receptors. Stimulates erythroid proliferation and differentiation by interacting with receptors on red cell progenitors. Also induces release of reticulocytes from bone marrow. Produced in kidney. Production increases in response to tissue hypoxia, and may correct anemia. In patients with chronic renal failure, cannot produce growth factor, and respond to exogenous form. Used for anemia associated with renal failure and sometimes effective for patients with other forms of anemia(ie. primary bone marrow disorders, or anemias secondary to cancer chemotherapy or HIV treatment, bone marrow transplantation, AIDS, or cancer).

Erythropoietin

Anemia Hematopoietic Growth Factor Member of JAK/STAT superfamily of cytokine receptors. Stimulates erythroid proliferation and differentiation by interacting with receptors on red cell progenitors. Also induces release of reticulocytes from bone marrow. Produced in kidney. Production increases in response to tissue hypoxia, and may correct anemia. In patients with chronic renal failure, cannot produce growth factor, and respond to exogenous form. Used for anemia associated with renal failure and sometimes effective for patients with other forms of anemia(ie. primary bone marrow disorders, or anemias secondary to cancer chemotherapy or HIV treatment, bone marrow transplantation, AIDS, or cancer). Banned by International Olympic Committee. Adverse - hypertension and thrombotic complications.

Deferoxamine

Anemia Iron chelator Acute iron toxicity is almost exclusively seen in young children who accidentally ingest iron tablets. They experience necrotizing gastroenteritis, vomiting, abdominal pain, and bloody diarrhea, which may be followed by shock, metabolic acidosis, coma, and death. Actions - Systemically given to bind iron already absorbed, and to promote excretion in urine and feces. Used to treat acute or chronic iron toxicity.

Deferasirox

Anemia Iron chelator Chronic iron toxicity,AKA hemochromatosis, results when excess iron deposits in heart, liver, pancreas, and other organs, leading to organ failure and death. Most commonly occurs with inherited hemochromatosis and those who receive many red cell transfusions over a long period of time(ie. patients with thalassemia major). Given parenterally. Used to treat patients with chronic iron toxicity to retard the iron accumulation.

Ferrous fumarate

Anemia Iron preparation - Oral Corrects anemia just as rapidly and completely as parenteral iron in most cases if absorption is normal. Ferrous iron is most efficiently absorbed. Should be continued for 3-6 months after correction of the cause of iron loss. Patients also develop black stools, having no clinical significance, but sometimes obscuring diagnosis. Used to correct hypochromic microcytic anemia due to iron deficiency. Adverse - nausea, epigastric discomfort, abdominal cramps, constipation, diarrhea.

Ferrous gluconate

Anemia Iron preparation - Oral Corrects anemia just as rapidly and completely as parenteral iron in most cases if absorption is normal. Ferrous iron is most efficiently absorbed. Should be continued for 3-6 months after correction of the cause of iron loss. Patients also develop black stools, having no clinical significance, but sometimes obscuring diagnosis. Used to correct hypochromic microcytic anemia due to iron deficiency. Adverse - nausea, epigastric discomfort, abdominal cramps, constipation, diarrhea.

Ferrous sulfate

Anemia Iron preparation - Oral Corrects anemia just as rapidly and completely as parenteral iron in most cases if absorption is normal. Ferrous iron is most efficiently absorbed. Should be continued for 3-6 months after correction of the cause of iron loss. Patients also develop black stools, having no clinical significance, but sometimes obscuring diagnosis. Used to correct hypochromic microcytic anemia due to iron deficiency. Adverse - nausea, epigastric discomfort, abdominal cramps, constipation, diarrhea.

Iron dextran

Anemia Iron preparation - Parenteral Should be reserved for patients with iron deficiency who are unable to tolerate or absorb oral iron, and for patients with extensive chronic anemia who cannot be maintained with oral iron alone. Used to correct hypochromic microcytic anemia due to iron deficiency.

Iron sucrose

Anemia Iron preparation - Parenteral Should be reserved for patients with iron deficiency who are unable to tolerate or absorb oral iron, and for patients with extensive chronic anemia who cannot be maintained with oral iron alone. Used to correct hypochromic microcytic anemia due to iron deficiency.

Sodium ferric gluconate complex

Anemia Iron preparation - Parenteral Should be reserved for patients with iron deficiency who are unable to tolerate or absorb oral iron, and for patients with extensive chronic anemia who cannot be maintained with oral iron alone. Used to correct hypochromic microcytic anemia due to iron deficiency.

Hydroxyurea

Anemia Sickle-Cell Disease Agent Actions - increases fetal hemoglobin levals, thus diluting abnormal hemoglobin S(HbS), which takes several months. Polymerization is delayed in treated patients so that painful crises are not caused by sickled cells blocking capillaries and causing tissue anoxia. Used to relieve painful clinical course of sickle-cell disease. Also currently being used to treat chronic myelogenous leukemia and polycythemia vera. Adverse - bone marrow suppression and cutaneous vasculitis.

Vitamin B12

Anemia Vitamin Cobalamin. Serves as a cofactor for several essential biochemical reactions in humans. Deficiency leads to megaloblastic anemia, and neurologic abnormalities. Active forms are deoxyadenosylcobalamin and methylcobalamin. Cyanocobalamin and hydroxocobalamin are found in found sources and converted to active forms and are available for therapeutic use. Average human has large storage pool(3000-5000ug) in liver. Normal daily requirement is only ~2ug, so megaloblastic anemia from storage exhaustion would take ~5 years. Complexes with intrinsic factor(IF), then gets absorbed in distal ileum by receptor-mediated transport system. Used to treat cobalamin deficiency. Deficiency is usually from malabsorption due to lack of IF or malfunction of distal ileal transporter. Rarely nutritional deficiency(strict vegans). Therefore parenteral injections are required. [Additional physiological review information on cobalamin in lecture notes.] Used to treat megaloblastic anemia. Treat together with folic acid if cause is unknown. Therapy must be continued for the remainder of life of pernicious anemia(defective IF secretion) patients. No adverse effects. Note: Deficiency can cause neurological syndrome beginning with paresthesias in peripheral nerves, weakness, progressing to spasticity, ataxia, and other dysfunctions.

Folic acid

Anemia Vitamin Reduced forms are required as cofactors for essential biochemical reactions. Deficiency is not uncommon, and easily corrected by administration. Deficiency consequences go beyond just anemia; they are implicated as cause of congenital malformations in newborns. Stores are low and requirements are high, therefore megaloblastic anemia can develop within 1-6 months. Cofactors are involved in DNA synthesis. Deficiency is often due to inadequate dietary intake, unlike Vit B12 deficiency. Can develop typically in alcoholics or those with liver disease and poor diet. Pregnant women and patients with hemolytic anemia have increased requirements. Evidence implicates maternal deficiency in occurrence of fetal neural tube defects. Can also be caused by drugs like methotrexate, trimethoprim, and pyrimethamine. Used to treat megaloblastic anemia. Treat together with Vit B12 if cause is unknown. Also used as supplement to prevent deficiency during pregnancy, in patients with alcohol dependence, hemolytic anemia, liver disease, skin diseases, or patients on renal dialysis Note: Deficiency does not cause neurological syndrome seen in Vit B12 deficiency.

Amlodipine

Anti-Anginals Calcium Channel Blocker - Dihydropyridine Due to induction of reflex tachycardia, used in combination with beta-blockers, when initialbeta-blocker therapy is not successful, or as beta-blocker substitute when contraindicated. Anti-anginal effects from increase in oxygen supply. Also able to dilate coronary arteries, preventing Prinzmetal coronary vasospasm. Has minimal effect on cardiac conduction or heart rate, and mainly used for vasodilator effects. Relieves symptom's of Prinzmetal's. Given orally, and approved only as sustained-release prep. Actions - Block voltage-gated L-type Ca2+ channels on vascular smooth muscle, reducing intracellular calcium. This causes vasodilation. Used to treat hypertension, angina, and arrhythmias. Used for chronic stable, unstable, and Prinzmetal's(variant) angina. Adverse - Reflex tachycardia, dizziness, flushing headache, hypotension, constipation, peripheral edema Note: Should be avoided unless combined with beta-blocker due to strong reflex tachycardia.

Felodipine

Anti-Anginals Calcium Channel Blocker - Dihydropyridine Due to induction of reflex tachycardia, used in combination with beta-blockers, when initialbeta-blocker therapy is not successful, or as beta-blocker substitute when contraindicated. Anti-anginal effects from increase in oxygen supply. Also able to dilate coronary arteries, preventing Prinzmetal coronary vasospasm. Has minimal effect on cardiac conduction or heart rate, and mainly used for vasodilator effects. Relieves symptom's of Prinzmetal's. Given orally, and approved only as sustained-release prep. Actions - Block voltage-gated L-type Ca2+ channels on vascular smooth muscle, reducing intracellular calcium. This causes vasodilation. Used to treat hypertension, angina, and arrhythmias. Used for chronic stable, unstable, and Prinzmetal's(variant) angina. Adverse - Reflex tachycardia, dizziness, flushing headache, hypotension, constipation, peripheral edema Note: Should be avoided unless combined with beta-blocker due to strong reflex tachycardia.

Verapamil

Anti-Anginals Calcium Channel Blocker - Diphenalkylamine Anti-anginal effects from increase in oxygen supply and decrease in oxygen demand. Also able to dilate coronary artieries, preventing/reversing coronary vasospasm in Prinzmetal's. Given orally. Has greatest negative inotropic action of CCBs, but weaker vasodilator. Actions - Block voltage-gated L-type Ca2+ channels on vascular smooth muscle, cardiac myocytesb, and cardiac nodal tissue, reducing intracellular calcium. This causes vasodilation, and decreased contractility and heart rate. Used to treat hypertension, angina, and arrhythmias. Used for chronic stable, unstable, and Prinzmetal's(variant) angina. Adverse - Cardiac conduction abnormalities, such as: bradycardia, AV block, heart failure. Anorexia, nausea, peripheral edema, and hypotension. Constipation in ~7% patients. Contraindications: Bradycardia, conduction defects, heart failure. Can also increase digoxin levels.

Isosorbide dinitrate

Anti-Anginals Organic Nitrate Longer half-life(>1 hour) than nitroglycerin. More useful in long-term management and prophylaxis of angina. Actions - Nitrous oxide(NO) is primarily produced by vascular endothelial cells to activate guanylyl cyclase to convert GTP to cGMP, resulting in smooth muscle relaxation. Also activates K+ channels, leading to hyperpolariziation. cGMP also stimulates cGMP-dependent protein kinase, that activates MLC phosphatase, which dephosphorylates MLC, leading to relaxation. NO relaxes vascular smooth muscle(vasodilator), inhibits platelet aggregation(anti-thrombotic), and inhibits leukocyte-endothelial interactions(anti-inflammatory). This drug mimics actions of NO by releasing or forming NO. Has more effect on veins than arteries. Dilating coronary arteries can relieve variant angina symptoms. Used to treat stable, unstable, and variant angina. Adverse - hypotension, reflex tachycardia(at high doses), headache(cerebral vasodilation), facial flushing. Contrindications: Should not be taken alongside sildenafil(cGMP-dependent phosphodiesterase) Note: Tolerance develops rapidly. Can be overcome by using smallest dose possible, with infrequent or irregular dosing.

Isosorbide mononitrate

Anti-Anginals Organic Nitrate Longer half-life(>1 hour) than nitroglycerin. More useful in long-term management and prophylaxis of angina. Nearly 100% oral bioavailability. Given orally for prophylaxis(sustained release preps available) Actions - Nitrous oxide(NO) is primarily produced by vascular endothelial cells to activate guanylyl cyclase to convert GTP to cGMP, resulting in smooth muscle relaxation. Also activates K+ channels, leading to hyperpolariziation. cGMP also stimulates cGMP-dependent protein kinase, that activates MLC phosphatase, which dephosphorylates MLC, leading to relaxation. NO relaxes vascular smooth muscle(vasodilator), inhibits platelet aggregation(anti-thrombotic), and inhibits leukocyte-endothelial interactions(anti-inflammatory). This drug mimics actions of NO by releasing or forming NO. Has more effect on veins than arteries. Dilating coronary arteries can relieve variant angina symptoms. Used to treat stable, unstable, and variant angina. Adverse - hypotension, reflex tachycardia(at high doses), headache(cerebral vasodilation), facial flushing. Contrindications: Should not be taken alongside sildenafil(cGMP-dependent phosphodiesterase) Note: Tolerance develops rapidly. Can be overcome by using smallest dose possible, with infrequent or irregular dosing.

Nitroglycerin

Anti-Anginals Organic Nitrate Undergoes significant first-pass metabolism(taken sublingually, transdermally, buccal, IV). Has rapid onset(2-5 in) sublingually, which lasts only 30 min. Transdermal patches are longer acting preps(12-24 hours). Given IV for unstable angina and acute heart failure. Given sublingually, or via spray as first-line therapy for acute anginal symptoms. Actions - Nitrous oxide(NO) is primarily produced by vascular endothelial cells to activate guanylyl cyclase to convert GTP to cGMP, resulting in smooth muscle relaxation. Also activates K+ channels, leading to hyperpolariziation. cGMP also stimulates cGMP-dependent protein kinase, that activates MLC phosphatase, which dephosphorylates MLC, leading to relaxation. NO relaxes vascular smooth muscle(vasodilator), inhibits platelet aggregation(anti-thrombotic), and inhibits leukocyte-endothelial interactions(anti-inflammatory). This drug mimics actions of NO by releasing or forming NO. Has more effect on veins than arteries. Dilating coronary arteries can relieve variant angina symptoms. Used to treat stable, unstable, and variant angina. Adverse - hypotension, reflex tachycardia(at high doses), headache(cerebral vasodilation), facial flushing. Contrindications: Should not be taken alongside sildenafil(cGMP-dependent phosphodiesterase) Note: Tolerance develops rapidly. Can be overcome by using smallest dose possible, with infrequent or irregular dosing.

Sodium Nitroprusside

Anti-Anginals Organic Nitrate Very useful in ICU and emergency settings. Has rapid onset of actio. Only available as IV continuously. Actions - Nitrous oxide(NO) is primarily produced by vascular endothelial cells to activate guanylyl cyclase to convert GTP to cGMP, resulting in smooth muscle relaxation. Also activates K+ channels, leading to hyperpolariziation. cGMP also stimulates cGMP-dependent protein kinase, that activates MLC phosphatase, which dephosphorylates MLC, leading to relaxation. NO relaxes vascular smooth muscle(vasodilator), inhibits platelet aggregation(anti-thrombotic), and inhibits leukocyte-endothelial interactions(anti-inflammatory). This drug mimics actions of NO by releasing or forming NO. Has more effect on veins than arteries. Dilating coronary arteries can relieve variant angina symptoms. Used to treat stable, unstable, and variant angina. Adverse - hypotension, reflex tachycardia(at high doses), headache(cerebral vasodilation), facial flushing. Cyanide toxicity(rare) Contrindications: Should not be taken alongside sildenafil(cGMP-dependent phosphodiesterase) Note: Tolerance develops rapidly. Can be overcome by using smallest dose possible, with infrequent or irregular dosing.

Ranolazine

Anti-Anginals Sodium Channel Blocker Metabolized by CYP 3A4 Actinos - Blocks late inward Na+ currents in cardiomyocytes, preventing Ca2+ overload within cells, leading to improved coronary blood flow. Also, thought to have effects on fatty acid oxidation. Has no significant effects on either heart rate or arterial pressure. Used as an alternative option for patients with chronic angina that have failed all other therapies. Adverse - QT prolongation, nausea, vomiting, dizziness, constipation. Contraindications: QT prolongation, due to risk of torsades de pointes and ventricular tachyarrhythmias.

Acebutolol

Anti-Anginals beta-Antagonist (Partial agonist? ISA like Pindolol?)

Propranolol

Anti-Anginals beta-Antagonist (Non-selective) Recommended in all patients with stable angina who have had an acute coronary syndrome or who have left ventricular dysfunction, unless contraindicated. There is no reflex tachycardia due to their negative inotropic/chronotropic effects. Reduces both frequency and severity of anginal attacks. Also decreases mortality after MI. Given orally. Extensive first-pass metabolism. Actions - Decreases myocardial contractility, heart rate, and cardiac output, and reduces renin secretion. Used to treat hypertension, angina, myocardial infarction, arrhythmias, and heart failure. Adverse - Abrupt cessation may produce unstable angina, MI, or even death in patients with coronary disease, or tachycardia, sweating, and malaise in patients without. Bradycardia, reduced exercise capacity, heart failure, hypotension, AV block, disturbed lipid metabolism, hypoglycemia, bronchoconstriction, and CNS effects. Contraindications: Prinzmetal (variant) angina, asthma, COPD, sinus bradycardia, partial AV block, heart failure, diabetes mellitus.

Atenolol

Anti-Anginals beta1-Antagonist Recommended in all patients with stable angina who have had an acute coronary syndrome or who have left ventricular dysfunction, unless contraindicated. There is no reflex tachycardia due to their negative inotropic/chronotropic effects. Reduces both frequency and severity of anginal attacks. Also decreases mortality after MI. Less likely to cause bronchospasm and vasoconstriction than non-selective beta-blockers. May be safer in patients with asthma, COPD, and diabetes. Most commonly used beta-blockers for angina. Given orally. Actions - Decreases myocardial contractility, heart rate, and cardiac output, and reduces renin secretion. Used to treat hypertension, angina, myocardial infarction, arrhythmias, and heart failure. Adverse - Abrupt cessation may produce unstable angina, MI, or even death in patients with coronary disease, or tachycardia, sweating, and malaise in patients without. Bradycardia, reduced exercise capacity, heart failure, hypotension, AV block, disturbed lipid metabolism, hypoglycemia, bronchoconstriction, and CNS effects. Contraindications: Prinzmetal (variant) angina, sinus bradycardia, partial AV block, heart failure.

Metoprolol

Anti-Anginals beta1-Antagonist Recommended in all patients with stable angina who have had an acute coronary syndrome or who have left ventricular dysfunction, unless contraindicated. There is no reflex tachycardia due to their negative inotropic/chronotropic effects. Reduces both frequency and severity of anginal attacks. Also decreases mortality after MI. Less likely to cause bronchospasm and vasoconstriction than non-selective beta-blockers. May be safer in patients with asthma, COPD, and diabetes. Most commonly used beta-blockers for angina. Given orally. Extensive first-pass metabolism. Actions - Decreases myocardial contractility, heart rate, and cardiac output, and reduces renin secretion. Used to treat hypertension, angina, myocardial infarction, arrhythmias, and heart failure. Adverse - Abrupt cessation may produce unstable angina, MI, or even death in patients with coronary disease, or tachycardia, sweating, and malaise in patients without. Bradycardia, reduced exercise capacity, heart failure, hypotension, AV block, disturbed lipid metabolism, hypoglycemia, bronchoconstriction, and CNS effects. Contraindications: Prinzmetal (variant) angina, sinus bradycardia, partial AV block, heart failure.

Captopril

Anti-Hypertensives ACE Inhibitors First-line agents for primary hypertension. Drug of choice for patients with hypertension and diabetes, as they have been shown to slow development and progression of diabetic glomerulopathy. Block the conversion of angiotensin I to angiotensin II, thus reducing angiotensin II vasoconstriction and aldosterone secretion, resulting in a reduction in bp, without elicitng reflex tachycardia. Do not reflexively increase cardiac output, rate, or contractility. Actions - decrease Na+ and water retention, increase bradykinin levels(potent vasodilator). Used to treat primary hypertension and hypertension caused by unilateral renal artery stenosis. Also very effective in treatment of chronic heart failure, and patients following MI. Also have a particularly useful role in treating patients with chronic kidney disease. Adverse - dry cough, hypotension, hyperkalemia(rarely clinically important, but can be serious in patients with chronic kidney disease), angioedema, acute renal failure(in patients with bilateral renal artery stenosis). Contraindications: Pregnancy, hyperkalemia, and bilateral renal artery stenosis.

Methyldopa

Anti-Hypertensives Centrally Acting Adrenergic Drug Choice of treatment of pregnancy-induced hypertension. Not first-line therapy because of side effects associated with their actions within the brain. Actions - Reduces sympathetic outflow by acting on presynaptic alpha2 receptors, leading to a decrease in PVR. Does not decrease renal blood flow or GFR. Used to treat chronic hypertension and hypertensive crises. Adverse - sedation, drowsiness, dizziness, nausea, headache, weakness, fatigue, sexual dysfunction, nightmares, mental depression, vertigo, hemolytic anemia, hepatitis.

Enalapril

Anti-Hypertensives ACE Inhibitors First-line agents for primary hypertension. Drug of choice for patients with hypertension and diabetes, as they have been shown to slow development and progression of diabetic glomerulopathy. Block the conversion of angiotensin I to angiotensin II, thus reducing angiotensin II vasoconstriction and aldosterone secretion, resulting in a reduction in bp, without elicitng reflex tachycardia. Do not reflexively increase cardiac output, rate, or contractility. Actions - decrease Na+ and water retention, increase bradykinin levels(potent vasodilator). Used to treat primary hypertension and hypertension caused by unilateral renal artery stenosis. Also very effective in treatment of chronic heart failure, and patients following MI. Also have a particularly useful role in treating patients with chronic kidney disease. Adverse - dry cough, hypotension, hyperkalemia(rarely clinically important, but can be serious in patients with chronic kidney disease), angioedema, acute renal failure(in patients with bilateral renal artery stenosis). Contraindications: Pregnancy, hyperkalemia, and bilateral renal artery stenosis.

Lisinopril

Anti-Hypertensives ACE Inhibitors First-line agents for primary hypertension. Drug of choice for patients with hypertension and diabetes, as they have been shown to slow development and progression of diabetic glomerulopathy. Block the conversion of angiotensin I to angiotensin II, thus reducing angiotensin II vasoconstriction and aldosterone secretion, resulting in a reduction in bp, without elicitng reflex tachycardia. Do not reflexively increase cardiac output, rate, or contractility. Actions - decrease Na+ and water retention, increase bradykinin levels(potent vasodilator). Used to treat primary hypertension and hypertension caused by unilateral renal artery stenosis. Also very effective in treatment of chronic heart failure, and patients following MI. Also have a particularly useful role in treating patients with chronic kidney disease. Adverse - dry cough, hypotension, hyperkalemia(rarely clinically important, but can be serious in patients with chronic kidney disease), angioedema, acute renal failure(in patients with bilateral renal artery stenosis). Contraindications: Pregnancy, hyperkalemia, and bilateral renal artery stenosis.

Losartan

Anti-Hypertensives Angiotension II Receptor Blocker Not yet approved for post-MI. Has same beneficial effects in patients with left ventricular failure or with nephropathy due to type 1 diabetes. Good alternative to ACEI in patients who experience bradykinin mediated cough. Actions - directly block the angiotensin type 1 receptor that mediate the effects of angiotensin II. Does not block breakdown of bradykinin, which contributes to both the vasodilation by ACEI and the dry cough. Used to treat hypertension and heart failure similarly to ACEI. Adverse - lowest incidence of side effects compared with other antihypertensive agents. Hypotension, hyperkalemia, acute renal failure angioedema. Contraindications: pregnancy, bilateral renal artery stenosis, hyperkalemia.

Valsartan

Anti-Hypertensives Angiotension II Receptor Blocker Not yet approved for post-MI. Has same beneficial effects in patients with left ventricular failure or with nephropathy due to type 1 diabetes. Good alternative to ACEI in patients who experience bradykinin mediated cough. Actions - directly block the angiotensin type 1 receptor that mediate the effects of angiotensin II. Does not block breakdown of bradykinin, which contributes to both the vasodilation by ACEI and the dry cough. Used to treat hypertension and heart failure similarly to ACEI. Adverse - lowest incidence of side effects compared with other antihypertensive agents. Hypotension, hyperkalemia, acute renal failure angioedema. Contraindications: pregnancy, bilateral renal artery stenosis, hyperkalemia.

Diltiazem

Anti-Hypertensives Calcium Channel Blocker - Benzothiazepine First-line agents. Useful in patients with angina or diabetes. Blocks voltage-sensitive L-type calcium channels located on vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue. Actions - vascular smooth muscle relaxation(vasodilation), decreased myocardial force generation, and decreased heart rate. Intermediate between verapamil and the dihydropyridines in selectivity. Having both cardiac depressant and vasodilator actions, able to reduce arterial pressure without producing the same degree of reflex tachycardia as the dihydropyridines Used to treat hypertension, angina, and arrhythmias. Adverse - bradycardia, AV block, heart failure, anorexia, nausea, peripheral edema, hypotension, constipation. Contraindications: bradycardia, conduction defects, heart failure.

Amlodipine

Anti-Hypertensives Calcium Channel Blocker - Dihydropyridine First-line agents. Useful in patients with angina or diabetes. Blocks voltage-sensitive L-type calcium channels located on vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue. Actions - vascular smooth muscle relaxation(vasodilation), decreased myocardial force generation, and decreased heart rate. More slective for vascular smooth muscle than other CCBs, and has less effect on cardiac muscle. More likely to evoke reflex tachycardia. Primarily used for treatment compared to verapamil or diltiazem. Used to treat hypertension, angina, and arrhythmias. Adverse - reflex tachycardia, dizziness, flushing, headache, gingival hyperplasia, peripheral edema. Contraindications: bradycardia, conduction defects, heart failure.

Nifedipine

Anti-Hypertensives Calcium Channel Blocker - Dihydropyridine First-line agents. Useful in patients with angina or diabetes. Blocks voltage-sensitive L-type calcium channels located on vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue. Actions - vascular smooth muscle relaxation(vasodilation), decreased myocardial force generation, and decreased heart rate. More slective for vascular smooth muscle than other CCBs, and has less effect on cardiac muscle. More likely to evoke reflex tachycardia. Primarily used for treatment compared to verapamil or diltiazem. Used to treat hypertension, angina, and arrhythmias. Adverse - reflex tachycardia, dizziness, flushing, headache, gingival hyperplasia, peripheral edema. Contraindications: bradycardia, conduction defects, heart failure.

Verapamil

Anti-Hypertensives Calcium Channel Blocker - Diphenylalkylamine First-line agents. Useful in patients with angina or diabetes. Blocks voltage-sensitive L-type calcium channels located on vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue. Has greatest depressant effect on heart and may decrease heart rate and cardiac output Actions - vascular smooth muscle relaxation(vasodilation), decreased myocardial force generation, and decreased heart rate. Relatively selective for the myocardium. More commonly used for the treatment of angina and cardiac arrhythmias. Used to treat hypertension, angina, and arrhythmias. Adverse - bradycardia, AV block, heart failure, anorexia, nausea, peripheral edema, hypotension, constipation. Contraindications: bradycardia, conduction defects, heart failure.

Doxazosin

Anti-Hypertensives alpha1-Antagonists All alpha antagonists are only advised to be used in combination with primary antihypertensive angents. Blocks alpha1 receptors in arterioles and venules, and reduces vasoconstriction and PVR, resulting in decreased blood pressure. NE is left to exert unopposed negative feedback on its own release via alpha2 receptors and results in less reflex tachycardia than non-selective antagonists(binding to beta1-receptors). Vasodilator effect is more pronounced in arterial resistance vessels. Used to treat primary hypertension, although use is not as widespread as other antihypertensive drugs. Adverse - Na+ and water retention can occur with chronic administration, dizziness, drowsiness, lack of energy, nausea, palpitations. Note: First dose can cause precipitous drop in standing blood pressure, so first dose should be small and given at bedtime.

Prazosin

Anti-Hypertensives alpha1-Antagonists All alpha antagonists are only advised to be used in combination with primary antihypertensive angents. Blocks alpha1 receptors in arterioles and venules, and reduces vasoconstriction and PVR, resulting in decreased blood pressure. NE is left to exert unopposed negative feedback on its own release via alpha2 receptors and results in less reflex tachycardia than non-selective antagonists(binding to beta1-receptors). Vasodilator effect is more pronounced in arterial resistance vessels. Used to treat primary hypertension, although use is not as widespread as other antihypertensive drugs. Adverse - Na+ and water retention can occur with chronic administration, dizziness, drowsiness, lack of energy, nausea, palpitations. Note: First dose can cause precipitous drop in standing blood pressure, so first dose should be small and given at bedtime.

Terazosin

Anti-Hypertensives alpha1-Antagonists All alpha antagonists are only advised to be used in combination with primary antihypertensive angents. Blocks alpha1 receptors in arterioles and venules, and reduces vasoconstriction and PVR, resulting in decreased blood pressure. NE is left to exert unopposed negative feedback on its own release via alpha2 receptors and results in less reflex tachycardia than non-selective antagonists(binding to beta1-receptors). Vasodilator effect is more pronounced in arterial resistance vessels. Used to treat primary hypertension, although use is not as widespread as other antihypertensive drugs. Adverse - Na+ and water retention can occur with chronic administration, dizziness, drowsiness, lack of energy, nausea, palpitations. Note: First dose can cause precipitous drop in standing blood pressure, so first dose should be small and given at bedtime.

Pindolol

Anti-Hypertensives beta-Antagonists - beta-Antagonist(Non-selective partial agonist) Preferred beta-blocker for use in pregnancy. First line therapy only for patients with coronary artery disease or left ventricular dysfunction. Used only as add-on therapy to first line agents in primary prevention patients. Given orally. Actions - decreases CO, contractility, and heart rate. Inhibits both release of NE and renin (beta1). There is no reflex tachycardia, due to negative inotropic/chronotropic actions. Unfortunately does not reduce CV events as well as other beta-blockers and may increase risk after MI. Used to treat hypertension, angina, myocardial infarction, arrhythmias, and heart failure. Adverse - abrupt cessation may produce unstable angina, MI, or even death in patients with coronary disease(must taper off). Bradycardia, heart failure, hypotension, AV block, and reduced exercise capacity. Hypolgycemia from beta2(tachycardia, which is normally a warning sign for insulin-induced hypoglycemia, may be masked because of beta1 blockade). Bronchoconstriction. Contraindications in patients with reactive airway disease(asthma, COPD) and patients with sinus bradycardia and partial AV block.

Propranolol

Anti-Hypertensives beta-Antagonists - beta-Antagonist(Non-selective) First line therapy only for patients with coronary artery disease or left ventricular dysfunction. Used only as add-on therapy to first line agents in primary prevention patients. Given orally. Extensive first-pass metabolism. Actions - decreases CO, contractility, and heart rate. Inhibits both release of NE and renin (beta1). There is no reflex tachycardia, due to negative inotropic/chronotropic actions. Used to treat hypertension, angina, myocardial infarction, arrhythmias, and heart failure. Adverse - abrupt cessation may produce unstable angina, MI, or even death in patients with coronary disease(must taper off). Bradycardia, heart failure, hypotension, AV block, and reduced exercise capacity. Increases TAGs, decreases HDLs. Hypolgycemia from beta2(tachycardia, which is normally a warning sign for insulin-induced hypoglycemia, may be masked because of beta1 blockade). Bronchoconstriction. Contraindications in patients with reactive airway disease(asthma, COPD) and patients with sinus bradycardia and partial AV block.

Atenolol

Anti-Hypertensives beta-Antagonists - beta1-Antagonist Most widely used. First line therapy only for patients with coronary artery disease or left ventricular dysfunction. Used only as add-on therapy to first line agents in primary prevention patients. Given orally. Actions - decreases CO, contractility, and heart rate. Inhibits both release of NE and renin (beta1). There is no reflex tachycardia, due to negative inotropic/chronotropic actions. Used to treat hypertension, angina, myocardial infarction, arrhythmias, and heart failure. Adverse - abrupt cessation may produce unstable angina, MI, or even death in patients with coronary disease(must taper off). Bradycardia, heart failure, hypotension, AV block, and reduced exercise capacity. Increases TAGs, decreases HDLs. Contraindications in patients with reactive airway disease(asthma, COPD) and patients with sinus bradycardia and partial AV block.

Metoprolol

Anti-Hypertensives beta-Antagonists- beta1-Antagonist Most widely used. First line therapy only for patients with coronary artery disease or left ventricular dysfunction. Used only as add-on therapy to first line agents in primary prevention patients. Given orally. Extensive first-pass metabolism. Actions - decreases CO, contractility, and heart rate. Inhibits both release of NE and renin (beta1). There is no reflex tachycardia, due to negative inotropic/chronotropic actions. Used to treat hypertension, angina, myocardial infarction, arrhythmias, and heart failure. Adverse - abrupt cessation may produce unstable angina, MI, or even death in patients with coronary disease(must taper off). Bradycardia, heart failure, hypotension, AV block, and reduced exercise capacity. Increases TAGs, decreases HDLs. Contraindications in patients with reactive airway disease(asthma, COPD) and patients with sinus bradycardia and partial AV block.

Procainamide

Antiarrhythmics Class IA - Na+ Channel Antagonist Class IA has intermediate kinetics. May or may not affect conduction at normal heart rates. Has weak anticholiergic effects. A percentage is acetylated to NAPA, which has class III activity and thus prolongs duration of action potential. Class IA has largely been replaced by safer antiarrhythmics. Actions - bind and block fast Na+ channels responsible for phase 0 depolarization, decreasing automaticity, decreasing the slope of phase 4 depolarization, raising the threshold for action potential firing, and slowing the rate of depolarization. Because nodal tissue action potentials do not rely on fast Na+ channels, Class I drugs do not have any direct effect. Also blocks K+ channels(phase 3) resulting in prolongation of the refractory period. Used to treat atrial fibrillation, supraventricular and ventricular tachyarrhythmias. Adverse - tachycardia, dry mouth, urinary retention, blurred vision, and constipation. Chronic use associated with high incidence of adverse effects including reversible lupus-like syndrome, GI intolerance, aggravation of underlying HF, induction of ventricular arrhythmias, depression, hallucinations, and psychosis. Contraindications: Patients with hypersensitivity, complete heart block, 2nd degree AV block, SLE, and torsades de pointes. Advise caution in patients with heart failure and hypertension.

Lidocaine

Antiarrhythmics Class IB - Na+ Channel Antagonist Class IB has fast kinetics. Drug of choice for termination of ventricular tachycardia and prevention of ventricular fibrillation after cardioversion in the setting of acute ischemia. Not very potent antiarrhythmic and has minimal effects on atrial tissue. Can only be given IV due to extensive first-pass metabolism. Actions - bind and block fast Na+ channels responsible for phase 0 depolarization, decreasing automaticity, decreasing the slope of phase 4 depolarization, raising the threshold for action potential firing, and slowing the rate of depolarization. Because nodal tissue action potentials do not rely on fast Na+ channels, Class I drugs do not have any direct effect. Only exert effects at fast heart rates, so do not affect tissue functioning at normal rhythm at normal rate. More likely to affect ischemic or diseased tissue. Cause slight reduction in refractory period by increasing K+ efflux. Used to treat ventricular arrhythmias. Adverse - wide toxic-therapeutic ratio, so little risk. Dizziness, sedation, slurred speech, blurred vision, paresthesia, muscle twitching, confusion, nausea, vomiting, seizures, psychosis, sinus arrest, and aggravation of underlying conduction disturbances. Overdoses result in convulsions and coma.

Mexiletine

Antiarrhythmics Class IB - Na+ Channel Antagonist Class IB has fast kinetics. Not very potent antiarrhythmic and has minimal effects on atrial tissue. Can only be given IV due to extensive first-pass metabolism. Actions - bind and block fast Na+ channels responsible for phase 0 depolarization, decreasing automaticity, decreasing the slope of phase 4 depolarization, raising the threshold for action potential firing, and slowing the rate of depolarization. Because nodal tissue action potentials do not rely on fast Na+ channels, Class I drugs do not have any direct effect. Only exert effects at fast heart rates, so do not affect tissue functioning at normal rhythm at normal rate. More likely to affect ischemic or diseased tissue. Cause slight reduction in refractory period by increasing K+ efflux. Used to treat ventricular arrhythmias. Adverse - Mainly CNS and GI side effects. Diarrhea, nausea, headache, dizziness.

Tocainide

Antiarrhythmics Class IB - Na+ Channel Antagonist Class IB has fast kinetics. Not very potent antiarrhythmic and has minimal effects on atrial tissue. Can only be given IV due to extensive first-pass metabolism. Actions - bind and block fast Na+ channels responsible for phase 0 depolarization, decreasing automaticity, decreasing the slope of phase 4 depolarization, raising the threshold for action potential firing, and slowing the rate of depolarization. Because nodal tissue action potentials do not rely on fast Na+ channels, Class I drugs do not have any direct effect. Only exert effects at fast heart rates, so do not affect tissue functioning at normal rhythm at normal rate. More likely to affect ischemic or diseased tissue. Cause slight reduction in refractory period by increasing K+ efflux. Used to treat ventricular arrhythmias. Adverse - severe hematological and pulmonary toxicities.

Flecainide

Antiarrhythmics Class IC - Na+ Channel Antagonist Class IC has slow kinetics. Actions - bind and block fast Na+ channels responsible for phase 0 depolarization, decreasing automaticity, decreasing the slope of phase 4 depolarization, raising the threshold for action potential firing, and slowing the rate of depolarization. Because nodal tissue action potentials do not rely on fast Na+ channels, Class I drugs do not have any direct effect. Express effects at all heart rates due to slow kinetics, making them most potent of all Class I drugs. Used to treat life-threatening supraventricular tachyarrhythmias and ventricular tacyharrhythmias. Also used for the prevention of paroxysmal atrial fibrillation and the maintenance of normal sinus rhythm in patients with symptomatic atrial fibrillation. Adverse - Recently seen to increase mortality more than two-fold in post MI patients treated for premature contractions(CAST, cardiac arrhythmia suppression trial). Use is reserved for sever symptomatic arrhythmias. Blurred vision, dizziness, dyspnea, headache, tremor, nausea, aggravation of existing heart failure(due to negative inotropic effect), and conduction disturbances. Also can induce life-threatening ventricular arrhythmias.

Propafenone

Antiarrhythmics Class IC - Na+ Channel Antagonist Class IC has slow kinetics. Actions - bind and block fast Na+ channels responsible for phase 0 depolarization, decreasing automaticity, decreasing the slope of phase 4 depolarization, raising the threshold for action potential firing, and slowing the rate of depolarization. Because nodal tissue action potentials do not rely on fast Na+ channels, Class I drugs do not have any direct effect. Express effects at all heart rates due to slow kinetics, making them most potent of all Class I drugs. Used to treat life-threatening supraventricular tachyarrhythmias and ventricular tacyharrhythmias. Also used for the prevention of paroxysmal atrial fibrillation and the maintenance of normal sinus rhythm in patients with symptomatic atrial fibrillation. Adverse - Recently seen to increase mortality more than two-fold in post MI patients treated for premature contractions(CAST, cardiac arrhythmia suppression trial). Use is reserved for sever symptomatic arrhythmias. Dizziness, fatigue, bronchospasm(slight beta-blocking effect), headache, taste disturbances, GI upset, AV block, aggravation of underlying heart failure(beta-blocking and slight Ca2+ channel blocking activity), conduction disturbances, or arrhythmias can all occur.

Propranolol

Antiarrhythmics Class II - beta Antagonist (Non-selective) Affect predominantly slow-response tissues(SA and AV nodes). Antiarrhythmic properties related to ability to inhibit sympathetic tone, particularly at beta1. Actions - Decrease rate of automaticity, slow conduction velocity, and prolong refractory period. HR slowed, PR interval lengthened, repolarization is prolonged at AV node. Used to treat supraventricular arrhythmias(atrial flutter, atrial fibrillation, and AV-nodal re-entrant tachycardia). Also used to treat ventricular tachyarrhythmias. Use has been shown to reduce incidence of sudden arrhythmic death after MI. Adverse - Usually well tolerated. Adverse effects include sleep disturbance, GI upset, bradycardia, hypotension, and CNS effects. Contraindications: CHF, severe bradycardia or heart block(due to negative inotropic effect), and severe hyperactive airway disease(due to blockade of beta2)

Metoprolol

Antiarrhythmics Class II - beta1 Antagonist Affect predominantly slow-response tissues(SA and AV nodes). Antiarrhythmic properties related to ability to inhibit sympathetic tone, particularly at beta1. Actions - Decrease rate of automaticity, slow conduction velocity, and prolong refractory period. HR slowed, PR interval lengthened, repolarization is prolonged at AV node. Used to treat supraventricular arrhythmias(atrial flutter, atrial fibrillation, and AV-nodal re-entrant tachycardia). Also used to treat ventricular tachyarrhythmias. Use has been shown to reduce incidence of sudden arrhythmic death after MI. Adverse - Usually well tolerated. Adverse effects include sleep disturbance, GI upset, bradycardia, hypotension, and CNS effects. Contraindications: CHF, and severe bradycardia or heart block(due to negative inotropic effect)

Esmolol

Antiarrhythmics Class II - beta1 Antagonist Affect predominantly slow-response tissues(SA and AV nodes). Antiarrhythmic properties related to ability to inhibit sympathetic tone, particularly at beta1. Short-acting(half-life = 9min.), so useful in treatment of acute arrhythmias occurring during surgery or in emergency situations. Actions - Decrease rate of automaticity, slow conduction velocity, and prolong refractory period. HR slowed, PR interval lengthened, repolarization is prolonged at AV node. Used to treat supraventricular arrhythmias(atrial flutter, atrial fibrillation, and AV-nodal re-entrant tachycardia). Also used to treat ventricular tachyarrhythmias. Use has been shown to reduce incidence of sudden arrhythmic death after MI. Adverse - Usually well tolerated. Adverse effects include sleep disturbance, GI upset, bradycardia, hypotension, and CNS effects. Contraindications: CHF, and severe bradycardia or heart block(due to negative inotropic effect)

Sotalol

Antiarrhythmics Class III - K+ Channel Antagonist By blocking K+ channels responsible for phase 3 repolarization, able to prolong action potential duration and increase effective refractory period in both fast- and slow-response tissues, causing QT-interval prolongation. Actions - Has potent non-selective class II(beta-blocking) activity. Used to treat life-threatening ventricular arrhythmias. Also used to maintain sinus rhythm in patients with atrial fibrillation and atrial flutter who are currently in sinus rhythm. Due to its pro-arrhythmic effects, not used for asymptomatic arrhythmias. Adverse - Has lowest rate of long-term or acute adverse effects. Has similar effects to all beta-blockers as well as dizziness, weakness, and fatigue.

Dofetilide

Antiarrhythmics Class III - K+ Channel Antagonist By blocking K+ channels responsible for phase 3 repolarization, able to prolong action potential duration and increase effective refractory period in both fast- and slow-response tissues, causing QT-interval prolongation. Actions - very potent K+ channel blocker and has virtually no extracardiac pharmacological effects. Used for maintenance of normal sinus rhythm in patients with chronic atrial fibrillation/flutter of longer than 1-week duration who have been converted to normal sinus rhythm. Also used for conversion of atrial fibrillation/flutter to normal sinus rhythm. Adverse - Headache and dizziness. Ventricular tachycardia and torsades de pointes can also occur.

Amiodarone

Antiarrhythmics Class III - K+ Channel Antagonist By blocking K+ channels responsible for phase 3 repolarization, able to prolong action potential duration and increase effective refractory period in both fast- and slow-response tissues, causing QT-interval prolongation. Can be taken IV or orally. Very long half-life(25-60 days), requires loading dose. Full effects take ~6 weeks. Actions - class I(Na+ channel blocking), II(beta-blocking), III(K+ channel blocking), and IV(Ca2+ channel blocking) activity and therefore decreases slope of phase 4 and conduction velocity in addition to phase 3 effects. Dominant effect is class III. Due to wide range, one of the most commonly employed antiarrhythmic drugs. Used to treat severe supraventricular and ventricular arrhythmias. Adverse - Mostly dose-related, and can be resolved by decreasing dose. Tremor, ataxia, parasthesia, GI disturbances, bradycardia, AV block, hyper- or hypothyroidism(serum TSH tested before intiation), interstitial pulmonary fibrosis, arrhythmias, liver toxicity, photosensitivity, blue-gray skin discoloration, and hypotension(IV only). Contraindications: Due to class II and class IV effects: bradycardia, SA or AV block, severe hypotension, severe respiratory failure. Also able to alter concentrations of digoxin, theophylline, warfarin, and quinidine, and dosage adjustments may be necessary.

Diltiazem

Antiarrhythmics Class IV - Ca2+ Channel Antagonist 'Cardiac-selective' Ca2+ channel blockers. Actions - decrease Ca2+ dependent action potentials in slow-response tissues(decreased rate of phase 4 spontaneous depolarization) and thus decrease the rate of automaticity, slow conduction velocity, and prolong the effective refractory period. HR slowed, PR interval lengthened, prolonged repolarization at AV node. Used to treat supraventricular tachycardia. Also used in the reduction of ventricular rate in atrial fibrillation & atrial flutter. Adverse - Excessive bradycardia, impaired electrical conduction, depressed contractility. Can also cause transient decrease in BP due to some effects on vascular smooth muscle. Also nausea, constipation, headache, fatigue, dizziness. Contraindications: Pre-existing depressed cardiac function.

Verapamil

Antiarrhythmics Class IV - Ca2+ Channel Antagonist 'Cardiac-selective' Ca2+ channel blockers. Slightly higher selectivity for myocardium than diltiazem. Actions - decrease Ca2+ dependent action potentials in slow-response tissues(decreased rate of phase 4 spontaneous depolarization) and thus decrease the rate of automaticity, slow conduction velocity, and prolong the effective refractory period. HR slowed, PR interval lengthened, prolonged repolarization at AV node. Used to treat supraventricular tachycardia. Also used in the reduction of ventricular rate in atrial fibrillation & atrial flutter. Adverse - Excessive bradycardia, impaired electrical conduction, depressed contractility. Can also cause transient decrease in BP due to some effects on vascular smooth muscle. Also nausea, constipation, headache, fatigue, dizziness. Contraindications: Pre-existing depressed cardiac function. Can increase concentrations of other CV drugs, such as digoxin, dofetilide, simvastatin, and lovastatin.

Digoxin

Antiarrhythmics Miscellaneous - Cardiac glycoside Very narrow therapeutic window. Half-life is 36-40 hours. Has large volume of distribution, including CSF(accumulates in muscle). Loading dose required. Does not increase survival. Actions - Both positively inotropic(selective inhibitor of Na+/K+ ATPase) and negatively chronotropic. Activates vagal efferent nerves to the heart(parasympathomimetic effect), resulting in reduction in conduction of electrical impulses within the AV node, decreasing ventricular rate. Also prolongs effective refractory period within AV node. Can also cause baroreceptor sensitization, offsetting desensitization in HF. Used to control ventricular response rate in atrial fibrillation and flutter with impaired left ventricular function or heart failure. Adverse - Cardiac arrhythmia, especially atrial tachycardias and AV block. Toxic doses can cause ectopic ventricular beats leading to ventricular tachycardias & ventricular fibrillation. Also anorexia, nausea, vomiting, headache, fatigue, confusion, blurred or yellow vision, alteration of color perception, and halo on dark objects. Contraindications: Patients with diastolic or right-sided HF, uncontrolled hypertension, bradyarrhythmia, hypokalemia, non-responders or intolerance. Interactions: K+ decreases affinity of Na+/K+ ATPase for digoxin, therefore, hypokalemia enhances therapeutic and toxic effects, and hyperkalemia reduces. Hypercalcemia ehnahces digoxin-induced increases in intracellular Ca2+, leading to overloading and arrhythmias. Hypomagnesia sensitizes the heart to digoxin-induced arrhythmias, since Mg2+ antagonizes effects of Ca2+. Quinidine(class IA), Amiodarone(class III), Verapamil(CCB), and NSAIDs compete with digoxin for binding sites and depress renal clearance. Diuretics can indirectly interact, since the can decrease plasma potassium. Hypothyroidism can cause higher concentrations. Hyperthyroidism can cause lower concentrations. Renal failure requires closely monitored levels. Treatment of toxcity - Withdraw drug, or lower dose. Adjust electrolyte status. Treat ventricular arrhythmias with lidocaine and/or Mg2+. If severe, treat with digitalis antibodies(Digoxine immune fab or Digibind).

Adenosine

Antiarrhythmics Miscellaneous - Endogenous molecular compound. Drug of choice for treatment. Naturally present throughout body. AV node is more sensitive than SA node. Only IV. Half-life = 15s Actions - Stimulates P1 class of purinergic receptors, opens G protein-coupled K+ channel, and inhibits SA nodal, atrial, and AV nodal conduction by increasing K+ conductance. Also inhibits cAMP-mediated Ca2+ influx, suppressing Ca2+ dependent action potentials. Net result is decreased conduction velocity, prolongation of refractory period, and decreased automaticity in AV node. Used to abolish acute supraventricular tachycardia. Adverse - Low incidence of toxicity, and most are transient. Flushing, headache, chest pain, excessive AV or SA nodal inhibition. Bronchoconstriction can occur for up to 30 min in patients with asthma.

Magnesium

Antiarrhythmics Miscellaneous - Mineral Important ion in many enzymatic reactions, including cardiac Na+/K+ ATPase. Actions - Hypomagnesia can inhibit Na+/K+ ATPase, leading to cellular depolarization. Functions as 'Ca2+ antagonist', preventing influx of Ca2+ into cell. Also thought to exert some effects on other Na+, K+, and Ca2+ channels(although not understood). Used for treatment of torsades de pointes, digitalis-induced arrhythmia, prophylaxis of arrhythmia in acute MI

Atropine

Antiarrhythmics Miscellaneous - Muscarinic Antagonist Muscarinic blocker. Actions - Inhibits effects of excessive vagal activation on the heart. Can temporarily revert sinus bradycardia to normal sinus rhythm, and reverse AV nodal blocks by removing vagal influences. Used in bradyarrhythmias to decrease vagal tone.

Colesevelam

Antihyperlipidemic Bile Acid-Binding Resin Better tolerated than Cholestyramine or Colesevelam. Drug of choice for children and woman planning to become pregnant. Little effect on plasma LDL in individuals who completely lack functional LDL receptors. Useful only in hyperlipoproteinemias involving isolated increases in LDL. In patients with hypertriglyceridemia as well as elevated LDL, VLDL may be further increased during treatment. Water insoluble and large molecular weights prevent them from being either absorbed, or metabolically altered in intestine, thus are totally excreted in feces. Actions - Bind to anionic bile acids in intestinal lumen and are excreted as the complex, preventing bile acids from returning to liver. Bile acid reduction increases hepatic conversion of cholesterol to bile acids, decreasing intracellular cholesterol, upregulating hepatic LDL receptors, decreasing plasma LDL levels. HDL rises modestly. Used with statins or niacin to increase LDL reduction. Adverse - bloating, nausea, cramping, constipation. Contraindications: hypertriglyceridemia. Pregnancy Category B(Only if clearly needed)

Cholestyramine

Antihyperlipidemic Bile Acid-Binding Resin Drug of choice for children and woman planning to become pregnant. Little effect on plasma LDL in individuals who completely lack functional LDL receptors. Useful only in hyperlipoproteinemias involving isolated increases in LDL. In patients with hypertriglyceridemia as well as elevated LDL, VLDL may be further increased during treatment. Water insoluble and large molecular weights prevent them from being either absorbed, or metabolically altered in intestine, thus are totally excreted in feces. Actions - Bind to anionic bile acids in intestinal lumen and are excreted as the complex, preventing bile acids from returning to liver. Bile acid reduction increases hepatic conversion of cholesterol to bile acids, decreasing intracellular cholesterol, upregulating hepatic LDL receptors, decreasing plasma LDL levels. HDL rises modestly. Used with statins or niacin to increase LDL reduction. Adverse - bloating, nausea, cramping, constipation, interfere with absorption of other drugs and Vitamins A, D, E, & K. Contraindications: hypertriglyceridemia. Pregnancy Category C

Colestipol

Antihyperlipidemic Bile Acid-Binding Resin Drug of choice for children and woman planning to become pregnant. Little effect on plasma LDL in individuals who completely lack functional LDL receptors. Useful only in hyperlipoproteinemias involving isolated increases in LDL. In patients with hypertriglyceridemia as well as elevated LDL, VLDL may be further increased during treatment. Water insoluble and large molecular weights prevent them from being either absorbed, or metabolically altered in intestine, thus are totally excreted in feces. Actions - Bind to anionic bile acids in intestinal lumen and are excreted as the complex, preventing bile acids from returning to liver. Bile acid reduction increases hepatic conversion of cholesterol to bile acids, decreasing intracellular cholesterol, upregulating hepatic LDL receptors, decreasing plasma LDL levels. HDL rises modestly. Used with statins or niacin to increase LDL reduction. Adverse - bloating, nausea, cramping, constipation, interfere with absorption of other drugs and Vitamins A, D, E, & K. Contraindications: hypertriglyceridemia. Pregnancy Category C

Ezetimibe

Antihyperlipidemic Cholesterol Absorption Inhibitor Inhibits intestinal absorption of cholesterol and phytosterols. Also causes small increases in HDL and mild decrease in TAGs. Complementary actions to statins. Combination provides additive reductions in LDl levels. Actions - selective inhibitor of a trasport protein(NPC1L1) in jejunal enterocytes, which takes up cholesterol from the lumen. Reduces cholesterol absorption by 54%, causing a compesatory increase in cholesterol synthesis(inhibited by statins), which reduces chylomicrons, which may decrease atherogenesis directly, since chylomicrons are very atherogenic lipoproteins. Also leads to upregulation of LDL receptors, enhancing plasma LDL clearance. Used to lower plasma LDL levels. Adverse - reversible impaired hepatic function(low incidence, slightly increased when given with statin), myositis. Pregnancy Category C

Fenofibrate

Antihyperlipidemic Fibrate Derivative Derivative of first-generation fibric acid clofibrate. Lowers VLDL levels and increases HDL levels. Actions - Activate nuclear transcription receptor, peroxisome proliferator-activated receptor-alpha(PPAR-alpha), expressed in liver and brown adipose(and, to a lesser extent, kidney, heart, skeletal muscle). Activation results in a decrease in plasma TAGs(increased muscle cell expression of LPL, decreased hepatic expression of apoCIII, and increased hepatic oxidation of fatty acids) and moderate increase in plasma HDL. Used to treat hypertriglyceridemias, in which VLDL predominate, and in dysbetalipoproteinemia. Adverse - Mild GI disturbances, myositis(renal insufficiency patients at risk), rhabdomyolysis(rare), lithiasis. Pregnancy Category C

Gemfibrozil

Antihyperlipidemic Fibrate Derivative Derivative of first-generation fibric acid clofibrate. Lowers VLDL levels and increases HDL levels. Actions - Activate nuclear transcription receptor, peroxisome proliferator-activated receptor-alpha(PPAR-alpha), expressed in liver and brown adipose(and, to a lesser extent, kidney, heart, skeletal muscle). Activation results in a decrease in plasma TAGs(increased muscle cell expression of LPL, decreased hepatic expression of apoCIII, and increased hepatic oxidation of fatty acids) and moderate increase in plasma HDL. Used to treat hypertriglyceridemias, in which VLDL predominate, and in dysbetalipoproteinemia. Adverse - Mild GI disturbances, myositis(renal insufficiency patients at risk), rhabdomyolysis(rare), lithiasis. Pregnancy Category C

Lovastatin

Antihyperlipidemic HMG-CoA Inhibitor (Statin) Analogs of 3-OH-3-methylglutarate(HMG). Competitive inhibitor of HMG-CoA reductase, enzyme that catalyzes first committed step of cholesterol biosynthesis. Marked first-pass metabolism in liver. A prodrug that must be hydrolyzed in GIT to yield active beta-hydroxyl derivative. Not as useful in patients homozygous for familiar hypercholesterolemia and lack functional LDL receptors. Useful alone or in combination with bile acid-binding resins, niacin, or ezetimibe. Actions - Inhibits de novo cholesterol synthesis, depleting intracellular supply, upregulating LDL receptors, resulting in increased clearance of LDL from the blood. Also cause modest decrease of plasma TAGs and small increase in HDL. Other effects: improves endothelial function, decreases platelet aggregation, reduces inflammation, decreases plasma levels of C-reactive protein. Used as drug of choice for LDL reduction in all types of hyperlipidemias to reduce cardiovascular mortality. Adverse - elevation of aminotransferases, myopathy, and rhabdomyolysis. Contraindications: Pregnant, lactating, or likely to become pregnant.

Simvastatin

Antihyperlipidemic HMG-CoA Inhibitor (Statin) Analogs of 3-OH-3-methylglutarate(HMG). Competitive inhibitor of HMG-CoA reductase, enzyme that catalyzes first committed step of cholesterol biosynthesis. Marked first-pass metabolism in liver. A prodrug that must be hydrolyzed in GIT to yield active beta-hydroxyl derivative. Not as useful in patients homozygous for familiar hypercholesterolemia and lack functional LDL receptors. Useful alone or in combination with bile acid-binding resins, niacin, or ezetimibe. Actions - Inhibits de novo cholesterol synthesis, depleting intracellular supply, upregulating LDL receptors, resulting in increased clearance of LDL from the blood. Also cause modest decrease of plasma TAGs and small increase in HDL. Other effects: improves endothelial function, decreases platelet aggregation, reduces inflammation, decreases plasma levels of C-reactive protein. Used as drug of choice for LDL reduction in all types of hyperlipidemias to reduce cardiovascular mortality. Adverse - elevation of aminotransferases, myopathy, and rhabdomyolysis. Contraindications: Pregnant, lactating, or likely to become pregnant.

Rosuvastatin

Antihyperlipidemic HMG-CoA Inhibitor (Statin) Analogs of 3-OH-3-methylglutarate(HMG). Competitive inhibitor of HMG-CoA reductase, enzyme that catalyzes first committed step of cholesterol biosynthesis. Marked first-pass metabolism in liver. Along with atorvastatin, most potent statins. Not as useful in patients homozygous for familiar hypercholesterolemia and lack functional LDL receptors. Useful alone or in combination with bile acid-binding resins, niacin, or ezetimibe. Actions - Inhibits de novo cholesterol synthesis, depleting intracellular supply, upregulating LDL receptors, resulting in increased clearance of LDL from the blood. Also cause modest decrease of plasma TAGs and small increase in HDL. Other effects: improves endothelial function, decreases platelet aggregation, reduces inflammation, decreases plasma levels of C-reactive protein. Used as drug of choice for LDL reduction in all types of hyperlipidemias to reduce cardiovascular mortality. Adverse - elevation of aminotransferases, myopathy, and rhabdomyolysis. Contraindications: Pregnant, lactating, or likely to become pregnant.

Atorvastatin

Antihyperlipidemic HMG-CoA Inhibitor (Statin) Analogs of 3-OH-3-methylglutarate(HMG). Competitive inhibitor of HMG-CoA reductase, enzyme that catalyzes first committed step of cholesterol biosynthesis. Marked first-pass metabolism in liver. Along with rosuvastatin, most potent statins. Not as useful in patients homozygous for familiar hypercholesterolemia and lack functional LDL receptors. Useful alone or in combination with bile acid-binding resins, niacin, or ezetimibe. Actions - Inhibits de novo cholesterol synthesis, depleting intracellular supply, upregulating LDL receptors, resulting in increased clearance of LDL from the blood. Also cause modest decrease of plasma TAGs and small increase in HDL. Other effects: improves endothelial function, decreases platelet aggregation, reduces inflammation, decreases plasma levels of C-reactive protein. Used as drug of choice for LDL reduction in all types of hyperlipidemias to reduce cardiovascular mortality. Adverse - elevation of aminotransferases, myopathy, and rhabdomyolysis. Contraindications: Pregnant, lactating, or likely to become pregnant.

Pravastatin

Antihyperlipidemic HMG-CoA Inhibitor (Statin) Analogs of 3-OH-3-methylglutarate(HMG). Competitive inhibitor of HMG-CoA reductase, enzyme that catalyzes first committed step of cholesterol biosynthesis. Marked first-pass metabolism in liver. Not as useful in patients homozygous for familiar hypercholesterolemia and lack functional LDL receptors. Useful alone or in combination with bile acid-binding resins, niacin, or ezetimibe. Actions - Inhibits de novo cholesterol synthesis, depleting intracellular supply, upregulating LDL receptors, resulting in increased clearance of LDL from the blood. Also cause modest decrease of plasma TAGs and small increase in HDL. Other effects: improves endothelial function, decreases platelet aggregation, reduces inflammation, decreases plasma levels of C-reactive protein. Used as drug of choice for LDL reduction in all types of hyperlipidemias to reduce cardiovascular mortality. Adverse - elevation of aminotransferases, myopathy, and rhabdomyolysis. Contraindications: Pregnant, lactating, or likely to become pregnant.

Fluvastatin

Antihyperlipidemic HMG-CoA Inhibitor (Statin) Analogs of 3-OH-3-methylglutarate(HMG). Competitive inhibitor of HMG-CoA reductase, enzyme that catalyzes first committed step of cholesterol biosynthesis. Marked first-pass metabolism in liver. Very useful in patients homozygous for familiar hypercholesterolemia and lack functional LDL receptors. Not as useful alone or in combination with bile acid-binding resins, niacin, or ezetimibe. Actions - Inhibits de novo cholesterol synthesis, depleting intracellular supply, upregulating LDL receptors, resulting in increased clearance of LDL from the blood. Also cause modest decrease of plasma TAGs and small increase in HDL. Other effects: improves endothelial function, decreases platelet aggregation, reduces inflammation, decreases plasma levels of C-reactive protein. Used as drug of choice for LDL reduction in all types of hyperlipidemias to reduce cardiovascular mortality. Adverse - elevation of aminotransferases, myopathy, and rhabdomyolysis. Contraindications: Pregnant, lactating, or likely to become pregnant.

Lovaza

Antihyperlipidemic Omega-3 Fatty Acids FDA-approved omega-3 product. Ethyl ester of omega-3 fatty acids. Reduces plasma TAGs in a dose-dependent way. Actions - Reduces TAG biosynthesis(incompletely understood molecular mechanism) and increases fatty acid oxidation in liver. With long-term intake, may increase HDL. May increase total LDL as it lowers TAGs. Used as an adjunct to diet to reduce TAG levels in adult patients with very high(>500mg/dL) TAG levels.

DHA (Docosahexaenoic Acid)

Antihyperlipidemic Omega-3 Fatty Acids Fish oil. Reduces plasma TAGs in a dose-dependent way. Actions - Reduces TAG biosynthesis(incompletely understood molecular mechanism) and increases fatty acid oxidation in liver. With long-term intake, may increase HDL. May increase total LDL as it lowers TAGs. Used over the counter as nutritional supplements.

EPA (Eicosapentaenoic Acid)

Antihyperlipidemic Omega-3 Fatty Acids Fish oil. Reduces plasma TAGs in a dose-dependent way. Actions - Reduces TAG biosynthesis(incompletely understood molecular mechanism) and increases fatty acid oxidation in liver. With long-term intake, may increase HDL. May increase total LDL as it lowers TAGs. Used over the counter as nutritional supplements.

Niacin

Antihyperlipidemic Vitamin Nicotinic acid. Favorably affects virtually all lipid parameters, decreasing VLDL, LDL, and Lp(a), and often increasing HDL significantly. Most effective agent for increasing HDL and only agent that may reduce Lp(a). Actions - inhibits adenylyl cyclase in adipocytes through Gi receptor, leading to inhibition of adipocyte hormone-sensitive lipase, reducing transport of fatty acids to liver and decreasing hepatic TAG synthesis. Reducing TAG synthesis, leads to decrease in hepatic VLDL production and release, resulting in decrease in LDL levels. Also increases LPL activity, and decreases catabolic rate for HDL. Also decreases fibrinogen levels, and increases levels of tPA, reversing some endothelial cell dysfunction contributing to thrombosis associated with hypercholesterolemia and atherosclerosis. Used to improve all lipid parameters. Adverse - intense cutaneous flush after each dose(aspirin 30 min. prior decreases flush, which is prostaglandin-mediated), pruritus, rashes, dry skin, acanthosis nigricans, hepatotoxicity, hyperglycemia, gout. Pregnancy Category C

1. Stimulant laxative 2. Prokinetic.

Bisacodyl 1. Mechanism of action 2. Use

1. Selectively binds to an ulcer and coats and protects it from acid and pepsin 2. Used to treat peptic ulcers caused by H. pylori infections

Bismuth subsalicylate (Bismuth) 1. Mechanism of action 2. Use

1. Inhibits the helminths electron transport chain 2. Drug of choices for fasciolosis

Bithionol 1. Mechanism of action 2. Use

Spironolactone

Congestive Heart Failure Aldosterone Antagonist - K+ Sparing Diuretic Diuretic therapy is recommended in all HF patients with evidence of fluid retention, but not mandatory for patients without, because they do not alter disease progression or prolong survival. Diuretic effects are minimal and are instead more used for attenuation of cardiac fibrosis and remodeling. Shown to decrease mortality and morbidity when combined with ACEI and other standard therapy. Research suggests also reduces systemic proinflammatory state and oxidative stress caused by aldosterone. Actions - Acts on CD. Prevents K+ secretion by antagonizing effects of aldosterone at DCT and CCD through competitive inhibition. Used to offset the effects of other diuretics that increase K+ excretion, to treat heart failure, hypertension, primary aldosteronism, and edema. Adverse - diarrhea, gastritis, gastric bleeding, peptic ulcers, antiandrogenic effects, such as gynecomastia, impotence, decreased libido, hirsutism, deepening of voice, and menstrual irregularities, hyperkalemia, hyperchloremic metabolic acidosis, drowsiness, lethargy, ataxia, confusion, and headache. Note: Slow onset of action(takes several days to reach full effect). Has some affinity towards progesterone and androgen receptors, where it acts as an antagonist and thereby induces side effects

Eplerenone

Congestive Heart Failure Aldosterone Antagonist - K+ Sparing Diuretic Diuretic therapy is recommended in all HF patients with evidence of fluid retention, but not mandatory for patients without, because they do not alter disease progression or prolong survival. Diuretic effects are minimal and are instead more used for attenuation of cardiac fibrosis and remodeling. Shown to decrease mortality and morbidity when combined with ACEI and other standard therapy. Research suggests also reduces systemic proinflammatory state and oxidative stress caused by aldosterone. Actions - Acts on CD. Prevents K+ secretion by antagonizing effects of aldosterone at DCT and CCD through competitive inhibition. Used to offset the effects of other diuretics that increase K+ excretion, to treat heart failure, hypertension, primary aldosteronism, and edema. Adverse - hyperkalemia, hyperchloremic metabolic acidosis, drowsiness, lethargy, ataxia, confusion, and headache.

Valsartan

Congestive Heart Failure Angiotensin II Receptor Antagonist ACC/AHA guidelines recommend use of ARBs only in patients with Stage A, B, or C HF who are intolerant of ACE inhibitors. Addition of an ARB may be considered in patients who remain symptomatic despite receiving optimal conventional therapy. Used to treat hypertension and heart failure similarly to ACEI. Adverse - lowest incidence of side effects compated with other antihypertensive agents. Hypotension, hyperkalemia, acute renal failure angioedema. Contraindications: pregnancy, bilateral renal artery stenosis, hyperkalemia.

Candesartan

Congestive Heart Failure Angiotensin II Receptor Antagonist ACC/AHA guidelines recommend use of ARBs only in patients with Stage A, B, or C HF who are intolerant of ACE inhibitors. Addition of an ARB may be considered in patients who remain symptomatic despite receiving optimal conventional therapy. Used to treat hypertension and heart failure similarly to ACEI. Adverse - lowest incidence of side effects compated with other antihypertensive agents. Hypotension, hyperkalemia, acute renal failure angioedema. Contraindications: pregnancy, bilateral renal artery stenosis, hyperkalemia. Note: May have added benefit when added to ACEI, however, there is also increased risk of adverse effects.

Nitrates(Isosorbide Dinitrate)

Congestive Heart Failure Direct Vasodilator Concurrent use of two oral vasodilators has been shown to produced sustained improvement in LVEF. Mortality, hospitalizations, and quality of life is improved in African Americans who receive these along with standard therapy. Current guidelines recommend adding as part of standard therapy in African Americans with moderately severe-severe HF. Usually given along with diuretic and beta-blocker to counteract side effects. Actions - can enhance SV and ejection fraction. Combined with hydralazine because of hydralazine's vasodilator effects, along with its own venodilator effects. Used with hydralazine to improve LVEF and treat moderately severe-severe HF(especially in African Americans, and possibly other ethnicities). Also can be used as first-line therapy in patients unable to tolerate ACEI or ARBs due to renal insufficiency or hyperkalemia. Note: All patients taking this should first receive beta-blocker and diuretic to attenuate effects of reflex tachycardia and sodium retention. Adverse - hypotension, reflex tachycardia, Na+ and water retention, headache, dizziness, and GI disturbances.

Hydralazine

Congestive Heart Failure Direct Vasodilator Concurrent use of two oral vasodilators has been shown to produced sustained improvement in LVEF. Mortality, hospitalizations, and quality of life is improved in African Americans who receive these along with standard therapy. Current guidelines recommend adding as part of standard therapy in African Americans with moderately severe-severe HF. Usually given along with diuretic and beta-blocker to counteract side effects. Actions - can enhance SV and ejection fraction. Combined with isosorbide dinitrate because of isosorbide dinitrate's venodilator effects, along with its own vasodilator effects. Used with isosorbide dinitrate to improve LVEF and treat moderately severe-severe HF(especially in African Americans, and possibly other ethnicities). Also can be used as first-line therapy in patients unable to tolerate ACEI or ARBs due to renal insufficiency or hyperkalemia. Note: All patients taking this should first receive beta-blocker and diuretic to attenuate effects of reflex tachycardia and sodium retention. Adverse - hypotension, reflex tachycardia, Na+ and water retention, headache, dizziness, and GI disturbances.

Ethacrynic Acid

Congestive Heart Failure Diuretics (Loop) Diuretic therapy is recommended in all HF patients with evidence of fluid retention, but not mandatory for patients without, because they do not alter disease progression or prolong survival. Usually necessary to restore and maintain euvolemia in HF. Unlike thiazides, maintain effectiveness in presence of impaired renal function. Most efficacious diuretic agents currently available. Actions - Acts on TAL. Selective inhibition of NaCl reabsoroption by inhibiting NKCC2. Also induces expression of COX-2, which helps synthesize prostaglandins, which appear to mediate diuretic/natriuretic action. Used as diuretic of choice to reduce acute pulmonary edema associated with HF and hepatic or renal disease. Also treats hypertension. Adverse - ototoxicity, hyperuricemia, acute hypovolemia, K+ depletion, hypomagenesemia, allergic reactions.

Milrinone

Congestive Heart Failure Inotropic Agent - Phosphodiesterase(PDE) III Inhibitor Actions - inhibit myocardial PDE activity, resulting in increase in cAMP levels, producing a positive inotropic effect and increased cardiac output. Also possess systemic and pulmonary vasodilator effects, reducing both preload and afterload. Shown to slightly increase AV conduction. Used for short-term therapy in patients with intract failure. Adverse - Long term therapy with PDE inhibitors has been shown to increase mortality. arrhythmia, hypotension.

Furosemide

Congestive Heart Failure Diuretics (Loop) Diuretic therapy is recommended in all HF patients with evidence of fluid retention, but not mandatory for patients without, because they do not alter disease progression or prolong survival. Usually necessary to restore and maintain euvolemia in HF. Unlike thiazides, maintain effectiveness in presence of impaired renal function. Most efficacious diuretic agents currently available. Actions - Acts on TAL. Selective inhibition of NaCl reabsoroption by inhibiting NKCC2. Also induces expression of COX-2, which helps synthesize prostaglandins, which appear to mediate diuretic/natriuretic action. Used as diuretic of choice to reduce acute pulmonary edema associated with HF and hepatic or renal disease. Also treats hypertension. Adverse - ototoxicity, hyperuricemia, acute hypovolemia, K+ depletion, hypomagenesemia, allergic reactions.

Torsemide

Congestive Heart Failure Diuretics (Loop) Diuretic therapy is recommended in all HF patients with evidence of fluid retention, but not mandatory for patients without, because they do not alter disease progression or prolong survival.Usually necessary to restore and maintain euvolemia in HF. Unlike thiazides, maintain effectiveness in presence of impaired renal function. Most efficacious diuretic agents currently available. Actions - Acts on TAL. Selective inhibition of NaCl reabsoroption by inhibiting NKCC2. Also induces expression of COX-2, which helps synthesize prostaglandins, which appear to mediate diuretic/natriuretic action. Used as diuretic of choice to reduce acute pulmonary edema associated with HF and hepatic or renal disease. Also treats hypertension. Adverse - ototoxicity, hyperuricemia, acute hypovolemia, K+ depletion, hypomagenesemia, allergic reactions.

Hydrochlorothiazide

Congestive Heart Failure Diuretics (Thiazide) Diuretic therapy is recommended in all HF patients with evidence of fluid retention, but not mandatory for patients without, because they do not alter disease progression or prolong survival. Relatively weak diuretic and infrequently used alone in HF. May be preferred over loop diuretics in patients with only mild fluid retention and elevated BP because of more persistent antihypertensive effects. Actions - Acts on DCT. Inhibits NaCl reabsorption by blocking NCCT. Also increases K+ and acid excretion and calcium reabsorption. Used to treat mild-moderate heart failure, hypertension, hypercalciuria, diabetes insipidus, and premenstrual edema. Adverse - hypokalemia, hyponatremia, volume depletion(postural hypotension), hyperuricemia, hyperglycemia, hyperlipidemia, hypersensitivity.

Chlorthalidone

Congestive Heart Failure Diuretics (Thiazide) Diuretic therapy is recommended in all HF patients with evidence of fluid retention, but not mandatory for patients without, because they do not alter disease progression or prolong survival. Relatively weak diuretic and infrequently used alone in HF. May be preferred over loop diuretics in patients with only mild fluid retention and elevated BP because of more persistent antihypertensive effects. Actions - Acts on DCT. Inhibits NaCl reabsorption by blocking NCCT. Also increases K+ and acid excretion and calcium reabsorption. Used to treat mild-moderate heart failure, hypertension, hypercalciuria, diabetes insipidus, and premenstrual edema. Adverse - hypokalemia, hyponatremia, volume depletion(postural hypotension), hyperuricemia, hyperglycemia, hyperlipidemia, hypersensitivity. Note: Long duration of action. Half-life is about 40-60 hours.

Metolazone

Congestive Heart Failure Diuretics (Thiazide) Diuretic therapy is recommended in all HF patients with evidence of fluid retention, but not mandatory for patients without, because they do not alter disease progression or prolong survival. Relatively weak diuretic and infrequently used alone in HF. May be preferred over loop diuretics in patients with only mild fluid retention and elevated BP because of more persistent antihypertensive effects. Actions - Acts on DCT. Inhibits NaCl reabsorption by blocking NCCT. Also increases K+ and acid excretion and calcium reabsorption. Used to treat mild-moderate heart failure, hypertension, hypercalciuria, diabetes insipidus, and premenstrual edema. Adverse - hypokalemia, hyponatremia, volume depletion(postural hypotension), hyperuricemia, hyperglycemia, hyperlipidemia, hypersensitivity. Note: Most potent of thiazides. Causes Na+ excretion in advanced kidney failure.

Glucagon

Congestive Heart Failure Inotropic Agent Able to produce same effects as beta agonist without activating beta receptors. Actions - stimulates adenylyl cyclase, increasing cAMP levels, resulting in positive inotropic and chronotropic effects. Used as cardiac stimulant in management of severe cases of beta-blocker overdosage.

Dobutamine

Congestive Heart Failure Inotropic Agent Administered as racemic mixture. (-)-isomer is alpha1 agonist and weak beta1 agonist. (+)-isomer is alpha1 antagonist and beta1 agonist. Stimulation of beta1 receptors predominate, leading to potent inotropic effect(with little change in HR). Net vascular effect is usually vasodilation(beta2). Actions - increases cardiac output without significantly elevating oxygen demands of myocardium. Used in short-term management of patients with cardiac decompensation(cardiogenic shock, MI). Adverse - less arrhythmogenic than dopamine.

Dopamine

Congestive Heart Failure Inotropic Agent Useful in shock due to it raising BP by stimulating the heart and increasing blood flow to the kidneys(vasodilation) Actions - Dose dependant dopaminergic(D1) and adrenergic agonist(alpha1, beta1, beta2). At low doses D1 mediated vasodilation occurs. As dosing increases, both dopaminergic and inotropic effects by beta1 become prominent. At high doses, chronotropic effects and alpha1 vasoconstricting effects become prominent. Also causes NE release from nerve terminal. Used in the treatment of shock(eg. MI, open heart surgery, renal failure, cardiac decompensation) which persists after adequate fluid volume replacement. Adverse - cardiac arrhythmia and, at higher doses, can increase myocardial oxygen demand, and potentially decrease myocardial blood flow, worsening ischemia in some patients with CAD.

Digoxin

Congestive Heart Failure Inotropic Agent - Cardiac Glycoside Indicated in patients with HF and supraventricular tachyarrhythmias such as a-fib. Should be considred early in therapy to help control ventricular response rate. Does not increase survival. Determining optimal level may be difficult, because of narrow therapeutic window. Half-life is 36-40 hours. Has large volume of distribution, including CSF(accumulates in muscle. Loading dose required Actions - Both positively inotropic(increases contractility) and negatively chronotropic(decreases heart rate). As a positive inotrope, is a selective and potent inhibitor of cellular Na+/K+ ATPase. Digoxin causes a rise in intracellular Na+, reducing the transmembrane gradient that normally drives Ca2+ out during repolarization, increasing intracellular Ca2+ levels, which increases myocardial contractility. Inhibition of the Na+/K+ ATPase in vascular smooth muscle causes depolarization, which causes smooth muscle contraction and vasoconstriction. At therapeutic doses, decreases automaticity and increases maximal diastolic resting membrane potential in atrial and AV nodal tissues, due to an increase in vagal tone and decrease in SNS activity. Causes prolongation of effective refractory period and decrease conduction velocity in AV nodal tissue. At higher doses, can increase SNS activity and directly affect automaticity, contributing to atrial and ventricular arrhythmias. Can also cause baroreceptor sensititzation, offsetting desensitization in HF. Used to decrease symptoms of HF, increase exercise tolerance and decrease rate of hospitalization(in addition to ACEI and beta-blocker) Adverse - digoxin toxicity, cardiac arrhythmias(especially atrial tachycardias and AV block), anorexia, nausea, vomiting, headache, fatigue, confusion, blurred, or yellow vision, alteration of color perception, halo on dark objects. Contraindications: Patients with diastolic or right-sided HF, uncontrolled hypertension, bradyarrhythmia, hypokalemia, or non-responders or intolerance. Interactions: K+ decreases affinity of Na+/K+ ATPase for digoxin, therefore, hypokalemia enhances therapeutic and toxic effects, and hyperkalemia reduces. Hypercalcemia ehnahces digoxin-induced increases in intracellular Ca2+, leading to overloading and arrhythmias. Hypomagnesia sensitizes the heart to digoxin-induced arrhythmias, since Mg2+ antagonizes effects of Ca2+. Quinidine(class IA), Amiodarone(class III), Verapamil(class IV/CCB), and NSAIDs compete with digoxin for binding sites and depress renal clearance. Diuretics can indirectly interact, since the can decrease plasma potassium. Hypothyroidism can cause higher concentrations. Hyperthyroidism can cause lower concentrations. Renal failure requires closely monitored levels. Treatment of toxcity - Withdraw drug, or lower dose. Adjust electrolyte status. Treat ventricular arrhythmias with lidocaine and/or Mg2+. If severe, treat with digitalis antibodies(Digoxine immune fab or Digibind).

Inamrinone

Congestive Heart Failure Inotropic Agent - Phosphodiesterase(PDE) III Inhibitor Actions - inhibit myocardial PDE activity, resulting in increase in cAMP levels, producing a positive inotropic effect and increased cardiac output. Also possess systemic and pulmonary vasodilator effects, reducing both preload and afterload. Shown to slightly increase AV conduction. Used for short-term therapy in patients with intract failure. Adverse - Long term therapy with PDE inhibitors has been shown to increase mortality. arrhythmia, hypotension, thrombocytopenia.

Carvedilol

Congestive Heart Failure beta-Antagonist (Mixed with alpha1) Mixed with alpha1-blocking effects, but substantially more potent beta effects, than alpha1. Also has antioxidant properties. Slows disease progression, decreases hospitalizations, and reduces mortality in patients with HF. ACC/AHA guidelines recommend use of beta blockers in all stable patients with HF and a reduced LVEF in absence of contraindications or a clear history of beta-blocker intolerance. Patients should receive a beta-blocker even if symptoms are mild or well-controlled with ACEI and diuretic therapy. Also recommended for asymptomatic patients with a reduced LVEF(Stage B) to decrease risk of progression to HF. Beneficial in treatment of diastolic HF by slowing HR, reducing myocardial oxygen demand, and reducing BP. Actions - Blocks excessive, chronic sympathetic influences on heart, harmful to the failing heart. Has negative inotropic effects, and should thus be started in very low doses and slowly titrated upwards. Used for management of patients with acute myocardial infarction to reduce cardiovascular mortality. Also used for long-term management of patients with angina pectoris, for management of hypertension, and for arrhythmias. Adverse - Drug withdrawal(abrupt cessation may be harmful), bradycardia, reduced exercise capacity, heart failure, hypotension, AV block, disturbed lipid metabolism, hypoglycemia, bronchoconstriction, CNS effects. Contraindications: Asthma, COPD, sinus bradycardia, partial AV block.

Metoprolol

Congestive Heart Failure beta1-Antagonist Slows disease progression, decreases hospitalizations, and reduces mortality in patients with HF. ACC/AHA guidelines recommend use of beta blockers in all stable patients with HF and a reduced LVEF in absence of contraindications or a clear history of beta-blocker intolerance. Patients should receive a beta-blocker even if symptoms are mild or well-controlled with ACEI and diuretic therapy. Also recommended for asymptomatic patients with a reduced LVEF(Stage B) to decrease risk of progression to HF. Beneficial in treatment of diastolic HF by slowing HR, reducing myocardial oxygen demand, and reducing BP. Actions - Blocks excessive, chronic sympathetic influences on heart, harmful to the failing heart. Has negative inotropic effects, and should thus be started in very low doses and slowly titrated upwards. Used for management of patients with acute myocardial infarction to reduce cardiovascular mortality. Also used for long-term management of patients with angina pectoris, for management of hypertension, and for arrhythmias. Adverse - Drug withdrawal(abrupt cessation may be harmful), bradycardia, reduced exercise capacity, heart failure, hypotension, AV block, disturbed lipid metabolism, hypoglycemia, bronchoconstriction, CNS effects. Contraindications: Asthma, COPD, sinus bradycardia, partial AV block.

1. ADH antagonist 2. Used to treat patients with hyponatremia due to elevated ADH Both

Conivaptan 1. Mechanism of action 2. Use Does this drug act on V1 or V2 receptors?

Mestranol

Contraceptives Estrogen One of two types of estrogen. Must be converted by the liver to ethinyl estradiol. Actions - Combined OCPs work primarily before fertilization by preventing ovulation by suppressing LH and FSH release. The progestin portion also thickens cervical mucus, preventing sperm penetration, and inducing endometrial changes that make embryo implantation unlikely. Used to prevent pregnancy. Also reduces risk of endometrial and ovarian cancer, ovarian cysts, symptomatic PID, relieves benign breast disease, and improves regulation of menstruation and acne control. Adverse - nausea, bloating, breakthrough bleeding, headache, melasma, amenorrhea, dyslipidemia, CV disorders(including thromboembolism, thrombophlebitis, HTN, increased incidence of MI, and cerebral and coronary thrombosis), carcinogenicity, depression. Absolute contraindications for combined OCPs: Hx of thromboembolic disease, stroke, CAD, breast CA, any estrogen-dependent neoplasm, hepatic tumors, undiagnosed abnormal uterine bleeding, pregnancy, heavy smokers (>15/day), or acute liver disease. Relative contraindications: Light smokers(<15/day), Hx of migraine headache disorder, HTN, fibroid tumors of uterus, breast-feeding, diabetes. Interactions - Rifampin reduces efficacy by inducing hepatic P450 enzymes and increasing metabolism of estrogen. Carbamazepine, oxcarbazepine, phenytoin, phenobarbital, primidone, topiramate, vigabatrin, and St. John's Wort are P450 inducers as well.

Ethinyl estradiol

Contraceptives Estrogen One of two types of estrogen. Pharmcologically active. Combined oral contraceptives most commonly used today are called "low-dose", and contain 35 micrograms or less. Actions - Combined OCPs work primarily before fertilization by preventing ovulation by suppressing LH and FSH release. The progestin portion also thickens cervical mucus, preventing sperm penetration, and inducing endometrial changes that make embryo implantation unlikely. Available in transdermal contraceptive patch (Ortho-Evra) with a progestin. Also in transvaginal delivery system(NuvaRing) with a progestin. Used to prevent pregnancy. Also reduces risk of endometrial and ovarian cancer, ovarian cysts, symptomatic PID, relieves benign breast disease, and improves regulation of menstruation and acne control. Adverse - nausea, bloating, breakthrough bleeding, headache, melasma, amenorrhea, dyslipidemia, CV disorders(including thromboembolism, thrombophlebitis, HTN, increased incidence of MI, and cerebral and coronary thrombosis), carcinogenicity, depression. Absolute contraindications for combined OCPs: Hx of thromboembolic disease, stroke, CAD, breast CA, any estrogen-dependent neoplasm, hepatic tumors, undiagnosed abnormal uterine bleeding, pregnancy, heavy smokers (>15/day), or acute liver disease. Relative contraindications: Light smokers(<15/day), Hx of migraine headache disorder, HTN, fibroid tumors of uterus, breast-feeding, diabetes. Interactions - Rifampin reduces efficacy by inducing hepatic P450 enzymes and increasing metabolism of estrogen. Carbamazepine, oxcarbazepine, phenytoin, phenobarbital, primidone, topiramate, vigabatrin, and St. John's Wort are P450 inducers as well. There is also a small risk of interaction with antibiotics.

Medroxyprogesterone acetate

Contraceptives Progestin AKA Depo-Provera. Progestin-only injectable contraceptive that contains only DMPA. Administered IM Q3months. Extremely effective in preventing pregnancy. Used to prevent pregnancy. Adverse - menstrual irregularities(including amenorrhea) and weight gain at a higher incidence than combined OCPs. Also, significant bone mineral density(BMD) loss(potentially irreversible).

Drospirenone

Contraceptives Progestin One of the many different progestins found in various oral contraceptives. Has antiandrogenic activity. Actions - Combined OCPs work primarily before fertilization by preventing ovulation by suppressing LH and FSH release. The progestin portion also thickens cervical mucus, preventing sperm penetration, and inducing endometrial changes that make embryo implantation unlikely. Used to prevent pregnancy. Also reduces risk of endometrial and ovarian cancer, ovarian cysts, symptomatic PID, relieves benign breast disease, and improves regulation of menstruation and acne control. Adverse - nausea, bloating, breakthrough bleeding, headache, insulin resistance(rarely), hirsutism, amenorrhea, dyslipidemia, carcinogenicity, depression. Absolute contraindications for combined OCPs: Hx of thromboembolic disease, stroke, CAD, breast CA, any estrogen-dependent neoplasm, hepatic tumors, undiagnosed abnormal uterine bleeding, pregnancy, heavy smokers (>15/day), or acute liver disease. Relative contraindications: Light smokers(<15/day), Hx of migraine headache disorder, HTN, fibroid tumors of uterus, breast-feeding, diabetes.

Levonorgestrel

Contraceptives Progestin One of the many different progestins found in various oral contraceptives. Has highest level of androgenic activity. Involved in both Plan B and Next Choice. Also many OCPs containing this can be used in higher-than-usual doses for emergency contraception. Also available as a intrauterine system that steadily releases it(Mirena). Actions - Combined OCPs work primarily before fertilization by preventing ovulation by suppressing LH and FSH release. The progestin portion also thickens cervical mucus, preventing sperm penetration, and inducing endometrial changes that make embryo implantation unlikely. Used to prevent pregnancy. Also used as emergency postcoital contraception after unprotected sexual intercourse. Also reduces risk of endometrial and ovarian cancer, ovarian cysts, symptomatic PID, relieves benign breast disease, and improves regulation of menstruation and acne control. Adverse - nausea, bloating, breakthrough bleeding, headache, insulin resistance(rarely), hirsutism, amenorrhea, dyslipidemia, carcinogenicity, depression. Absolute contraindications for combined OCPs: Hx of thromboembolic disease, stroke, CAD, breast CA, any estrogen-dependent neoplasm, hepatic tumors, undiagnosed abnormal uterine bleeding, pregnancy, heavy smokers (>15/day), or acute liver disease. Relative contraindications: Light smokers(<15/day), Hx of migraine headache disorder, HTN, fibroid tumors of uterus, breast-feeding, diabetes.

Norgestrel

Contraceptives Progestin One of the many different progestins found in various oral contraceptives. Has highest level of androgenic activity. Substance in progestin-only contraceptive pills(AKA minipills). Actions - Combined OCPs work primarily before fertilization by preventing ovulation by suppressing LH and FSH release. The progestin portion also thickens cervical mucus, preventing sperm penetration, and inducing endometrial changes that make embryo implantation unlikely. Used to prevent pregnancy. Also reduces risk of endometrial and ovarian cancer, ovarian cysts, symptomatic PID, relieves benign breast disease, and improves regulation of menstruation and acne control. Adverse - nausea, bloating, breakthrough bleeding, headache, insulin resistance(rarely), hirsutism, amenorrhea, dyslipidemia, carcinogenicity, depression. Absolute contraindications for combined OCPs: Hx of thromboembolic disease, stroke, CAD, breast CA, any estrogen-dependent neoplasm, hepatic tumors, undiagnosed abnormal uterine bleeding, pregnancy, heavy smokers (>15/day), or acute liver disease. Relative contraindications: Light smokers(<15/day), Hx of migraine headache disorder, HTN, fibroid tumors of uterus, breast-feeding, diabetes.

Norethindrone

Contraceptives Progestin One of the many different progestins found in various oral contraceptives. Has lower androgenic activity than levonorgestrel and norgestrel. Substance in progestin-only contraceptive pills(AKA minipills). Actions - Combined OCPs work primarily before fertilization by preventing ovulation by suppressing LH and FSH release. The progestin portion also thickens cervical mucus, preventing sperm penetration, and inducing endometrial changes that make embryo implantation unlikely. Used to prevent pregnancy. Also reduces risk of endometrial and ovarian cancer, ovarian cysts, symptomatic PID, relieves benign breast disease, and improves regulation of menstruation and acne control. Adverse - nausea, bloating, breakthrough bleeding, headache, insulin resistance(rarely), hirsutism, amenorrhea, dyslipidemia, carcinogenicity, depression. Absolute contraindications for combined OCPs: Hx of thromboembolic disease, stroke, CAD, breast CA, any estrogen-dependent neoplasm, hepatic tumors, undiagnosed abnormal uterine bleeding, pregnancy, heavy smokers (>15/day), or acute liver disease. Relative contraindications: Light smokers(<15/day), Hx of migraine headache disorder, HTN, fibroid tumors of uterus, breast-feeding, diabetes.

Desogestrel

Contraceptives Progestin One of the many different progestins found in various oral contraceptives. Third-gerneration progestin. Has lower androgen activity than norethindrone. Actions - Combined OCPs work primarily before fertilization by preventing ovulation by suppressing LH and FSH release. The progestin portion also thickens cervical mucus, preventing sperm penetration, and inducing endometrial changes that make embryo implantation unlikely. Used to prevent pregnancy. Also reduces risk of endometrial and ovarian cancer, ovarian cysts, symptomatic PID, relieves benign breast disease, and improves regulation of menstruation and acne control. Adverse - nausea, bloating, breakthrough bleeding, headache, insulin resistance(rarely), hirsutism, amenorrhea, dyslipidemia, carcinogenicity, depression. Absolute contraindications for combined OCPs: Hx of thromboembolic disease, stroke, CAD, breast CA, any estrogen-dependent neoplasm, hepatic tumors, undiagnosed abnormal uterine bleeding, pregnancy, heavy smokers (>15/day), or acute liver disease. Relative contraindications: Light smokers(<15/day), Hx of migraine headache disorder, HTN, fibroid tumors of uterus, breast-feeding, diabetes.

Norgestimate

Contraceptives Progestin One of the many different progestins found in various oral contraceptives. Third-gerneration progestin. Has lower androgen activity than norethindrone. Actions - Combined OCPs work primarily before fertilization by preventing ovulation by suppressing LH and FSH release. The progestin portion also thickens cervical mucus, preventing sperm penetration, and inducing endometrial changes that make embryo implantation unlikely. Used to prevent pregnancy. Also reduces risk of endometrial and ovarian cancer, ovarian cysts, symptomatic PID, relieves benign breast disease, and improves regulation of menstruation and acne control. Adverse - nausea, bloating, breakthrough bleeding, headache, insulin resistance(rarely), hirsutism, amenorrhea, dyslipidemia, carcinogenicity, depression. Absolute contraindications for combined OCPs: Hx of thromboembolic disease, stroke, CAD, breast CA, any estrogen-dependent neoplasm, hepatic tumors, undiagnosed abnormal uterine bleeding, pregnancy, heavy smokers (>15/day), or acute liver disease. Relative contraindications: Light smokers(<15/day), Hx of migraine headache disorder, HTN, fibroid tumors of uterus, breast-feeding, diabetes.

1. ACTH analog 2. Used to differentiate between primary adrenal insufficiency (Addisons disease) and secondary adrenal insufficiency as a result of inadequate ACTH secretion. Limited utility as a therapeutic agent because it is less predictable and convenient than corticosteroid therapy. 3. Similar to glucocorticoids

Corticotropin 1. Mechanism of action 2. Use 3. Adverse effects

1. ACTH analog 2. Used to differentiate between primary adrenal insufficiency (Addisons disease) and secondary adrenal insufficiency as a result of inadequate ACTH secretion. Limited utility as a therapeutic agent because it is less predictable and convenient than corticosteroid therapy. 3. Similar to glucocorticoids.

Cosyntropin 1. Mechanism of action 2. Use 3. Adverse effects

1. This is a combination of trimethoprim and sulfamethoxazole 2. Drug of choice for uncomplicated UTIs, pneumocyxtic carinii pneumonia, nocardiosis, and can be used as an alternative treatment for toxoplasmosis. TMP-SMX Can not be given to pregnant women as it reduces the utilization of folic acid through the trimethoprim activity and can lead to fetal complications.

Cotrimoxazole 1. Mechanism of action 2. Use What is another name for this drug? What is a contraindication of this drug and why?

Plastic and jewelry manufacturing and when natural compounds like wool or silk are burned. Respiratory failure It has a high affinity for Fe3+ and binds to Fe3+ in the heme of cytochrome a,a3 in the electron transport chain inhibiting oxygen from serving as the final electron acceptor. This inhibits cellular respiration causing lactic acidosis and cytotoxic hypoxia. An antidote kit which aims at providing a large pool of ferric iron to compete for cyanide. The kits also have inhaled amyl nitrite and IV sodium nitrite both of which oxidize hemoglobin to methemoglobin. Methemoglobin competes with cytochrome oxidase for cyanide forming cyanmethemoglobin which restores cytochrome oxidase activity. Sodium thiosulfate is also given which promotes the conversion of cyanide to thiocyanate which is easily excreted in the urine.

Cyanide toxicity is common in what industries? What is the cause of death in these patients? How does it cause adverse effects? How is this treated?

1. H1 receptor blocker (antihistamine). 2. Can be used to treat motion sickness and chemotherapy induced nausea

Cyclizine 1. Mechanism of action 2. Use

1. Strong antimuscarinic agent 2. Used for the relief of acute muscle spasm caused by local trauma or strain

Cyclobenzaprine 1. Mechanism of action 2. Use

1. It is an alkylating agent (anti-cancer drug) that kills proliferating lymphoid cells 2. Immunosuppression For Wegener's granulomatosis, SLE and other autoimmune diseases.

Cyclophosphamide 1. Mechanism of action 2. Is it used for immunosuppression or immune stimulation? In what sort of conditions would you use this drug to cause immunosuppression?

1. Cross-links DNA and prevents cell replication 2. Used only to treat the most severe cases of RA 3. Bone marrow suppression, infertility, and hemorrhagic cystitis. Infection and malignancy

Cyclophosphamide 1. Mechanism of action 2. Use 3. Adverse effects Long term used of this drug increases the risk of what?

Acrolein which can cause hemorrhagic cystitis and can be prevented by concomitant administration of MESNA and increased water intake to maintain a urine output of >3L/day. Yes, because it is more potent it has more of a potential to cause this condition.

Cyclophosphamide needs to be activated by hepatic enzymes. A toxic compound is produced. What is this compound, what conditions can this lead to, and how do you treat the condition? Does ifosfmaide also carry this risk?

1. Inhibits release of IL-2 from activated T-cells by binding to cyclophilin which inhibits calcineurin which leads to the lack of activation of NFAT and decreased production of IL-2. 2. Can be helpful in treating patients with RA It can cause nephrotoxicity in the majority of patients being treated with this drug and it is involved many drug interactions

Cyclosporine 1. Mechanism of action 2. Use Why is its use limited?

1. Binds to an intracellular protein called cyclophilin which inhibits calcineurin thereby preventing activation of NFAT and inhibits cytokine (IL-2) production 2. Used as an immunosuppressant 3. Nephrotoxicity Gum hyperplasia which can lead to the development of gingivitis By CYP3A4 which means that its levels are directly effected by Lymphoma and squamous cell skin cancer

Cyclosporine 1. Mechanism of action 2. Use 3. Adverse effect What is a fairly unique side effect of cyclosporine use? How is this drug metabolized? Chronic use of this drug puts patients at risk of developing what neoplastic conditions?

Androgen receptor antagonists To treat hirsutism. Cyproterone is a common component in the hormone therapy of male-to-female transexual people.

Cyproterone and sprionolactone are both what types of drugs? What are they used to treat?

Phenytoin

Cytochrome P450 inducer CAR receptor Gene target: CYP2B6, CYP3A4 Displays zero-order kinetics

Phenobarbital

Cytochrome P450 inducer PXR & CAR receptors Gene target: CYP3A4, CYP3A7 CYP2B6,

Rifampin

Cytochrome P450 inducer PXR receptor Gene target: CYP3A4, CYP3A7

Chloramphenicol

Cytochrome P450 inhibitor

Cimetidine

Cytochrome P450 inhibitor

Erythromycin

Cytochrome P450 inhibitor

Ketoconazole

Cytochrome P450 inhibitor

1. Non-competitive inhibitors of HIV-1 reverse transcriptase and cause inhibition of RNA and DNA dependent DNA polymerase 2. Used to treat HIV but not as widely used as other NNRTIs due to its short half life 3. Development of a hypersensitivity rash and it is a teratogen Inhibitor of CYP3A4

Delaviradine 1. Mechanism of action 2. Use 3. Adverse effects Is this an inducer or inhibitor of CYP3A4?

1. Monoclonal antibody that inhibits the RANKL secreted by osteoblasts which prevents the stimulation of osteoclast differentiation and function 2. Used to treat osteoporosis 3. Increased risk of infections

Denosumab 1. Mechanism of action 2. Use 3. Adverse effects

Plasma fractions

Disorders of Coagulation Drugs used to treat bleeding Deficiencies in plasma coagulation factors can cause bleeding. Spontaneous bleeding occurs when factor activity is less than 5-10% of normal. Factor VIII(hemophilia A) and IX(hemophilia B) deficiency account for most of the heritable coagulation defects.

Dalteparin

Disorders of Coagulation Anticoagulant - Low-Molecular-Weight Heparin (LMWH) Heterogenous compound produced by chemical or enzymatic depolymerization of UFH. Free of some drawbacks associated with UFH, thus replacing UFH in many clinical situations. Equal efficacy, superior bioavailability, longer half-life, and less frequent dosing requirements than UFH. Dosing of LMWH results in predictable plasma levels, so it is not usually necessary to monitor LMWH blood levels, except with renal insufficiency, obesity, and pregnancy. Does not cross the placenta, and has not been associated with fetal malformations, therefore is safe anticoagulation choice for pregnancy. Actions - Inhibit Factor Xa, but has less effect on thrombin than UFH. Used to initiate treatment of venous thrombosis and pulmonary embolism, usually concurrently with warfarin, while heparin is continued for at least 5 days. Also used to initially manage patients with unstable angina or acute myocardial infarction, and during coronary balloon angioplasty to prevent thrombosis. Adverse - bleeding, hypersensitivity reactions, heparin-induced thrombocytopenia(HIT). HIT type I is mild and not serious, but type II is a systemic hypercoagulable state in patients treated with UFH for a minimum of 7 days. Antibodies recognize heparin complexes and Platelet Factor 4, leading to platelet aggregation and release of platelet contents. The risk is lower in patients solely treated with LMWH. Also, mild liver transaminase elevations, and osteoporosis in long-term full therapy patients. Note: Excessive anticoagulant action is treated by discontinuance, but if bleeding occurs, administration of a specific antagonist, such as protamine sulfate, is indicated.

Tinzaparin

Disorders of Coagulation Anticoagulant - Low-Molecular-Weight Heparin (LMWH) Heterogenous compound produced by chemical or enzymatic depolymerization of UFH. Free of some drawbacks associated with UFH, thus replacing UFH in many clinical situations. Equal efficacy, superior bioavailability, longer half-life, and less frequent dosing requirements than UFH. Dosing of LMWH results in predictable plasma levels, so it is not usually necessary to monitor LMWH blood levels, except with renal insufficiency, obesity, and pregnancy. Does not cross the placenta, and has not been associated with fetal malformations, therefore is safe anticoagulation choice for pregnancy. Actions - Inhibit Factor Xa, but has less effect on thrombin than UFH. Used to initiate treatment of venous thrombosis and pulmonary embolism, usually concurrently with warfarin, while heparin is continued for at least 5 days. Also used to initially manage patients with unstable angina or acute myocardial infarction, and during coronary balloon angioplasty to prevent thrombosis. Adverse - bleeding, hypersensitivity reactions, heparin-induced thrombocytopenia(HIT). HIT type I is mild and not serious, but type II is a systemic hypercoagulable state in patients treated with UFH for a minimum of 7 days. Antibodies recognize heparin complexes and Platelet Factor 4, leading to platelet aggregation and release of platelet contents. The risk is lower in patients solely treated with LMWH. Also, mild liver transaminase elevations, and osteoporosis in long-term full therapy patients. Note: Excessive anticoagulant action is treated by discontinuance, but if bleeding occurs, administration of a specific antagonist, such as protamine sulfate, is indicated.

Enoxaparin

Disorders of Coagulation Anticoagulant - Low-Molecular-Weight Heparin (LMWH) Heterogenous compound produced by chemical or enzymatic depolymerization of UFH. Free of some drawbacks associated with UFH, thus replacing UFH in many clinical situations. Equal efficacy, superior bioavailability, longer half-life, and less frequent dosing requirements than UFH. Dosing of LMWH results in predictable plasma levels, so it is not usually necessary to monitor LMWH blood levels, except with renal insufficiency, obesity, and pregnancy. Does not cross the placenta, and has not been associated with fetal malformations, therefore is safe anticoagulation choice for pregnancy. Actions - Inhibit Factor Xa, but has less effect on thrombin than UFH. Used to initiate treatment of venous thrombosis and pulmonary embolism, usually concurrently with warfarin, while heparin is continued for at least 5 days. Also used to initially manage patients with unstable angina or acute myocardial infarction, and during coronary balloon angioplasty to prevent thrombosis. Adverse - bleeding, hypersensitivity reactions, heparin-induced thrombocytopenia(HIT). HIT type I is mild and not serious, but type II is a systemic hypercoagulable state in patients treated with UFH for a minimum of 7 days. Antibodies recognize heparin complexes and Platelet Factor 4, leading to platelet aggregation and release of platelet contents. The risk is lower in patients solely treated with LMWH. Treat with DTI or fondaparinux. Also, mild liver transaminase elevations, and osteoporosis in long-term full therapy patients. Note: Excessive anticoagulant action is treated by discontinuance, but if bleeding occurs, administration of a specific antagonist, such as protamine sulfate, is indicated.

Fondaparinux

Disorders of Coagulation Anticoagulant - Selective Factor Xa Inhibitor Synthetic pentasaccharide that can bind to antithrombin III and induce conformational change in antithrombin required to bind to factor Xa. Has negligible antithrombin activity. Available as once-daily SC injection. Used for prophylaxis of DVT, treatment of acute DVT and acute pulmonary emobolism when administered in conjunction with warfarin.

Heparin

Disorders of Coagulation Anticoagulant - Unfractionated Heparin (UFH) Injectable, rapidly acting anticoagulant used acutely to interfere with formation of thrombi. Mixture of straight-chain anionic glycosaminoglycans. Monitoring therapy with activated partial thromboplastin time(aPTT) assay is important for maintaining anticoagulant effect within therapeutic range and prevent bleeding. aPTT tests the integrity of the intrinsic and common pathways of coagulation, evaluating factors XII, XI, IX, VIII, X, V, II, and fibrinogen. Does not cross the placenta, and has not been associated with fetal malformations, therefore is safe anticoagulation choice for pregnancy. Actions - binds to antithrombin III, an alpha-globulin, which normally slowly inhibits clotting factor proteases, especially thrombin IXa, and Xa. Heparin binding causes a 1000x acceleration. Used to initiate treatment of venous thrombosis and pulmonary embolism, usually concurrently with warfarin, while heparin is continued for at least 5 days. Also used to initially manage patients with unstable angina or acute myocardial infarction, and during coronary balloon angioplasty to prevent thrombosis. Adverse - bleeding, hypersensitivity reactions, heparin-induced thrombocytopenia(HIT). HIT type I is mild and not serious, but type II is a systemic hypercoagulable state in patients treated with UFH for a minimum of 7 days. Antibodies recognize heparin complexes and Platelet Factor 4, leading to platelet aggregation and release of platelet contents. Also, mild liver transaminase elevations, and osteoporosis in long-term full therapy patients. Note: Excessive anticoagulant action is treated by discontinuance, but if bleeding occurs, administration of a specific antagonist, such as protamine sulfate, is indicated.

Clopidogrel

Disorders of Coagulation Platelet Aggregation Inhibitor - ADP Receptor Blocker Effective in preventing cerebrovascular and cardiovascular as well as peripheral vascular disease. Like, aspirin, is irreversible platelet inhibitor, increasing risk of bleeding for 5-7 days after drug cessation. Can cause prolonged bleeding for which there is no antidote. Has largely replaced ticlopidine because of superior side effect profile and dosing requirements. Prodrug converted and activated by CYP2C19. Actions - Irreversibly inhibits P2Y12, one of the two subtypes of ADP receptors on platelet surfaces, reducing platelet aggregation by irreversibly inhibiting ADP binding. Inhibits cytochrome P450, and interferes with other drugs' metabolism. Used to reduce the rate of stroke, MI, and death in patients with recent MI or stroke, established peripheral arterial disease, or acute coronary syndrome. Adverse - Thrombocytopenic purpura. Fewer than ticlopidine, and rarely associated with neutropenia. CYP2C19 poor metabolizers have lower plasma levels, and exhibit higher cardiovascular event rates if with acute coronary syndrome, or undergoing percutaneous coronary intervention along with drug. Contraindications: Omeprazole is a CYP2C19 inhibitor, and concurrent use should be avoided.

Ticlopidine

Disorders of Coagulation Platelet Aggregation Inhibitor - ADP Receptor Blocker Has largely been replaced by clopidogrel because of superior side effect profile and dosing requirements. Effective in preventing cerebrovascular and cardiovascular as well as peripheral vascular disease. Like, aspirin, is irreversible platelet inhibitor, increasing risk of bleeding for 5-7 days after drug cessation. Can cause prolonged bleeding for which there is no antidote. Inhibits cytochrome P450, and interferes with other drugs' metabolism. Used to prevent cerebrovascular, cardiovascular, and peripheral vascular disease. Adverse - Neutropenia. Thrombocytopenic purpura.

Aspirin

Disorders of Coagulation Platelet Aggregation Inhibitor - Cyclooxygenase Inhibitor Other salicylates and other NSAIDs also inhibit COX, but have shorter duration because they cannot acetylate COX. Their action is also reversible. Actions - Inhibits TXA2 synthesis by irreversible acetylation of the COX enzyme, interfeime.ring with platelet aggregation and prolonging bleeding. Used to in the prophylactic treatment of transient cerebral ischemia, to reduce the incidence of recurrent myocardial infarction, and to decrease mortality in postmyocardial infarction patients. Displays zero-order kinetics at high doses.

Dipyridamole

Disorders of Coagulation Platelet Aggregation Inhibitor - Phosphodiesterase Inhibitor Coronary vasodilator. Has little or no beneficial effect by itself. Combination of aspirin and extended-release preparation is available for secondary prophylaxis of cerebrovascular disease. Also used in combination with warfarin. Actions - increases cAMP levels by inhibiting PDE and/or by blocking uptake of adenosine(which acts at A2 receptors to activate platelet adenylyl cyclase). Used to prophylactically treat angina pectoris. Indicated as adjunct to warfarin in prevention of postoperative thromboembolic complications of cardiac valve replacement.

Cilostazol

Disorders of Coagulation Platelet Aggregation Inhibitor - Phosphodiesterase Inhibitor Promotes vasodilation and inhibition of platelet aggregation. Actions - increases cAMP levels by inhibiting PDE, causing vasodilation. Used to treat intermittent claudication.

Abciximab

Disorders of Coagulation Platelet Aggregation Inhibitor - Platelet GPIIb/IIIa Receptor Blocker Chimeric mouse-human monoclonal antibody against GPIIb/IIIa receptor. Binding is essentially irreversible, with a dissociation half-time of 18-24 hours. Used in patients with acute coronary syndromes.

Eptifibatide

Disorders of Coagulation Platelet Aggregation Inhibitor - Platelet GPIIb/IIIa Receptor Blocker Cyclic peptide reversible antagonist of GPIIb/IIIa receptor. Used in patients with acute coronary syndromes.

Tirofiban

Disorders of Coagulation Platelet Aggregation Inhibitor - Platelet GPIIb/IIIa Receptor Blocker Nonpeptide tyrosine analogue. Reversible antagonist of GPIIb/IIIa receptor. Used in patients with acute coronary syndromes.

Urokinase

Disorders of Coagulation Thrombolytic Human enzyme synthesized by the kidney and found in urine. Originally used to treat DVT, serious pulmonary embolism, acute MI, and peripheral arterial thrombosis, but now used less frequently. Actions - convert inactive zymogen plasminogen to active protease plasmin. Used to lyse blood clots and thereby restore the patency of an obstructed vessel before distal tissue necrosis occurs. Approved for lysis of pulmonary emboli. Adverse - Also has potential to dissolve not only pathologic, but physiologically appropriate thrombi. Contraindications: healing wounds, pregnancy, history of cerebrovascular accident or metastatic cancer.

Anistreplase

Disorders of Coagulation Thrombolytic Information not found. [Actions - convert inactive zymogen plasminogen to active protease plasmin. Used to reduce mortality associated with acute MI. Adverse - Also has potential to dissolve not only pathologic, but physiologically appropriate thrombi. Contraindications: healing wounds, pregnancy, history of cerebrovascular accident or metastatic cancer.]

Reteplase

Disorders of Coagulation Thrombolytic Modified recombinant human tPA. Less fibrin-selective than tPA. Tissue plasminogen activator(tPA) activates plasminogen bound to fibrin in a thrombus or hemostatic plug. Said to be "fibrin selective". Can be given as "double bolus" because of longer half-life than alteplase. Actions - convert inactive zymogen plasminogen to active protease plasmin. Used to manage acute MI. Adverse - Also has potential to dissolve not only pathologic, but physiologically appropriate thrombi. Contraindications: healing wounds, pregnancy, history of cerebrovascular accident or metastatic cancer.

Tenecteplase

Disorders of Coagulation Thrombolytic Mutant form of tPA. Less fibrin-selective than tPA. Tissue plasminogen activator(tPA) activates plasminogen bound to fibrin in a thrombus or hemostatic plug. Said to be "fibrin selective". Can be given as single IV bolus, because of longer half-life than reteplase. Actions - convert inactive zymogen plasminogen to active protease plasmin. Used to reduce mortality associated with acute MI. Adverse - Also has potential to dissolve not only pathologic, but physiologically appropriate thrombi. Contraindications: healing wounds, pregnancy, history of cerebrovascular accident or metastatic cancer.

Ethacrynic Acid

Diuretic Loop Diuretic Acts on thick ascending Loop of Henle(TAL). Selective inhibition of NaCl reabsorption in TAL by inhibiting luminal Na+/K+/2Cl- cotransporter (NKCC2). Most efficacious diuretic agents currently available, thus sometimes called "high-ceiling diuretics." Also shown to induce expression of COX-2, which helps synthesize prostaglandins, which appear to mediate the diuretic/natriuretic action. Rapidly absorbed with short half-life via IV and oral preparations. Action - decreased renal vascular resistance, increased prostaglandin synthesis. Urinary excretion: increased Na+, K+, Ca2+, Mg2+, and urine volume. Used as diuretic of choice to reduce acute pulmonary edema associated with heart failure and hepatic or renal disease. Also used to treat hypertension. Adverse - Ototoxicity, hyperuricemia, acute hypovolemia, K+ depletion, hypomagnesemia, allergic reactions.

Torsemide

Diuretic Loop Diuretic Acts on thick ascending Loop of Henle(TAL). Selective inhibition of NaCl reabsorption in TAL by inhibiting luminal Na+/K+/2Cl- cotransporter (NKCC2). Most efficacious diuretic agents currently available, thus sometimes called "high-ceiling diuretics." Also shown to induce expression of COX-2, which helps synthesize prostaglandins, which appear to mediate the diuretic/natriuretic action. Rapidly absorbed with short half-life via IV and oral preparations. Action - decreased renal vascular resistance, increased prostaglandin synthesis. Urinary excretion: increased Na+, K+, Ca2+, Mg2+, and urine volume. Used as diuretic of choice to reduce acute pulmonary edema associated with heart failure and hepatic or renal disease. Also used to treat hypertension. Adverse - Ototoxicity, hyperuricemia, acute hypovolemia, K+ depletion, hypomagnesemia, allergic reactions.

Furosemide

Diuretic Loop Diuretic Acts on thick ascending Loop of Henle(TAL). Selective inhibition of NaCl reabsorption in TAL by inhibiting luminal Na+/K+/2Cl- cotransporter (NKCC2). Most efficacious diuretic agents currently available, thus sometimes called "high-ceiling diuretics." Also shown to induce expression of COX-2, which helps synthesize prostaglandins, which appear to mediate the diuretic/natriuretic action. Rapidly absorbed with short half-life via IV and oral preparations. Action - decreased renal vascular resistance, increased renal blood flow and prostaglandin synthesis. Urinary excretion: increased Na+, K+, Ca2+, Mg2+, and urine volume. Used as diuretic of choice to reduce acute pulmonary edema associated with heart failure and hepatic or renal disease. Also used to treat hypertension. Adverse - Ototoxicity, hyperuricemia, acute hypovolemia, K+ depletion, hypomagnesemia, allergic reactions. Note: Has been shown to increase renal blood flow.

Mannitol

Diuretic Osmotic Acts everywhere in the nephron. Administered in large enough doses to significantly increase the osmolality of plasma and tubular fluid, expanding ECF volume, decreasing blood viscosity, and inhibiting renin release. Does not affect Na+ excretion. Must be given IV. Actions - raises plasma osmotic pressure and draws water out of body tissues. Urinary excretion: increase Na+, K+, Ca2+, Mg2+, Cl-, HCO3-, phosphate, and urine volume. Used to increase urine flow in patients with acute renal failure, reduce increased intracranial pressure and treat cerebral edema, and promote excretion of toxic substances. Adverse - extracellular water expansion leading to hyponatremia, and tissue dehydration. Contraindicated in patients with active cranial bleeding.

Eplerenone

Diuretic Potassium Sparing - Aldosterone Antagonist Acts on Collecting Duct(CD). Prevents K+ secretion by antagonizing the effects of aldosterone at the late distal tubule and cortical collecting duct. Competitively inhibits binding of aldosterone to receptor. Potassium levels must be closely monitored. Actions - Urinary excretion: decrease K+; increase Na+, urine volume. Used primarily to offset the effects of other diuretics that increase K+ excretion. Also used to treat heart failure, hypertension, primary hyperaldosteronism, and edema. Adverse - hyperkalemia, hyperchloremic metabolic acidosis, CNS effects, such as drowsiness, lethargy, ataxia, confusion, and headache.

Spironolactone

Diuretic Potassium Sparing - Aldosterone Antagonist Acts on Collecting Duct(CD). Prevents K+ secretion by antagonizing the effects of aldosterone at the late distal tubule and cortical collecting duct. Competitively inhibits binding of aldosterone to receptor. Potassium levels must be closely monitored. Has some affinity towards progesterone and androgen receptors, where it acts as an antagonist and thereby induces side effects. Actions - Urinary excretion: decrease K+; increase Na+, urine volume. Used primarily to offset the effects of other diuretics that increase K+ excretion. Also used to treat heart failure, hypertension, primary hyperaldosteronism, and edema. Adverse - diarrhea, gastritis, gastric bleeding, peptic ulcers, antiandrogenic effects such as, gynecomastia, impotence, decreased libido, hirsutism, deepening of voice, and menstrual irregularities, hyperkalemia, hyperchloremic metabolic acidosis, CNS effects, such as drowsiness, lethargy, ataxia, confusion, and headache. Note: Slow onset of action(takes several days to reach full effect). Active metabolite: Canrenone - prolongs effects of parent drug.

Triamterene

Diuretic Potassium Sparing - Inhibitors of Renal Epithelial Na+ Channels Acts on Collecting Duct(CD). Does not rely on presence of aldosterone. Competitively inhibit epithelial sodium channels(ENaC) in the late distal tubule and collecting duct, thus reducing Na+ reabsorption. Also inhibits K+ secretion, and prevents K+ loss associated with thiazides and furosemide. Not very efficacious(used in combination). Actions - Urinary excretion: decrease K+; increase Na+, urine volume. Used primarily to offset the effects of other diurectics that increase K+ excretion. Also used to treat heart failure, and hypertension. Adverse - hyperkalemia, hyponatremia, can reduce glucose tolerance, induce photosensitization, and has been associated with interstitial nephritis and renal stones.

Amiloride

Diuretic Potassium Sparing - Inhibitors of Renal Epithelial Na+ Channels Acts on Collecting Duct(CD). Does not rely on presence of aldosterone. Competitively inhibit epithelial sodium channels(ENaC) in the late distal tubule and collecting duct, thus reducing Na+ reabsorption. Also inhibits K+ secretion, and prevents K+ loss associated with thiazides and furosemide. Not very efficacious(used in combination).Eliminated predominantly by urinary excretion of intact drug. Actions - Urinary excretion: decrease K+; increase Na+, urine volume. Used primarily to offset the effects of other diurectics that increase K+ excretion. Also used to treat heart failure, and hypertension. Adverse - hyperkalemia, hyponatremia

Hydrochlorothiazide

Diuretic Thiazide "Ceiling diuretics" since dose above normal does not promote further response. Acts on distal tubule(DCT). Inhibit NaCl reabsorption in the DCT by blocking Na+/Cl- cotransporter(NCCT). Also increases the excretion of K+ and acid. Also able to increase reabsorption of calcium, thus decreasing calcium excretion. May also cause mild magnesuria. Orally effective and long half-life of about 40hrs, thus taking 1-3 weeks to produce stable drop in bp. Actions - decrease peripheral vascular resistance. Urinary excretion: decrease Ca2+; increase Na+, Cl-, K+, Mg2+, urine volume. Used to treat hypertension(either alone or with other antihypertensives), heart failure(mild-moderate), hypercalciuria, diabetes insipidus, and premenstrual edema Adverse - hypokalemia, hyponatremia, volume depletion(postural hypotension), hyperuricemia, hyperglycemia, hyperlipidemia, and hypersensitivity.

Chlorthalidone

Diuretic Thiazide "Ceiling diuretics" since dose above normal does not promote further response. Acts on distal tubule(DCT). Inhibit NaCl reabsorption in the DCT by blocking Na+/Cl- cotransporter(NCCT). Also increases the excretion of K+ and acid. Also able to increase reabsorption of calcium, thus decreasing calcium excretion. May also cause mild magnesuria. Orally effective and long half-life of about 40hrs, thus taking 1-3 weeks to produce stable drop in bp. Actions - decrease peripheral vascular resistance. Urinary excretion: decrease Ca2+; increase Na+, Cl-, K+, Mg2+, urine volume. Used to treat hypertension(either alone or with other antihypertensives), heart failure(mild-moderate), hypercalciuria, diabetes insipidus, and premenstrual edema Adverse - hypokalemia, hyponatremia, volume depletion(postural hypotension), hyperuricemia, hyperglycemia, hyperlipidemia, and hypersensitivity. Note: Long duration of action. Half-life is about 40-60hrs(used to treat hypertension once daily).

Metolazone

Diuretic Thiazide "Ceiling diuretics" since dose above normal does not promote further response. Acts on distal tubule(DCT). Inhibit NaCl reabsorption in the DCT by blocking Na+/Cl- cotransporter(NCCT). Also increases the excretion of K+ and acid. Also able to increase reabsorption of calcium, thus decreasing calcium excretion. May also cause mild magnesuria. Orally effective and long half-life of about 40hrs, thus taking 1-3 weeks to produce stable drop in bp. Actions - decrease peripheral vascular resistance. Urinary excretion: decrease Ca2+; increase Na+, Cl-, K+, Mg2+, urine volume. Used to treat hypertension(either alone or with other antihypertensives), heart failure(mild-moderate), hypercalciuria, diabetes insipidus, and premenstrual edema Adverse - hypokalemia, hyponatremia, volume depletion(postural hypotension), hyperuricemia, hyperglycemia, hyperlipidemia, and hypersensitivity. Note: Most potent. Causes Na+ excretion in advanced kidney failure.

Immunosuppressant They inhibit the cell cycle and induce apoptosis in activated T-cells which inhibits both the cellular and humoral immune response. Prednisone Adrenal suppression, Cushing-like presentation, and OSTEOPOROSIS. CORticosteroids (Cushing-like presentation, Osteoporosis and adRenal suppression.

Do corticosteroids act as an immunosuppressant or a immune stimulant? How do they act in this manner? What drug is commonly given for this purpose? What are some common side effects?

1. Hyper 2. Hyper 3. Hypo 4. Hypo 5. Hyper 6. Hyper 7. Hypo

Do the following drugs cause hypo or hyperglycemia. How does this occur? 1. Epinephrine 2. Glucocorticoids 3. Ethanol 4. Salicylates 5. Atypical antipsychotics 6. HIV protease inhibitors 7. Beta blockers

1. Dihydrofolate reductase 2. Dihydropteroate synthase 3. Both Trimethoprim and sulfonamides are both bacteriostatic but cotrimoxazole is combination of the two which acts on two enzymes in the same pathway which makes it activity bactericidal.

Do the following drugs inhibit dihydrofolate reductase or dihydropteroate synthase in the pathway of bacterial nucleic acid synthesis? 1. Trimethoprim 2. Sulfonamides 3. Cotrimoxazole What is unique about the bacteriostatic and bactericidal activity of these drugs.

1. Inhibitor 2. Inducer 3. Inhibitor

Do the following drugs that are used to treat mycobacterial infections induce or inhibit CYP P450 enzymes? 1. Dapsone 2. Rifampin 3. Isoniazid

1. 30S (reversibly) 2. 50S 3. 30S (irreversibly) 4. 50S (reversibly) 5. 30S (reversibly) 6. 50S (reversibly) 7. 50S 8. 50S (binding to the 23S ribosomal RNA)

Do the following inhibitors of protein synthesis bind to the 30S or 50S ribosomal subunit? 1. Tetracycline 2. Dalfopristin/Quinupristin 3. Aminoglycosides 4. Macrolide 5. Tigecycline 6. Chloramphenicol 7. Clindamycin 8. Linezolid

1. SNRI (serotonin and norepinephrine reuptake inhibitor) 2. Used as an adjuvant for pain management 3. Nausea, sexual dysfunction, and somnolence (a state of near sleep)

Duloxetine 1. Mechanism of action 2. Use

1. Serotonin & norepinephrine reuptake inhibitor (inhibits both equally) 2. May be effective in treating depression in patients whose depression is not well controlled by SSRIs They do not block H1, muscarinic, and α-adrenergic receptors which gives them a lower adverse effect profile.

Duloxetine 1. Mechanism of action 2. Use How does this drug differ from TCAs?

No, propofol acts as an anti-emetic so the co-administration of ondansetron is not necessarily required although it may be recommended in order to prevent aspiration of stomach contents during surgical procedures.

During an anesthesiology rotation the attending administers propofol and ondansetron to a patient to initiate and maintain anesthesia. Are both of these agents necessary?

1. Acts on motilin receptors of GIT when given IV 2. Used to cause gastric emptying before upper GI endoscopic procedures

Erythromycin 1. Mechanism of action 2. GI use

1. Macrolide drug that reversibly binds to the 50S ribosomal subunit and inhibits translocation 2. Used in empiric therapy of community-acquired pneumonia and to treat upper respiratory tract and soft-tissue infections (ex. Staph, H. influenza, S. pneumonia, and enterococci) Whooping cough (B. pertussis)

Erythromycin 1. Mechanism of action 2. Use This is the drug of choice for what condition?

1. Short acting beta blocker 2. Used to control an intra-operative thyroid storm

Esmolol 1. Mechanism of action 2. Use

Ovaries, adrenal gland, placenta, and in the blood from aromatization. Estradiol

Estradiol, estrone, and estriol are derived from what sources? Which is the most potent?

1. Synthetic pyrimidine that is taken up by cytosine permease (found in fungal cells but not human cells) and is converted to 5-flurouracil which has two functions: Inhibits thymidylate synthetase which blocks synthesis of dTMP and inhibits protein synthesis. 2. Only used to treat serious infections caused by susceptible strains of candida and cryptococcus. 3. Because it is converted to 5-FU it can cause bone marrow toxicity No, because of the synergistic actions seen with Amphoteracin B and to avoid the development of resistance. It should be used in combination with amphoteracin B for the treatment of systemic candidiasis and cryptococcosis.

Flucytosine 1. Mechanism of action 2. Use 3. Adverse effects Is this drug used alone?

1. Benzodiazepine receptor antagonist which blocks the effects of benzodiazepines 2. Used to reverse CNS depressant effects of benzodiazepine overdose and to quicken recovery when the drugs are used for anesthetic and diagnostic procedures. It has a rapid onset but a short duration so frequent administration may be required in order to maintain the reversal of long-acting benzodiazepine drugs

Flumazenil 1. Mechanism of action 2. Use What is the half life of this drug like and, as a result, how should it be administered?

1. Androgen receptor antagonist 2. Used to treat prostate cancer by inhibition testosterones prostatic hyper plastic activity

Flutamide 1. Mechanism of action 2. Use

1. Recombinant FSH 2. Used to treat male and female infertility 3. Ovarian hyperstimulation syndrome, multiple pregnancies, and precocious puberty 4. Gynecomastia

Follitropin 1. Mechanism of action 2. Use 3. Adverse effects in women 4. Adverse effects in men

1. Inhibit peripheral conversion of T4 to T3 2. Used as part of treatment in patients with a thyroid storm

Glucocorticoids 1. Mechanism of action 2. Use

1. Inhibit the production of a variety of inflammatory mediators 2. Controversial use in treating RA because of the complications associated with long-term use Used in short courses of low-doses for symptomatic relief until the beneficial effects of DMARDs become apparent

Glucocorticoids 1. Mechanism of action 2. Use How are they used by rheumatologists to treat RA?

1. Anti-inflammatory and immunosuppressive effects 2. Used to treat attacks of acute gouty arthritis When an attack of acute gouty arthritis is unresponsive to NSAIDs or colchicine depot preparations of glucocorticoids can be injected directly into the site of inflammation.

Glucocorticoids 1. Mechanism of action 2. Use When and how is this used to treat acute gout attacks?

1. Second generation sulfonylurea drug 2. Used to treat type II diabetes and is effective at reducing fasting plasma glucose and HbA1c levels 3. Hypoglycemia and weight gain

Glyburide 1. Mechanism of action 2. Use 3. Adverse effects

1. Muscarinic (cholinergic) agonists. 2. Used to treat IBS

Glycopyrrolate 1. Mechanism of action 2. Use

1. Forms gold salts that are taken up by macrophages and suppress phagocytosis and lysosomal enzyme activity which inhibits progression of bone and articular destruction 2. Used to treat RA IM Because of their toxicity

Gold sodium thiomalate 1. Mechanism of action 2. Use How is this drug administered? Why are gold compounds used infrequently today?

1. Gonadotropin releasing hormone 2. To treat male infertility and rarely female infertility. Can also be used to diagnose a patients LH responsiveness to GnRH Inhibition of FSH and LH release leading to hypogonadism The analogs are more poten and have a longer lasting effect than Gonadorelin

Gonadorelin 1. Mechanism of action 2. Use What can occur if this drug is administered in a non-pulsitile manner? This drug is not an analog but other drugs are. Which is more potent and which lasts longer?

1. GnRH analog 2. Used to treat prostatic cancer It should be given by a pulsatile dose as a continuous dose of this drug can lead to reversible medical castration

Goserelin 1. Mechanism of action 2. Use How should this drug be administered and why?

1. Drug is rapidly hydrolyzed to 6-MAM which is then hydrolyzed to morphine. 2. Drug of abuse Both heroin andn 6-MAM are more liposoluble than drugs like morphine and they therefor enter the brain through the BBB more readily.

Heroin 1. Mechanism of action 2. Use Why does heroin have increased CNS effects not seen which some other opioid drugs?

Astemizole

Histamine Antagonist H1 Receptor Antagonist - Second Generation Withdrawn from the US market because it induces potentially fatal arrhythmia, torsades de pointes. Has sedative effects and is more likely to block autonomic receptors. Historically considered to be H1-receptor antagonists, but recently shown to be inverse agonists. Histamine-induced bronchoconstriction and GI muscle contraction can be completely blocked. Have additional effects unrelated to H1 antagonism, probably reflecting binding to cholinergic, alpha-adrenergic, serotonin, and local anesthetic receptor sites. Used to treat allergies in the past, but in combination with ketoconazole, itraconazole, or macrolide antibiotics such as erythromycin, patients would get significant cardiac toxicity, including potentially lethal ventricular arrhythmias. These antimicrobials inhibit CYP3A4, which causes an increase in blood levels.

Terfenadine

Histamine Antagonist H1 Receptor Antagonist - Second Generation Withdrawn from the US market because it induces potentially fatal arrhythmia, torsades de pointes. Has sedative effects and is more likely to block autonomic receptors. Historically considered to be H1-receptor antagonists, but recently shown to be inverse agonists. Histamine-induced bronchoconstriction and GI muscle contraction can be completely blocked. Have additional effects unrelated to H1 antagonism, probably reflecting binding to cholinergic, alpha-adrenergic, serotonin, and local anesthetic receptor sites. Used to treat allergies in the past, but in combination with ketoconazole, itraconazole, or macrolide antibiotics such as erythromycin, patients would get significant cardiac toxicity, including potentially lethal ventricular arrhythmias. These antimicrobials inhibit CYP3A4, which causes an increase in blood levels. Adverse - Grapefruit juice also inhibits CYP3A4 and increases blood levels.

Famotidine

Histamine Antagonist H2 Receptor Antagonist Actions - Competitive, reversible inhibition of H2 receptors. Completely inhibits gastric acid secretion induced by histamine or gastrin, and partially inhibits secretion by muscarinic agonists. Used to inhibit gastric acid secretion. To promote healing of duodenal and gastric ulcers, manage acute stress ulcers, and to prevent and treat heart-burn(gastroesophageal reflux in GERD) Adverse - Extremely safe. Occurs in < 3%. Can cross placenta, and should be given only when absolutely necessary. Rapid IV infusion may cause bradycardia and hypotension through blockade of cardiac H2 receptors.

Nizatidine

Histamine Antagonist H2 Receptor Antagonist Actions - Competitive, reversible inhibition of H2 receptors. Completely inhibits gastric acid secretion induced by histamine or gastrin, and partially inhibits secretion by muscarinic agonists. Used to inhibit gastric acid secretion. To promote healing of duodenal and gastric ulcers, manage acute stress ulcers, and to prevent and treat heart-burn(gastroesophageal reflux in GERD) Adverse - Extremely safe. Occurs in < 3%. Can cross placenta, and should be given only when absolutely necessary. Rapid IV infusion may cause bradycardia and hypotension through blockade of cardiac H2 receptors.

Ranitidine

Histamine Antagonist H2 Receptor Antagonist Actions - Competitive, reversible inhibition of H2 receptors. Completely inhibits gastric acid secretion induced by histamine or gastrin, and partially inhibits secretion by muscarinic agonists. Used to inhibit gastric acid secretion. To promote healing of duodenal and gastric ulcers, manage acute stress ulcers, and to prevent and treat heart-burn(gastroesophageal reflux in GERD) Adverse - Extremely safe. Occurs in < 3%. Can cross placenta, and should be given only when absolutely necessary. Rapid IV infusion may cause bradycardia and hypotension through blockade of cardiac H2 receptors.

Cimetidine

Histamine Antagonist H2 Receptor Antagonist Actions - Competitive, reversible inhibition of H2 receptors. Completely inhibits gastric acid secretion induced by histamine or gastrin, and partially inhibits secretion by muscarinic agonists. Used to inhibit gastric acid secretion. To promote healing of duodenal and gastric ulcers, manage acute stress ulcers, and to prevent and treat heart-burn(gastroesophageal reflux in GERD) Adverse - Extremely safe. Occurs in < 3%. Inhibits Cytochrome P450. Binds to androgen receptors and has antiandrogenic effects, such as gynecomastia and reduced sperm count in men, galactorrhea in women. Can cross placenta, and should be given only when absolutely necessary. Rapid IV infusion may cause bradycardia and hypotension through blockade of cardiac H2 receptors.

Epinephrine

Histamine Antagonist Physiological Antagonist Smooth muscle actions opposite to those of histamine, acting on different receptors. Used for counteracting systemic anaphylaxis, and other conditions where massive release of histamine occurs.

Cromolyn

Histamine Antagonist Release Inhibitor Reduces degranulation of mast cells that results from antigen-IgE interaction. Used to treat asthma.

Nedocromil

Histamine Antagonist Release Inhibitor Reduces degranulation of mast cells that results from antigen-IgE interaction. Used to treat asthma.

Only for short-term or intermittent use to treat anxiety Diazepam Clonazepam Lorazepam and diazepam

How are benzodiazepines typically used to treat anxiety? Which benzodiazepine is useful in the treatment of skeletal muscle spasms and to treat spasticity from degenerative disorders like MS and cerebral palsy? Which benzodiazepine is used to treat some types of epileptic seizures? Which are used to treat status epilepticus?

It is not preferred for long term treatment but it can be used with antidepressants in early treatment or to acutely reduce panic symptoms. It may cause rebound anxiety between doses and could cause withdrawal if used for a long period with symptoms that include seizure.

How are benzodiazepines used in the treatment of panic disorder? Although alprazolam is commonly used for an immediate effect on symptoms, what is the problem with this treatment?

1. Mild to moderate opioid receptor agonist 2. Used as an antitussive and to treat pain It is less efficacious than morphine

Hydrocodone 1. Mechanism of action 2. Use How does this drug efficacy in treating pain compare to that of morphine?

1. Corticosteroid which inhibit TNFα, IL-1, and IL-8. 2. Used to treat Crohn's disease and UC

Hydrocortisone 1. Mechanism of action 2. GI Use

1. Strong opioid receptor agonist 2. Useful in treating severe pain High affinity for µ receptor and a lower affinity for the δ and κ receptors.

Hydromorphone 1. Mechanism of action 2. Use What is the affinity of this drug for the µ, δ, and κ opioid receptors?

1. Mechanism of action is unclear 2. Used to treat RA 3. Hemolysis in patients with a G6PD deficiency and retinal damage Ophthalmological exam should be undertaken before the initiation of treatment and annually in all patients at high risk (>60, with liver disease, and/or retinal disease) Every 5 years Methotrexate and sulfasalazine

Hydroxychloroquine 1. Mechanism of action 2. Use 3. Adverse effects To avoid AE how should these patients be monitored? How often should patients at low risk be monitored? This drug is commonly used in conjunction with which drugs to treat RA?

1. It is a urea analog that inhibits ribonucleotide reductase which results in depletion of dNTP which inhibits DNA synthesis 2. Used to treat melanoma, CML, and sickle cell disease (it increases HbF levels) S phase

Hydroxyurea 1. Mechanism of action 2. Use What phase of the cell cycle does this drug act in?

1. H1 receptor blocker 2. Used in the treatment of symptomatic anxiety

Hydroxyzine 1. Mechanism of action 2. Sedative-hypnotic use

1. Muscarinic (cholinergic) agonists 2. Used to treat IBS

Hyoscyamine 1. Mechanism of action 2. Use

They cause corrosive effects on the upper and lower airways Cough, stridor, wheezing, and pneumonia 100% oxygen

Irritant gases include chlorine, ammonia, sulfur dioxide, and nitrogen oxides. What does toxicity with these agents cause? What are the clinical features? How is it treated?

Yes

Is Chloroquine safe for the treatment of malaria in pregnant women and young children?

A narrow spectrum antibiotic is preferred in order to reduce the risk of the development of resistance. They should have blood cultures drawn and be treated with broad spectrum antibiotics that cover the most likely organism(s) causing the infection and once blood culture are returned they should be moved to a narrow spectrum antibiotic that specifically targets the offending organism.

Is a broad spectrum or narrow spectrum antibiotic preferred and why? How should patient with a severe infection be treated?

1. A stereoisomer of dopa which can be converted to dopamine by the remaining dopaminergic neurons restoring dopamine levels in extrapyramidal centers 2. Used for symptomatic control of Parkinson's disease as the effect only lasts while the drug is present in the body. 3. Nausea, vomiting, cardiac arrhythmias, and hypotension Carbidopa

Levodopa 1. Mechanism of action 2. Use 3. Adverse effects This drug is coadministered to patients receiving levodopa?

3-ο-methyl dopa HVA (homovanillic acid)

Levodopa is metabolized to what compound? Dopamine is eventually metabolized to what compound?

1. Fluoroquinolone drug that inhibits bacterial DNA replication by interfering with topoisomerase II (DNA gyrase) and topoisomerase IV 2. Used to treat prostatitis, STDs (not syphilis), skin infections, acute sinusitis, bronchitis, and TB 3rd

Levofloxacin 1. Mechanism of action 2. Use Generation?

1. Fluoroquinolone 2. Recommended for use against first-line drug resistant strains but always used in combination No, it is teratogenic

Levofloxacin 1. Mechanism of action 2. Use in TB treatment Use in pregnancy?

1. Strong µ receptor agonist, NMDA receptor antagonist, and a serotonin and norepinephrine reuptake inhibitor 2. Used in detoxification clinics It is a compound related to methadone that has an even longer half life.

Levomethadyl acetate 1. Mechanism of action 2. Use Why is this drug useful?

1. Binds to the 23S ribosomal subunit of the 50S ribosome and inhibits the formation of the 70S initiation complex. 2. Used in the treatment of multi-drug resistant infections 3. Should be used with caution in patients taking adrenergic and serotonergic drugs None Most Gram-positive organisms with moderate activity against Mycobacterium tuberculosis It is a weak reversible inhibitor of MAO

Linezolid 1. Mechanism of action 2. Use 3. Contraindications What drugs does this drug share cross resistance with? This drug is useful against what types of bacteria? What enzymatic interaction does this drug have?

Can inhibit the release of hormone and cause thyroid enlargement

Lithium Affect on the thyroid gland?

They require actively proliferating bacteria which are synthesizing a cell wall or these drugs will not be effective.

Mammalian cells do not have a cell wall so inhibitors of cell wall synthesis are selective for bacteria. What do these drugs require in order for them to be affective?

Quinine, Quinidine, or halofantrine

Mefloquine should never be co-administered with which drugs?

1. Selective COX-2 inhibitor 2. 1. Non-selecive reversible COX inhibitor 2. Antipyretic, analgesic, and anti-inflammatory.

Meloxicam 1. Mechanism of action 2. Use

1. Purified extract of FSH and LH ( mixture of the two) 2. Used to treat male and female infertility 3. Ovarian hyperstimulation syndrome, multiple pregnancies, and precocious puberty 4. Gynecomastia

Menotropins 1. Mechanism of action 2. Use 3. Adverse effects in women 4. Adverse effects in men

1. Strong µ receptor agonist 2. No longer recommended for the treatment of chronic pain due to metabolite toxicity Can cause seizures Meperidine has a half life of 3 hours so chronic use of this drug would require frequent dosing. Meperidines metabolic product normeperidine has a half life of 15-20 hours so the dosing required for meperidine to be effect would result in accumulation of normeperidine which could eventually lead to the development of seizures

Meperidine 1. Mechanism of action 2. Use This drug is metabolized to normeperidine. At high concentrations what are the adverse effects of this metabolite? Why should this drug not be used at large doses or for prolonged periods?

1. Promotes apoptosis of the immune response cells 2. Used to treat moderate to severe Crohn's disease and UC

Mercaptopurine 1. Mechanism of action 2. Use

1. β-lactam inhibitor of cell wall synthesis (carbapenem) 2. Used for serious infections that require broad spectrum antibiotics. No, it does not form a nephrotoxic metabolite like Imipenem.

Meropenem 1. Mechanism of action 2. Use Does this drug require co-administration with Cilastatin?

Projects from the midbrain to the prefrontal cortex Negative and cognitive symptoms are likely the result of reduced activity of this pathway Blocking this pathway may worsen the negative and cognitive symptoms

Mesocortical pathway Where does this pathway travel in the brain? What role is it believed that this pathway plays in schizophrenia? Blocking of D2 receptors in this pathway could result in what?

Projects from the midbrain to limbic system Emotional behaviors Hyperactivity of this pathway is thought to cause positive symptoms Blockade can mediate antipsychotic effects of antipsychotic drugs

Mesolimbic pathway Where does this pathway travel in the brain? This pathway is believed to play an important role in what behaviors? What role is it believed that this pathway plays in schizophrenia? Blocking of D2 receptors in this pathway could result in what?

~1% Patients should be started on a combination of two non-insulin agents or with insulin itself

Monotherapy for type 2 diabetics with most non-insulin anti diabetic agents can reduce HbA1c levels by how much? Patients with an HbA1c level greater than 9% are unlikely to achieve their goals with monotherapy. As a result, what should be done?

1. Strong opioid receptor agonist 2. Useful in treating severe pain High affinity for µ receptor and a lower affinity for the δ and κ receptors

Morphine 1. Mechanism of action 2. Use What is the affinity of this drug for the µ, δ, and κ opioid receptors?

In patients with conditions that involve air within the body or body cavities (ex. pneumothorax, air embolus, obstructed loop of the bowel, etc). This is because nitrous oxide enters cavities quicker than nitrogen and can lead to increases in volume and pressure within the cavity.

Nitrous oxide should be avoided in what patients and why?

Warfarin

Pharmacogenomics Pharmacokinetics + Pharmacodynamics (Multiple Genes) Widely prescribed oral anticoagulant. Narrow therapeutic window with wide interindividual variability. Under-coagulation results in thrombosis and over-coagulation results in bleeding episodes. Pharmacokinetics - Racemic mixture. S-isomer is 3-5x more potent than R-isomer. Both are metabolized by different enzymes. Metabolism of S-isomer is mainly via CYP2C9, and R-isomer is via CYP3A4 and other isoforms. CYP2C9 is highly polymorphic, and variant allelles can have much lower activity than the wild-type allele. Patients with variant alleles, require decreased doses, and have increased risk for hemorrhage. Pharmacodynamics - Vitamin K epoxide reductase is the molecular target. The gene encoding the enzyme is vitamin K epoxide reductase complex 1(VKORC1), which shows many polymorphisms that affect dosing. Dose may vary two-fold.

CYP3A4 Their levels will require monitoring when being administered with NNRTIs as these drugs are inducers/inhibitors of CYP enzymes including CYP3A4 Potent inhibitors (for the most part) They are substrates for P-glycoprotein pumps.

Pharmacokinetics for protease inhibitors is important. What CYP enzyme are they a substrate for? How will this affect its co-administration with other antiretroviral drugs? Are these drugs inducers or inhibitors of CYP P450 enzymes? What other interaction is important for these drugs bioavailability?

1. Block voltage gated sodium channels which leads to a decrease in the transmission of excitatory glutamatergic neuronal signaling and blocks post synaptic glutamate receptors 2. Second line drug used in the treatment of simple and complex partial seizures and generalized tonic-clonic seizures 3. Induction of CYP P450 enzymes

Phenobarbital 1. Mechanism of action 2. Use 3. Adverse effects

1. Block voltage gated sodium channels which leads to a decrease in the transmission of excitatory glutamatergic neuronal signaling 2. Used in the treatment generalized tonic-clonic seizures, simple and complex partial seizures, and secondarily generalized tonic-clonic seizures 3. Induction of CYP P450 enzymes, gingival hyperplasia, hirsituism, and coarsening of facial features in children.

Phenytoin 1. Mechanism of action 2. Use 3. Adverse effects

1. Aminoglycoside drug that irreversibly binds to the 30S ribosomal subunit prior to ribosome formation 2. Commonly used as an initial treatment of an unknown infection for a short period of time and is discontinued after the offending organism is identified For treatment of the plague (Y. pestis)

Streptomycin 1. Mechanism of action 2. Use This is the drug of choice for what condition?

1. 2. Used as a second line therapy (not used much right now) in the treatment of drug-resistant strains of TB Because of increasing frequency of resistance

Streptomycin 1. Mechanism of action 2. Use 3. Adverse effects What is currently limiting the use of this drug?

Red as a beet (skin flushed), hot as a hare (hyperthermia), dry as a bone (dry mucous membranes & no sweating), blind as a bat (blurred visions, cycloplegia, and pupillary dilation), and mad as a hatter (confusion & delirium) Tachycardia Physostigmine but it should not be given to patients with a TCA overdose as it can aggregate cardiotoxicity resulting in a heart block or asystole.

The classic anticholinergic syndrome can be remembered using what pneumonic? What is another sign these patients present with? What is the treatment for anticholinergic toxicity?

It is a combination of hemolysis and hemoglobinuria that results from death of the P. falciparum parasite during treatment. Quinine and Quinidine

What is blackwater fever? What drugs is it associated with?

Malignant hyperthermia Dantrolene

The combination of succinylcholine and halogenated anesthetics can lead to the development of what condition in susceptible patients? What is the treatment for this condition?

Magnesium sulfate

Uterine Agents Tocolytic No tocolytic is first-line choice. Mother should be monitored for toxic effects, such as respiratory depression and cardiac arrest. Can also cross placenta and cause respiratory and motor depression in neonate. Actions - uncouples excititation-contraction in myometrial cells through inhibition of cellular action potentials. Used widely as primary tocolytic due to similar efficacy to terbutaline with better tolerance. Adverse - (Maternal) flushing, nausea, headache, drowsiness, blurred vision. Mother should be monitored for toxic effects, such as respiratory depression and cardiac arrest. Can also cross placenta and cause respiratory and motor depression in neonate. Contraindications: acute fetal distress(except during intrauterine resuscitation), chorioamnionitis, eclampsia, or severe preeclampsia, fetal demise(of singleton pregnancy), fetal maturity, and maternal hemodynamic instability.

Atosiban

Uterine Agents Tocolytic Peptide oxytocin analogue. Not available in US. Actions - Competitive antagonist at oxytocin receptors. Used to decrease and stop uterine contractions.

Terbutaline

Uterine Agents Tocolytic beta2 Agonist(Only one used as tocolytic in US). No tocolytic is first-line choice. Given SQ or IV Actions - Activates adenylyl cyclase, causing a rise in cAMP, activating protein kinase A. PKA phosphorylates smooth-muscle MLCK(SmMLCK), preventing it from phosphorylating myosin, and the myometrial smooth muscle relaxes. Used as tocolytic to delay delivery. Adverse - palpitations, tremor, nausea, vomiting, nervousness, anxiety, chest pain, shortness of breath, hyperglycemia, hypokalemia, hypotension. Serious complications include pulmonary edema, cardiac insufficiency, arrhythmias, myocardial ischemia, and maternal death. Contraindications: acute fetal distress(except during intrauterine resuscitation), chorioamnionitis, eclampsia, or severe preeclampsia, fetal demise(of singleton pregnancy), fetal maturity, and maternal hemodynamic instability.

1. Prodrug of Acyclovir 2. Treatment of choice for HSV encephalitis, with activity against most herpes viruses (1-4) and commonly used for genital herpes infections and as prophylaxis in immunocompromised transplant patients. Valacyclovir

Valacyclovir 1. Mechanism of action 2. Use Does acyclovir or valacyclovir have a greater oral bioavailability?

1. Prodrug of Ganciclovir 2. Drug of choice for CMV retinitis and CMV prophylaxis in immunocompromised patients Valganciclovir

Valganciclovir 1. Mechanism of action 2. Use Does ganciclovir or valganciclovir have a greater oral bioavailability?

1. Block voltage gated sodium channels which leads to a decrease in the transmission of excitatory glutamatergic neuronal signaling and blocks T-type calcium channels 2. Drug of choice in the treatment of myoclonic seizures and also used in the treatment generalized tonic-clonic seizures, secondarily in the treatment of simple and complex partial seizures, secondarily generalized tonic-clonic seizures, and absence seizures 3. Hepatotoxicity and inhibition of CYP P450 enzymes

Valproate 1. Mechanism of action 2. Use 3. Adverse effects

Antiepileptic Carbamazepine & lamotrigine Lithium Atypical antipsychotics including olanzapine, aripiprazole, quetiapine, risperidone, & ziprasidone.

Valproate is what type of drug and what condition can it be used as an alternative to treat? What other drugs in this class can be used to treat bipolar disorder? These are used as an alternative to what drug in the treatment of bipolar disorder? What other types of drugs can be used in the treatment of this condition?

1. Non-β-lactam inhibitor of cell wall synthesis 2. Used to treat serious infections caused by β-lactam resistant gram-positive organisms like MRSA, used to treat gram-positive infections in patients with a severe β-lactam allergy, and used in combination with amino glycosides as empirical treatment for infective endocarditis, for enterococcal endocarditis, and penicillin resistant Strep. pneumoniae. Gram-positives only It binds D-Ala-D-Ala on the bacterial peptidoglycan wall. Some bacteria have developed a D-Ala-D-lactate modification that keeps this drug from being effective.

Vancomycin 1. Mechanism of action 2. Use Is this drug affective against gram-negative, gram-positive, or both? What is the binding property of this drug and how has this lead to the development of VRSA or VRE?

Used as an initial treatment against infective endocarditis (until the offending organism is identified), for treatment of Enterococcal endocarditis, and for penicillin resistant Strep. pneumoniae To treat C. difficile pseudomembranous colitis because it is poorly absorbed so easily makes it to the offending area of the colon where the C. difficile infection is occurring.

Vancomycin and aminoglycosides are used in combination to treat what condition? For what condition is vancomycin given orally and why?

1. Partial agonist at nicotinic receptors in the CNS 2. Used to treat nicotine addiction

Varenicline 1. Mechanism of action 2. Use

1. Rifampin, pyrazinamide, and ethambutol and a fluoroquinolone (levofloxacin) can be added to strengthen the treatment 2. Fluoroquinolone (levofloxacin), pyrazinamide, ethambutol, with an injectable agent with or without a second-line agent 3. Fluoroquinolone (levofloxacin) and ethambutol or pyrazinamide (whichever the strain is susceptible to) with an injectable agent with or without two second-line agents 4. Isoniazid, ethambutol, fluoroquinolone (levofloxacin) with supplemented with pyrazinamide for the first 2 months The more resistant the strain is to the typical drugs that treat TB the longer the duration of treatment (because the treatment will not be as directed).

What drugs can be given to treat TB with the following patterns of drug resistance? 1. Isoniazid (+/- streptomycin) 2. Isoniazid & Rifampin (+/- streptomycin 3. Isoniazid, Rifampin (+/- streptomycin), ethambutol or pyrazinamide 4. Rifampin How does treating strains with more and more resistance affect the duration of treatment?

These drugs LEACH calcium form the bone. Lithium ETOH Anastrozole Corticosteroids Heparin PE Phenytoin Etidronate

What drugs cause osteoporosis and how can you remember them? What drugs cause osteomalacia and how can you remember them?

Valproate and lamotrigine Corticotropin or glucocorticoids are commonly used with an unknown MOA and vigabatrin can also be effective

What drugs may be useful in the treatment of atonic seizures? What drugs are recommended to treat infantile seizures?

Diazepam, lorazepam, or phenobarbital.

What drugs should be used to treat drug-induced seizures in non-epileptic patients?

1. Inhibits synthesis (iodination and condensation of thyroid hormone) 2. Inhibits synthesis by inhibiting iodination of thyroglobulin and inhibits the proteolytic release of hormones 3. Inhibits synthesis (iodination and condensation of thyroid hormone)

What effect do the following have on the synthesis and secretion of thyroid hormone? 1. Propylthiouracil 2. Elevated iodide 3. Methimazole

The metabolism of some of the long acting and intermediate acting drugs yields active metabolites so the drug action continues. Most undergo phase 1 reactions though CYP3A4 and the metabolites are then conjugated to form glucuronides It is a metabolite of several clinically used benzodiazepines that has a half life of over 40 hours LOT (lorazepam, temazepam, and oxazepam

What gives the benzodiazepine drugs various lengths of activity? How are the majority of them metabolized? What is desmethyldiazepam? Which benzodiazepine drugs are conjugated direct and are not metabolized by P450 enzymes?

Opioids PCP

What group of drugs being used would you suspect if you had a patient that presented with pinpoint pupils and sedation? What group of drugs being used would you suspect if you had a patient that presented with pinpoint pupils and agitation?

They are initially asymptomatic but later they develop fulminant liver failure causing hepatic encephalopathy and death. N-acetycysteine It increases glutathione production which helps to detoxify NAPQI and prevent it from being shunted into the pathway whose product causes cell death.

What happens to patients with acetaminophen poisoning? What is the antidote for acetaminophen poisoning? How does this antidote work?

Its lipid solubility (the more lipid soluble the better it can cross), its molecular weight (lower molecular weight, the better its ability to cross), and protein binding of the drug. 1. Lipid soluble 2. Low lipid solubility 3. Lipid soluble

What influences the ability of a drug to penetrate the blood-brain-barrier? Of the following drugs, which are lipid soluble and which have low lipid solubility? 1. Fluoroquinolones 2. Penicillin 3. Metronidazole

It is a live attenuated vaccine against tuberculosis. It is given after the resection of a superficial bladder cancer intravesically to induce granuloma formation in the area where the tumor was resected in order to prevent recurrence.

What is BCG (Bacillus Calmette-Guerin)? When is this given and why?

It is a mixture of iodine and potassium iodide used to inhibit thyroid hormone production and release prior to surgery for hyperthyroidism.

What is Lugol's solution?

It is thinning of the lateral 1/3 of the eyebrows and it is associated with hypothyroidism.

What is Queen Anne's sign and what condition is it associated with?

It is a condition that causes fatty liver, hypoglycemia, coma, and childhood hepatic encephalopathy in children with a viral infection treated with aspirin. Acetaminophen

What is Reye's syndrome and what is it caused by? What drug should be used to treat the symptoms of a viral illness in children?

Hemolysis in patients with a G6PD deficiency Primaquine No, we withhold therapy and treat relapses as necessary but we will not be able to remove the dormant liver form of this parasite.

What is a adverse drug reaction of almost all the antimalarial drugs that you should remember? What is the most likely drug to cause this adverse effect? If a patient is found to be G6PD deficient and infected with P. vivax or P. ovale, can we treat them with primaquine?

They have a high incidence of hypersensitivity reactions (eg. rash) which can develop into Stevens-Johnson syndrome and they are all CYP3A4 substrates that can act as inducers, inhibitors, or both of CYP P450 enzymes.

What is a major disadvantage of the NNRTIs (non-nucleotide reverse transcriptase inhibitors)?

It is an anti-T lymphocyte antibody that is obtained from horses and sheep which is used to suppress immunity before transplantation and in the treatment of acute graft rejection

What is a polyclonal antibody and what is its use?

Hyperkalemia as a result of the loss of tissue potassium during depolarization which can lead to cardiac arrest and/or circulatory collapse. Patients with burns and muscle trauma. As a result, succinylcholine is contraindicated in these patients.

What is a potentially fatal adverse effect of succinylcholine? Which patients have an increased risk of developing this adverse effect?

Chemotherapy that is added in addition to surgery or radiotherapy Chemotherapy that is given before surgery to decrease the size of the target tumor

What is adjuvant chemotherapy? What is neo-adjuvant chemotherapy?

Can produce tachycardia and arrhythmias as a result of muscarinic receptor blockades. Pancuronium

What is an adverse effect of ammonio steroids and how does it develop? Which is most likely to cause moderate tachycardia due to a blockade of cardiac M2 receptors?

Ethosuximide and valproate Only valproate can be used for both tonic-clonic and absence seizure treatment. Valproate Valproate

Which two drugs can be used to treat absence seizures? Can both of these drugs also be used to treat tonic-clonic seizures as well? As a result, what drug is recommended for patients who have both tonic-clonic and absence seizures? What is the preferred drug for the treatment of atypical absence seizures?

Prolactin and GH

Which two hormones act via Jak/Stat receptors?

1. Activity against gram-positive cocci, P. mirabilis, E. coli, and K. pneumonia 2. Extended gram-negative coverage with greater activity against H. influenzae, Enterobacter, and Neisseria spp. Weak activity against gram-positives 3. Enhanced activity against gram-negative cocci with less activity against most gram-positive organisms 4. Wide antibacterial spectrum with the gram-positive activity of the 1st generation and gram-negative activity of the 3rd generation. 5. MRSA and the same gram-negative activity as the 3rd generation

Which types of bacteria are the following cephalosporins active against? 1. 1st Generation 2. 2nd Generation 3. 3rd Generation 4. 4th Generation 5. 5th Generation

Atypical antipsychotics

Which types of drug have been found to be helpful as an adjunct for the treatment of major depressive disorder?

SSRIs OCD, panic disorder, GAD, PTSD, social anxiety disorder, PMDD, and bulimia. Increased serotonergic activity in the gut causes nausea, GI upset, diarrhea. In the spinal cord, increased serotonergic activity can cause sexual dysfunction and loss of interest, and some patients gain weight as a result of using these drugs.

Which types of drugs are the drugs of choice for treating depression? What other conditions does this drug treat? What are the adverse effects of these drugs?

Aztreonam (a monobactam). It is used to treat CF patients with Pseudomonas respiratory infections. In the urine It leaves unmetabolized as the parent compound so renal issues can lead to toxic levels of this drug building up.

Which β-lactam drug is given by inhalation and what is it used for? How is this drug excreted? Why is this important?

Opioids can cause respiratory depression which can lead to acute respiratory failure in patients with pre-existing pulmonary function impairment These drugs are metabolized in the liver (either for excretion or to metabolites which therapeutic activity) and impaired liver function can cause a reduction in this necessary metabolism The half-life of the drugs may be prolonged as a result of an impairment in excretion of the drugs and their metabolites Patients with adrenal insufficiency or hypothyroidism may have prolonged and exaggerated responses to these drugs.

Why should opioid drugs not be used in patients with impaired pulmonary function? Why should opioid drugs be used with caution in patients with impaired hepatic function? Why should opioid drugs be used with caution in patients with impaired renal function? Why should opioid drugs be used with caution in patients with endocrine disease? Which endocrine diseases should you be wary of?


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