Cardiovascular Flashcards
Which drug has this MOA?
Drug x stimulates alpha-2 receptors in the brain stem resulting in reduced sympathetic outflow: reduced NE, other neurotransmitters, resulting in decr in vasoconstriction and cardiac output and heart rate. This drug does not alter normal hemodynamic response to exercise at recommended doses.
A) Clonidine
B) Atenolol
C) Valsartan
D) hydrochlorothiazide
A) Clonidine
Which drug competitively blocks Beta1 receptors without an effect on Beta2 receptors. It blocks the sympathetic NS catecholamines (NE and E), resulting in reduced renin and aldosterone release and fluid balance. This leads to reduced resting and exercise-induced heart rate and myocardial contractility via reduced velocity of impulse conduction through AV node.
A) Propanolol
B) Atenolol
C) Valsartan
D) Digoxin
B) Atenolol
Drug x has a positive inotropic activity. N+, K+ -ATPase inhibition prevents K+ being pumped into the cell, and Na+ out of the cell, resulting in increased intracellular Na+ suppressing Na+-Ca2+ exchanger, leading to decreased Na+ influx and Ca2+ efflux, where Ca2+ accumulating inside the cell (enhancing contractility). This cardiac glycoside increases parasympathetic outflow at SA and AV nodes, leading to decr heart rate
A) Valsartan
B) Gemfibrozil
C) Digoxin
D) Clonidine
C) Digoxin
Drug x blocks angiotensin II receptors, preventing aldosterone production, decreasing peripheral vascular resistance and effective circulating volume in the body.
A) Valsartan
B) Lisinopril
C) Spironolactone
D) Furosemide
A) Valsartan (ARB)
Drug x competitively inhibits HMG-CoA reductase (catalyzed first step in cholesterol synthesis in liver, converts HMG-CoA –> mevalonic acid). Causes increase in [LDL receptors] on hepatocytes (end result: incr HDL-C, decr LDL-C, decr total cholesterol, decr TGs)
A) Furosemide
B) Amiodarone
C) Gemfibrozil
D) Atorvastatin
D) Atorvastatin
Drug x blocks K+, Na+, Ca2+ channels and adrenergic beta-receptors; prolongs cardiac repolarization: increases refractory period of atrial and ventricular tissue; slows heart rate; increases PR and QT intervals.
A) Spironolactone
B) Atenolol
C) Amiodarone
D) Clonidine
C) Amiodarone
Drug x is converted to nitric oxide by vascular endothelium. Which second messenger system does drug x use?
A) tyrosine kinase; adenylate cyclase, cAMP
B) IP3, DAG
C) guanylate cyclase, cGMP
Nitroglycerin; guanylate cyclase, cGMP
GC incr cGMP, which decr intracellular calcium, resulting in relaxation of vascular smooth muscle.
Drug x stimulates lipoprotein lipase, an enzyme that breaks down triglycerides into VLDL and chylomicrons, which are then removed from circulation. This drug has also been implicated in decreasing hepatic cholesterol biosynthesis
A) Spironolactone
B) Atrovostatin
C) Valsartan
D) Gemfibrozil
D) Gemfibrozil
Drug x competitively blocks Beta1 and Beta2 receptors, decreasing heart rate and contractility, and increasing respiratory smooth muscle resulting in bronchoconstriction, respectively.
A) Lisinopril
B) Propanolol
C) Atenolol
D) Valsartan
B) Propanolol
Drug x competitively inhibits Angiotensin converting enzyme (ACE) which converts angiotensin 1 to Ang 2 (potent vasoconstrictor). This increases plasma renin activity and reduces aldosterone secretion.
A) Spironolactone
B) Lisinopril
C) Atenolol
D) Valsartan
B) Lisinopril
Drug x inhibits reabsorption of sodium and chloride (in the medullary portion of ascending loop of Henle), causing excretion of water, calcium, magnesium, sodium, chloride, potassium, ammonia: while uric acid excretion is reduced. This increases plasma renin, secondary hyperaldosteronism may result. Reduced BP in hypertensive and normotensives
A) Hydrochlorothiazide
B) Furosemide
C) Spironolactone
D) Valsartan
B) Furosemide
Drug x blocks voltage-gated calcium channels of cardiac and vascular smooth muscle, inhibiting flow of calcium into cells. Result: decr muscle contraction with resulting peripheral vasodilation and Decr myocardial contractility
A) Valsartan
B) Digoxin
C) Amlodipine
D) Furosemide
C) Amlodipine (CCB)
Drug x inhibits NaCl transporter in distal tubule; increases excretion of Na+, K+, Cl-; decreases Ca2+ excretion in persons with Ca2+ type kidney stones.
A) Furosemide
B) Hydrochlorothiazide
C) Amlodipine
D) Atrovastatin
B) Hydrochlorothiazide
Drug x adverse effects include: dizziness (most common); H/A, fatigue, cough, URTI; dry persistent and nonproductive cough; rash; chest pain; orthostatic effects; hypotension, hyperkalemia; increased serum creatinine (Decr GFR); teratogenic (may cause fetal renal damage if used in pregnancy). Potentially fatal: severe hypotension, angioedema, liver failure.
A) Amlodipine
B) Atenolol
C) Clondine
D) Lisinopril/Captopril
D) Lisinopril/Captopril
Which drug is indicated for clinical use in: Hypertension, CHF, Edema (Dt CHF/hepatic cirrhosis esp with high levels of aldosterone), Low plasma levels of potassium (hypokalemia), primary hyperaldosteronism.
A) Valsartan
B) Atorvastatin
C) Spironolactone
D) Gemfibrozil
C) Spironolactone
HELP fight against aldosterone
Which drug is indicated for clinical use in: hypertension, Prinzmetal’s angina, stable angina. Off-label use: Raynaud phenomenon.
A) Amlodipine
B) Atenolol
C) Propanolol
D) Lisinopril
A) Amlodipine