Cardiovascular

Question 1

Amlodipine, nimodipine, nifedipine

Answer 1

Dihydropyridine calcium channel blockers. Block V-dependent L-type Ca channels of cardiac and smooth muscle.

Superior effect on vessels vs. non-dihydropyridines

Amlodipine and nifedipine treat HTN, angina (including Prinzmetal), Raynaud phenomenon

Nimodipine treats subarachnoid hemorrhage (prevents cerebral vasospasm)

Toxicity: cardiac depression, hyperprolactinemia

Question 2

Diltiazem, verapamil

Answer 2

Non-dihydropyridine calcium channel blockers

Superior effect on heart vs. dihydropyridines; verapamil is most cardiac-selective Ca blocker

Treat HTN, angina, A-fib/flutter

Toxicity: AV block, gingival hyperplasia, constipation, hyperprolactinemia

Question 3

Hydralzine

Answer 3

Vasodilates arterioles>veins. Increases cGMP.

Treats severe HTN, (first-line in pregnancy), CHF.

Coadministered with beta-blocker to prevent reflex tachycardia

Toxicity: Lupus-like syndrome

Question 4

Nitroprusside

Answer 4

Short-acting vasodilator. Direct release of NO causes increased cGMP.

Treats HTN emergency

Toxicity: cyanide toxicity (treat with sulfur)

Question 5

Fenoldopam

Answer 5

Selective dopamine D1 receptor agonist with no alpha/beta properties (unlike dopamine). Results in vasodilation and naturiuresis.

Treats HTN emergency

Question 6

Nitroglycerin, isosorbide dinitrate

Answer 6

Direct release of NO causes increased cGMP. Venodilation>>vasodilation. Decreases preload.

Treats angina, ACS, pulmonary edema.

Coadministered with beta-blocker to prevent reflex tachycardia.

Question 7

Lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin

Answer 7

HMG-CoA reductase inhibitors; inhibit conversion of HMG-CoA to mevalonate

Decreases LDL, trigs; increases HDL

Toxicity: hepatotoxicity, rhabdomyolysis (especially when used with niacin and fibrates)

Question 8

Vitamin B3 (Niacin)

Answer 8

Inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis

Decreases LDL, trigs; increases HDL

Toxicity: hyperglycemia, hyperuricemia, hypotension and flushed face (due to release of prostaglandins; inhibited by aspirin)

Question 9

Cholestyramine, colestipol, colesevelam

Answer 9

Bile acid resins; prevent intestinal reabsorption of bile

Decreases LDL

Toxicity: hypertriglyceridemia, cholesterol gallstones, bad taste, impaired absorption of vitamins and drugs

Question 10

Ezetimibe

Answer 10

Prevents cholesterol absorption at small intestine brush border

Decreases LDL

Toxicity: diarrhea

Question 11

Gemfibrozil, Clofibrate, Bezafibrate, Fenofibrate

Answer 11

Fibrates upregulate lipoprotein lipase to increase TG clearance. Activates PPAR-alpha to induce HDL synthesis

Decreases triglycerides; increases HDL

Toxicity:

• myositis (increased risk with concurrent statins)
• hepatotoxicity,
• cholesterol gallstones (increased risk with concurrent bile acid resins)

Question 12

Digoxin

Answer 12

Cardiac glycoside that directly inhibits Na/K ATPase and indirectly inhibits Na/Ca exchanger, resulting in increased inotropy.

Acts on the vagus nerve to increase parasympathetic tone, resulting in decreased AV conduction.

Treats CHF (increased contractility) and A-fib (depresses SA node and decreases conductance via AV node)

Question 13

Digoxin toxicity

Answer 13

Symptoms: n/v/d, blurry yellow vision, increased PR, decreased QT, arrhythmia, AV block

Factors predisposing to toxicity: renal failure, hypokalemia (digoxin binds at K site on Na/K ATPase), hypovolemia, verapamil, amiodarone, quinidine (decreased clearance)

Antidote: normalize K+, anti-digoxin Fab fragments, Mg

Question 14

Quinidine, Procainamide, Disopyramide

Answer 14

Class 1A antiarrhythmics (intermediate association/disassociation) - lengthens the AP, increase effective refractory period, increase QT interval

Treats atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT

Toxicity: Torsades due to increased QT interval. Quinidine can cause tinnitus. Procainamide can cause SLE-like syndrome. Disopyramide can cause CHF

Question 15

Lidocaine, Mexiletine, Phenytoin

Answer 15

Class 1B antiarrhythmics (fast association/disassociation) - shortens the AP, preferentially affects ischemic or depolarized Purkinje and ventricular tissue

Treats ventricular arrhytmias, especially post-MI, and digitalis-induced arrhythmias

Toxicity: CNS stimulation/depression, increased risk of systole

Question 16

Flecainide, Propafenone

Answer 16

Class 1C antiarrhythmics (slow association/disassociation) - no effect on AP; prolongs refractory period in AV node

Treats SVTs, including A-fib Toxicity: pro-arrhythmic, especially post-MI!

Contraindicated in structural and ischemic heart disease

Question 17

Metoprolol, propanolol, esmolol, atenolol, carvedilol

Answer 17

Class 2 antiarrhythmics - decrease SA and AV nodal activity by decreasing cAMP, Ca currents, slope of phase 4. Results in decreased HR and increased PR interval

Treats SVT. Carvedilol reduces mortality in CHF (unique in that it blocks beta1, beta2, and alpha1)

Toxicity: Metoprolol can cause dyslipidemia. Propanolol can exacerbate vasospasm in Prinzmetal angina. Treat overdose with glucagon.

Question 18

Amiodarone, Ibutilide, Dofetilide, Sotalol

Answer 18

Class 3 antiarrhythmics - K+ channel blockers that lengthen AP, increase QT interval (like class Ia antiarrhythmics)

Atrial fibrillation, atrial flutter

Amiodarone and sotalol also treat VT

Toxicity: sotalol and ibutilide can cause torsades

Question 19

Amiodarone toxicity

Answer 19

Side effects may include pulmonary fibrosis, hepatotoxicity, hypothryoidism/hyperthryoidism, corneal deposits, blue/gray skin deposits, neurologic effects, constipation, CV effects

Unlike other Class III and Class 1A antiarrhythmics, amiodarone does not increase risk of torsades

Always check PFTs, LFTs, TFTs

Question 20

Verapamil, diltiazem

Answer 20

Class 4 antiarrhythmics - non-dihydropyridine calcium channel blockers; decrease conduction velocity and increase PR interval

Prevents nodal arrhytmias (SVT) and used as rate control in A-fib

Question 21

Adenosine

Answer 21

Hyperpolarizes the cell by expelling K+. Acts on phase 4 of the nodal cell action potential to reduce rate of spontaneous depolarization in cardiac pacemaker cells. Used to diagnose/abolish SVTs

Blocked by theophylline and caffeine

Question 22

Magnesium as CV treatment

Answer 22

Used to treat torsades de points and digoxin toxicity

Question 23

Cilostazol

Answer 23

Phosphodiesterase inhibitor (PDE3) with therapeutic focus on increasing cAMP, which directly inhibits platelet aggregation. Also act as a vasodilator.

Treats intermittent claudication

Toxicity: headache, diarrhea, increased HR

Question 24

Captopril, enalapril, lisinopril

Answer 24

ACE inhibitors

Prevent activation of angiotensin II –> vasodilation, decreased filtration fraction, decreased aldosterone, decreased ADH

Prevents inactivation of bradykinin (angioedema, cough), unlike Angiotensin II receptor blockers

Treats HTN, CHF, proteinuria, diabetic nephropathy

Contrindications: C1 esterase inhibitor deficiency (angioedema), pregnancy (fetal renal malformations), bilateral renal artery stenosis (renal failure)