med chem final exam

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what is elevated blood pressure?

120-129/<80

what is stage 1 hypertension

130-139/80-89

What is normal blood pressure?

<120/<80

what is stage 2 hypertension

> or = 140/90

Which of the following statements would be most​ consistent with the results expected of a pharmacological antagonist ​of the vasopressin​ V2 receptor? A) A decreased water reabsorption by the collecting duct cells, similar to the effect caused by prostaglandin E2 action on these cells B) An increased insertion of H2O channels into the luminal membrane of collecting duct cells C) An inhibition of cyclic nucleotide gated cation channels D) A large increased natriuresis E) A decreased urinary excretion of Ca2+ and Mg2+

A) A decreased water reabsorption by the collecting duct cells, similar to the effect caused by prostaglandin E2 action on these cells

4- Elevated levels of which of the following molecules would most likely contribute to a hypokalemia? A) Aldosterone B) A direct renin inhibitor C) An angiotensin converting enzyme inhibitor D) A potassium sparing diuretic E) A beta-adrenergic receptor antagonist

A) Aldosterone

Renin secretion is stimulated by:

A. Decreased renal perfusion (or reduced blood pressure). B. Reduced sodium concentration in the distal tubule. C. Beta-1 adrenergic receptor activation.

I am the only approved drug to inhibit renin.

Aliskiren

I am the only short acting ACE inhibitor.

Captopril

I block both the alpha and beta. I am also an anti-oxidant

Carvedilol

I am a centrally-acting alpha-2 agonist. If a patient suddenly stops taking me, his blood pressure will go very high.

Clonidine

3-All the following autonomic drug classes may cause bradycardia EXCEPT: A) Non-selective beta adrenoceptor antagonists. B) Selective beta-1 adrenoceptor antagonists. C) Selective alpha-1 adrenoceptor agonists. D) Non-selective alpha adrenoceptor antagonists. E) Selective alpha-2 adrenoceptor agonists.

D) Non-selective alpha adrenoceptor antagonists.

I am the only ACE inhibitor that does not need dose adjustment in patients with renal impairment.

Fasinopril

what is the chemical reaction that is catalyzed by carbonic anhydrase.

H2O + CO2 <--> H2CO3

What are the two main functions of the angiotensin converting enzyme (ACE)?

It activates the renin angiotensin aldosterone system (RAAS) or activates angiotensin I to angiotensin II. B. It inactivates bradykinins

Which of the following is not true of losartan? a. It is a competitive inhibitor of the AT1 receptor b. Its metabolism by CYP3A4 gives rise to an active metabolite c. It is a prodrug that must be converted to an active species by esterases d. Unlike angiotensin II, it is not a peptide e. It antagonizes the effects of angiotensin II

It is a prodrug that must be converted to an active species by esterases

I block the alpha and beta adrenergic receptors, and I can be used safely in pregnant women.

Labetalol

9) Which of the following drugs is an appropriate initial antihypertensive therapy in an otherwise healthy adult with mild arterial hypertension? a. Chlorthalidone b. Eplerenone c. Triamterene d. Furosemide e. Acetazolamide

a. Chlorthalidone

Which of the following best describes the mechanism of action of spironolactone? a. Competitive antagonist of aldosterone at mineralocorticoid receptor b. Inhibitor of Na+/Cl- symporter in distal tubule of the nephron c. Inhibitor of Epithelial sodium channel (ENaC) in collecting tubule of nephron d. Inhibitor of the Na+/K+/2Cl- transporter in the thick ascending loop of Henle e. Inhibitor of Na+/H+ transporter in the proximal tubule of the nephron

a. Competitive antagonist of aldosterone at mineralocorticoid receptor

The administration of aliskiren will: a. Decrease plasma renin activity and increase plasma renin concentration b. Increase both plasma renin activity and plasma renin concentration c. Decrease both plasma renin activity and plasma renin concentration d. Increase plasma renin activity and decrease plasma renin concentration e. Not have any effect of plasma renin activity and plasma renin concentration

a. Decrease plasma renin activity and increase plasma renin concentration

Which of the following statements is NOT true? a. Minoxidil acts by inhibiting PDE 4 b. Sodium nitroprusside releases cyanide (CN- ) when it is broken down in blood c. Hydralazine is metabolized by N-acetyltransferase d. Minoxidil must be converted to its active species metabolically e. KATP-channel activators bring about hyperpolarization in vascular smooth muscle cells

a. Minoxidil acts by inhibiting PDE 4

name two carbonic anhydrase inhibitors

acetazolimide, dorzolamide, brinzolamide, methazolamide

when do you use drug therapy in hypertension?

at stage 1 HTN when ASCVD 10 year risk is 10 % or higher or at stage 2

which drug can antagonize the effects of digoxin?

atropine

Rank the Ca2+ channel blockers according to their direct actions on the heart relative to vascular smooth muscle (1=most active on heart and 3=most active on vascular smooth muscle) a. (1) amlodipine>(2) verapamil> (3) diltiazem b. (1) verapamil >(2) diltiazem > (3) amlodipine c. (1) diltiazem> (2) amlodipine>(3) verapamil d. (1) verapamil> (2) amlodipine> (3) diltiazem e. (1) amlodipine> (2) diltiazem> (3) verapamil

b. (1) verapamil >(2) diltiazem > (3) amlodipine

Which of the following endogenous mediators would be MOST likely to increase the number of functional collecting duct epithelial sodium channels and thus favor increased Na+ reabsorption from the nephron? a. Arginine vasopressin b. Aldosterone c. Prostaglandin E2 d. Dopamine e. Adenosine

b. Aldosterone

Which of the following agents is most likely to induce hyperkalemia? a. Hydrochlorothiazide b. Amiloride c. Mannose d. Acetozolamide e. Furosemide

b. Amiloride

7) When furosemide is administered to a patient with pulmonary edema, there is often rapid relief of symptoms, i.e. within a few minutes. This relief is primarily due to . . . . a. A rapid diuretic effect and the resultant decrease in plasma volume b. An increase in venous capacitance c. A direct, positive cardiac inotropic effect d. Enhanced furosemide-induced metabolism of vasodilator prostaglandins e. Psychological effects

b. An increase in venous capacitance

Amiloride a. Is an antagonist of the mineralocorticoid receptor b. Blocks the epithelial Na+ -channel c. Inhibits of the Na+ -K+ -2Cl- symport system d. Inhibits carbonic anhydrase e. Inhibits the Na+ -Cl- symporter

b. Blocks the epithelial Na+ -channel

Which agent exerts its diuretic effect by inhibiting the Na+/Cl- symport system? a. Dorzolamide b. Chlorthalidone c. Amiloride d. Torsemide e. Eplerenone

b. Chlorthalidone

12) The following are known or hypothetical mechanisms whereby drugs could act on molecular targets to affect blood pressure regulation. Which action would be expected to INCREASE blood pressure? a. Inhibition of kininase II (the same protein as ACE) and inhibition of neprilysin (i.e., as is afforded by sacubitril) b. Decreased hydrolysis/inactivation of asymmetric dimethyl arginine (ADMA) c. Binding of brain natriuretic peptide (BNP) to vsm NPR- A receptors d. Blockade of vsm endothelin ETA receptors e. Drug action that fosters activation of myosin light chain phosphatase

b. Decreased hydrolysis/inactivation of asymmetric dimethyl arginine (ADMA)

11) Which of the following can be caused by both "loop diuretics" and thiazides? a. Metabolic acidosis b. Hypokalemia c. A decrease in the plasma concentration of Ca2+ d. A decrease in the plasma concentrations of both glucose and urate e. A rapid decrease in cardiac left ventricular end diastolic pressure (LVEDP) due to dilatation of veins

b. Hypokalemia

Which of the following best describes the mechanism of action of furosemide (Lasix)? a. Inhibitor of carbonic anhydrase b. Inhibitor of Sodium-Potassium-Two Chloride (Na-K-2Cl) transporter c. Inhibitor of sodium-Chloride (Na-Cl) transporter d. Inhibitor of endothelial Na channel (ENaC) e. Antagonist of aldosterone an mineralocorticoid receptor

b. Inhibitor of Sodium-Potassium-Two Chloride (Na-K-2Cl) transporter

2) A new imaginary drug (drug X) is designed to inhibit ACE activity toward Angiotensin I (AngI), without affecting its activity in breaking down bradykinin and other inflammatory mediators. Compared to traditional ACE inhibitors, drug X will cause: a. More reduction in blood pressure and less dry cough. b. Less reduction in blood pressure and less dry cough. c. More reduction in blood pressure and more dry cough. d. Less reduction in blood pressure and more dry cough. e. Similar reduction in blood pressure and less dry cough.

b. Less reduction in blood pressure and less dry cough.

Icatibant is a bradykinin receptor antagonist. If icatibant and an ACE inhibitor are given together to a hypertensive patient, icatibant will cause: a. More reduction in blood pressure and less dry cough. b. Less reduction in blood pressure and less dry cough. c. More reduction in blood pressure and more dry cough. d. Less reduction in blood pressure and more dry cough. e. Similar reduction in blood pressure and less dry cough

b. Less reduction in blood pressure and less dry cough.

Which of the following phosphodiesterase inhibitors is used in the treatment of chronic obstructive pulmonary disease (COPD)? a. Milrinone b. Roflumilast c. Anagrelide d. Crisaborole e. Avanafil

b. Roflumilast

Which of the following drugs is a selective inhibitor of neutral endopeptidase Angiotensin converting enzyme a. Cilazapril b. Sacubitril c. Eposartan d. Captopril e. Brinzolamide

b. Sacubitril

All the following autonomic drug classes reduce arterial blood pressure, EXCEPT: a. Selective α1-adrenoceptor antagonists. b. Selective α2-adrenoceptor antagonists. c. Non-selective α-adrenoceptor antagonists. d. Selective β1-adrenoceptor antagonists. e. Non-selective β-adrenoceptor antagonists

b. Selective α2-adrenoceptor antagonists.

One would see an increase in renin secretion under the following condition? a. Increased blood pressure b. Stimulation of β1 receptors c. Elevated levels of angiotensin II d. Elevated levels of atrial natriuretic peptide e. All of the above

b. Stimulation of β1 receptors

Which statement is TRUE? a. Any signaling pathway leading to stimulation of myosin light chain kinase (MLCK) activity in vascular smooth muscle cells is predicted to promote vasodilation b. Vascular endothelial cells supply vascular smooth muscle cells with an array of vasoconstrictors (e.g., endothelin/ET-1) and vasodilators (e.g., prostacyclin/PGI2) c. Any signaling pathway leading to stimulation of cAMP levels in vascular smooth muscle cells is predicted to promote vasoconstriction d. Organic nitrates like glyceryl trinitrate (nitroglycerin) promote vasodilation by suppressing the activity of myosin light chain phosphatase e. Angiotensin Converting Enzyme (ACE) inhibitors and Angiotensin Receptor Blockers (ARBs) evoke vasodilation by enhancing the activity of an endogenous vasodilatory signaling pathway in vascular smooth muscle cells.

b. Vascular endothelial cells supply vascular smooth muscle cells with an array of vasoconstrictors (e.g., endothelin/ET-1) and vasodilators (e.g., prostacyclin/PGI2)

Which of the following endogenous mediators would be most likely to increase the number of functional collecting duct epithelial sodium channels and thus favor increased Na+ reabsorption from the nephron. A) Arginine vasopressin B) Aldosterone C) Prostaglandin E2 D) Dopamine E) Adenosine

b. aldosterone

Which of the following best describes the mechanism of action of furosemide (Lasix)? A) Inhibitor of carbonic anyhdrase B) Inhibitor of Sodium-Potassium-Two Chloride (Na-K-2Cl) transporter C) Inhibitor of sodium-Chloride (Na-Cl) transporter D) Inhibitor of endothelial Na channel (ENaC) E) Antagonist of aldosterone an mineralocorticoid receptor

b. inhibitor of sodium-Potassium-Two Chloride (Na-K-2Cl) transporter

which of the following long acting ACE inhibitors is NOT a prodrug? a. captopril b. lisinopril c. fosinopril d. enalapril e. ramipril

b. lisinopril

all of the following can result from beta activation except: a. tachycardia b. reduced stroke volume c. increased cardiac output d. renin secretion e. activation of RAAS

b. reduced stroke volume

all of the following are side effects of Angiotensin I converting enzyme (ACE) inhibitors EXCEPT: a. dry cough b. tachycardia c. hypotension d. hyperkalemia e. angioedema

b. tachycardia

8) Via an action in the collecting duct, prostaglandin E2 causes an effect on urine composition and output/volume that is most like the effect caused by . . . . a. An angiotensin converting enzyme inhibitor b. A thiazide c. A pharmacological antagonist acting at the V2 vasopressin receptor. d. An inhibitor of epithelial sodium channels in the late distal tubule/collecting duct e. A carbonic anhydrase inhibitor

c. A pharmacological antagonist acting at the V2 vasopressin receptor.

A 71 year old female patient receiving diuretic therapy to treat congestive heart failure is diagnosed with an acute, potentially life-threatening case of Steven-Johnson Syndrome. Which of the following agents is most likely responsible? a. Mannitol b. Furosemide (Lasix) c. Acetazolamide (Diamox) d. Amiloride e. Spironolactone (Aldactone)

c. Acetazolamide (Diamox)

Which of the drugs listed below has a relatively long T1/2 , lacks direct cardiac effects when used in typical clinical doses, does not affect contractility of veins, and is an effective, orally-active agent for the chronic treatment of primary hypertension? a. Verapamil b. Diltiazem c. Amlodipine d. Nitroglycerin e. digoxin

c. Amlodipine

Amlodipine is used clinically for all of the following conditions except: a. Stable angina b. Variant angina c. Atrial flutter d. Hypertension e. Raynaud's Syndrome

c. Atrial flutter

What underlies the vasodilatory impact of neprilysin inhibition? a. Reduction of prostacyclin levels b. Competitive inhibition of alpha-1 adrenergic receptors c. Increased level and influence of natriuretic peptides d. Increased endothelin production by vascular smooth muscle cells e. Increased metabolism of bradykinin

c. Increased level and influence of natriuretic peptides

Which of the following diuretic agents is only effective if administered intravenously (i.e. is not efficacious following oral administration)? a. Hydrochlorothiazide b. Amiloride c. Mannose d. Acetozolamide e. Furosemide

c. Mannose

What endogenous mediator impacts vasopressin's effect on the aquaporin of the collecting duct in a manner that is most similar to a V2 vasopressin receptor antagonist? a. Arginine vasopressin b. Aldosterone c. Prostaglandin E2 d. Dopamine e. Adenosine

c. Prostaglandin E2

In addition to treating erectile dysfunction, a phosphodiesterase 5 (PDE5) inhibitor is used in treating which of the following? a. Essential thrombocytosis b. Psoriatic arthritis c. Pulmonary arterial hypertension d. Male pattern baldness e. None of the above

c. Pulmonary arterial hypertension

A 71 year old female patient receiving diuretic therapy to treat congestive heart failure is diagnosed with an acute, potentially life-threatening case of Steven-Johnson Syndrome. Which of the following agents is most likely responsible? A) Mannitol B) Furosemide (Lasix) C) Acetazolamide (Diamox) D) Amiloride E) Spironolactone (Aldactone)

c. acetazolamide (diamox)

Which of the following drugs acts as an osmotic diuretic? a. Metolazone b. Torsemide c. Mannitol d. Brinzolamide e. None of the above

c. mannitol

NSAIDs may impair the hypotensive effect of ACE inhibitors, by inhibiting the synthesis of: a.bradykinin b. nitric oxide c. prostacylcin d. angiotensin 1-7 e. alamandine

c. prostacyclin

Which of the following conditions would be MOST appropriate to treat with a hypotensive drug according to the 2017 ACC/AHA hypertension treatment guidelines? a. systolic pressure =131 mm Hg; ASCVD (atherosclerotic cardiovascular disease) 10 year risk = 4% b. diastolic pressure =83 mm Hg; ASCVD 10 year risk = 6% c. systolic pressure = 120 mm Hg; diastolic blood pressure = 92 mm Hg d. systolic pressure = 125 mm Hg; diastolic pressure = 79 mm Hg e. systolic pressure = 131 mm Hg; diastolic pressure = 81 mm Hg

c. systolic pressure = 120 mm Hg; diastolic blood pressure = 92 mm Hg

i am an alpha agonist, but i can reduce your blood pressure. if you suddenly stop taking me, bad things can happen. who am I?

clonidine

name 2 alpha 2 agonists

clonidine and methyldopa

All the following autonomic drug classes may cause bradycardia EXCEPT: A) Non-selective beta adrenoceptor antagonists. B) Selective beta-1 adrenoceptor antagonists. C) Selective alpha-1 adrenoceptor agonists. D) Non-selective alpha adrenoceptor antagonists. E) Selective alpha-2 adrenoceptor agonists.

d) non-selective alpha adrenoceptor antagonists

antagonism of all the following receptors will reduce arterial blood pressure in hypertensive patients EXCEPT: a. alpha 1 adrenergic receptors b. beta 1 adrenergic receptors c. AT1 receptors d. AT2 receptors e. Endothelin receptors

d. AT2 receptors

Which of the following investigational approaches can have a beneficial therapeutic effect in hypertensive patients? a. Kallikrein inhibitors. b. Chymase activators. c. ACE2 inhibitors. d. AT2-receptor agonists. e. MAS receptor antagonists.

d. AT2-receptor agonists.

Which of the following agents is a selective endothelin (ETA) A receptor antagonist? a. Bosentan b. Milrinone c. Cilostazol d. Ambrisentan e. Sildenafil

d. Ambrisentan

The inhibition of phosphodiesterase 3 (PDE3) results in the which of the following effects a. A decrease in platelet aggregation b. A decrease in cardiac muscle contraction c. Vasodilation d. Both a and c e. Both b and c

d. Both a and c

Which functional group in the angiotensin converting enzyme inhibitor below complexes with the zinc atom within the enzyme's active site. a. Amino group 1 b. Carbonyl group 2 c. Carboxylic acid group 3 d. Carboxylic acid group 4 e. None of the above groups as there is no zinc atom in angiotensin converting enzyme

d. Carboxylic acid group 4

Choose the correct pairing of drug and mechanism of action relevant to vasodilation: a. Phentolamine: competitive antagonism of AT1 receptors b. Bosentan: inhibition of phosphodiesterase 5 (PDE5), suppressing cGMP metabolism in vascular smooth muscle cells c. Sildenfil: decreased production of endothelin (ET-1) d. Lisinopril: inhibition of angiotensin converting enzyme leads to suppression of angiotensin II (ATII) production and increased levels of bradykinin e. Losartan: competitive antagonism of alpha adrenergic receptors found on vascular smooth muscle cells

d. Lisinopril: inhibition of angiotensin converting enzyme leads to suppression of angiotensin II (ATII) production and increased levels of bradykinin

5) What is the molecular target of tolvaptan? a. Angiotensin converting enzyme b. Angiotensin II AT1 receptor c. Na+-channel in the late distal tubule/collecting duct d. V2 vasopressin receptor e. Phosphodiesterase 5

d. V2 vasopressin receptor

which of the following antihypertensive medications can be used safely by pregnant women? a. methyldopa only b. labetalol only c. enalapril only d. a and b e. a and c

d. a and b

All the following are side effects of alpha-1 adrenoceptor antagonists, EXCEPT: a. Postural hypotension. b. Salt and water retention. c. Impotence. d. Bradycardia. e. Nasal congestion

d. bradycardia

all the following can contribute to angiotensin II induced increase in blood pressure EXCEPT a. direct vasoconstrictive effect b. increased norepinephrine release c. increased aldosterone secretion d. increased renin secretion e. increased tubular sodium reabsorption

d. increased renin secretion

the concurrent use of aliskerin with ACE inhibitors may dangerously increase the blood level of: a. angiotensin I b. bradykinin c. sodium d. potassium e. aliskerin

d. potassium

all of the following autonomic drug classes can be used in the treatment of hypertension except: a. selective beta 1 antagonist b. non-selective beta antagonist c. selective alpha 1 antagonist d. selective alpha 2 antagonist e. non selective alpha antagonist

d. selective alpha 2 antagonist

dry cough is a common side effect of ACE inhibitors. Which of the following statements is TRUE regarding ACE inhibitors induced dry cough a. it is caused by the accumulation of Angiotensin I b. It always happens within one month of initiating the ACE inhibitor therapy c. all drugs inhibiting the Renin Angiotensin Aldosterone System (RAAS) have dry cough as a side effect d. several inflammatory mediators contribute to the pathogenesis of ACE inhibitors induced dry cough e. It is a serious side effect and the patient should stop taking the ACE inhibitor immediately

d. several inflammatory mediators contribute to the pathogenesis of ACE inhibitors induced dry cough

what is the mechanism of action for osmotics?

decrease Na+ and H2O reabsorption

4) All the following are theoretical advantages of Angiotensin Receptor Blockers (ARBs) over ACE inhibitors, EXCEPT: a. ACE inhibitors increase renin and Angiotensin I (AngI) levels, which may overcome their inhibitory effect b. ACE is not the only enzyme that converts angiotensin I (AngI) to angiotensin II (AngII) c. ARBs selectively block AT1 receptors, thereby preserving the protective effects of AT2 receptor d. ARBs cause less dry cough and angioedema. e. ARBs can be used in patients with bilateral renal artery stenosis

e. ARBs can be used in patients with bilateral renal artery stenosis

Which of the following is true concerning the structure-activity relationships of the thiazide and hydrothiazide diuretics? a. The sulfamoyl group at position 7 is a prerequisite for diuretic activity b. Reduction of the 3-4 double bond yields the more active hydrothiazides c. Lipophilic moieties at position 3 (R2) increase potency d. The sulfonyl group at position 1 can be replaced with a carbonyl group e. All of the above

e. All of the above

Which of the following statements is TRUE regarding the conversion of angiotensin I (Ang I) to angiotensin II (Ang II)? a. The conversion of Ang I to Ang II is the rate limiting step in activating the Renin Angiotensin Aldosterone System (RAAS). b. Angiotensin converting enzyme (ACE) is the only enzyme capable of converting Ang I to Ang II. c. The conversion of Ang I to Ang II is mediated by endopeptidase enzymes. d. Ang I is a more potent vasoconstrictor molecule than Ang II. e. Ang II activates both AT1 and AT2 receptors.

e. Ang II activates both AT1 and AT2 receptors.

3) All the following conditions increase the risk of hyperkalemia in patients treated with ACE inhibitors, EXCEPT: a. Diabetes b. Concurrent use of aldosterone antagonists c. Renal insufficiency d. Concurrent use of potassium supplement e. Concurrent use of loop diuretics

e. Concurrent use of loop diuretics

All the following conditions increase the risk of hyperkalemia in patients treated with angiotensin receptor blockers (ARBs), EXCEPT: a. Diabetes. b. Concurrent use of aldosterone antagonists. c. Renal insufficiency. d. Concurrent use of potassium supplements. e. Concurrent use of thiazide diuretics.

e. Concurrent use of thiazide diuretics.

Which drug is a carbonic anhydrase inhibitor used to treat glaucoma? a. Hydrochlorothiazide b. Triamterene c. Tolvaptan d. Bumetanide e. Dorzolamide

e. Dorzolamide

1) Which of the following cardiac parameters is reduced by beta 1-adrenoceptor activation? a. Heart rate b. Conductivity c. Contractility d. Automaticity e. Efficiency

e. Efficiency

When a patient with primary arterial hypertension is treated with a thiazide diuretic, all of the following are likely EXCEPT: a. The initial hypotensive effect seen in the first 1-2 weeks of treatment results from a decrease of extracellular fluid volume and cardiac output. b. The delayed, sustained hypotensive effect that occurs after several weeks of therapy is due to a decrease in peripheral vascular resistance. c. After arterial pressure is reduced, hypokalemia remains a problem. d. Hyperuricemia may occur. e. Hypoglycemia may occur.

e. Hypoglycemia may occur.

The following are known or hypothetical mechanisms whereby drugs could act on molecular targets to affect blood pressure regulation. Which action would be most expected to INCREASE blood pressure? a. Inhibition of the Na+-Cl- transporter of the distal convoluted tubule b. Inhibition of renin release c. Activation of α2 receptors in the CNS d. Blockade of the endothelin ETA receptors in the vascular smooth muscle e. Inhibition of the myosin light chain phosphatase in the vascular smooth muscle

e. Inhibition of the myosin light chain phosphatase in the vascular smooth muscle

6) Furosemide increases the excretion of all of the following EXCEPT . . . a. Na+ b. K+ c. Ca++ and Mg++ d. Cl - e. Uric acid

e. Uric acid

renin secretion is stimulated by all of the following EXCEPT a. reduction in arterial blood pressure b. reduction in sodium concentration in the distal tubule c. increase in sympathetic activity d. the use of loop diuretics e. angiotensin II

e. angiotensin II

Which of the following is true of tolvaptan? a. It increases water channel (aquaporin) expression in membranes b. It antagonizes V2 vasopressin receptors c. It is effective in treating hyponatremia associated with congestive heart failure d. Both a and b are true e. Both b and c are true

e. both b and c are true

which of the following cardiac parameters is reduced by beta 1 adrenoceptor activation? a. heart rate b. conductivity c. contractility d. automaticity e. efficiency

e. efficiency

all of the following may lower the heart rate except: a. atenolol b. phenylephrine c. digoxin d. clonidine e. prazosin

e. prazosin

Which of the following drug classes would NOT generally be considered a first-line treatment of essential hypertension in the absence of comorbidities. a. thiazide or thiazide -type diuretics b. calcium channel blockers c. ACE inhibitors d. ARBs (angiotensin II receptor blockers) e. β - blockers

e. β - blockers

what does alpha 2 antagonists do?

elevates blood pressure (yohimbine)

true or false: beta blockers vasodilate

false

what can reverse beta blocking effects that cause cardiac depression

glucagon

Describe two mechanisms by which drugs could reduce PR by decreasing the influence of certain endogenous vasoconstrictors

i) Reduce effects of norepinephrine (NE) on resistance vessels - Pharmacological mechanisms that decrease the synthesis, storage, release or binding of NE to alpha 1 adrenoceptors will decrease PR. (Note that these mechanisms could include ganglionic blocking agents, reserpine, and guanethidine [obsolete agents], as well as centrally-acting drugs [see 2. below] and alpha 1 adrenoceptor antagonists that are still used today) - Delivery of a drug that causes agonist action on alpha 2 adrenoceptors in the vasomotor center ii) Reduce effects of angiotensin II on resistance vessels - Pharmacological mechanism that inhibits the formation of angiotensin I, i.e. inhibition of renin activity - Pharmacological mechanism that inhibits the formation of angiotensin II, i.e. inhibition of ACE - Pharmacological antagonism of Ang II binding at the AT1 receptor iii) Reduce effects of endothelin (ET) on resistance vessels (Note that ET is primarily important with respect to the pulmonary circulation) - Block ET receptors on vsm, e.g. by bosentan or other -"entan" drugs. - Block ET "converting enzyme" (potential drug), reducing metabolism of "Big ET" to ET

what is the mechanism of action for carbonic anhydrase inhibitors?

inhibit the carbonic anhydrase which decreases Na+ and HCO3- reabsorption

what is the mechanism of action for thiazides?

inhibition of Na+/Cl- symporter

what is the mechanism of action of potassium sparing diuretics?

inhibition of aldosterone or blockade of Na+ channel

what is the mechanism of action of loop diuretics?

inhibition of the Na+/K+/Cl- transport system

which beta blocker is safe in pregnancy

labetalol

what beta blocker has beta 1 blocking effect and is a beta 3 agonist?

nebivolol

i reduce your blood pressure and slow your heart rate, but take care if you have asthma, who am I?

non-selective beta blocker

what class of diuretics is mannitol?

osmotics

which non-selective alpha antagonist is irreversibly bound?

phenoxybenzamine

which non-selective alpha antagonist is reversible

phentolamine

I increase your blood pressure and lower your heart rate. If you have a recent cardiac transplant, you may get a different effect

phenylephrine

name 2 alpha 1 agonists

phenylephrine and midodrine

what are the effects of a beta 1 agonist

positive inotropic and chronotropic (dobutamine)

what is an alpha 1 antagonist that has a short half life

prazosin

what site of action does carbonic anhydrase inhibitors attack?

proximal tubule

where is mannitol's site of action?

proximal tubule, loop of Henle, and the collecting duct

what are two serious adverse effects of acetazolamide?

stevens-johnson syndrome, metabolic acidosis

what happens when the Na+/K+/Cl- symport is inhibited?

the Na+ reabsorption is stopped and increases Ca2+ and Mg2+ excretion

what does the carbonic anhydrase inhibitor attack?

the zinc metalloenzyme

true or false: methyldopa can be used in pregnant women

true


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