PHARM EXAM QUESTIONS WITH 100%
CORRECT ANSWERS [GRADED A+]
Nitrates (mechanism, use, toxicity) - ✔✔Cause NO release -> vasodilation
(veins >>> arteries); used in angina; fast tolerance, hypotension, flushing,
headache
Adverse effects of statins - ✔✔Hepatoxicity and muscle breakdown
Niacin (mechanism, use, toxicity) - ✔✔Inhibits lipolysis and reduces VLDL
secretion, lowering LDL and raising HDL; hyperlipidemia; flushing and
hyperuricemia
Cholestyramine, colestipol, colesevelam (mechanism, use, toxicity) -
✔✔Inhibits reabsorption of bile acids -> lower LDL with slight increase in
HDL; unpigmented gallbladder stones and malabsorption
©morren2025/2026.Year published 2026.
,Ezetimibe - ✔✔Prevents cholesterol reabsorption -> lower LDL
Fibrates (gemfibrozil + -fibrates) (mechanism, use, toxicity) -
✔✔Upregulates LPL -> lower triglycerides, slightly inc. HDL and slightly
dec. LDL; myositis and hepatoxicity
Digoxin and digitoxin (mechanism, use, toxicity) - ✔✔Inhibits Na/K
ATPase -> indirectly inhibits Na/Ca exchanger -> inc. calcium levels -> inc.
contractility; stimulates the vagus; causes cholinergic symptoms and
hyperkalemia
Class 1A antiarrhythmics - ✔✔Quinidine, procainamide, and
disopyramide; inc. AP duration and QT interval; can cause torsades de
pointes, cinchonism (qunidine), procainamide (drug-induced lupus)
Class 1B antiarrhythmics - ✔✔Lidocaine, mexiletine, and tocainide; dec.
AP duration especially in depolarized/ischemia tissue; best following MI
©morren2025/2026.Year published 2026.
,Class 1C antiarrhythmics - ✔✔Flecainide, propafenone; no effect on AP,
used in ventricular tachycardias; do not use post-MI due to risk for
arrhythmias
Class 1 antiarrhythmics (general mechanism and toxicity) - ✔✔Blocks Na
channels, decreasing the slope of phase 0 depolarization; toxicity
exacerbated by hyperkalemia
Class 2 antiarrhythmics - ✔✔Beta-blockers; reduces cAMP, slowing SA
and AV node activity, increases PR interval; adverse effects include
impotence, asthma exacerbation, sedation
Class 3 antiarrhythmics - ✔✔Amiodarone, ibutilide, dofetilide, sotalol; K
channel blockers; inc. AP duration and QT interval
Toxicity of amiodarone - ✔✔Pulmonary fibrosis, hepatotoxicity, thyroid
dysfunction
©morren2025/2026.Year published 2026.
, Class 4 antiarrhythmics - ✔✔Ca channel blockers; verapamil and
diltiazem; dec. conduction velocity and inc. PR interval; cause constipation,
flushing, and edema
Adeosine (mechanism, use, toxicity) - ✔✔Inc. K efflux, hyperpolarizing the
cell; used in supraventricular tachycardias; can cause flushing,
hypotension, and chest pain
Magnseium (mechanism, use, toxicity) - ✔✔Used in torsades de pointes
and digoxin toxicity
Treatment for prolactinoma - ✔✔Bromocriptine or cabergoline (dopamine
agonists)
Treatment of secondary hyperaldosteronism - ✔✔Spironolactone (or other
AT2 antagonist)
Treatment of carcinoid syndrome - ✔✔Octreotide (somatostatin
analogues)
©morren2025/2026.Year published 2026.
CORRECT ANSWERS [GRADED A+]
Nitrates (mechanism, use, toxicity) - ✔✔Cause NO release -> vasodilation
(veins >>> arteries); used in angina; fast tolerance, hypotension, flushing,
headache
Adverse effects of statins - ✔✔Hepatoxicity and muscle breakdown
Niacin (mechanism, use, toxicity) - ✔✔Inhibits lipolysis and reduces VLDL
secretion, lowering LDL and raising HDL; hyperlipidemia; flushing and
hyperuricemia
Cholestyramine, colestipol, colesevelam (mechanism, use, toxicity) -
✔✔Inhibits reabsorption of bile acids -> lower LDL with slight increase in
HDL; unpigmented gallbladder stones and malabsorption
©morren2025/2026.Year published 2026.
,Ezetimibe - ✔✔Prevents cholesterol reabsorption -> lower LDL
Fibrates (gemfibrozil + -fibrates) (mechanism, use, toxicity) -
✔✔Upregulates LPL -> lower triglycerides, slightly inc. HDL and slightly
dec. LDL; myositis and hepatoxicity
Digoxin and digitoxin (mechanism, use, toxicity) - ✔✔Inhibits Na/K
ATPase -> indirectly inhibits Na/Ca exchanger -> inc. calcium levels -> inc.
contractility; stimulates the vagus; causes cholinergic symptoms and
hyperkalemia
Class 1A antiarrhythmics - ✔✔Quinidine, procainamide, and
disopyramide; inc. AP duration and QT interval; can cause torsades de
pointes, cinchonism (qunidine), procainamide (drug-induced lupus)
Class 1B antiarrhythmics - ✔✔Lidocaine, mexiletine, and tocainide; dec.
AP duration especially in depolarized/ischemia tissue; best following MI
©morren2025/2026.Year published 2026.
,Class 1C antiarrhythmics - ✔✔Flecainide, propafenone; no effect on AP,
used in ventricular tachycardias; do not use post-MI due to risk for
arrhythmias
Class 1 antiarrhythmics (general mechanism and toxicity) - ✔✔Blocks Na
channels, decreasing the slope of phase 0 depolarization; toxicity
exacerbated by hyperkalemia
Class 2 antiarrhythmics - ✔✔Beta-blockers; reduces cAMP, slowing SA
and AV node activity, increases PR interval; adverse effects include
impotence, asthma exacerbation, sedation
Class 3 antiarrhythmics - ✔✔Amiodarone, ibutilide, dofetilide, sotalol; K
channel blockers; inc. AP duration and QT interval
Toxicity of amiodarone - ✔✔Pulmonary fibrosis, hepatotoxicity, thyroid
dysfunction
©morren2025/2026.Year published 2026.
, Class 4 antiarrhythmics - ✔✔Ca channel blockers; verapamil and
diltiazem; dec. conduction velocity and inc. PR interval; cause constipation,
flushing, and edema
Adeosine (mechanism, use, toxicity) - ✔✔Inc. K efflux, hyperpolarizing the
cell; used in supraventricular tachycardias; can cause flushing,
hypotension, and chest pain
Magnseium (mechanism, use, toxicity) - ✔✔Used in torsades de pointes
and digoxin toxicity
Treatment for prolactinoma - ✔✔Bromocriptine or cabergoline (dopamine
agonists)
Treatment of secondary hyperaldosteronism - ✔✔Spironolactone (or other
AT2 antagonist)
Treatment of carcinoid syndrome - ✔✔Octreotide (somatostatin
analogues)
©morren2025/2026.Year published 2026.
