Pharm Test 2

How can HTN treatment adherence be improved?

Cost Side effects Patient education Health promotion DASH Exercise Smoking cessation Medications Home BP monitoring Encouragement!

Describe high intensity statin therapy

Daily dose lowers LDL-C by approx >50% Atorvastatin (Lipitor) 40-80mg Rosuvastatin (Crestor) 20-40mg

What are the two main types of heart failure?

"There are two main types of heart failure. They are defined based on whether the "ejection fraction" (which indicates how well the left ventricle is able to pump) is preserved or reduced: ●In "heart failure with reduced ejection fraction" (also called "HFrEF" or "systolic heart failure"), the heart is too weak. When the heart pumps, it doesn't squeeze normally. ●In "heart failure with preserved ejection fraction" (also called "HFpEF" or "diastolic heart failure"), the heart is too stiff. When the heart pumps, it doesn't relax and fill with blood normally." Per Patient education UpToDate, 2018

What are examples, MOA, contraindications, and adverse effects of calcium channel blockers?

(-ipine suffix) Amlodipine, felodipine MOA: Inhibit movement of calcium across cell membranes Decrease contractility of myocardial and smooth muscle Contraindications No proven benefit in heart failure (may be used for other reasons) Adverse Events Headache, flushing, palpitations, peripheral edema

What are examples, MOA, and adverse effects of alpha-beta adrenergic antagonists

(-lol) suffix: Carvedilol, labetalol MOA: Block adrenergic β-1, β-2, alpha-1 receptor sites, blunt catecholamine response Adverse events Same as non-cardioselective beta-blocker for airway disease & DM Less insulin resistance compared to BB Taper over 10-14 days Carvedilol is used for treating HTN and CHF. It functions much like labetolol. Carvedilol blocks stimulation of beta1 (myocardial) and beta2 (pulmonary, vascular, and uterine)-adrenergic receptor sites. Also has alpha1 blocking activity, which may result in orthostatic hypotension. Therapeutic Effect(s): Decreased heart rate and BP. Improved cardiac output, slowing of the progression of HF and decreased risk of death. Alpha/Beta Blockers: Carvedilol and Labetalol. "Carvedilol and labetalol are unusual in that they can block alpha1 receptors as well as beta receptors. Blood pressure reduction results from a combination of actions: (1) alpha1 blockade promotes dilation of arterioles and veins, (2) blockade of cardiac beta1 receptors reduces heart rate and contractility, and (3) blockade of beta1 receptors on juxtaglomerular cells suppresses release of renin. Presumably, these drugs also share the ability of other beta blockers to reduce peripheral vascular resistance. Like other nonselective beta blockers, labetalol and carvedilol can exacerbate bradycardia, AV heart block, and asthma. Blockade of venous alpha1 receptors can produce postural hypotension." (Lehne, 2016) "Labetalol HCl combines both selective, competitive, alpha1-adrenergic blocking and nonselective, competitive, beta-adrenergic blocking activity in a single substance. Both the alpha- and beta-blocking actions of orally administered labetalol HCl contribute to a decrease in blood pressure in hypertensive patients. Labetalol HCl consistently, in dose-related fashion, blunted increases in exercise-induced blood pressure and heart rate, and in their double product. The pulmonary circulation during exercise was not affected by labetalol."

What are examples, MOA, adverse effects of beta-adrenergic antagonists (beta-blockers)

(-olol or -lol suffix): atenolol, metoprolol, propranolol, etc. MOA β-1 receptors (heart & kidneys) - stimulating effect β-2 receptors (lungs, liver, pancreas, arteriolar smooth muscle) - relaxing effect Cardioselective bind specifically to β-1 receptors Non-cardioselective bind to β-1 and β-2 receptors Adverse events Use with caution in untreated heart block May cause bronchospasm May worsen insulin resistance May mask hypoglycemia Risk vs benefit? With discontinuation: taper over 10-14 days

What are examples, MOA, contraindications, and adverse effects of angiotensin-converting enzyme inhibitors (ACEI)

(-pril siffix) Mechanism of Action Inhibit Angiotensin Converting Enzyme; decrease conversion of angiotensin I to angiotensin II (potent vasoconstrictor). Contraindications Renal artery stenosis (bilateral/unilateral) History of angioedema Pregnancy category D Adverse Events Chronic dry cough, rashes, dizziness Hyperkalemia Angioedema, laryngeal edema

What are examples, MOA, contraindications, and adverse effects of Angiotensin II Receptor Blockers (ARB)

(-sartan suffix) Losartan, telmisartan MOA: Selectively bind to angiotensin II receptors Block vasoconstricting and aldosterone-secreting effects of angiotensin II Contraindications Pregnancy category D ACE inhibitor-related angioedema (unless good justification to use) Impaired kidney or liver function Adverse Events Angioedema, cough, hyperkalemia Fatigue, diarrhea, respiratory tract infections

What are 3 types of lipoproteins?

-high-density lipoproteins (HDLs) -low density lipoproteins (LDLs) -very low density lipoproteins (VLDL) HDL-The Good LDL-The Bad VLDL-The Ugly

What are pathophysiological factors that influence BP?

1. Baroreceptors in aorta, carotid sinus, LV wall Monitor level of arterial pressure by sensing stretch in blood vessel...send signal to CNS Lower or elevate systemic arterial pressure (decrease or increase HR; vasoconstriction or vasodilation) Have short term effect; desensitized with essential HBP 2. Regulation of body fluid volume Healthy kidneys either retain fluid if patient hypotensive or excrete fluid if hypertensive 3. Renin-angiotensin system Angiotensin II vasoconstricts and controls aldosterone release Aldosterone causes kidneys to reabsorb sodium and inhibit fluid loss = Increased blood volume and BP 4. Vascular autoregulation Helps keep tissue perfusion relatively constant Has role in HBP (poorly understood)

JNC 8 BP goals

1. If age > 60, target < 150/90; Corollary if doing well at < 140/90, continue current RX 2. If age < 60, target DBP < 90 3. If age < 60, target SBP < 140 4. If CKD, target SBP < 140, DBP < 90 5. If DM, target SBP < 140, DBP < 90

What are nine recommendations by the JNC-8

1. If age > 60, target < 150/90; Corollary if doing well at < 140/90, continue current RX 2. If age < 60, target DBP < 90 3. If age < 60, target SBP < 140 4. If CKD, target SBP < 140, DBP < 90 5. If DM, target SBP < 140, DBP < 90 6. First agent of choice, if non-black: thiazide type diuretic, CCB, ACEI, ARB 7. First agent of choice, if black: thiazide type diuretic, CCB 8. First agent of choice, if CKD: ACEI, ARB 9.Medication titration options "JNC 8" - 2014 Evidence Based Guidelines Nine Recommendations Patients >60 years of age - Start treatment if BP > 150/90. Goal BP <150/90 <60 years, treatment initiation. BP goals should be 140/90 mm Hg. Nonblack patients with HTN initial treatment = thiazide-type diuretic, CCB, ACE inhibitor, or ARB. Black population - initial treatment = thiazide-type diuretic, CCB, ACE inhibitor, or ARB, Pt. >18 years with CKD, initial or add-on therapy should be ACE inhibitor or ARB, regardless of race or diabetes status. In patients <60 years, treatment initiation and goals should be 140/90 mm Hg, the same threshold used in patients >18 years with either chronic kidney disease (CKD) or diabetes. "JNC 8" - 2014 Evidence Based Guidelines Nine Recommendations JNC 8 is essentially in line with European Society of Hypertension (ESH) guidelines released early 2017, which suggested target of <140 mm Hg systolic BP for "all" patients, with some caveats. In patients with diabetes, ESH guidelines suggest a diastolic BP of <85 mm Hg, and for patients under 80 years, they suggest a target of between 140 and 150, going lower only if the patient is fit and in good health.

How is HTN diagnosed?

12 lead ECG Urinalysis with urinary albumin Blood glucose and hematocrit Serum potassium Creatinine & estimated GFR Serum calcium Lipid profile

What are identifiable causes of HTN

2 - 5% have an identifiable cause Chronic Kidney Disease Coarctation of the Aorta Cushing's Syndrome Obstructive uropathy Pheochromocytoma Primary aldosteronism Coarctation of the aorta is a narrowing of the aorta. When this occurs, the heart must pump harder to force blood through the narrow part of the aorta. Coarctation of the aorta is generally present at birth (congenital). Coarctation of the aorta can range from mild to severe, and might not be detected until adulthood, depending on how narrowed the aorta is. Coarctation of the aorta often occurs along with other heart defects. While treatment for coarctation of the aorta is usually successful, it's a condition that requires careful follow-up through adulthood. Obstructive uropathy is a structural or functional hindrance of normal urine flow, sometimes leading to renal dysfunction (obstructive nephropathy). A pheochromocytoma (see the image below) is a rare, catecholamine-secreting tumor that may precipitate life-threatening hypertension. Primary aldosteronism now is considered one of the more common causes of secondary HTN Renovascular hypertension Sleep apnea Thyroid or Parathyroid Disease Drug induced or drug related: NSAIDS, COX 2 inhibitors, sympathomimetics, OCs, cyclosporine and tacrolimus, erythropoietin, adrenal steroid hormones, cocaine, amphetamines, licorice, OTC supplements (e.g. ephedra, ma huang, bitter orange). Tacrolimus is an immunosuppressive drug used mainly after allogeneic organ transplant to lower the risk of organ rejection.

Dosing and amount of elemental iron for Ferrous gluconate (Fergon)

240 mg tablet (contains 27 mg elemental iron per tablet). Recommend 1 tab/day. Do not give if < 12 years old

Dosing and amount of elemental iron ferrous fumarate

324 or 325 mg tablet (contains 106 mg elemental iron per tablet).

Dosing and amount of elemental iron ferrous sulfate (feosol)

325 mg tablet (contains 65 mg elemental iron per tablet). Adults -1 tab tid-qid 220 mg/5 mL oral elixir (contains 44 mg elemental iron per 5 mL). Children (1-11 years of age) 2.5 -5ml tid

Compare HBP in 2001 to 2011

46765 in 2001 compared to 65123 in 2011 13% increase in HBP related deaths "a mere 10 percent increase in hypertension treatment would prevent about 14,000 deaths every year, the report noted. For most people, the American Heart Association recommends treatment if blood pressure is 140/90 or higher, and research shows that lowering blood pressure by just 5 points reduces the overall risk of death from any cause by 7 percent

Triglycerides (fats) levels

< 150 mg/dL Optimal <150-200 Borderline >200 High

Total cholesterol levels

< 200 Desirable 200 - 239 Borderline high > 240 High

HDL cholesterol levels

< 40 Low > 60 High (Desirable) But remember that we WANT high levels of HDL because they're the "good" guys

LDL Cholesterol levels

<100 mg/dL Optimal 100 - 129 Near / above optimal 130 - 159 Borderline high 160 - 189 High >190 Very high

Describe pt education regarding lifestyle for angina

Attain Ideal body weight Increase aerobic physical activity w/in limits Reduce daily sodium intake (< 1500mg) Maintain adequate dietary K intake (60meq) Reduce saturated fats and cholesterol Stop smoking Limit alcohol

Megaloblastic anemia

A megaloblast is a large, nucleated, embryonic type of cell that is a precursor of erythrocytes in an abnormal erythropoietic process observed in pernicious anemia Megaloblastic anemia is a type of anemia (number of red blood cells is lower than normal). Of course you know that when your body doesn't have enough red blood cells, your tissues and organs don't get enough oxygen. Megaloblastic anemia is characterized by red blood cells that are larger than normal. There also aren't enough of them. It's known as vitamin B-12 or folate deficiency anemia, or macrocytic anemia, as well. Megaloblastic anemia is caused when red blood cells aren't produced properly. Because the cells are too large, they may not be able to exit the bone marrow to enter the bloodstream and deliver oxygen. In non-megaloblastic anemia, there is an increase in RBC size without megaloblasts present in the bone marrow.

Pharmacodynamics of Class I: sodium channel blockers

A: lengthens the duration of action potential (ex: Quinidine, procainamide) B: shortens the duration of action potential (ex: Lidocaine) C: minimally increases action potential (ex: Propafenone)

meds for heart failure?

ACE inhibitor (End-stage: loop diuretic)

Meds for htn with cv disease?

ACE inhibitor AND thiazide diuretic

Meds for post-mi?

ACE inhibitor, beta-blocker

Describe ACE Inhibitors for angina

ACEIs act on the renin-angiotensin- aldosterone system. Decreased peripheral vascular resistance Decreased afterload ACEIs indirectly reduce the secretion of aldosterone. Decreased sodium and water retention Reducing extracellular fluid volume and preload ACE Inhibitors- "-pril" Most common S/e: cough Worst case scenario, angioedema! Educate pt of s/s. Ex) Lisiniporil, captopril ACE Inhibitors cause ↓ aldosterone secretion Patho Review: Aldosterone causes retention of Na+ and H20, SOOOOO the opposite of that would be ↓ Na+ and ↓H20 in circulatory system, so now allows for ↓ return of blood to heart so ↓ preload.

Treatment of stage C heart failure

ACEIs and beta blockers Loop Diuretics For volume overload, NYHA class II-IV pts Digoxin 3rd line drug Indicated for worsening HF due to LVD despite ACEI, BB, & diuretic therapy Persistently symptomatic, African-American, NYHA class II-IV patients Add hydralazine and isosorbide dinitrate Aldosterone antagonist (spironolactone, eplerenone) NYHA class II-IV patients, provided estimated GFR>30 ml/min and K+ < 5.0 mEq/dL Anticoagulation: for patients with permanent/persistent/paroxysmal Afib and an additional risk factor for cardioembolic stroke (may be reasonable without additional risk factor) Omega-3 fatty acid supplement: unless contraindicated, to reduce mortality and cardio-vascular hospitalizations Antiarrhythmics, CCBs (except amlodipine), NSAIDs and TZDs should be avoided or withdrawn if possible Nonpharmacological Specific education to facilitate HF self-care Exercise training / physical activity to improve functional status if able to participate Sodium restriction to reduce congestive symptoms CPAP can increase LVEF and improve functional status in patients with HF and sleep apnea Cardiac rehab in clinically stable patients to improve functional status, exercise duration, health-related quality of life (HR-QOL), and mortality

Treatment of stage B heart failure

ACEIs in all patients, ARBs for those who cannot tolerate an ACEI Beta blockers in most pts carvedilol, metoprolol succinate, or bisoprolol Nondihydropyridine calcium channel blockers with negative inotropic effects (verapamil, diltiazem) may be HARMFUL in asymptomatic patients with low LVEF and no symptoms of HF after MI The ejection fraction is a measurement doctors very commonly use to assess how well the heart is able to pump blood. Specifically, the ejection fraction is the proportion of blood that is pumped from the left ventricle (the main pumping chamber of the heart) with each heart beat.

Examples of drugs for stable angina

ACEIs(-pril) Recommended for all symptomatic patients with chronic stable angina to prevent MI or death and to reduce symptoms. Angiotensin II receptor blocker (-sartan) For patients who are intolerant to ACE inhibitors BBs (-lol) Recommended as initial therapy by all the guidelines for all patients CCBs (-pine) Initial drugs of choice for coronary artery vasospasm associated angina This pretty much summarizes your general rules for prescribing for angina. Also remember, Short acting sublingual nitrates can be used for pts with mild, stable CAD for immediate relief on a PRN basis

What are examples, MOA, contraindications, and adverse effects of renin inhibitors?

Aliskiren (Tekturna) Mechanism of Action Blocks conversion of angiotensinogen to angiotensin I Contraindications: Pregnancy Adverse Events Diarrhea Angioedema

What is automaticity

Ability of a heart cell to spontaneously depolarize and generate an action potential May be altered, enhanced, decreased by Cell damage, biochemical disturbance, pharmacological agents, environmental toxins Target for antiarrhythmic drugs SA nodes, AV nodes, His-Purkinje, special atrial cells

Describe prophylaxis of hypercoaguable states like VTE prophylaxis

Acutely ill, medical, increased risk of thrombosis or critically ill Not bleeding/risk - LMWH, low-dose UFH, fondaparinux (Arixtra) Bleeding/high risk - graduated compression stocking/intermittent pneumatic compression

meds for htn with diabetes without chronic kidney disease?

African-American: CCB and/or Thiazide Non African-American: ACEI, ARBs, Thiazide, CCB

What are CV risk factors?

Age (Men > 55, Women > 65) Diabetes Mellitus Elevated LDL or low HDL cholesterol Estimated GFR < 60 ml/min Family history of premature CVD Microalbuminuria Obesity (BMI > 30) Physical inactivity Tobacco usage (esp. cigarettes)

How are those with clinical ASCVD managed with statins?

Age <75: high-intensity statin Age > 75 OR not candidate for high-intensity statin: moderate-intensity statin Statins are first line treatment for elders b/c well tolerated and can be taken once daily. CV events reduced even after only a few weeks/months of therapy.

What are examples and MOA of coronary vasodilators?

Agents that serve to increase myocardial oxygen supply Nitrates (nitroglycerin, isosorbide) Prototype: nitroglycerine (NTG) Calcium channel blockers (CCBs) Ex) amlodipine NTG and CCBs promote vasodilation, thus opening the vessels allowing more blood flow. More blood=more O2 being delivered and quickly! Short acting sublingual nitrates can be used for pts with mild, stable CAD for immediate relief on a PRN basis

Meds for htn with BPH?

Alpha-1 receptor blockers "-zocin"

Warfarin drug interactions that cause increased INR

Analgesics - acetaminophen, ASA, tramadol Antiarrhythmics - amiodorone, propafenone Antibiotics - most Anticonvulsants - phenytoin (early on), valproate Antidepressants - duloxetine, venlafaxine, SSRIs Antifungals - azoles Antihyperlipidemics - ezetimibe, fluvastatin, rosuvastatin, fibrates Other - allopurinol, cimetidine, oral corticosteroids, PPIs, thyroid supplements

Describe aspirin and statins for angina

Aspirin decreases platelet aggregation to prevent cycle of vasoconstriction and platelet buildup. Statins Preventive Reduction in low-density lipoprotein (LDL) cholesterol levels plays a significant role in decreasing the formation of atherosclerotic plaque. ASA-anti-aggregate Statins-prevent plaques! "There is growing experimental and clinical evidence pointing to the anti-ischemic and anti-anginal properties of statins. Some data suggest that the degree of anti-ischemic efficacy of statins may be comparable to the current standard pharmacologic and mechanical strategies "Statins have demonstrated favorable modification of both biochemical markers (oxidative stress, inflammatory and coagulation markers/factors) and clinical symptoms (anginal and ischemic) of the disease

What is anemia of chronic disease and how is it treated?

Anemia of chronic disease Occurs due to a disease process Older adults Patients with renal failure, osteomyelitis, tuberculosis, rheumatoid diseases, hepatitis, carcinoma, myeloma, lymphoma, and leukemia at risk "The anemia of chronic disease (ACD, also called the anemia of inflammation, anemia of chronic inflammation, or hypoferremia of inflammation) was initially thought to be associated primarily with infectious, inflammatory, or neoplastic disease. However, other observations have shown that ACD can be seen in a variety of conditions, including chronic kidney disease, severe trauma, diabetes mellitus, anemia of older adults, and in those with acute or chronic immune activation. The anemia is typically normochromic, normocytic, hypoproliferative, and mild in degree." Treatment If associated with chronic renal failure or zidovudine-treated HIV: epoetin alfa 50 to 100 units/kg in adults and 50 units/kg in children dosed three times a week Epoetin alpha dose is titrated to keep Hgb level between 10 and 12 g/dL. Dosage is increased by 25% if Hgb is less than 10 g/dL. Epoetin alpha dose is decreased by 25% if Hgb approaches 12 g/dL or increases more than 1 g/dL in any 2 week period.

Describe angina monitoring

Angina episodes Presence, characteristics, and timing Evaluate every 4 to 6 months during the first year of therapy. Questions to ask Has the patient's level of physical activity decreased since the last visit? How well is the patient tolerating therapy? How successful has the patient been in modifying risk factors and improving knowledge about ischemic heart disease? Has the patient developed any new comorbid illnesses or has the severity or treatment of known comorbid illnesses worsened the patient's angina? Consider "PQRST" or "OLD CARTS" to evaluate chest pain (CP)

Descirbe MOA, effects, drug interactions, adrs for ranolazine (Ranexa) for angina

Anti-ischemic agent for management of chronic angina MOA: reduces sodium-induced calcium overload in myocytes, which leads to myocyte dysfunction & angina Effects: Reduces angina symptoms Increases exercise capacity Minimal effects on HR or BP May prolong QT interval Reserved for pts refractory to other meds (expensive) Ranolazine=Refractory pts Drug interactions: CYP450 3A4 inhibitors/inducers (ketoconazole, clarithromycin, rifampin) ADRs: Dizziness, constipation, h/a, nausea Liver Liver Liver! Avoid prescribing the following meds if patient is taking ranazoline: ketoconazole (Nizoral®), itraconazole (Sporanox®, Onmel®); clarithromycin (Biaxin®); rifampin (Rifadin®), rifabutin (Mycobutin®), rifapentine (Priftin®); phenobarbital, phenytoin (Phenytek®, Dilantin®, Dilantin‐125®), carbamazepine (Tegretol®) or St. John's wort

Black box warning of amiodarone (Cordarone)

Appropriate Use: hospitalize to administer loading dose. Consider dose change, D/C, or switch to alternate tx due to variable amiodarone absorption/prolonged elimination; restrict use to life-threatening arrhythmias due to drug-associated toxicity Pulmonary Toxicity: hypersensitivity pneumonitis or interstitial/alveolar pneumonitis; abnormal diffusion capacity w/o symptoms -can be fatal Hepatotoxicity: common but usually mild w/ only elev. LFTs; overt hepatic failure can occur Proarrhythmic Effects: arrhythmias worsen This is almost erbatim from Epocrates: Appropriate Use: hospitalize to administer loading dose. Consider for dose change, D/C, or switch to alternate tx due to variable amiodarone absorption/prolonged elimination; restrict use to life-threatening arrhythmias due to drug-assoc. toxicity; try alternative agents 1st!! Proarrhythmic Effects: arrhythmias worsened, significant heart block, or sinus bradycardia in 2-5% of pts; effects prolonged vs. other antiarrhythmics Hepatotoxicity: common but usually mild w/ only elev. LFTs; overt hepatic failure can occur w/ few fatal cases Pulmonary Toxicity: hypersensitivity pneumonitis or interstitial/alveolar pneumonitis in 10-17% of pts; abnormal diffusion capacity w/o sx more common; fatal in 10% of pts

What is the physiology of dysrhythmias?

Arrhythmias-physiological and/or anatomical consequences that prevent normal cardiac action potentials. Normal HR depends on intrinsic electrical impulses initiated at the sinoatrial (SA) node and conducted to the AV node and over the ventricles.

Target organ damage of HTN

Brain: TIA, stroke Eye: Retinopathy Arteries/veins: PVD Kidneys: renal failure Heart: LVH, CHD, HF

What is the treatment goal for all individuals for BP?

BP < 130/80

Tests to be done before starting statins

Baseline ALT before starting statin therapy Baseline CK for patients at increased risk for adverse muscle events Liver functions or CK during statin therapy for symptoms Evaluate for diabetes according to recommended screening Evaluate for other source of muscle pain if occurs Evaluate for other causes of confusion or memory impairment if occur Check CK for fear of rhabdomyolysis....So if pt c/o muscle pain and is on statin therapy, evaluate!!!

How do you initiate warfain?

Baseline labs: PT, INR, aPTT, urinalysis, CBC, liver functions Weigh risks/benefits: Nonadherence Falls alcohol use memory impairment support system Prothrombin Time (PT) The partial thromboplastin time (PTT) or activated partial thromboplastin time (aPTT or APTT) is a medical test that characterizes blood coagulation. ACCP guideline of 10mg loading dose x 2 days Start at 5 mg daily 2.5mg for elderly, CHF, malignancy, renal or hepatic impairment, interacting drugs, bleeding risk)

Describe beta blockers for angina

Beta blockers (BBs) decrease the force of myocardial contractility and decrease heart rate and conduction velocity. BBs decrease systemic vascular resistance and BP (afterload). Decreased myocardial oxygen demand = decreased anginal pain BBs ↓ force of systole, HR, and conduction----basically slows it all down. Think about patho, they're literally blocking the beta receptors from getting stimulated. The MOA is in the name. BBs ↓ afterload Thus, heart isn't working as hard so it has ↓ O2 demand ↓ CP (chest pain)

What meds for stable angina?

Beta-blocker Long-acting calcium channel blocker (2nd choice)

What meds for acute coronary syndrome

Beta-blocker AND ACE inhibitor

Approaches to anticoagulation for prosthetic heart valves

Bioprosthetic valves Depends on site and circumstances first 3 months After 3 months ASA Mechanical valves Warfarin with INR goal 2.5 - 3.5 Add low dose ASA (50-100 mg) for mechanical mitral or aortic valve with low risk of bleeding

Class IV: calcium channel blockers (CCBs) -"pine" pharmacodynamics

Block the influx of calcium, reduction in contractility (negative inotropism), decrease SA and AV node conduction Significantly reduce afterload but little effect on preload Verapamil, diltiazem, Nicardipine, amlodipine (Norvasc) "All the big Pine trees block the calcium channel trails!"

Pharmacokinetcis of iron preparations along with precautions/contrainidications, ADRs, drug interactions, clinical use/dosing, monitoring, pt education, outcome evaluation for iron deficiency anemia

Build serum iron and iron storage in the body Pharmacokinetics Enhanced absorption if iron stores low Ferrous form is absorbed more readily. Food affects absorption. Eliminated via shedding of GI mucosal cells or via bleeding Precautions and contraindications Hemochromatosis and hemolytic anemia ADRs GI symptoms (constipation, GI upset) Acute toxicity possible especially in children Drug interactions Chelation Decreased absorption Clinical use and dosing Iron deficiency anemia Adults: 120 mg elemental iron daily x 3 months Children: 3 mg per kg per day; up to 60 mg elemental iron per day. Premature infants: 2 to 4 mg/kg/day Continue for 3 months after anemia corrected in adults Monitoring Reticulocyte count 7 to 10 days after starting therapy Hgb at 2 weeks, then based on individual risk Reticulocyte count 5 to 10 days after starting therapy Hgb, hematocrit (Hct), ferritin at 4 weeks, then at 3 months and annually One Ferrous sulfate 325 mg tablet contains 65 mg elemental iron. The dosage of elemental iron required to treat iron deficiency anemia in adults is 120 mg per day for three months; the dosage for children is 3 mg per kg per day, up to 60 mg per day. An increase in hemoglobin of 1 g per dL after one month of treatment shows an adequate response to treatment and confirms the diagnosis. In adults, therapy should be continued for three months after the anemia is corrected to allow iron stores to become replenished Patient education Prevention Adequate intake of iron in diet Administration Take on empty stomach, if tolerated. Take with vitamin C to enhance absorption. Avoid taking with dairy products, calcium, antacids Three times per day is best Constipation (may need a stool softener) Return to normal Hgb, Hct, and ferritin levels If Hgb, Hct, and ferritin do not return to normal levels the patient should be evaluated for a source of blood loss of other pathology.

How is BP calculated?

CO X PVR CO= SV X HR

Describe Calcium Channel Blockers for angina. Side effects? Examples?

Calcium channel blockers (CCBs) cause arterial smooth muscle relaxation, which leads to peripheral vasodilation and decreased afterload. CCBs may cause coronary vasodilation. Atherosclerotic vessels do not dilate. CCBs- "-pine" CCBs allow heart to not work as hard when pushing blood out, less resistance to push against so easier on heart muscle. Ex) amlodipine, Verapamil-S/E: constipation-encourage pt to increase fiber and fluids-consider adding on stool softener. SEs: -decreased BP -bradycardia -may precipitate av block -headache -abdominal discomfort (constipation, nausea) -peripheral edema Examples Amlodipine (Norvasc) Diltiazem (Cardizem, Tiazac, others) Felodipine. Isradipine. Nicardipine. Nifedipine (Adalat CC, Afeditab CR, Procardia) Nisoldipine (Sular) Verapamil (Calan, Verelan)

Patho of iron deficiency anemia

Caused by poor intake or blood loss (acute or chronic) Treated with iron replacement

Describe Bile acid sequestrants (resins). Examples, uses, side effects

Cholestyramine (Questran); Cilesevelam (Welchol); Colestipol (Colestid) Best for moderated elevated LDL and low CVD risk Do not use if TG >200 - 400. May be given along with statins. GI side effects. Give other meds at least 1 hour before or 4 hours after Often used as monotherapy for women who are pregnant or who may become pregnant "Bile acid sequestrants OK for the unborn Babies"

Describe HTN in pregnancy

Chronic HTN: diagnosed before pregnancy or before 20wks Stage I HTN: Lifestyle modifications Pharmacotherapy for BP 150-160 systolic or 100-110 diastolic Methyldopa: drug of choice for chronic HTN diagnosed in pregnancy Beta blockers: safe in 2nd & 3rd trimester Contraindicated: ACE, ARB, DRI

What is class, MOA, action, and uses of Quinidine?

Class 1A MOA: DECREASES SODIUM CONDUCTANCE ACTION: DECREASES MEMBRANE RESPONSIVENESS SLOWS IMPULSE CONDUCTION USES: ATRIAL, NODAL, OR VENTRICULAR DYSRHYTHMIAS

What is class, use, side effects of Procainamide

Class 1A USE: VENTRICULAR DYSRHYTHMIAS ALTERNATE IN ACLS SIMILAR TO QUINIDINE BUT LESS GI UPSET MAY PRODUCE LUPUS; BONE MARROW DEPRESSION

What is class, use, kinetics of Lidocaine?

Class 1B USE: VENTRICULAR DYSRHYTHMIAS EMERGENCIES (ALSO LOCAL ANESTH) SIMILAR TO QUINIDINE BUT DOES NOT SLOW AV CONDUCTION KINETICS: IV ONSET RAPID; SHORT DURATION METABOLIZED IN LIVER MEXILETINE "ORAL LIDOCAINE"

What are contraindications of warfarin and adverse effects

Contraindications: Pregnancy hemorrhagic stroke, risk of active major bleeding, recent trauma or traumatic surgery, immediately following CNS or ocular surgery, presence of spinal catheters, aneurysms or CNS tumors with a high bleeding risk Adverse effects: minor bleeding, major bleeding, intracranial hemorrhage

What class, use, main concern, and BB warning of Flecainide (Tambacor)

Class 1C: USE: ATRIAL OR VENTRICULAR DYSRHYTHMIAS "WHEN OTHER AGENTS FAIL" GIVEN PO MAIN CONCERN: PROARRHYTHMIC BB Warning: Excessive mortality or nonfatal cardiac arrest; Restrict use to life threatening ventricular arrhythmias. Not recommended for chronic atrial fib Flecaininde has a narrow therapeutic index of flecainide, physicians should be alert for signs of toxicity before life-threatening arrhythmias occur like torsades de pointes Flecainide has a very high affinity for lung tissue and is associated with drug-induced interstitial lung disease. Treatment of flecainide cardiac toxicity involves increasing the excretion of flecainide, blocking its effects in the heart, and (rarely) institution of cardiovascular support to avoid impending lethal arrhythmias. So, it is a dangerous drug & not utilized regularly. But, you might see a patient taking it. So, I would refer that patient to a cardiologist for quick evaluation and likely change to a different antiarrhythmic.

What class, onset of action, duration of action, excretion, dosing, uses, ADRs of Amiodarone

Class III Pharmacodynamic/kinetics Onset of action: oral - 2 days to 3 weeks Duration of action: 7 to 50 days (LONG half-life) Excreted: feces, 1% in urine Dosing: Watch grapefruit juice! Ventricular arrhythmias: 800 to 1,600 mg twice daily for 1 to 3 weeks then decreased to 300 to 400 mg twice daily, maintenance 400 mg/day Amiodarone's primary effect is to block the potassium channels, but it can also block sodium and calcium channels and the beta and alpha adrenergic receptors. Think K+! Grapefruit can raise the levels of amiodarone in the body and lead to dangerous side effects. Metabolized in liver by cytochrome P450, that's why so many drug interactions and to watch grapefruit juice! Again, if you understand the patho you will understand the MOA, drug interactions, etc. Start w/ loading dose: 800-1600 mg po daily x 1-3 weeks until response gained. If loading dose > 1000 mg/day, give in divided doses Usual Dose you will see your patients taking: 200-600 mg daily Ventricular fibrillation Ventricular tachycardia Atrial fibrillation Atrial flutter ADRS Severe-Interstitial pneumonitis, pulmonary fibrosis (lung damage not evident until advanced), prolonged QT, sinus bradycardia, Torsades De Pointes, optic neuropathy causing pain w/ eye movement, sun sensitivity, visual halos around light, blue skin discoloration, hyper or hypothyroidism, severe hypotension, abnormal liver functions Less Severe- N/V, constipation, involuntary quivering, anorexia, loss of coordination Drug interactions: multiple-from ABX to ASA to CV drugs Amiodarone has multiple effects on myocardial depolarization and repolarization that makes it an extremely effective antiarrhythmic drug. Its primary effect is to block the potassium channels, but it can also block sodium and calcium channels and the beta and alpha adrenergic receptors Hypokalemia and amiodarone can be a lethal combo-can contribute to the development of polymorphous ventricular tachycardia, Torsade de pointes.

What is the patho of stable angina?

Clinical syndrome characterized by chest and/or arm discomfort Caused by an imbalance between myocardial oxygen supply and demand (ischemia) Associated with coronary artery disease (CAD) Pain is reproducible with physical exertion or emotional stress Lasts a short time (5 mins or less) Relieved by nitroglycerine (NTG) or rest. Angina in women does NOT always manifest as chest/arm pain, women are atypical, instead can present as stomach/abdominal pain, weakness, fatigue, and SOB w/o CP. Many women think they're suffering from indigestion. ANY woman that comes in with abd pain consider EKG. Angina d/t Ischemia, not infarction....yet at least.

What are examples, MOA, and adverse effects of centrally acting agents?

Clonidine, methyldopa MOA Works at brain BP control center Adverse events Sedation risk Abrupt withdrawal of clonidine can lead to rebound HTN

Describe Sacubitril/Valsartan (entresto)

Combination of a neprilysin inhibitor and an angiotensin receptor blocker (ARB) To reduce risk of CV death and the rate of hospitalization in patients with chronic heart failure (New York Heart Association [NYHA] class II to IV) and reduced ejection fraction. ADRs: hypotension, renal dysfunction, & hyperkalemia. Should not be used together w/ an ACE inhibitor due to increased risk of angioedema, or with another ARB, or with aliskiren (Tekturna) in patients with diabetes mellitus. When switching from an ACE inhibitor, patients should wait 36 hours before starting sacubitril/valsartan. Sacubitril/valsartan therapy may increase serum lithium concentrations if taking lithium The cost of a one-month supply of sacubitril/valsartan is approximately $413. Sacubitril/valsartan provides a small mortality benefit and decreases heart failure-related hospitalizations over and above an ACE inhibitor.

Describe multidrug therapy of BBs and CCBs

Combinations of BBs and CCBs have been shown to be more effective than the individual drugs used alone. Combinations of a long-acting nitrate and a BB are safe, effective, and low in cost. Combining long-acting nitrates and CCBs is rarely used because of the high risk for hypotension and additive adverse reaction profiles. BBs+CCBs=Better together! "Bonnie and Clyde" Ex) long acting form of nifedpine (Procardia XL) + Propranolol (Inderal) pg. 312-----b/c the BB suppresses the reflex tachycardia that may occur with Type II CCBs Long acting Nitrate+BB=Safe and affordable

Describe the pathophysiology of heart failure

Complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricles to fill or eject blood (cardiac output - CO) Determinants of ventricular function Preload, afterload Contractility, stroke volume, CO Heart rate

Describe pt education r/t warfarin

Compliance Interactions with food Interactions with drugs Take same time every day No alcohol Safety Pregnancy

Describe low intensity statin therapy

Daily dose lowers LDL-C by <30% Simvastatin 10mg Pravastatin 10-20mg Lovastatin 20mg Fluvastatin20-40mg Pitavastatin 1mg

Describe moderate intensity statin therapy

Daily dose lowers LDL-C by approx 30-50% Atorvastatin 10-20mg Rosuvastatin 5-10mg Simvastatin (Zocor) 20-40mg Pravastatin (Pracachol) 40-80 Lovastatin (Mevacor) 40mg Fluvastatin XL (Lescol XL) 80 Fluvastatin 40mg BID Pitavastatin (Livalo) 2-4mg

Warfarin drug interactions that cause decreased INR

Decreased INR Antibiotics - rifampin Antidepressants - trazodone Anticonvulsants - carbamazepine, phenobarbital, primidone, phenytoin (later on) Other - antithyroid agents, cholestyramine Other Increased Bleeding Risk Analgesics - aspirin, COX-2 inhibitors, NSAIDs Anticoagulants / Antiplatelet agents Antidepressants - SSRIs

meds for htn with chronic kidney disease? and how is ckd defined?

Defined by: Creatinine >1.3 in females, 1.5 in males Albuminuria > 300 mg/day ACE inhibitors or ARBs offer best protection

What are examples, MOA, contraindications, and adverse effects of nonDHP calcium channel blockers

Diltiazem, verapamil Mechanism of Action As with other CCBs Slows conduction at AV node, slows heart rate Contraindications Heart failure Adverse Events Peripheral edema Bradycardia, atrioventricular block Constipation Non-dihydropyridines, of which there are only two currently used clinically, comprise the other two classes of CCBs. Verapamil (phenylalkylamine class), is relatively selective for the myocardium, and is less effective as a systemic vasodilator drug. This drug has a very important role in treating angina (by reducing myocardial oxygen demand and reversing coronary vasospasm) and arrhythmias. Diltiazem (benzothiazepine class) is intermediate between verapamil and dihydropyridines in its selectivity for vascular calcium channels. By having both cardiac depressant and vasodilator actions, diltiazem is able to reduce arterial pressure without producing the same degree of reflex cardiac stimulation caused by dihydropyridines. Retrieved from: http://cvpharmacology.com/vasodilator/CCB

What are drug type, MOA, indications, contraindication, ae, and interactions of Dabigatran (Pradaxa)?

Direct thrombin inhibitor Binds to active site of thrombin Prevents generation of additional thrombin Decreases platelet activation Prevents conversion of fibrinogen to fibrin Blocks activation of factors V, VII, VIII, IX, XIII Directly inhibits free and clot-bound thrombin Indications Reduction of risk of stroke and systemic embolism in non-valvular atrial fibrillation Peak: 1 hour Half life: 12-17 hrs Elimination: Urine Initiation Baseline labs: CBC and renal function 150mg by mouth twice per day Severe renal impairment: 75mg BID Contraindications: active serious bleeding, severe renal disease, prosthetic heart valve Adverse events: bleeding (FFP if severe), GI Interactions: quinidine & amiodarone increase plasma levels, rifampin reduces plasma levels

Switching drugs from warfarin to dabigatran

Discontinue warfarin, INR<2, start dabigatran

What are different classes of antihypertensives

Diuretics Thiazide/thiazide-like Loop Potassium-sparing Calcium Channel Blockers Angiotensin Converting Enzyme (ACE) Inhibitors Angiotensin II Receptor Blockers (ARBs) Direct Renin Inhibitor Beta-blockers Alpha-1 Receptor Blockers (peripheral) Alpha-2 Receptor Agonists (central) Adrenergic Antagonists Direct vasodilators

What are cardinal manifestations of heart failure?

Dyspnea and fatigue - may limit exercise tolerance Fluid retention - may lead to pulmonary and/or splanchnic congestion and/or peripheral edema Patients may not have all symptoms May result from disorders of: pericardium, myocardium, endocardium, heart valves, great vessels, or certain metabolic abnormalities If the HF is due to cardiomyopathy, the first rule in treating dilated cardiomyopathy (DCM) is to identify and treat the underlying cause. Treating the underlying cause can often slow, stop, or even reverse the progression of DCM

Describe initial assessment of angina

ECG-Remember, ECGs show us the electrical functioning of the heart not the physical activity-though it gives us a good idea. Fasting lipid levels- High lipids could indicate high possibility of plaque build up in coronary arteries CXR-could reveal non-cardiac component to CP-is heart being pushed by mass? Could it be Pneumonia, PE, pneumothroax, since also prevents as CP? CBC-could reveal concurrent source of concern such as infections ex) pneumonia, endocarditis, pericarditis, etc. Thyroid-remember certain thyroid conditions and medications directly influence heart function (ex: hyperthyroidism and tachycardia, hypothyroidism and use of synthroid) Renal- ppl with bad kidney fxn retain K+ b/c cant excrete it, how would excess K+ effect heart activity?

What are goals of drug therapy for angina?

Elimination of angina pain Blood pressure (BP) within normal limits (WNL) and pulse > than 70 bpm. Treatment is aimed at: Increasing myocardial O2 supply Reducing myocardial O2 demand Minimizing or removing the occlusion Overall goal: Reduce the risks of myocardial infarction (MI) and ultimately, death. BP Goal: varies based on pt age New guidelines say Healthy BP < 120/80, but may not be feasible for elderly pt

How are those with clinical LDL >190mg/dl managed with statins?

Evaluate for secondary causes of hyperlipidemia High-intensity statin (moderate-intensity if not candidate for high-intensity statin) May add non-statin if needed to further lower LDL-C

Who are the 4 groups that benefit from statins?

Evidence of Clinical ASCVD Primary LDL > 190 mg/dl DM pts w/ LDL 70 - 189 mg/dl without clinical ASCVD (aged 40 - 75 years) Age 40 -75 without DM or ADCVD with a 10-year ASCVD risk of 7.5% or higher and LDL 70-189 mg/dL

Describe nicotinic acid (niacin) vitamin B3

Extended release are RX only Decrease LDL 5 - 25%, TG 20 - 50% Increase HDL 15 - 35% Can be used with statin, or bile acid sequestrant Avoid in liver disease, PUD, arterial bleeding Can increase glucose, PT, uric acid, decrease phosphorus, platelets. Causes flushing and itching of the neck and face (325 mg of Aspirin 30 minutes before dose may help). Be careful with DM pts, Hx PUD, alcohol abuse. Niacin, is known to raise blood glucose levels when consumed in large quantities Taking Niacin on an empty stomach increases side effects (such as flushing, nausea). Once a day, extended-release Niacin preparation (available by prescription only as Niaspan) helps limit flushing. Take325 mg. ASA 30 minutes prior

What are examples, uses, and what to watch for for Cholesterol absorption inhibitors

Ezetamide (Zetia) is only one on the market Inhibits absorption of cholesterol by the small intestine. Decrease LDL 18%, TG 8% Can be added to statin or fenofibrate If taken with bile acid sequestrant take 2 hours before or 4 hours after. Monitor liver function Vytorin (combination with simvastatin) - decrease LDL 50 - 60%

What are simvastatin warnings?

FDA warnings due to risk of myopathy. No new patients on 80 mg Avoid w/ itraconazole, ketoconazole, posaconazole, erythromycin, clarithromycin, telithromycin, nefazodone, gemfibrozil, cyclosporine, danazol. No more than 10 mg with amiodarone, verapamil, diltiazem No more than 20 mg with amlodipine

Describe MOA, Baseline labs, pregnancy categories, drug interactions of, Rivaroxaban (Xarelto)

Factor Xa inhibitor Oral MOA: Blocks active site of factor Xa Baseline labs: CBC, PT, INR, aPTT, renal functions Pregnancy category: C Avoid administration with combined P-gp and strong CYP3A4 inhibitors (ketoconazole, itraconazole, ritonavir, and conivaptan) ; increased pharmacodynamic effects of Xarelto Avoid administration with combined P-gp and strong CYP3A4 inducers (carbamazepine, phenytoin, rifampin, St. John's wort); decreased pharmacodynamic effects of Xarelto Caution with renal impairment and combined P-gp and weak or moderate CYP3A4inhibitors (amiodarone, diltiazem, verapamil, quinidine, ranolazine, dronedarone, felodipine, erythromycin, azithromycin); increased pharmacodynamic effects of Xarelto Avoid with other anticoagulants (unless benefit>risk), caution with antiplatelet agents

Describe MOA, Baseline labs, pregnancy categories of Fondaparinum (Arixtra)

Factor Xa inhibitor subcutaneous MOA: subcutaneous Baseline labs: CBC, PT, INR, aPTT, renal functions Pregnancy: B

Risk assessment for atherosclerosis

Fasting lipid profile every 5 years starting at age 20 (also at age 9 -11, and 17 - 21 [AAP, 2011]) LDL Total HDL Triglycerides Non fasting cholesterol Total HDL

Describe examples, uses, and cautions for fibric acids (fibrates)

Fenofibrate (Tricor, Trilipix); Gemfibrozil (Lopid) Effective triglyceride lowering drug Modestly lower LDL Raise HDL Do not use with severe renal or hepatic disease Watch for gallstones, myopathy Caution with anticoagulants (fenofibrates) Gemfibrozil cannot be added to a statin GI side effect Really just best for lowering triglycerides, everything else is kinda just an added bonus. Be careful with liver, kidney and bleedy ppl Warn pt about GI S/E

How can statin therapy be optimized?

For patients intolerant of statin at high or moderate intensity, use maximum tolerated intensity Those with less than anticipated response: Reinforce adherence to lifestyle and medications Exclude secondary causes of hyperlipidemia Those at higher risk for ASCVD, maximum tolerated statin dose, less than anticipated response, or those who are completely statin intolerant: Add non-statin "shown to reduce ASCVD events in Randomized control trials" Does not specify which to add in the guideline. Niacin and cholestyramine (Questran), a bile acid sequestrant have been shown to reduce ASCVD events and can be added to a statin Gemfibrozil (Lopid)-works by decreasing amt of fat made by liver has been shown to reduce ASCVD events; should NOT be added to a statin. Fenofibrate (Tricor) + statin has not shown decreased ASCVD events (Prevention Guidelines Clinical Vignettes). Do not prescribe if liver, gallbladder, severe kidney disease & nursing mothers "Cholestyramine (Questran) is known as a bile acid-binding resin. MOA: removes bile acid from the body. In people with hyperlipidemia, this causes the liver to make more bile acid by using cholesterol in the blood. This helps to lower the cholesterol levels". https://www.webmd.com/drugs/2/drug-4803/cholestyramine-light-oral/details Gemfibrozil (Lopid) is a fibric acid derivative. Fibric acid derivatives activate peroxisome proliferator activated receptor α (PPAR-α). The primary role of these agents in clinical practice is for the management of hypertriglyceridemia. Gemfibrozil Warnings. ... You shouldn't combine gemfibrozil with any drug in the statin family of cholesterol-reducing medicines because that could increase the risk of a condition known as rhabdomyolysis (muscle injury), which can cause kidney damage and even death. Dec 19, 2014. The major concern when using a statin-fibrate combination is the potential increased risk for myopathy and rhabdomyolysis.

Describe management of elevated INR

For target INR 2-3, no bleeding 3.1-3.9 Decrease dose 5-10% Recheck in 7-14 days 4.0-4.9 Hold for 0-1 day then decrease dose 10% Recheck in 4-8 days For target INR 2.5-3.5, no bleeding 3.6-4.5 Decrease dose 5-10%; consider holding 1 dose Recheck in 7-14 days 4.5-6.0 Hold for 1-2 days then decrease 5-15% Recheck in 2-8 days

Describe management of low INR

For target INR 2-3, no bleeding <1.5 Increase 10-20% or extra dose Recheck 4-8 days 1.5-1.9 Increase 5-10% Recheck 7-14 days For target INR 2.5-3.5, no bleeding <1.5 Increase 10-20% or extra dose Recheck 4-8 days 1.5-2.4 Increase 5-10% Recheck 7-14 days

Describe low molecular weight heparin, considerations

Fragments of unfractionated heparin Enoxaparin (Lovenox), dalterparin (Fragmin), tinzaparin (Innohep) Inhibits activation of factor X, minimal effect on thrombin (due to small size) Baseline labs: CBC, PT, INR, aPTT, renal functions Response is predictable, do not need monitoring aPTT. May check anti-Xa levels in patients with renal dysfunction, morbid obesity, pregnancy. Check CBC periodically Standard dosing daily or BID (depends on drug), reduced by 50% if CrCl <30 ml/min Contraindications: active major bleeding, indwelling epidural catheters, hypersensitivity to pork products, HIT associated with LMWH Adverse events: bleeding (use protamine if severe), thrombocytopenia, elevated LFTs

Describe monitoring of heart failure

Functional capacity Fluid status Weight changes Jugular venous distension Cardiac rhythm Labs Electrolytes Creatinine Thyroid and liver function

Examples, MOA, contraindications, SEs Loop Diuretics

Furosemide, bumetanide, torsemide Mechanism of Action Furosemide & ethacrynic acid inhibit reabsorption of sodium and chloride in proximal and distal tubules and loop of Henle. Bumetanide has more effect on reabsorption of chloride. Clinical use: Edema, HF, Renal Disease, Cirrhosis Furosemide: start low for HF at 40mg twice daily, titrate dose to promote wt loss of 0.5 to 1 kg daily Contraindications Anuria, hepatic coma, severe electrolyte depletion Hypersensitivity to loop diuretics or sulfonamides Ethacrynic acid contraindicated in infants Adverse Events Similar to thiazides, less effect on glucose and lipids, may cause hypocalcemia Electrolyte and volume depletion

Prophylaxis of general hypercoagulable states

General/abdominal pelvic surgery - depends on risk of thrombosis vs. risk of bleeding Major trauma - LMWH/LDUH unless contraindicated Orthopedic surgery: THA, TKA, Hip Fracture Surgery Antithrombotic therapy minimum of 10 - 14 days LMWH preferred agent Also use IPCD at least 18 hours/day

Describe clinical use and dosing of nitro for acute angina attack

Give nitroglycerin (NTG). Sublingual NTG, a short-acting form, is 0.3 to 0.6 mg every 5 minutes for up to three doses.

Choosing the best drug for Atrial fibrillation/flutter

Goal to prevent cardioembolic stroke Based on risk: CHADS2 score (1 each for CHF, HTN, Age ≥ 75, Diabetes, 2 for Stroke symptoms previously/TIA) Non-rheumatic AF: CHADS2 = 0: No therapy/ASA 75-325 mg daily CHADS2 = 1: Oral anticoagulation; ASA +/- clopidigrel if unsuitable/unwilling to take CHADS2 = 2: Oral anticoagulation; ASA & clopidigrel if unsuitable/unwilling to take ACCP recommends dabigatran in preference to warfarin Other recommendations with comorbidities

Describe HTN in older adults

Goal: 130/80 Monitor Orthostatic hypotension Cognitive Dysfunction Dementia

Describe rational drug selection for angina

Grading of Angina by the New York Heart Association and the Canadian Cardiovascular Society All patients with angina should be on aspirin 81 to 162 mg/day. If patient cannot tolerate aspirin then clopidogrel (Plavix) 75 mg daily may be substituted. NTG for exertional angina Sublingual tablet 0.3 to 0.6 mg SL q5min prn; Max 3 doses w/in 15 min translingual spray 1-2 sprays SL q5min; Max 3 sprays w/in 15min If allergic to ASA give Plavix! For pts with angina only on exertion, a normal resting ECG, and symptoms that can be controlled by rest and intermittent nitro--start lifestyle modifications and have aggravating factors treated For pts with known CAD, age 65 or older, with ECG changes on exertion, or with diabetes are considered high risk for unstable angina-- start on both life style modifications and drug therapy

Classes of medications for hyperlipidemia

HMG-CoA Reductase Inhibitors (Statins) ex)atorvastatin Block conversion of HMG-CoA to mevalonate, thereby limiting the rate of production of cholesterol in the liver. Bile Acid Resins (Bile Acid Sequestrants) ex)Cholestyramine (Questran) Decreases return of cholesterol to liver by binding bile acids into an insoluble compound that is excreted in the feces. Increased LDL receptors on liver decrease serum LDL, but will increase VLDL & triglyceride level. Niacin (Nicotinic Acid) [Vitamin and sold OTC] Unknown MOA. Decreases VLDL synthesis in liver, inhibits lipolysis in adipose tissue, increases lipoprotein lipase activity. Cholesterol Absorption Inhibitors ex) Ezetamide (Zetia) Works on brush border of small intestine thereby decreasing absorption of cholesterol and decreasing delivery to liver. Reduces stores in liver and increases clearance of cholesterol from the blood. Fibric Acid Derivatives AKA Fibrates ex) Fenofibrate (Tricor) Unclear MOA. Good in combo with statin. Lowers triglyceride levels and modestly lowers LDLs and raises HDL. Omega-3 Fatty Acids [Available OTC] May reduce VLDL-TG synthesis &/or secretion from liver. May enhance TG clearance from circulating VLDL. Pt may c/o "fish burp"

Describe HTN in pediatrics

HTN defined by percentile system (age, ht, M/F) Elevated BP: BP 90th-95th % or BP >120/90 Stage I HTN: 95th-99th percentile Stage II HTN: 99th plus 5 mm Hg Monitor prior to age 3 yrs with: CKD Glomerulonephritis Kawasaki disease Identifiable causes for HTN: Cardiac defects Adrenal problems Recreational use of OTC cold medications Illegal purchase of stimulants Anabolic steroid abuse

What is preeclampsia

HTN with proteinuria after 20 wks gestation Bedrest Control of BP Seizure prophylaxis Timely delivery Antihypertensive therapy: prescribed only for maternal safety Delivery > 48hrs away: methyldopa, labetalol, CCB Imminent delivery: Parenteral hydralazine, labetalol

What is gestational htn? and transient htn?

HTN without proteinuria after 20 wks Careful monitoring for preeclampsia BP normal by 12 wks postpartum

Describe the clotting cascade

Hemostasis maintained by: Endothelial cells Platelets Coagulation proteins Clotting cascade In response to damage to the endothelial cells or contact with foreign surface (two pathways) Inactivated clotting factors sequentially converted to activated form; final step is activation of prothrombin to thrombin, leads to conversion of fibrinogen to fibrin and formation of a fibrin clot Causes: Injury to artery Atherosclerosis Inflammation Alteration in blood flow Low BP Obstructions

What are effects of hypertension

Higher the BP, greater the chance of heart attack, heart failure, stroke, and kidney disease. Pre-hypertensive BPs are associated with more than twice the relative risk of cardiovascular disease as compared to normal BPs. Until age 50, DBP is a more potent RF. After age 50, SBP is more important.

What is the prototype, examples, MOA, Contraindications, and adverse effects of thiazide/thiazide like diuretics

Hydrocholorthiazide (prototype), chlorthalidone, bendroflumethazide, Cyclopenthiazide and Indapamide MOA: Low volume sodium depletion that leads to PVR reduction. act on the nephron mainly at the proximal part of the distal tubule. Sodium excretion and urine volume are increased by interference with transfer across cell membranes. The result is a reduction in blood volume. Contraindications Anuria (CrCl<30 ml/minute), renal decompensation Hypersensitivity to thiazides or sulfonamides Adverse events: Potential for negative impact on dislipidemia, glucose control Monitor for Na+, K+, Mg+ depletion Elevated calcium, uric acid, glucose, cholesterol Hypokalemia due to urinary potassium loss. Hyperuricemia due to interference with renal clearance of uric acid. (Risk of acute gout) Hyperglycemia possibly related to hypokalemia. (Risk of new onset diabetes) Hypercalcemia due to reduced renal clearance of calcium Erectile dysfunction by an unknown mechanism. Thrombocytopenia and skin rashes. Rare (Fall in serum potassium > 0.3 mmol/l with low-dose thiazide or thiazide-like diuretics raises suspicion of primary hyperaldosteronism if serum sodium is in high-normal range: refer for investigation).

What are NY Heart Association classifications of heart failure?

I No objective evidence of cardiovascular disease. No symptoms and no limitation in ordinary physical activity. II Objective evidence of minimal cardiovascular disease. Mild symptoms and slight limitation during ordinary activity. Comfortable at rest. III Objective evidence of moderately severe cardiovascular disease. Marked limitation in activity due to symptoms, even during less-than-ordinary activity. Comfortable only at rest. IV Objective evidence of severe cardiovascular disease. Severe limitations. Experiences symptoms even while at rest.

Antiarrhythmic Agents

I. Membranes stabilizing agents (sodium channel blockers) A. Quinidine, procainimide, disopyramide B. Lidocaine, phenytoin C. Encainide, Iorcainide, flecainide II. Beta blockers Propranolol, metoprolol, sotalolol, and others III. Agents which prolong duration of the action potential (potassium channel blockers) Amiodarone, bretylium IV. Calcium channel blockers Verapamil, diltiazem Bepridil would be included in the Calcium channel blocker group, but it is no longer sold in the US

Describe management of significantly elevated INR with and without bleeding

INR 5.0-8.9, no bleeding: hold 1-2 doses and reduce 10-20%; monitor frequently Alternate: consider Vit K 1-2.5mg orally (AAFP) INR 9.0 or above, no bleeding: hold and give oral Vitamin K 5 to 10mg; monitor frequently (AAFP) Resume lower dose when INR in target range ACCP does not recommend oral Vit K until INR>10 if no evidence of bleeding

What are drugs for arrhythmias used for?

Ideally in primary care setting consult with cardiology team Pharmacological management of arrhythmias requires an office that is prepared, ready, and able to handle emergencies. You will see these patients for infections, depression, anemia, fatigue, etc. SO Be aware of action and adverse drug potentials.

Take home points about atherosclerosis and hyperlipidemia

Identify pts at high risk of ascvd through thresholds get ldl-c as low as possible with drugs that are effective and safe -high intensity statin (if tolerate), adherence, optimized diet, exericse, lifestyle modifications -consider non statin treatment with ezetimeibe or psk9 inhibitor for additional ldl-c reduction, per latest treatment guidelines engage in clinician patient discussion document all pt info for insurance coverage

2013 guidelines for statins

In 2016 the United States Preventative Task Force recommended statins for those who have at least one risk factor for coronary heart disease, are between 40 and 75 years old, and have at least a 10% 10-year risk of heart disease.

What are some warfarin food, herb, supplement interactions

Increased INR Alcohol (binge), cranberry juice/extract, fish oil, garlic, glucosamine +/- chondroitin, grapefruit, mango, papaya extract, birch, chitosan, danshen, dong quai Decreased INR Alcohol (chronic), coenzyme Q10, ginseng, smoking, St. John's wort, Vitamin C, Vitamin K Other Increased Bleeding Risk Alcohol (heavy drinkers) Garlic supplements

Describe antiplatelet agents

Inhibit platelet aggregation (various MOAs) Baseline labs: CBC, LFTs Aspirin (most common) 75 - 325 mg/day Contraindicated with active stroke/stroke in progress, active GI bleed Aspirin + dipyridamole (Aggrenox) BID dosing Clopidigrel (Plavix), Ticlopidine (Ticlid) Ongoing debate on effect of omeprazole/ esomeprazole (CYP2C19 inhibitor) on clopidigrel

What does warfarin do?

Inhibits activation of clotting factors in liver that depend on Vitamin K for synthesis (factors II, VII, IX, and X and coagulation inhibitor proteins C and S) Does not affect function of existing clotting factors, and has no effect on existing clots Warfarin is an oral anticoagulant- it prevents formation of clots by reducing the production of factors II, VII, IX & X, Protein C & Protein S (factors produced by liver which promote clotting). Adequate Vitamin K is required for production of these clotting factors. Warfarin blocks Vitamin K which reduces production of Factors II, VII, IX & X, Proteins C & S Indication: Prevention and treatment of venous thrombosis Systemic embolism PE Atrial Fibrillation

What does unfractionated heparin do, indications, initiation, contraindication, ae, patient safety

Inhibits reactions that lead to clotting without altering concentration of normal clotting factors Binds to antithrombin III, increases inactivation rate of factors XII, XI, X, IX, thrombin Inactivates thrombin, prevents conversion of fibrinogen to fibrin Cannot inactivate clot-bound thrombin or activated factor X that is bound to platelets In therapeutic doses, it acts as an anticoagulant, preventing the formation of clots and extension of existing clots within the blood. While heparin does not break down clots that have already formed, it allows the body's natural clot lysis mechanisms to work normally to break down clots that have formed. Indications Preventive of post-op thromboembolism Intravenous administration Onset: 20-60 min Peak: 1h Half Life: 1-3h (dose dependent) Elimination: urine, reticuloendothelial system Initiation Baseline labs: aPTT, PT, INR, CBC 5,000 IU 2h pre-op 5,000 U q8-12 h post-op Monitor aPTT every 6 hours until stable, then every 12 hours (aPTT of 1.5 to 2.5 x control) Advantages: rapidly reversed. If turn off infusion, ½ life is 30 minutes, so APTT returns to normal in bout 30 minutes. Disadvantage: Binds unpredictably & non-specifically to plasma proteins, macrophages & endothelium so has unpredictable response to dosing. Binding to plasma proteins can lead to heparin resistance where very large heparin doses are required to achieve anticoagulation. Heparin in a fixed, low dose of 5000 U subcutaneously (SC) every 8 or 12 hours reduces the risk of venous thrombosis and fatal PE by 60% to 70% and is an effective and safe form of prophylaxis in medical and surgical patients at risk of VTE. Although low-dose heparin is also effective in reducing deep-vein thrombosis after hip surgery, it is not as effective as LMWH in this setting. Contraindications: active bleeding, severe thrombocytopenia, history of HIT Adverse events: bleeding (IV protamine sulfate if severe), osteoporosis (extended use), thrombocytopenia Patient safety: pay attention to order sets! Different concentrations Unfractionated heparin exerts its anticoag effect via antithrombin. Heparin binds to and produces a conformational change in antithrombin. Anticoagulant effect reversed with protamine sulfate ADR: Heparin-Induced Thrombocytopenia (HIT)

How should statin recommendations be monitored?

Initial fasting lipid panel Repeat 4 to 12 weeks after initiation of statin therapy to determine patient's adherence Repeat every 3 to 12 months as clinically indicated Consider decreasing statin dose when 2 consecutive LDL-C levels are < 40 mg/dl

Choosing the best drug for ischemic stroke

Initial treatment: IV recombinant tissue plasminogen activator (r-tPA) Within 4.5 hours of onset of symptoms if meet criteria IntraArterial r-tPA Within 6 hours of onset of sx if not eligible for IV Start ASA therapy (160 -325 mg) within 48 hours For VTE prevention (ischemic/hemorrhagic stroke) Intermittent pneumatic compression devices +/- LMWH in preference to UFH (start between days 2 and 4 if given with hemorrhagic stroke)

Describe HTN treatment initiation for general population 60 & older

Initiate pharmacologic treatment to lower BP if SBP 150 mmHg or higher or a DBP of 90 mmHg or higher, and treat patients to a goal SBP lower than 150 mmHg and a goal DBP lower than 90 mmHg

Compelling indications for HTN treatment

Ischemic heart disease Heart failure Left ventricular hypertrophy Diabetes mellitus Chronic kidney disease Cerebrovascular disease Peripheral artery disease Benign prostatic hypertrophy (BPH)

Describe left ventricular dysfunction

Left ventricular dysfunction Increase in end systolic volume Increase in end diastolic volume Pulmonary congestion Decreased CO, hypo perfusion Compensatory systems Sympathetic activation Renin-angiotensin-aldosterone system

Describe treatment of all types of angina

Lifestyle changes Surgical intervention (ex: percutaneous intervention [PCI]) Pharmacological management Coronary vasodilators: Nitrates and Calcium channel blockers (CCBs) Beta blockers (BBs) Angiotensin-converting enzyme (ACE) inhibitors Statins Aspirin (ASA)

Treatment of stage A heart failure

Lifestyle modification: dyslipidemia, diabetes, hypertension (diuretics or angiotensin-converting enzyme inhibitors - ACEIs) ACEIs are drug of choice in patients with diabetes. Angiotensin II receptor blockers (ARBs) are considered in ACEI-intolerant patients, but more expensive.

What is lipoprotein (a), homocysteine, prothrombotic and proinflammatory factors, and subclinical atherscerlotic disease and how does it relate to atherosclerosis?

Lipoprotein (a) - modified form of LDL. Impairs fibrinolysis, promotes deposition of cholesterol in atherosclerotic plaques. Routine screening not recommended. Decrease with Niacin. Homocysteine -amino acid, has atherogenic and prothrombotic effects. Creates an inflammatory response, which worsens vessels integrity. Routine screening not recommended. Decrease with Folate, B6 & B12. Per Lipoprotein a Society: "Lipoprotein(a) is a type of lipoprotein/cholesterol and high levels increase your risk for atherosclerosis (build up of fatty deposits in the wall of the artery, also called atherosclerotic cardiovascular disease or CVD) including coronary heart disease (blockages in your heart arteries) or heart attack, peripheral vascular disease (PAD, blockages in the leg arteries), aortic stenosis (damage to the aortic valve of the heart), thrombosis (blood clots) and stroke (blockages in the neck arteries). In children, a high level of Lp(a) is a leading risk factor for strokes but strokes are very rare in any child, even those with a high level of Lp(a)."

Describe examples, uses, and cautions for omega 3 fatty acids

Lovaza (omega-3-acid ethyl esters) Vascepa (ecosapent ethyl) Omacor Indicated for reduction of TG in adults with severe hypertriglyceridemia (>500 mg/dl) May elevate LDL Monitor liver enzymes Lovaza has warning about atrial fib/flutter Can add to a statin

What is MOA, ADRs, drug interactions, and precautions/contraindications of nitrates?

Low doses of NTG dilate the veins, decreasing venous return to the heart. Decreases preload Higher doses dilate arterial vessels. Decreased vascular resistance (afterload) Some dilation of coronary arteries Atherosclerotic vessels do not dilate. (B/c they physically can't) ↓ doses NTG (Dilate VEINS)=↓ preload ↑ doses NTG (Dilate ARTERIES)=↓ afterload ADRs Headache (HA) Orthostatic hypotension with potential for syncope and tachycardia (direct result of therapeutic vasodilation) Contact dermatitis d/t transdermal patches. Drug interactions Concurrent use with the vasodilators, or erectile dysfunction drugs sildenafil (Viagra), tadalafil (Cialis), or vardenafil (Levitra) contraindicated Additive hypotension with antihypertensives, alcohol, BBs, CCBs (consider risks vs benefit) S/E: Pt will c/o massive HA, remind them this is normal and expected. HA may be severe and persists in up to 50% of patients. Hypotension may lead to decrease in diastolic filling pressure and tachycardia may lead to decrease in diastolic filling time, which may lead to myocardial ischemia, arrhythmias, and rebound hypertension. Consider asking pt in private about use of drugs for erectile dysfunction. Real Life example: Man embarrassed to admit Viagra use in front of wife, bottomed out when given NTG. Not cool. Contraindicated in hypersensitivity or idiosyncratic responses For the transdermal patches, allergy to adhesive may limit their use. Pregnancy category C

Describe drug interactions with digoxin

Macrolides & tetracycline, ranolazine, verapamil, quinidine, indomethacine, alprazolam, spironolactone, itraconazole, furosemide (hypokalemia or hypomagnesemia can cause dysrhythmia), omeprazole may all lead to digoxin intoxication by elevating the serum concentration of digoxin. *Avoid ordering digoxin and beta blocker or calcium channel blockers together (R/T bradycardia) Antacids and antidiarrheal agents may interfere with absorption of digoxin. Avoid licorice root, hawthorn, St John's Wort, Ginko balboa, & Siberian ginseng

Describe NY Heart Assoc and canadian cardiovascual society grading of CLASS III Angina

Marked limitations: angina during less-than-routine physical activity (walking short distances) Marked limitations of ordinary activity.

What is the JNC 8 titration strategy?

Maximize first medication before adding second OR Add second medication before reaching max dose of first OR Start with 2 medication classes separately or as fixed combo At blood pressure goal? Reinforce medication and lifestyle adherence For strategies A & B Add & titrate thiazide/ACEI/ARB/CCB For strategy C Titrate dose of initial med to max At blood pressure goal yet? Reinforce medication and lifestyle adherence Add and titrate thiazide/ACEI/ARB/CCB At goal BP yet? Reinforce medication and lifestyle adherence Add med: B-blocker, aldosterone antagonist, or others And/or refer to specialist

Describe NY Heart Assoc and canadian cardiovascual society grading of CLASS II Angina

Mild symptoms: angina and slight limitation during ordinary activity Slight limitation of ordinary activity. Angina occurs on walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, in cold wind, under emotional stress, or only during the few hours after awakening.

What are uses, action, kinetics, ADRs of Adenosine

Misc. antidysrhythmics USE: SUPRAVENTRICULAR ARRHYTHMIAS TERMINATE PSVT ACTION: INHIBITS SA & AV NODE CONDUCTION MAY STOP HEART KINETICS: VERY RAPID ONSET VERY BRIEF (HALF-LIFE < 10 SEC.) SE/ADR: FACIAL FLUSH; DYSPNEA Adenosine-one of the very few meds we ever get to "slam" it, IVP rapidly, preferably in LAC since closest to the heart. Will freak you out cause pt may flat line for a few secs which makes you want to flat line, then all of a sudden a beautiful normal HR shows on your tele then you remember to breathe again before you yourself become a pt. SHORT HALF LIFE. So watch the pt, may go back into arrhythmia.

How are those with age 40-75 with diabetes managed with statins?

Moderate intensity statin (high intensity if≥ 7.5% 10-yr ASCVD risk) Weigh individual risks and benefits for older or younger patients

How are those with 7.5% 10 year ASCVD risk and age 40-75 managed with statins?

Moderate to high intensity statin

Describe monitoring of digoxin

Monitoring Diagnosis of toxicity is based on both clinical and laboratory data. Toxicity commonly occurs with serum levels greater than 2 ng/mL. Monitor potassium levels. Patient education Take at same time each day. Do not double doses. Monitor for signs of toxicity. Take pulse hold for heart rate (HR) less than 60 or greater than 100. Digoxin acts by inhibiting the Na-K-ATPase pump, thus reducing the transport of sodium from the intracellular space in myocytes [4] as well as non-cardiac cells to the extracellular space [5]. This mechanism contributes to digoxin's hemodynamic, neurohumoral, and electrophysiologic effects

Describe monitoring and pt education for all antiarrhythmics

Monitoring -Potassium (K+), blood urea nitrogen (BUN), creatinine, therapeutic drug levels (ex: Warfarin) -Electrocardiogram (ECG) Patient education -Take exactly as prescribed, do not double doses. -Be aware of food and drug interactions. Monitor HR for regularity of rate and rhythm. -Monitor BP at home. (Ex: Interactions between Warfarin and high K foods) high K foods: bananas, avocados, and leafy greens like spinach and chard. (Educate pt how to take pulse) (Pt to Keep BP log)

Describe nitrates for long term control

Monotherapy generally should be avoided Pts unprotected during nitrate-free period each day Combine with either BB or CCB Protect your pt! Combine NTG with other therapies to protect from nitrate free period breakthrough symmptoms.

Describe supplements as they relate to hyperlipidemia

Niacin (500 mg BID increases HDL, decreases TG, 2000 mg/day decreases LDL) Fish Oil (12 x 1000 mg tablets/day) Red yeast rice (statin-like effects) Remember: supplements are not FDA approved.

Cost of treatment r/t angina

Nitrates cheapest BBs mid-range for cost Older drugs cheaper CCBs and ACEIs are the most expensive. Generics less expensive

Switching drugs between rivaroxaban to warfarin

No clinical trail data; manufacturer recommends starting both warfarin and parenteral anticoagulant when next dose of rivaroxaban would be scheduled

Describe BP categories per ACC/AHA updated Nov. 2017

Normal blood pressurewithin the normal (optimal) range of less than 120/80 mm Hg. Encourage a balanced diet and regular exercise. Elevated BPReadings are consistently ranging from 120-129 systolic and less than 80 mm Hg diastolic. People with elevated blood pressure are likely to develop high blood pressure unless steps to control BP. Encourage lifestyle changes & Check for meds that can increase BP (NSAIDs, SNRIs, estrogenm etc) Hypertension Stage 1Blood pressure is consistently ranging from 130-139 systolic or 80-89 mm Hg diastolic. Start w/ lifestyle changes if ACC/AHA 10 year CV risk (risk of atherosclerotic cardiovascular disease (ASCVD) such as heart attack or stroke) is <10%. Consider adding blood pressure medication for pts with CVD, DM, CKD or 10 yr CV risk ≥10%..  Hypertension Stage 2Blood pressure is consistently ranging 140/90 mm Hg or higher. At this stage of high blood pressure, likely need to prescribe a combination of blood pressure medications along with lifestyle changes. Hypertensive crisisIf blood pressure readings suddenly exceed 180/120 mm Hg - requires medical action!

Describe recommended HBP follow up

Normal: Recheck in 2 years. Prehypertension: Recheck in 1 year. Stage 1 HTN: Confirm within 2 months. Stage 2 HTN: Evaluate or refer within 1 month. If > 180/110 evaluate and treat immediately or within 1 week. Use your clinical judgment: consider history, risk factors, target organ disease.

Classification of BP for adults > 18 yrs.

Normal: SBP 90-120, and DBP 60-79. Prehypertension: SBP 120 - 139, or DBP 80-89. Stage 1 HTN: SBP 140 - 159, or DBP 90 - 99. Stage 2 HTN: SBP >160 or DBP > 100. Per Eighth Joint National Committee (JNC 8) in 2014 Categories of BP in Adults* Normal: SBP 90-120, and DBP 60-79. Prehypertension BP: SBP 120 - 139, or DBP 80-89. Stage 1 HTN: SBP 140 - 159, or DBP 90 - 99. Stage 2 HTN: SBP >160 or DBP > 100.

Pt education about anticoagulation

Notify if: Bleeding > 5minutes Nosebleeds/bleeding gums Red/pink tinged urine Faintness/weakness H/a Stomach pains Unusual bruising Red, black, or tarry stools

What is hypertensive crisis?

Often occurs when patients are not following medication regimen True medical emergency Clinical Manifestations (S, Sx, Dx) severe HA, anxiety extremely high BP (>240 mm Hg systolic, >120 mm Hg diastolic) blurred vision dizziness disorientation epistaxis (nosebleed) possibly obtunded patient This is when high blood pressure requires medical attention. If blood pressure readings suddenly exceed 180/120 mm Hg, wait five minutes and test again. If readings are still unusually high, experiencing hypertensive crisis. If blood pressure is higher than 180/120 mm Hg & Pt. experiencing signs of possible organ damage such as chest pain, shortness of breath, back pain, numbness/weakness, change in vision, difficulty speaking, you have a medical emergency.

Patient variables regarding med treatment for angina

Older adults ACEIs and BBs if the patient has congestive heart failure (CHF) CCBs will make CHF worse Women No gender-based difference in therapy Women undertreated ACEI+BBs= ✓ for CHF "A+B=C" DO NOT GIVE CCB to CHFer! Not cool! Will worsen condition. Women undertreated b/c often present with abnormal symptoms, not classic CP symptoms.

What is the onset, peak, duration, half life, and elimination of warfarin

Onset: dependent on both ½-life of warfarin and time it takes to deplete clotting factors Peak: 3-5 days Duration: 2-5 days Half life: 36 to 42 hours Elimination: urine

What are admin routes for nitroglycerin?

Oral Sublingual tablet Extended-release buccal tablet Extended-release capsule Lingual aerosol Chewable tablet Ointment Transdermal topical systems Wear gloves when applying the patch/ointment! Easily absorbed through skin, then you're working the rest of the day with a HA

Describe long acting nitrates

Oral or patch (transdermal) Used for patients intolerant to BBs Isosorbide dinitrate (Isordil) given 2 or 3 times/day With a 10 to 12 hour nitrate-free interval to prevent nitrate tolerance Timing of the nitrate-free interval should coincide with the time of fewest episodes of angina.****

Describe digoxin use in antidysrhythmic drugs

Other antidysrhythmic drug category Used more for heart failure treatment Suppresses dysrhythmias by decreasing conduction through the AV node& by decreasing automaticity in the SA node

Racial factors r/t BP

Over 40 % of African American adults have HTN. Starts earlier in life and is more severe. Caucasian: 31% Mexican American: 28% American Indian / Alaskan: 21% Hispanic / Latino: 18% Asian: 17% "The adjusted relative risk of stroke, for example, is more than twice as high in hypertensive blacks aged 45 to 64 years as compared with similarly aged hypertensive whites."

How should hypertensive crisis be treated?

Patient in semi-Fowlers' position Order O2 Order IV antihypertensives nitroprusside (Nipride) nicardipine (Cardene IV) labetalol (Normodyne) Monitor BP closely and frequently - q 5-15 min Assess for neurologic or CV complications: seizure - LOC, pupillary rx numbness, weakness, tingling of extremities chest pain dysrhythmias - monitor ECG

What is secondary prevention for stroke

Patients with history of stroke or TIA Noncardioembolic ischemic stroke/TIA Clopidogrel or ASA/dypiridamole preferred Ischemic stroke/TIA and AF Oral anticoagulation with dabigatran preferred History of ICH/hemorrhagic stroke Long-term use of antithrombotic therapy NOT recommended (may consider with CHADS2 >4

Pernicious anemia cause, prevention, monitoring, pt education

Pernicious anemia is caused by inadequate vitamin B12. Defective secretion of gastric intrinsic factor, which is necessary for vitamin B12 absorption Vitamin B12 malabsorption occurs in 10% to 30% of adults over age 50 due to reduced pepsin activity and gastric acid secretion. Prevention Eat foods high vitamin B12, such as mollusks (e.g., clams), fortified breakfast cereals, liver, trout, salmon, milk, and eggs. Pernicious anemia is an autoimmune illness which causes autoimmune destruction of the parietal cells (which produce intrinsic factor) & leads to reduced vitamin B-12 absorption from the GI tract Monitoring Reticulocyte counts, Hgb and Hct, iron, folic acid, and vitamin B12 serum levels prior to treatment, at 5 to 7 days of therapy, then frequently until the Hgb and Hct are normal Monitor potassium levels. Liver function tests every 2 to 4 weeks to monitor for hepatotoxicity Patient education Disease process and need for lifelong therapy Vitamin B12 therapy regimen Monitoring

Describe anticoagulation in special populations

Pregnancy LMWH 1st line anticoagulant (ACCP) Older Adult Falls Dementia Risk vs benefit

What is the JNC 8 newest guideline r/t meds for htn?

Prescribing medication for Stage 1 hypertension (SBP 130-139 DBP 80-89) only if a patient has already had a cardiovascular event such as a heart attack or stroke, or is at high risk of heart attack or stroke based on age, the presence of diabetes mellitus, chronic kidney disease or calculation of atherosclerotic risk; recognizing that many patients will need two or more types of medications to control their blood pressure, and that people may take their pills more consistently if multiple medications are combined into a single pill; and identifying socioeconomic status and psychosocial stress as risk factors for HBP, which should be considered in a patient's plan of care.

Prevention and treatment of iron deficiency anemia

Prevention Adequate intake via iron-rich diet Monitor in periods of rapid growth (infancy, adolescence, pregnancy). Treatment Iron replacement based on age Divide dose in three doses per day. Patients with an underlying condition that causes iron deficiency anemia should be treated or referred to a subspecialist (e.g., gynecologist, gastroenterologist) for definitive treatment.

Vitamin B12 Clinical use

Prevention of deficiency Pregnancy 2.2 mcg/day, lactation 2.6 mcg/day Infants 0.3 to 0.5 mcg/day Children age 1 to 10 years: 0.7 to 1.4 mcg/day Treatment of deficiency 1000 mcg oral cobalamin daily or 1000 mcg. IM monthly for 6 to 12 weeks B-12 deficiency can present with peripheral neuropathy & neuropsychiatric complaints (dementia). Can see in poor dietary intake, strict vegans, elderly, Patients w/ malabsorption, hx of gastric resection or bypass, & Patient w/ chronic metformin or proton pump inhibitors. Pernicious anemia Initial dose 1000 mcg/day IM or SC x 7 days, then 100 to 1000 mcg IM per week for a month Maintenance: 1000 mcg IM once monthly 500 mcg intranasal cyanocobalamin weekly 1000 mcg PO daily (absorption increased if taken on empty stomach) In pernicious anemia, the body can't make enough healthy red blood cells because it doesn't have enough vitamin B12.

What is the significance of heart failure?

Primary or contributing cause in about 261,000 U.S. deaths (2002). Direct & indirect costs $59.7 billion (AHA). As many as 65 million Americans aged 6 or over have HTN. Nearly 1/3 of U.S. adults have HTN. About 59 million (28%) U.S. adults have prehypertension. Fewer Americans are dying from heart disease and stroke, but deaths caused by high blood pressure are on the rise, according to new statistics from the American Heart Association (AHA, 2018).

How is ASHD, MI, stroke, vascular death

Primary prevention: 50 years or older without symptomatic cardiovascular disease, recommend aspirin 75 -100 mg daily Established CAD: different recommendations depending on circumstances

Pharmacodynamics of Class III: postassium channel blockers

Prolong effective refractory period and reduce speed of conduction Ex: Amiodarone Class III: Think about the pathophys behind the dysrhythmia, block the excitation (Movement of K+), block the dysrhythmia! HENCE amiodarone is often called an anti-arrhythmic.

Describe NY Heart Assoc and canadian cardiovascual society grading of CLASS I Angina

Proven coronary artery disease without symptoms Ordinary physical activity, such as walking or climbing stairs, does not cause angina.

Duration of treatment for DVT/PE

Provoked by surgery/transient risk factor - 3 mo. Unprovoked - 3 mo., then evaluate risk/benefit Choice of drug: Warfarin if no cancer (next preferred LMWH) LMWH if active cancer (next preferred warfarin) Extended therapy (using same drug) for: 2nd unprovoked DVT with low/moderate bleeding risk DVT with active cancer

What do HMG COA reductase inhibitors (statins) do?

Reduce LDL 15 - 55% Increase HDL 5 - 15% Decrease TG 7 - 30% Risk of myopathy (DC for CK > 10 x normal) Myalgias (treat low Vit D, CoQ10 may help) Increased liver enzymes (DC if >3xULN) Contraindicated with liver disease, caution with heavy alcohol use Pregnancy category X Drug interactions (CYP system)

Pharmacodynamic Class II: beta blockers (BBs) "-lol"

Reduce adrenergic activity in the heart Sotalol: considered a class II and III drug Ex) Labetolol, metoprolol

Goals of BP treatment

Reduce cardiovascular and renal morbidity and mortality. 35 - 40 % reduction in stroke 20 - 25 % reduction in MI >50 % reduction in heart failure Sustained 12 mmHg reduction in SBP over 10 years (stage 2 with other RF) will prevent 1 death for 11 patients treated. Most important non-pharmacologic interventions weight loss (1), the DASH (Dietary Approaches to Stop Hypertension) diet, sodium reduction, potassium supplementation, increased physical activity, and a reduction in alcohol consumption.

Therapeutic lifestyle changes for atherosclerosis?

Reduce saturated fats (< 7% of calories) Reduce cholesterol (< 200 mg/day) Increase soluble fiber (10 - 25 gm / day) Increase physical activity Weight control TLC diet: Avoidance of heavily saturated fats Plant stanols/sterols 2 g/d; plant sterols block cholesterol absorption Increased viscous (soluble) fiber to 10 to 25 g/d; viscous fibers increase bile-acid losses Total calories adjusted to maintain desirable body weight and prevent weight gain

What is the reentry phenomena?

Reentry is the cause of SOME arrhythmias. It depends on TWO anatomically or physiologically distinct electrical pathways. Normally, impulses from the AV node will be conducted down both pathways in the same direction, bifurcating to cover the entire ventricle. If action potential encounters a block in one of the pathways, then the impulse can only be conducted down the other pathway. (blocks can be due to damage from MI or prolonged refractory period) The impulse can return to the initial point of bifurcation and reexcite the myocardium. Short circuiting conducting tissue can occur and causes premature contraction. If reentry is repetitive, sustained ventricular arrhythmias such as V tachycardia can occur. Ex) repetitive PVCs V Tach YGD unless ACLS performed Real Life example: Old Lady at Out Pt appt passed out brought to ED, EKG looked OK but tele monitor would show occasional PVCs EKG missed, took 3 additional EKGs to show pt throwing PVCs, alerted MD, not concerned, coded 5 mins later. Got her back, but still, Not cool.

What is the absolute refractory period?

Regardless of the strength of a stimulus, the cell cannot be depolarized.

Patho of folic acid deficiency anemia

Seen in alcoholics, chronic malnutrition, fad diets, and diets low in vegetables Drugs: dilantin, sulfamethoxazole/trimethoprim, oral contraceptives, methotrexate

Goal of anemia treatment

Restore hemoglobin (Hgb) and red blood count to normal levels to maintain oxygen-carrying capacity of blood.

Describe children and statins

Review Figure 39-7 pg 1143 Goal: primary prevention Drug therapy consideration: consult with experienced provider in lipid disorders. < 10 yrs old: referral to specialist No statins under age of 10 yrs- males; onset of menses-females Remember: Category X Up to 25% of children have cholesterol >200, usually r/t same environmental factors responsible for adult hypercholesterolemia. Test levels in children with visible cutaneous xanthomas

Risk groups, prevention, drug therapy, monitoring, education, for folic acid deficiency anemia

Risk groups Infants fed goat's milk or powdered milk formula Vegetarians and vegans Pregnancy increases daily requirement need. Patients with Celiac sprue, Crohn's disease, giardial infections, and short bowel syndrome Patients taking drugs that affect folic acid absorption Prevention Adequate dietary intake Folic acid supplementation in pregnancy Drug therapy for deficiency Oral folic acid 1 to 2 mg/day for 4 to 5 weeks Hgb levels start to rise in a week Women of childbearing age and pregnant women should consume 0.4 to 0.8 mg/day. CDC recommends 0.4 mg (400 mcg) per day Monitoring Follow Hgb/Hct in 4 weeks and then regularly Education Need for folic acid Administration The U. S. Public Health Service and CDC recommend that all women of childbearing age consume 0.4 mg (400 micrograms) of folic acid daily to prevent two common and serious neural tube defects - spinal bifida and anencephaly. Per ACOG: Folic acid (AKA folate) is a B vitamin that is important for pregnant women. Before pregnancy and during pregnancy, they need 400 micrograms of folic acid daily to help prevent major birth defects of the fetal brain and spine called neural tube defects. Current dietary guidelines recommend that pregnant women get at least 600 micrograms of folic acid daily from all sources. It may be hard to get the recommended amount of folic acid from food alone. For this reason, all pregnant women and all women who may become pregnant should take a daily vitamin supplement that contains folic acid

From greatest to lowest impact on LDL how do the drugs go?

Rosuvastatin (Crestor) Atorvastatin (Lipitor) Simvastatin (Zocor) Lovastatin (Mevacor) Pravastatin (Pravachol) Fluvastatin (Lescol)

Examples of spontaneously depolarizing cells?

SA nodes, AV nodes, His-Purkinje, special atrial cells

What is low risk stable angina?

Severe angina=Class III & IV Comes as a "surprise"-unstable. Occurs at rest-unstable Lasts longer than stable angina Result of CAD, Often referred to as Acute Coronary Syndrome (ACS). "Low" risk b/c pt is nonsmoker, normotensive, low cholesterol, neg family history, normal echo, and good exercise tolerance tests.

Describe NY Heart Assoc and canadian cardiovascual society grading of CLASS IV Angina

Severe limitations: angina during minimal activity or rest Inability to carry on any physical activity without discomfort. Angina may occur at rest.

How should an elevated INR be managed?

Significant bleeding (regardless of INR): Hold warfarin give Vitamin K 10 mg slow IV infusion repeat q12 hours if needed. may need FFP, prothrombin complex concentrate, or recombinant factor VIIa

What are contributing factors for low HDL?

Smoking Drugs: Beta blockers, anabolic steroids, progestational agents Elevated triglycerides Genetic factors Overweight and obesity Physical inactivity Type II DM Very high carbohydrate intake Drugs that lower HDL: Beta blockers, anabolic steroids, pro-gestational agents-Many persons with hyperlipdemia also have HTN so keep comorbidities in mind when determining appropriate med to prescribe You can increase the HDL through Therapeutic Lifestyle Changes (TLC): Being active. Exercise can boost HDL level. Get at least 30 minutes a day of moderate activity, most days of the week. Losing extra weight. If overweight, losing extra pounds can help raise HDL levels, as well as lower LDL Choosing better fats. The healthier choices are monounsaturated and polyunsaturated fats. These are found in plants, nuts, and fish like salmon or tuna. Eat less healthy food choices in small portions. Fats pack a lot of calories in small amounts. Drinking alcohol in moderation. Drinking moderate amounts of alcohol is linked to higher HDL levels. Smoking cessation- Kicking the cigarette habit can raise HDL level.

What are examples, MOA, clinical use, contraindications, and adverse effects of Aldosterone Antagonists

Spirolactone, eplerenone Mechanism of Action Binds with receptors on the distal tubule, increases excretion of sodium and water, while potassium is retained Clinical use: HF, HTN Contraindications Anuria, acute renal insufficiency, hyperkalemia Addison's disease Adverse Events Gynecomastia, hirsuitism, menstrual irregularities

What are examples, MOA, and adverse effects of aldosterone antagonists?

Spironolactone, Eplerenone MOA: Block effects of aldosterone Better regulation of Na+ & water homeostasis Better maintenance of intravascular volume Adverse events: Hyperkalemia Gynecomastia with prolonged use Caution in renal impairment Eplerenone (INN) is a steroidal antimineralocorticoid of the spirolactone group that is used as an adjunct in the management of chronic heart failure. Brand name is Inspra

What are American College of Cardiology Foundation/American Heart Association Heart Failure Classification?

Stage A - High risk for development of heart failure; no underlying structural cardiac disease (hypertension, diabetes mellitus, hyperlipidemia, etc.) Stage B - Structural heart disease but asymptomatic Stage C - Structural heart disease with past or current symptoms of heart failure Stage D - Refractory heart failure

Treatment stage 4 heart failure

Stage C treatments Inotropes: dobutamine (hospitalized patient) Ventricular assist device, transplantation, hospice

Switching drugs from dabigatran to warfarin

Start warfarin 1-3 days before stopping dabigatran (depends on renal function)

What is refractoriness?

State of the cardiac cell which determines depolarization Damaged heart cells may maintain a constant rate of refractoriness or may not be refractory at all

What are safety recommendations for all statins?

Statins are Pregnancy Category X. Selection and dose of statins based on: patient characteristics ASCVD risk *AHA's ASCVD Risk Calculator Characteristics predisposing to statin adverse effects: Multiple/serious comorbidities (incl. liver and kidney) History of previous statin intolerance/muscle disorders Unexplained ALT elevation > 3 x upper limit of normal (ULN) Patient characteristics/concomitant use of drugs which affect statin metabolism >75 years of age Other: history of hemorrhagic stroke; Asian ancestry Increasing the dose of statin also increases the risk of adverse effects. Statin metabolized in the liver by CYP450 so no grapefruit juice! And monitor LFTs.

Switching drugs between rivaroxaban to other anticoagulants (oral/parenteral)

Stop rivaroxaban and start other agent when next dose due

Switching drugs from warfarin to rivaroxaban

Stop warfarin, INR<3, start rivaroxaban

What is the relative refractory period?

Stronger than normal stimulus can induce depolarization.

What are risk factors for coronary heart disease? (CHD) Major risk factors? Other risk factors?

Symptomatic carotid artery disease Peripheral arterial disease Abdominal aortic aneurysm (AAA) Type II Diabetes Cigarette smoking Hypertension (>140/90 or on meds) Low HDL cholesterol Family history of premature CHD (father or brother < 55; mother or sister < 65) Age (men > 44; women >54) Diabetes mellitus Type II Obesity Physical inactivity Atherogenic diet Metabolic syndrome Impaired fasting glucose (100 - 125) Obesity-Pay attention to your patient's BMI and TRENDS- where are they heading? Atherogenic diet (high fat high cholesterol content) Metabolic syndrome (AKA Pre-diabetes) Educate your pt on Therapeutic lifestyle changes (TLC) if have these risk factors.

What is hypertriglyceridemia?

TG >1000 can cause pancreatitis For very high triglycerides (>500), treat that first, then cholesterol. Look for causes: diabetes, alcohol abuse, hypothyroidism, CRF, obesity, medications, etc. Need very low fat diet Recommend fibric acids first line Nicotinic acid or Omega-3 fatty acids next Avoid bile acid sequestrants (elevate TG) Omega-3 fatty acids (Fish oils) need to give 4000 mg daily. Give in divided doses. I start with 1000 mg/ day because many patients cannot tolerate if you start too high. Burpless- fish oil caps have been developed. Use cautiously if ASA sensitivity, cirrhosis, concurrent anticoagulant use. With diabetes keep Fish oil dose < 3g/ day. Lovaza is a brand of fish oil Give w/ meals

Describe pt education r/t nitroglycerin

Take the drug exactly as prescribed. Eccentric dosing of some long-acting nitrates Use of sublingual NTG If anginal symptoms occur at night, the nitrate-free time is during day.*** Storage of NTG Avoid heat and moisture. NTG expiration date

Describe patient education for nitrates

Take the drug exactly as prescribed. Eccentric dosing schedule separated by 7 hours due to need to have nitrate-free period Take at 7 to 8 a.m. and 2 to 3 p.m. rather than "usual" twice daily regimen. Need nitrate-free interval of 10 to 12 hours. If anginal symptoms occur at night, have a daytime nitrate-free interval. Storage of NTG Adhere to the expiration date on the bottle, usually 6 months. Do not open the bottle frequently or keep bottles of tablets next to the body (in a shirt pocket). There is a NEED for NITRATE FREE period of 10-12 hours. Understand timing of dosing for nitrate free period in relation to timing of angina symptoms **** Do not open the bottle frequently b/c light sensitive, also don't carry it around in your pocket! BAD if next to the Body!

Describe different classes of DHP calcium channel blockers

There are three classes of CCBs. They differ not only in their basic chemical structure, but also in their relative selectivity toward cardiac versus vascular L-type calcium channels. The most smooth muscle selective class of CCBs are the dihydropyridines. Because of their high vascular selectivity, these drugs are primarily used to reduce systemic vascular resistance and arterial pressure, and therefore are used to treat hypertension. Extended release formulations or long-acting compounds are used to treat angina and are particularly effecting for vasospastic angina; however, their powerful systemic vasodilator and pressure lowering effects can lead to reflex cardiac stimulation (tachycardia and increased inotropy), which can offset the beneficial effects of afterload reduction on myocardial oxygen demand. Note that dihydropyridines are easy to recognize because the drug name ends in "pine." Dihydropyridines include the following specific drugs: amlodipine felodipine isradipine nicardipine nifedipine nimodipine Nitrendipine

Treat of heart failure based on stages

Treatment of stage A heart failure should focus on reducing modifiable risk factors, including management of hypertension and hyperlipidemia. To prevent symptomatic heart failure, ACE inhibitors and beta blockers should be used in all patients with stage B or C heart failure who have a reduced ejection fraction. Patients with stage C heart failure and fluid retention should be treated with diuretics in addition to ACE inhibitors and beta blockers.

Describe patient education regarding heart failure

Treatment plan Pathophysiology and chronicity of heart failure Home monitoring Drug therapy Take exactly as directed. Do not miss or double doses.

Gender factors r/t BP

Until age 55: Males > Females After age 55: Females > Males 2 - 3 times more common in women taking OCs, especially if older or obese, than those not taking them.

Describe clinical use and dosing of nitro for predictable angina

Use isosorbide. Isosorbide dinitrate: 10 to 40 mg orally 2 to 3 times daily; sustained-release form 40 to 80 mg daily Isosorbide mononitrate: Dosing is 20 mg twice daily. Eccentric scheduling to avoid development of tolerance

Describe examples, uses, ADRs of Class IV: Calcium channel blockers

VERAPAMIL (Calan, Isoptin) IV OR PO DILTIAZEM (Cardizem) IV USE: SUPRAVENTRICULAR ARRHYTHMIAS ADRs: Constipation, nausea, H/A, rash, pretibial & pedal edema, hypotension, dizziness, drowsiness, liver dysfunction, sexual dysfunction & gingival overgrowth SVTs Pt w/ HF- can exacerbate heart failure symptoms & decrease heart's pumping action.

Describe Class II: Beta Blockers

Various types include nonspecific beta antagonists, selective beta-antagonists, and those with and without intrinsic sympathomimetic activity (ISA) -In post-MI patients, cardioselective agents are preferred without ISA. -Some are used as antiarrhythmics. -Drugs with ISA may help avoid a decrease in CO and HR. May be preferred for patients who experience bradycardia with other beta blockers. More effective in African-American and older patients BBs may NOT be abruptly withdrawn, increases beta receptor sensitivity No longer first-line HTN drug choice Worry if abrupt discontinuation of BBs-Can cause rebound. Think about MOA- what is it actually doing to the beta receptors in the heart?

What are disorders requiring anticoagulation/antiplatelet therapy?

Venous Thromboembolism Deep Vein Thrombosis (DVT) Pulmonary Embolism (PE) Atrial Fibrillation Ischemic Stroke Prosthetic Heart Valve Prophylaxis of Hypercoagulable States Prevention of ASHD, MI, stroke, vascular death

What is the best drug treatment for VTE?

Venous thromboembolism (DVT/PE) Initial treatment with LMWH, fondaparinux, or UFH (least preferred) Start warfarin on day 1 Continue parenteral therapy 5 days AND until INR ≥2 for at least 24 hours Acute DVT of leg may be treated at home under suitable circumstances

Patho of pernicious anemia

Vitamin B12 deficiency leads to macrocytic-normochromic anemia. Vegetarians, vegans, genetic predisposition, autoimmune disease

Ineffective drug therapies for angina

Vitamin C & E supplementation Chelation therapy Garlic Acupuncture Coenzyme Q10

What are different types of anticoagulants?

Vitamin K Antagonists Direct Thrombin Inhibitors Unfractionated Heparin (UFH) Low molecular weight heparin (LMWH) Factor Xa Inhibitors Antiplatelet Agents

Lifestyle modifications for BP

Weight loss (5 - 20 mmHg / 10 kg) DASH diet (8 - 14 mmHg) www.nhlbi.nih.gov Reduce Sodium (2 - 8 mmHg) Regular aerobic activity (4 - 9 mmHg) Limit alcohol (2 - 4 mmHg) Stop smoking (overall CV risk reduction) Correcting poor diet, physical inactivity, and excessive alcohol consumption that cause high BP is an important approach to prevention and management of high BP, either on their own or in combination with pharmacological therapy. Prevention of HTN and treatment of established hypertension are complementary approaches to reducing CVD risk in the population, but prevention of hypertension provides the optimal means of reducing risk and avoiding the harmful consequences of hypertension. Nonpharmacological therapy alone is especially useful for prevention of hypertension, including in adults with elevated BP, and for management of high BP in adults with milder forms of hypertension men and women with elevated BP or HTN who also consume alcohol should be advised to drink no more than 2 and 1 standard drinks* per day, respectively

Microcytic

abnormally small red blood cell

What is mean corpuscular hemoglobin (mch)

average amount of hemoglobin in the typical red blood cell.

What is mean corpuscular hemoglobin concentration (mchc)

average concentration of hemoglobin in a specific amount of red blood cells.

What is mean corpuscular volume (MCV)

average volume of red blood cells or average amount of space each red blood cell fills. is a measure of the average volume of a red blood corpuscle (or red blood cell). The MCV measurement allows classification as either a microcytic anemia (MCV below normal range), normocytic anemia (MCV within normal range) or macrocytic anemia (MCV above normal range). Normocytic anemia is usually deemed so because the bone marrow has not yet responded with a change in cell volume. It occurs occasionally in acute conditions, namely blood loss and hemolysis.

Describe benefits, MOA, ADRs of cardiac glycoside: digoxin

can be beneficial, unless contraindicated, to decrease hospitalizations for CHF MOA: Highly selective inhibitors of the ATPase system. Inhibition of this pump results in sodium and calcium buildup inside the cell, which leads to increased contractility of heart muscle. Serum concentrations greater than 1 ng/mL have been linked to an increase in mortality. Initiate therapy at the lowest dose possible. New research shows digoxin may increase mortality in women. Benefits are best in patients with: severe HF, enlarged heart, third heart sound, and in patients who do not respond to ACEIs and BBs. levels >1 ng/ml (not mg/ml) have been shown to increase mortality. That number came from a study that found digoxin levels >1.2 ng/ml may be harmful (Goldberger & Goldberger, 2012). Due to the narrow therapeutic index of Digoxin, patients need to be closely monitored. The toxic range for digoxin for years has been levels greater than 2.5 ng/mL. About 10% of patients may show toxicities at levels less than 2 ng/mL (particularly in hypokalemia, hypomagnesemia, hypoxia, heart disease, and hypercalcemia. Well-absorbed orally NOT extensively metabolized, excreted unchanged by kidneys Half-life is 36 to 48 hours. In the absence of oral or intravenous loading, steady state is achieved in four half-lives or 1 week. Reduced clearance of digoxin with drug interaction: Quinidine, amiodarone, verapamil, diltiazem Clinical use in HF: Therapy with digoxin is commonly initiated and maintained at a dose of 0.125 to 0.25 mg daily. Doses of digoxin that achieve a plasma concentration of drug in the range of 0.5 to 0.9 ng/mL are suggested Digoxin acts by inhibiting the Na-K-ATPase pump, thus reducing the transport of sodium from the intracellular space in myocytes as well as non-cardiac cells to the extracellular space. This mechanism contributes to digoxin's hemodynamic, neurohumoral, and electrophysiologic effects ADRs: Gastrointestinal (GI) most common: anorexia, nausea/vomiting, diarrhea Central nervous system: fatigue, disorientation, depression, hallucinations, visual disturbances - yellow vision and green halos around lights Toxicity: atrial arrhythmias/tachycardia in children Cardiac: bradycardia, premature ventricular contractions, junctional and AV block arrhythmias, and bigeminy Avoid using in patients with normal left ventricular systolic function Digoxin possesses a narrow toxic to therapeutic window. Toxic effects include the induction of arrhythmias, conduction disturbances, and, in severe cases, constitutional symptoms such as nausea, vomiting, and visual disturbances. Digoxin-related cardiac arrhythmias and extracardiac symptoms can occur when the SDC is in the therapeutic or even subtherapeutic range; as a result, digoxin toxicity is a clinical concern irrespective of circulating levels (unless the value is zero)."

What is atherosclerosis?

deposits of cholesterol and lipoproteins on artery walls

What is red cell distribution width (RDW or RCDW)

describes shape and size of red blood cells.

What does zetia do?

ezetimibe inhibits cholesterol absorption at small intestine brush border

Describes HTN treatment initiation for those less than 60, general population

initiate pharmacologic treatment at a DBP of 90 mmHg or higher or an SBP of 140 mmHg or higher and treat to goals below these respective thresholds.

What is simvastatin?

is a derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.

Macrocytic

larger than normal red blood cell larger than normal, , such as the erythrocytes in macrocytic anemia.

Mean Platelet Volume (MPV)

measures and calculates the average size of platelets.

Table per AHA, 2018 Classification of blood pressure according to the 2017 ACC/AHA guideline

mostly new classification scheme for BP was a prominent feature of the new guideline; <120/80 (normal), 120-129/<80 (elevated), 130-139 or 80-89 (stage I hypertension), and ≥140 or >90 mm Hg (stage II hypertension). The guideline eliminates the category of prehypertension, which previously referred to an SBP between 120-139 mmHg or a DBP between 80-89 mmHg.

Platelet count

number of platelets (clotting)

What is hemoglobin? (hgb)

the main functional constituent of the RBC which serves as an oxygen-carrying protein.

What is hematocrit (hct)

the ratio of the volume of red blood cells to the total volume of blood. It determines how much of the total blood volume consists of red blood cells.