Cardio Drugs

Question 1

Antihypertensives

Answer 1

ACEI (Lisinopril), ARBs (sartans), CCB, Hydralazine

Question 2

ACEI

Answer 2

ex. Lisinopril
MOA: decrease GFR (dilate efferent arteriole)
S/E: cough and angioedema/laryngoedema - due to decreased breakdown of Bradykinin
20% increase in serum Cr, Hyperkalemia (decreased Aldosterone)
CI in pregnancy -> fetal kidney development abnl

Question 3

Hypertension with HF

Answer 3

Diuretics, ACEI/ARBs, Aldosterone antagonists, B blockers (compensated HF)

Question 4

HTN with DM

Answer 4

ACEI/ARBs, CCB, thiazide diuretics, B blockers

Question 5

HTN in pregnancy

Answer 5

Hydralazine, labetalol, methyldopa, nifedipine (DHP CCB)

Question 6

CCBs

Answer 6

Amilodipine, Nifedipine (DHPs - vascular smooth muscle)
Diltiazem, Verapamil - nonDHP - on heart

Moa: Block L type Ca channels in cardiac and smooth muscle -> decreased muscle contractility

Use: DHP: HTN, angina (also Prinzmetal), Raynaud phenomenon
non-DHP: HTN, angina, Afib/Aflutter

S/E: Cardiac depression, AV block (non DHP), constipation, gingival hyperplasia, peripheral edema, dizziness, Hyperprolactinoma (Verapamil)

Question 7

Nimodipine

Answer 7

CCB used in subarachnoid hemorrhage (prevents cerebral vasospasm)

Question 8

Clevidipine

Answer 8

CCB used in hypertensive urgency/ER

Question 9

Hydralazine

Answer 9

Moa: increase cGMP -> smooth muscle relaxation vasodilate arterioles > veins; afterload reduction

Use: acute HTN, HF. Have to use B blocker (prevent reflex tachycardia)

S/E: Reflex tachycardia/CI in CAD/angina, fluid retention, HA, angina, drug induced Lupus

Question 10

HTN emergency

Answer 10

Clevidipine, Fenoldapam, labetalol, nicardipine, nitroprusside

Question 11

Nitroprusside

Answer 11

Short acting; Increase cGMP via direct release of NO

SE: cyanide toxicity

Question 12

Fenoldapam

Answer 12

Dopamine D1 receptor agonist; Peripheral, Coronary, renal, splanchnic vasodilation -> Decrease BP and increase natriuresis

Question 13

Nitrates

Answer 13

Nitroglycerine, isosorbide di/mononitrate
Mononitrate (oral avail)

Moa: increase NO in vascular smooth muscle -> vasodllate by increasing cGMP

Veins» arterioles -> preload reduction (and decrease SV)
Use: Angina, Acute coronary syndrome, pulmonary edema

S/E: Reflex tachycardia (give B blocker), hypotension, HA, flushing

Question 14

Anti-anginal therapy

Answer 14

Goals: Reduce Myocardial O2 demand by: decreasing end-diastolic volume, HR, contractility, BP

Nitrates, B Blocker, CCB

Question 15

B Blockers

Answer 15

Decrease HR and contractility

Selective blocker; B1 on heart and B2 in lungs
Use: Afib/Flutter, HF and MI: prevent cardiac negative remodeling, anti-anginals, social phobias

Question 16

Lipid Lowering Drugs

Answer 16

Statins (HMG-CoA reductase inhibitors), Bile acid resins, Ezetimibe, Fibrates, Niacin (Vitamin B3)

Question 17

Statins

Answer 17

inhibit LDL synthesis by inhibiting HMG-CoA reductase in liver; liver increases LDL receptors to uptake peripheral circulating LDL in blood

Decrease mortality in CAD

S/E: increase LFTs, myopathy (rhabdomyolysis), kidney damage
Measure: CK, BUN/Cr due to kidney damage (fluid hydration tx)

Question 18

Fibrates

Answer 18

Gemfibrozil, clofibrate

Decrease TG by increasing TG clearance by upregulating LPL; activate PPAR-alpha to induce HDL synthesis

SE: myopathy, esp if given with statins; Cholesterol gallstones (because decreased TG precipitates cholesterol in bile)

Question 19

Bile acid resins

Answer 19

Cholestyramine, colestipol, colesevelam

Prevent reabsorption of bile acids -> liver must use cholesterol to make more bile acids -> decreased LDL, increased HDL, TG

SE: GI upset, decreased absorption of drugs and fat soluble vitamins

Question 20

Ezetimibe

Answer 20

Prevent Cholesterol absorption at small intestine brush border -> decrease LDL only

SE: increase LFTs, steatorrhea/malabsorption

Question 21

Niacin (Vitamin B3)

Answer 21

Inhibit lipolysis in adipose tissues -> decreased TG synthesis; decreased hepatic VLDL synthesis;
increased HDL synthesis ( most potent increase in HDL) and increased Prostaglandin synthesis

SE: Red, flushed face (decreased by NSAIDs - Aspirin), Hyperglycemia, Hyperuricemia

Question 22

Digoxin

Answer 22

Cardiac glycoside; antiarrhythmic; Use: HF

Blocks Na/K ATPase in cardiac myocytes, INa builds up, Na/Ca pump: pumps out Na and pumps in Ca -> Increased ICa concentration -> increased contractility

SE: Cholinergic effects, N/V/D, Blurry vision and weird color vision, decreases QT -> arrhythmia

Test: EKG to track QT (and prevent arrhythmia)
Tx: AntiDigoxin Antidote (Ab)