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?

25
What do fibrates decrease?
TG!!
26
Mechanism of fibrates?
Activates PPAR to induce HDL synthesis upregulates LPL
27
AE of fibrantes?
myopathy and cholesterol gallstones
28
Mechanism of niacin?
inhibits lipolysis in adipose tissue and reduces hepatic VLDL synthesis
29
What are the main AE of digoxin *cardiac glycosides)?
Cholinergic (N/V/D, blurry yellow vision), arrhythmias, AV block Hyperkalemia
30
What can predispose to digoxin toxicity?
renal failure, hypokalemia, verapamil, amiodarone, quinidine
31
Why is hypokalemia a risk factor for digoxin toxicitity?
Because K+ and digoxin both bind the same spot...so when there is low K+ digoxin can bind more
32
What is the treatment for digoxin toxicity?
Slowly normalize K+, cardiac pacer, antidigoxin Fab fragments, Mg2+
33
Name 2 class IIa antiarrhythmics?
quinidine and procainamide
34
What are 3 major AEs of quinidine and procainamide?
1- SLE like (P) 2- cinchonism (Q) 3- TdP (increased QT interval)
35
What is quinidine and procainamide used for?
Atrial and ventricular arrhythmias (SVT and VT)
36
Name 2 class IIb antiarrhythmics?
Lidocaine and mexiletine Phenytoin
37
Use of lidocaine and mexiletine?
acyte ventricular arrhythmias, digitalis induced arrhythmias POST MI!!
38
What type of tissue does lidocaine and mexiletine preferrentially affect?
preferentially affects ischemic or depolarizated purkinje and ventricular tissue
39
Name 2 class Ic antiarrhythmics?
Flecainde and propafenone
40
AE of flecainide and propafenone?
Arrhythmia!
41
Mechanism by which class II antiarrhymics work?
Beta blockers--> decreased SA and AV node activity by decreasee cAMP and decrease Ca currents
42
Name the class III antiarrhythmics (K channel blockers)?
Amiodarone, Sotalol
43
Use of amiodarone and sotalol?
Atrial fibrillation and atrial flutter Ventricular tachycardia
44
AE of sotalol?
TdP, excessive beta blockade
45
AE of amiodarone?
Pulmonary fibrosis Hepatotoxicity Hypothyroidism/ hyperthyroidism Corenal deposits Blue/ gray skin
46
Problem with amiodarone?
Extensive tissue binding....LONG half life
47
Name the class IV antiarrhythmics?
Verapamil and diltiazem
48
Use of verapamil and diltiazem?
prevention of nodal arrhythmias, and rate control in a fib
49
DOC for diagnosing and abolishing SVT?
adenosine
50
Use of Mg2+?
Effective in TdP and Digoxin toxicity