Cardiac Drugs

Question 1

How to identify dihydropyridine calcium channel blockers

Answer 1

-pines

Question 2

-pines
MOA
TU
Tox

Answer 2

MOA: Ca2+ channel blockers, dihydropyridines
TU: HTN, angina, Raynaud
Tox: peripheral edema, flushing, dizziness, gingival hyperplasia

Question 3

Diltiazem
MOA
TU
Toxp

Answer 3

diltiazem
MOA: Ca2+ channel blocker, non-dihydropyridine
TU: HTN, angina, A-fib, A-flutter
Tox: cardiac depression, AV block, hyperprolactinemia, constipation

Question 4

Verapamil
MOA
TU
Tox

Answer 4

Verapamil
MOA: Ca2+ channel blocker, non-dihydropyridine
TU: HTN, angina, A-fib, A-flutter
Tox: cardiac depression, AV block, hyperprolactinemia, constipation

Question 5

Hydralizine
MOA
TU
Tox

Answer 5

hydralizine
MOA: increase cGMP –> sm muscle relaxation, dilateds arterioles > veins, afterload reduction
TU: severe acute HTN, HF, safe during pregnancy, admin w/ β-blocker to prevent reflex tachycardia
Tox: compensatory tachycardia, fluid retention, headache, angina, Lupus-like syndrome

Question 6

Nitrates (nitro, isosorbide dinitrate, isosorbide mononitrate)
MOA
TU
Tox

Answer 6

MOA: increased cGMP in sm muscle -> vasodilation in veins > arterioles
TU: angina, acute coronary syndrome, pulmonary edema
Tox: reflex tachycardia (Tx: β-blockers), flushing, headache, “Monday disease” in workers exposed

Question 7

Ranolazine
MOA
TU
Tox

Answer 7

ranolazine
MOA: inhibits late phase of Na+ current thereby reducing diastolic wall tension and oxygen consumption, does not affect heart rate or contractility
TU: refractory angina
Tox: constipation, dizziness, headache, nausea, long QT

Question 8

Statins
MOA
TU
Tox

Answer 8

MOA: inhibit HMG-CoA reductase
TU: CAD
Tox: hepatotoxicity, myopathy esp w/ fibrates or niacin
**rhabdomyolysis

Question 9

Bile acid resins (cholestyramines, solestipol, colesevelam)
MOA
TU
Tox

Answer 9

MOA: prevent intestinal absorption of bile acids
TU: hypercholesterolemia
Tox: GI, decreased absorption of other drugs and fat-soluble vitamins

Question 10

Ezetimibe
MOA
TU
Tox

Answer 10

ezetimibe
MOA: prevent cholesterol absorption at small intestine brush border
TU: hypercholesterolemia
Tox: rare increase in LFTs, diarrhea

Question 11

Fibrates (gemfibrozil, benzafibrate, fenofibrate)
MOA
TU
Tox

Answer 11

fibrates
MOA: upregulate LPL –> increase TG clearance, activates PPAR-α to induce HDL synthesis
TU: hypercholesterolemia
Tox: myopathy (esp w/ statins), cholesterol gallstones

Question 12

Niacin
MOA
TU
Tox

Answer 12

niacin
MOA: inhibits lipolysis ie hormone-sensitive lipase in adipose, reduces hepatic VLDL synthesis
TU: hyperholesterolemia
Tox: red, flushed face, hyperglycemia, hyperuricemia

Question 13

Digoxin
MOA
TU
Tox

Answer 13

MOA: direct inhibition of Na+/K+ ATPase, indirect inhibition of Na+/Ca2+ exchanger, increased Ca2+ intracellular –> positive ionotropy (force of contraction), stimulates vagus nerve to decrease HR
TU: HF, A-fib (decrease conduction at AV node and depression of SA node)
Tox: cholinergic (N/V, diarrhea, blurry yellow vision, arrhythmias, AV block), hyperkalemia (means bad prognosis)

Question 14

Adenosine
MOA
TU
Tox

Answer 14

MOA: increased K+ out of cells, hyperpolarizes cell during ICa
TU: SVT Dx and Tx
Tox: effects blocked by caffeine and theophylline (both are adenosine receptor antagonists), flushing, hypotension, chest pain, sense of impending doom, bronchospasm

Question 15

Mg2+

TU

Answer 15

TU: tosades, digoxin toxicity