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Step 1 Review > Cardio Pharm High Yield > Flashcards

Cardio Pharm High Yield Flashcards

1
Q

4 types of drugs used to HTN in heart failure?

A

Diuretics

ACEi/ ARB

Beta bloclers

Aldosterone antagonisits

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2
Q

4 drugs to be used in HTN with diabetes mellitus?

A

ACEi/ ARB

Ca channel blocker

Thiazide diurects

Beta blocers

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3
Q

4 Drugs to be used in HTN of pregnancy?

A

Hydralazine

Labetalol

Methyldopa

Nifedipine

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4
Q

Name the major dihydropyridine Calcium channel blocker?

A

Amlodipine, nifedipine

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5
Q

Name the 2 non-dihydropyridine CCBs?

A

Diltiazem and verapamil

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6
Q

Mechanism of CCBs?

A

decreased contractility of the heart

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7
Q

Treatment for subarachnoid hemorrhage?

A

nimodipine (CCB)

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8
Q

3 main uses of dihydropyridine CCBs?

A

HTN, angina, Raynaud

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9
Q

3 Major uses of nondihydropridine CCBs?

A

HTN, angina, A. fib/ flutter

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10
Q

AE of amlodipine?

A

gingival hyperplasia

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11
Q

AE of nondihydropiridine CCBs?

A

Constipation, AV block, cardiac depression

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12
Q

Mechanism of Hydralazine?

A

increased cGMP to vasodilate (arterioles> veins) leading to afterload reduction

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13
Q

AE of hydralazine?

A

SLE like syndrome, fluid retention, compensatory tachycardia

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14
Q

Mechanism of nitroprusside?

A

increased cGMP to vasodilate (arterioles + veins) leading to afterload reduction

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15
Q

Main AE of nitroprusside treatment?

A

cyanide toxicity

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16
Q

2 drugs used in hypertensive emergencies?

A

Nitroprusside and fenoldapam

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17
Q

How do nitrates work?

A

vasodilation by increased NO–> increase in cGMP and smooth muscle relaxation

dilates veins&raquo_space;> arteries (decreased preload)

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18
Q

“monday disease”

A

development of tolerance to NO during the workweek due to industrial exposure and then loss of tolerance over the weekend

Tachycardia, dizziness, headache upon reesposure

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19
Q

Name 3 endogenous substances that increase release of NO?

A

ACh, bradykinin, 5HT

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20
Q

Name 3 endogenous substances that increase release of NO?

A

ACh, bradykinin, 5HT

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21
Q

Mechanism of cholestrymine?

A

Bile acid resins:

prevent intestinal reabsorption of bile acids (so liver must make more cholesterol)

22
Q

What is the mechanism of ezetimibe?

A

prevent cholesterol absorption at small intestine brush border

23
Q

AE of ezetimibe?

A

increased LFTs and diarrhea

24
Q

what does ezetimibe decrease?

A

LDL

25
Q

What do fibrates decrease?

A

TG!!

26
Q

Mechanism of fibrates?

A

Activates PPAR to induce HDL synthesis

upregulates LPL

27
Q

AE of fibrantes?

A

myopathy and cholesterol gallstones

28
Q

Mechanism of niacin?

A

inhibits lipolysis in adipose tissue and reduces hepatic VLDL synthesis

29
Q

What are the main AE of digoxin *cardiac glycosides)?

A

Cholinergic (N/V/D, blurry yellow vision), arrhythmias, AV block

Hyperkalemia

30
Q

What can predispose to digoxin toxicity?

A

renal failure, hypokalemia, verapamil, amiodarone, quinidine

31
Q

Why is hypokalemia a risk factor for digoxin toxicitity?

A

Because K+ and digoxin both bind the same spot…so when there is low K+ digoxin can bind more

32
Q

What is the treatment for digoxin toxicity?

A

Slowly normalize K+, cardiac pacer, antidigoxin Fab fragments, Mg2+

33
Q

Name 2 class IIa antiarrhythmics?

A

quinidine and procainamide

34
Q

What are 3 major AEs of quinidine and procainamide?

A

1- SLE like (P)

2- cinchonism (Q)

3- TdP (increased QT interval)

35
Q

What is quinidine and procainamide used for?

A

Atrial and ventricular arrhythmias (SVT and VT)

36
Q

Name 2 class IIb antiarrhythmics?

A

Lidocaine and mexiletine

Phenytoin

37
Q

Use of lidocaine and mexiletine?

A

acyte ventricular arrhythmias, digitalis induced arrhythmias

POST MI!!

38
Q

What type of tissue does lidocaine and mexiletine preferrentially affect?

A

preferentially affects ischemic or depolarizated purkinje and ventricular tissue

39
Q

Name 2 class Ic antiarrhythmics?

A

Flecainde and propafenone

40
Q

AE of flecainide and propafenone?

A

Arrhythmia!

41
Q

Mechanism by which class II antiarrhymics work?

A

Beta blockers–> decreased SA and AV node activity by decreasee cAMP and decrease Ca currents

42
Q

Name the class III antiarrhythmics (K channel blockers)?

A

Amiodarone, Sotalol

43
Q

Use of amiodarone and sotalol?

A

Atrial fibrillation and atrial flutter

Ventricular tachycardia

44
Q

AE of sotalol?

A

TdP, excessive beta blockade

45
Q

AE of amiodarone?

A

Pulmonary fibrosis Hepatotoxicity
Hypothyroidism/ hyperthyroidism
Corenal deposits
Blue/ gray skin

46
Q

Problem with amiodarone?

A

Extensive tissue binding….LONG half life

47
Q

Name the class IV antiarrhythmics?

A

Verapamil and diltiazem

48
Q

Use of verapamil and diltiazem?

A

prevention of nodal arrhythmias, and rate control in a fib

49
Q

DOC for diagnosing and abolishing SVT?

A

adenosine

50
Q

Use of Mg2+?

A

Effective in TdP and Digoxin toxicity

Step 1 Review (62 decks)

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