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First Aid Cardiovascular Chapter > Cardio Pharmacology I > Flashcards

Cardio Pharmacology I Flashcards

1
Q

B-blockers must be used with caution in what and are contraindicated in what?

A

decompensated heart failure

contraindicated in cardiogenic shock

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2
Q

what drugs are protective against diabetic nephropathy?

A

ACE inhibitors/ARBs

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3
Q

What drugs can be used for hypertension in pregnancy? (4)

A

Hydralazine, labetalol, methyldopa, nifedipine

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4
Q

Amlodipine and the other ‘dipines’ have what mechanism of action?

A

Block voltage-dependent L-type calcium channels of cardiac and smooth muscle -> decreasing muscle contractility

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5
Q

difference between dihydropyridines and non-dihydropyridines?

A

dihydropyridines act on vascular smooth muscle

non-dihydropyridines act on heart

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6
Q

name the non-dihydropyridines

A

diltiazem, verapamil

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7
Q

amlodipine = nifedipine > diltiazem > verapamil in regards to what function?

A

action on vascular smooth muscle

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8
Q

verapamil > diltiazem > amlodipine = nifedipine in regards to what function?

A

action on heart

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9
Q

which calcium channel blocker can be used for subarachnoid hemorrhage (prevents cerebral vasospasm)?

A

Nimodipine

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10
Q

which calcium channel blocker can be used for hypertensive urgency or emergency?

A

Clevidipine

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11
Q

Dihydropyridines can be use for what indications? (3)

A

hypertension, angina (including Prinzmetal), Raynaud phenomenon.

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12
Q

which dihydropyridine cannot be used for their normal indications?

A

Nimodipine

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13
Q

Non-dihydropyridines can be used for what indications? (3)

A

hypertension, angina, atrial fibrillation/flutter.

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14
Q

Adverse effects of cardiac depression, AV block, hyperprolactinemia, constipation are associated with what class of drugs?

A

Non-dihydropyridine CCB

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15
Q

Adverse effects of peripheral edema, ushing, dizziness, gingival hyperplasia are associated with what class of drugs?

A

Dihydropyridine CCB

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16
Q

Mechanism of Hydralazine?

A

increases cGMP -> smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction.

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17
Q

Why is hydralazine frequently co-administered with a B-blocker?

A

to prevent reflex tachycardia.

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18
Q

What are the indications for Hydralazine? (3)

A 
Severe hypertension (particularly acute), HF. 
hypertension in pregnancy.
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19
Q

What do you coadminister hydralazine with for HF?

A

organic nitrates

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20
Q

What are the contraindications for Hydralazine and why? (2)

A

Angina and CAD

compensatory tachycardia

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21
Q

What cardiac drug is known to cause drug-induced Lupus like syndrome?

A

Hydralazine

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22
Q

clevidipine, fenoldopam, labetalol, nicardipine, nitroprusside can all be used in what scenario?

A

Hypertensive Emergency

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23
Q

Mechanism of Nitroprusside?

A

Short acting; cGMP via direct release of NO

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24
Q

Adverse effect of Nitroprusside?

A

Can cause cyanide toxicity (releases cyanide)

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25
Q

What cardiac drug used in hypertensive emergency is a D1 receptor agonist?

A

Fenoldopam

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26
Q

What cardiac drug is used postoperatively as an antihypertensive?

A

Fenoldopam

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27
Q

What is the effect of Fenoldopam on the body?

A

coronary, peripheral, renal, and splanchnic vasodilation.

decreases BP and increases natriuresis.

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28
Q

Mechanism of Nitrates?

A

Vasodilator by increasing NO in vascular smooth muscle -> increase in cGMP and smooth muscle relaxation.
Dilate veins&raquo_space; arteries.
decreases preload.

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29
Q

What are the indications for Nitrates?

A

Angina, acute coronary syndrome, pulmonary edema.

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30
Q

What is Monday disease and it occurs with what drug class?

A

Nitrates
industrial exposure: development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend -> tachycardia, dizziness, headache upon reexposure.

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31
Q

What is the goal of anti-anginal therapy?

A

reduction of myocardial O2 consumption (MVO2)

32
Q

What are the determinants of MVO2 targeted in anti-anginal therapy? (4)

A

end-diastolic volume, BP, HR, contractility

33
Q

What B-blockers are contraindicated in angina?

A

Pindolol and acebutolol—partial β-agonists contraindicated in angina.

34
Q

What drug Inhibits the late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption?

A

Ranolazine

35
Q

How does Ranolazine effect heart rate and contractility?

A

Does not affect heart rate or contractility

36
Q

What drug do you use for angina refractory to all other medications?

A

Ranolazine

37
Q

What drug has the side effects of constipation, dizziness, headache, nausea, QT prolongation?

A

Ranolazine

38
Q

Mechanism of Statins?

A

Inhibit conversion of HMG- CoA to mevalonate, a cholesterol precursor

39
Q

Statins decrease mortality in what patients?

A

CAD patients

40
Q

Toxicity of Statins?

A

Hepatotoxicity/Hepatitis (increases LFTs), myopathy

41
Q

when are statins more susceptible to causing myopathy?

A

especially when used with fibrates or niacin

42
Q

What enzyme do statins inhibit?

A

HMG-CoA Reductase

43
Q

How do statins change LDL, HDL, and TG levels?

A

decreases LDL a lot
increases HDL
decreases TG

44
Q

Name the bile acid resins (3)

A

Cholestyramine, colestipol, colesnvelam

start with “Coles”

45
Q

What drugs prevent intestinal reabsorption of bile acids making the liver use cholesterol to make more?

A

Cholestyramine, colestipol, colesnvelam

Bile acid resins

46
Q

What drugs decrease the absorption of other drugs and decrease the absorption of fat-soluble vitamins?

A

Cholestyramine, colestipol, colesnvelam

Bile acid resins

47
Q

How do bile acid resins change LDL, HDL, and TG levels?

A

decreases LDL a lot
slightly increases HDL
slightly increases TG

48
Q

What drug prevents cholesterol absorption at small intestine brush border?

A

Ezetimibe

49
Q

What adverse effects does Ezetimibe have?

A

Rare LFTs, diarrhea

50
Q

How does Ezetimibe change LDL, HDL, and TG levels?

A

decreases LDL a lot

no change in HDL and TG

51
Q

Name the Fibrates (3)

A

Gemfibrozil, bezafibrate, fenofibrate

“fibr” in the middle

52
Q

What group of drugs upregulate LPL -> increases TG clearance?

A

Fibrates

53
Q

What group of drugs activates PPAR-α to induce HDL synthesis?

A

Fibrates

54
Q

What are the adverse effects of Fibrates?

A

Myopathy (risk with statins), cholesterol gallstones, hepatitis

55
Q

How do Fibrates change LDL, HDL, and TG levels?

A

decrease LDL
increase HDL
decrease TG a lot

56
Q

What vitamin is Niacin?

A

B3

57
Q

Mechanism of Niacin (B3)? (2)

A

Inhibits lipolysis (hormone- sensitive lipase) in adipose tissue; reduces hepatic VLDL synthesis

58
Q

What lipid lowering drug causes a red, flushed face?

A

Niacin

59
Q

WHICH adverse effect OF WHAT lipid lowering drug is decreased by NSAIDs or long-term use?

A

red, flushed face adverse effect of Niacin (B3)

60
Q

What lipid lowering agent causes hyperglycemia and hyperuricemia?

A

Niacin (B3)

61
Q

How does Niacin change LDL, HDL, and TG levels?

A

decreases LDL a lot
increases HDL a lot
decreases TG

62
Q

Digoxin directly inhibits what?

A

Na+/K+ ATPase

63
Q

Digoxin indirectly inhibits what?

A

Na+/Ca++ exchanger

64
Q

What is the net effect of digoxin’s inhibition of the transporters?

A

increased Ca++ concentration inside the myocyte -> positive inotropy (contractility)

65
Q

How does Digoxin increase cardiac contractility?

detailed explanation

A

by inhibition of the gradient formed by the Na/K ATPase, Ca++ is no longer released from cell -> accumulation of Ca++. This causes the SR to have Ca++-dependent Ca++ release, which then increases Troponin C binding Ca++ -> increased cardiac contraction

66
Q

Why does Digoxin cause a decrease in HR?

A

stimulates Vagus Nerve

67
Q

indication for Digoxin use?

A

HF and atrial fibrillation

68
Q

Explain why Digoxin works for its two indications

A

HF - increases contractility, helps the heart pump

Atrial Fib - decreases conduction at AV node and depresses SA node

69
Q

what type of adverse reactions are seen with Digoxin?

A

cholinergic - due to vagus nerve stimulation

70
Q

What odd side effect occurs with digoxin? (think Van Gogh)

A

blurry yellow vision

71
Q

What electrolyte disorder can be caused by digoxin?

A

Can lead to hyperkalemia, which indicates poor prognosis.

72
Q

Why does renal failure predispose someone to digoxin toxicity?

A

decreases excretion

73
Q

Why does hypokalemia predispose someone to digoxin toxicity?

A

no competition for digoxin binding at K+-binding site on Na+/K+ ATPase

74
Q

What drugs that displace digoxin from tissue-binding sites, and decreased clearance

A

verapamil, amiodarone, quinidine

75
Q

What are the antidotes for digoxin toxicity? (4)

A

Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+

First Aid Cardiovascular Chapter (6 decks)

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