Usmle - Cv Drugs

Front 1

What antihypertensive drug is protective against diabetic nephropathy?

Back 1

Beta blockers

Front 2

Hydralazine

Back 2

Increases cGMP, causing smooth muscle relaxation. Vasodilates arteries more so than veins, reducing afterload (which is unique).

Clinically used for severe hypertension, CHF. FIRST LINE FOR HTN IN PREGNANCY, with Methyldopa. Frequently coadministered with a beta blocker to prevent reflex tachycardia.

Toxicity includes compensatory tachycardia (contraindicated in CAD/angina), fluid retention, nausea, headache, angina. CAUSES DRUG INDUCED LUPUS!

Front 3

What drugs are given to pregnant women with HTN?

Back 3

Hydralazine and methyldopa

Front 4

Minoxidil

Back 4

K+ channel opener, which hyperpolarizes and relaxes vascular smooth muscle.

Used for severe HTN.

Toxicity include hypertrichosis (hair growth), pericardial effusion, reflex tachycardia, angina, and salt retention.

Front 5

Nifedipine

Back 5

Calcium channel blocker (dihydropyridine - works more on vasculature); blocks voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility.

Used for hypertension, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's.

Toxicity includes peripheral edema, flushing dizziness, and constipation.

Nifedipine avoids side effects causing cardiac depression and AV block.

Front 6

Amlodipine

Back 6

Calcium channel blocker (dihydropyridine - works more on vasculature); blocks voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility.

Used for hypertension, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's.

Toxicity includes peripheral edema, flushing dizziness, and constipation.

Avoids cardiac depression and AV block found with non-dihydropyridine CCBs that affect the heart more.

Front 7

Felodipine

Back 7

Calcium channel blocker (dihydropyridine - works more on vasculature); blocks voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility.

Used for hypertension, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's.

Toxicity includes peripheral edema, flushing dizziness, and constipation.

Avoids cardiac depression and AV block found with non-dihydropyridine CCBs that affect the heart more.

Front 8

Nicardipine

Back 8

Calcium channel blocker (dihydropyridine - works more on vasculature); blocks voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility.

Used for hypertension, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's.

Toxicity includes peripheral edema, flushing dizziness, and constipation.

Avoids cardiac depression and AV block found with non-dihydropyridine CCBs that affect the heart more.

Front 9

Nisoldipine

Back 9

Calcium channel blocker (dihydropyridine - works more on vasculature); blocks voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility.

Used for hypertension, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's.

Toxicity includes peripheral edema, flushing dizziness, and constipation.

Avoids cardiac depression and AV block found with non-dihydropyridine CCBs that affect the heart more.

Front 10

Verapamil

Back 10

Calcium channel blocker (non-dihydropyridine - works more on heart); blocks voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility.

Used for hypertension, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's.

Toxicity includes cardiac depression, AV block peripheral edema, flushing dizziness, and constipation.

Front 11

Diltiazem

Back 11

Calcium channel blocker (non-dihydropyridine - works more on heart); blocks voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility.

Used for hypertension, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's.

Toxicity includes cardiac depression, AV block peripheral edema, flushing dizziness, and constipation.

Front 12

Nitroglycerin

Back 12

Vasodilates by releasing NO in smooth muscle, causing an increase in cGMP and smooth muscle relaxation. Dilates veins more than arteries (opposite of hydralazine). DECREASES PRELOAD.

Clinically used for angina, pulmonary edema (cause fluid to leave lungs and pool in the periphery). Also used as an aphrodisiac and erection enhancer.

Toxicity includes reflex tachycardia, hypotension, flushing, headache, "Monday disease" in industrial workers. Development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend, resulting in tachycardia, dizziness, and headache on reexposure.

Front 13

Isosorbide dinitrate

Back 13

Vasodilates by releasing NO in smooth muscle, causing an increase in cGMP and smooth muscle relaxation. Dilates veins more than arteries (opposite of hydralazine). DECREASES PRELOAD.

Clinically used for angina, pulmonary edema (cause fluid to leave lungs and pool in the periphery). Also used as an aphrodisiac and erection enhancer.

Toxicity includes reflex tachycardia, hypotension, flushing, headache, "Monday disease" in industrial workers. Development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend, resulting in tachycardia, dizziness, and headache on reexposure.

Front 14

Nitroprusside

Back 14

Malignant hypertension treatment; short acting; increased cGMP via direct release of NO. CAN CAUSE CYANIDE TOXICITY (RELEASES CN).

Decreases preload AND afterload by dilating arteries and veins.

Front 15

Fenoladopam

Back 15

Malignant hypertension treatment; dopamine D1 receptor agonist - relaxes renal vascular smooth muscle.

Front 16

Diazoxide

Back 16

Malignant hypertension treatment; K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle. Can cause hyperglycemia (reduces insulin release).

Front 17

Statins

Back 17

HMG-CoA reductase inhibitors (enzyme in cholestrol synthesis); biggest effect is a large decrease on LDL. Also increases HDL and lowers triglycerides slightly.

Works by inhibiting cholesterol precursor mevalonate and increasing LDL receptors on liver.

Side effects include hepatotoxicity (increased LFTs), rhabdomyolysis, myalgias, and myositis.

Front 18

Niacin (for lipid lowering)

Back 18

Main effect is an increase in HDL, but also decreases LDL and triglycerides. Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation.

Side effects include red flushed face, which is decreased by aspirin or long term use, hyperglycemia (acanthosis nigrans), and hyperuricemia (exacerbates gout).

Front 19

Cholestyramine

Back 19

Bile acid resin. Decreases LDL and slightly increases HDL and triglycerides. Prevents intestinal reabsorption of bile acids; liver must use cholestrol to make more.

Patients hate this drug. Tastes bad, causes GI discomfort, decreases absorption of fat-soluble vitamins and causes CHOLESTROL GALLSTONES.

Front 20

Colestipol

Back 20

Bile acid resin. Decreases LDL and slightly increases HDL and triglycerides. Prevents intestinal reabsorption of bile acids; liver must use cholestrol to make more.

Patients hate this drug. Tastes bad, causes GI discomfort, decreases absorption of fat-soluble vitamins and causes CHOLESTROL GALLSTONES.

Front 21

Colesevelam

Back 21

Bile acid resin. Decreases LDL and slightly increases HDL and triglycerides. Prevents intestinal reabsorption of bile acids; liver must use cholestrol to make more.

Patients hate this drug. Tastes bad, causes GI discomfort, decreases absorption of fat-soluble vitamins and causes CHOLESTROL GALLSTONES.

Front 22

Ezetimibe

Back 22

Cholestrol absorption blocker; main effect is a decrease in LDL.

Prevents cholestrol reabsorption at the small intestine brush border. Rarely increases LFTs and plaque thickness.

Front 23

Do you ever give a fibrate with a statin?

Back 23

NO YOU NEVER GIVE A FIBRATE WITH A STATIN!!!

Front 24

Gemfibrozil

Back 24

Fibrate; main effect is a decrease in triglycerides.

It's MOA is to upregulate LPL and increase triglyceride clearance.

Side effects include myositis, hepatotoxicity (increase LFTs), and cholestrol gallstones.

Front 25

What lipid lowering agents cause myositis?

Back 25

Statins and fibrates; they are both also potentially hepatotoxic.

Front 26

Omega 3 fatty acids

Back 26

Lower triglycerides; shown to also reduce severity of some rheumatic diseases and reduce arrhythmias in heart disease patients.

Front 27

Digoxin

Back 27

Directly inhibits Na+/K+ ATPase leading to indirect inhibition of Na+/Ca2+ exchanger/antiport. Increases intracellular Ca2+ causing positive inotropy. Stimulates vagus nerve.

Clinically used for CHF (increases contractility) and A-fib (decreases conduction at AV node and depression of SA node). Does not help acute CHF.

Toxicity includes cholingeric (nausea, diarrhea, BLURRY YELLOW VISION. ECG will have increased PR, decreased QT, scooping, T-wave inversion, arrhythmia, hyperkalemia, bradycardia (most common).

Front 28

What are the class IA antiarrhythmics?

Back 28

Quinidine, Procainamide, and Disopyramide

Front 29

What are the class IA effects?

Back 29

Increased AP duration, increased effective refractory period (ERP), increased QT interval.

Front 30

What are quinidine's toxicities?

Back 30

Cinchonism (headache, tinnitus), thrombocytopenia, torsades de pointes due to increases QT interval)

Front 31

What are procainamide's toxicities?

Back 31

Reversible drug induced lupus

Front 32

What are the class IB antiarrhythmics

Back 32

Lidocaine, Mexiletine, and Tocainide

Front 33

What are the actions of class IB antiarrhythmics?

Back 33

Decrease AP duration; preferentially affect ischemic or depolarized Purkinje and ventricular tissue. Useful in acute ventricular arrhythmias (espcially post-MI) and in digitalis-induced arrhythmias.

Front 34

What are the class IC antiarrhythmics?

Back 34

Flecainide, Encainide, and Propafenone

Front 35

What are the effects of the class IC antiarrhythmics?

Back 35

No effect on AP duration. Useful in V-tachs that progress to VF and in intractable SVT. Usually only as last resort in refractory tachyarrhythmias. For patients without structural abnormalities.

Front 36

What electrolyte, when increased, causes increased toxicity for all class I drugs?

Back 36

K+

Front 37

Which class I group is best post-MI? Which is contraindicated post-MI?

Back 37

Class IB is Best post-MI; Class IC is Contraindicated.