Cardiac Pharm from FA (and UWorld questions) Flashcards Preview

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Flashcards in Cardiac Pharm from FA (and UWorld questions) Deck (102):
1

Digoxin: what does it directly inhibit?

what does this cause?

cardiac myocyte Na/K ATPase.

causes increased intracellular Na, which causes increased intracellular Ca due to loss of Na/Ca co-transporter activity.

2

generally, what are the 2 effects of Digoxin?

-increases intracellular Ca -> increases inotropy

-stimulates vagus nerve -> decreases HR

3

2 clinical uses for digoxin?

-CHF (because it will increase contractility)

-afib (because it will decrease conduction at the AV node and depress the SA node) -> incr diastolic filling time.

4

digoxin - toxicity?

Cholinergic toxocity ie nausea, vomiting, diarrhea, blurry yellow vision/yellow-green halos (think Van Gogh)

5

digoxin: changes to ECG?

increase PR, decrease QT, ST scooping, T wave inversion, arrythmia, AV block

6

Digoxin: what factors predispose patients to toxicity?

-renal failure

-hypokalemia (K and Dig compete for the same binding site)

-verapamil (Ca channel blocker)

-amiodarone (K channel blocker)

-quinidine (decreased digoxin clearance; displaces digoxin from tissue-binding sites)

7

Digoxin: antidote?

what not to do?

-slowly normalize K levels

-cardiac pacer

-anti-digoxin Fab fragments

-Mg2+

-DO NOT give calcium gluconate to patients with hyperK in setting of digoxin toxicity

8

Digoxin: class?

cardiac glycoside

aka digitalis

found in Foxglove plant in so many suburban gardens.

9

Big picture: what are the types of anti-arrhythmic drugs? (4 classes + misc)

-Class I: Na channel blockers (IA, IB, IC)

-Class II: Beta-blockers

-Class III: K channel blockers

-Class IV: Ca channel blockers

Other: Adenosine (kicks K out of cells) and Mg2+ (for Torsades and Digoxin toxicity)

10

Which classes of anti-arrhythmics cause QT prolongation?

IA (Na blockers)

III (K blockers)

11

Of the 4 Class III (K+ channel blocking) antiarrhythmics, which one also has beta-blocking ability?

Name the 4 K blocker anti-arrhythmics

-Sotalol (causes bradycardia)

-Class III (K+ channel blockers) = Amidarone, Ibutilide, Dofetilide, Sotalol

"AIDS" (can give you Kaposi's Sarcoma --- K association to remember the AIDS anti-arrhy drugs?!?) 

12

what do beta blockers do?

slow the heart rate, lower contractility by blocking AV nodal activity.

slow Phase 4 depolarization.

13

Of the 2 Class IV antiarrhythmics, which is more cardioselective?

Verapamil is more cardioselective than Diltiazem.

(these are Ca blockers)

both will cause slight decr in BP due to some action on peripheral vasculature

14

what is the mech of action for Aspirin?

If a pt is allergic to aspirin, what is a possible alternative for a patient with angina?

Irreversibly inhibits COX1 and COX2 (by acetylation). (-->prevents synth of thromboxane A2 and prostaglandins)

Platelets can't synth new cyclo-oxygenase enzyme so effect lasts until new platelets come on the scene.

One alternative = Clopidogrel - Irreversibly blocks ADP receptors on platelets -> inhibits platelet aggregation.

Aspirin and Clopidogrel are equally effective in prevention of thrombo-embolic disease.

15

Aspirin and Clopidogrel: synergistic effect? why/not?

Yes

because they have different mechanisms.

16

if you need to restore blood flow emergently post-MI or cerebrovascular incident, what is a possible drug to use?

Streptokinase

Thrombolytic agent

17

3 types of hypertension that are treated with different drug classes?

-Primary/essential HTN

-HTN with CHF

-HTN with diabetes

18

what classes of drugs are used to treat primary/essential HTN?

diuretics, ACE inhibitors/ARBs, Ca channel blockers

19

what classes of drugs are used to treat HTN with CHF?

Diuretics, ACE inhibitors, ARBs, beta-blockers, aldosterone antagonists

20

what classes of drugs are used to treat HTN with diabetes?

ACE inhibitors/ARBs, Ca channel blockers, diuretics, beta blockers, alpha blockers

21

for HTN with CHF, what drug do we use with caution in decompensated CHF? when is this drug contraindicated?

for decompensated CHF use beta blockers cautiously

they are contraindicated with cardiogenic shock

22

what drugs are protective against diabetic nephropathy?

ACE inhibitors/ARBs

23

what class of drugs prevents remodeling of the heart that may result from chronic HTN?

ACE inhibitors

24

MOA of Ca channel blockers? effect?

 blocks voltage-dependent L type Ca channels on cardiac and smooth muscle.

effect = reduce muscle contractility

25

name the 5 Ca channel blockers

which are dihydropyridines and which are not?

Amlodipine

Nimodipine

Nifedipine

Diltiazem

Verapamil

ANN = dihydropyridines

D/V = non-dihydropyridines

26

of the Ca channel blockers, which are most effective on vascular smooth muscle?

Amlodipine and Nifedepine

27

of the Ca channel blockers, which are most effective on heart?

Verapamil, then Diltiazem (the non-dihydropyridines)

"Verapamil -> Ventricle"

28

Amlodipine and Nifedipine: Clinical use?

Ca channel blockers

Use = HTN, angina (including Prinzmetal), Raynaud's

29

Nimodipine: clinical use?

Ca channel blocker

Use = subarachnoid hemorrhage. Prevents cerebral vasospasm.

30

Diltiazem, Verapamil: clinical use?

Ca channel blockers

HTN, angina, afib/atrial flutter

31

Calcium channel blockers: tox?

Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, constipation

32

Hydralazine: class?

anti-hypertensive

33

Hydralazine: clinical use?

severe HTN, CHF.

First line for HTN with pregnancy (along with methyldopa). 

Coadministered with a beta blocker to prevent reflex tachycardia.

34

Hydralazine: tox?

compensatory tachycardia, fluid retention, nausea, HA, angina, lupus-like syndrome

35

Hydralazine: contraindication?

in angina/CAD

due to compensatory tachycardia.

36

commonly used drugs in a hypertensive emergency? (5)

-nitroprusside

-nicardipine

-clevidipine

-labetolol

-fenoldopam

37

Nitroprusside: use?

mech? tox?

Used in hypertensive emergency

Mech: increases cGMP via direct release of NO. Short-acting.

Tox = releases cyanide (CN-, binds cytochrome C oxidase and stops cellular respiration)

38

Fenoldopam: use?

mech? tox?

used in hypertensive emergency.

Mech: Dopamine D1 receptor agonist. Vasodilates coronary, peripheral, renal, splanchnics.

Decr BP and incr naturiuresis.

39

Nitroglycerin, Isosorbide dinitrate

Mech?

Vasodilation

incr NO in vascular smooth muscle -> incr cGMP -> smooth muscle relaxation.

Dilates veins >>> arteries.

Decr preload.

40

Nitroglycerin, Isosorbide dinitrate

Use?

Angina, coronary artery syndrome, pulm edema

41

what is Monday Disease?

Secondary to industrial exposure: develop tolerance for Nitroglycerin/isosorbide dinitrate during the workweek (tolerance to vasodilating action). Then lose tolerance over weekend.

Monday re-exposure results in tachycardia, dizziness, headache.

42

Nitroglycerin/isosorbide dinitrate: tox?

Monday disease

Reflex tachy, hypotension, flushing, headache

43

Revlex tachycardia due to Nitroglycerin/isosorbide dinitrate: treatment?

beta blockers

44

what is the goal of antianginal therapy?

Reduce myocardial O2 consumption by decreasing 1 or more of these:

-end-diastolic volume

-blood pressure

-HR

-contractility

45

Nitrates affect Preload or Afterload?

effect on:

EDV?

BP?

contractility?

HR?

Ejection time?

MVO2?

Nitrates affect Preload

EDV? DECR

BP? DECR

contractility? INCR (reflex)

HR? INCR (reflex)

Ejection time? DECR

MVO2? DECR

46

Beta blockers affect Preload or Afterload?

EDV? 

BP? 

contractility? 

HR?

Ejection time? 

MVO2? 

Beta blockers affect Afterload

EDV? INCR

BP? DECR

contractility? DECR

HR? DECR

Ejection time? INCR

MVO2? DECR

47

Nitrates + beta blockers together - effect on:

EDV? 

BP? 

contractility? 

HR? 

Ejection time? 

MVO2? 

EDV? no effect

BP? DECR

contractility? no effect

HR? DECR

Ejection time? no effect

MVO2? DECR A LOT

(ie everything is either decreased or no effect)

48

what are 2 partial beta agonists that are contraindicated in angina?

-Pindolol

-Acebutolol

49

Nifedipine

effect is more similar to nitrates or beta blockers?

Nitrates

50

Verapamil

effect is more similar to nitrates or beta blockers?

Beta blockers

51

5 categories of lipid-lowering agents?

-HMG-CoA reductase inhibitors

-Niacin

-Bile acid resins

-Cholesterol absorption blockers

-Fibrates

52

what are the 5 HMG-CoA reductase inhibitors listed?

(unless there are differences between them, probably just need to know -STATINS)

Lovastatin

Pravastatin

Simpastatin

Atorvastatin

Rosuvastatin

53

HMG-CoA reductase inhibitors: Mechanism of action?

Inhibit conversion of HMG-CoA to mevalonate (which is a cholesterol precursor)

(remember that HMG-CoA is kind of in the middle between Acetyl-CoA/TCA, cholesterol synth, and ketone synthesis)

54

Statins: effect on LDL? HDL? TAGs?

LDL: decrease dramatically

HDL: increase

TAGs: decrease

55

Niacin: effect on LDL? HDL? TAGs?

LDL: decr

HDL: incr (niacin = best for this)

TAGs: decr

56

Bile Acid resins: effect on LDL? HDL? TAGs?

LDL: decr

HDL: incr (slight)

TAGs: incr (slight)

57

Cholesterol absorption blockers: effect on LDL? HDL? TAGs?

LDL: decr

HDL: no effect

TAGs: no effect

58

Fibrates: effect on LDL? HDL? TAGs?

LDL: decr

HDL: incr

TAGs: decrease A LOT (best for this)

59

Statins: SEs?

-Hepatotoxicity (increases LFTs)

-Rhabdomyolysis (esp when used with fibrates and niacin)

60

Niacin: Mech?

Inhibits lipolysis in adipose tissue

Reduces hepatic VLDL synthesis

61

Niacin: SEs?

-Red flushed face (will decrease with aspirin or long term use)

-Hyperglycemia (acanthosis nigricans)

-Hyperuricemia (exacerbates gout)

62

Bile acid resins: Mech?

Prevent intestinal re-absorption of bile acids

->liver must use more cholesterol to make more

63

Bile acid resins: SEs?

Patients hate these: they taste bad and they cause GI discomfort

also decr absorption of fat-sol vitamins

64

Ezetimibe: Mech?

Directly prevents chol absorption at the small intestine brush border

65

Ezetimibe: SEs?

-increased LFTs (rarely)

-diarrhea

66

Fibrates: mech?

-Upregulate LPL to increase clearance of TAGs from bloodstream

-Activates PPAR-alpha to induce HDL synthesis

67

Fibrates: SEs?

-Myositis (increased risk with concurrent statins)

-Hepatotoxicity (increases LFTs)

-Cholesterol gallstones (esp with concurrent bile acid resins)

68

Anti-arrhythmics Class IA, IB, IC (Na channel blockers)

Mech?

-Slow/block conduction, esp of depolarized cells.

-Decrease slope of Phase 0 depolarization, increase threshold for firing in abmornal pacemaker cells.

-State-dependent: they selectively depress tissue that is more frequently depolarized (eg in tachycardia)

69

Anti-arrhythmics Class IA, IB, IC (Na channel blockers)

what causes increased toxicity for all Class I drugs?

hyperkalemia

70

Class IA drugs: name them (3)?

Quinidine

Procainamide

Disopyramide

"The Queen Proclaims Diso's pyramid"

71

Class IA drugs (Quinidine, Procainamide, Disopyramide)

Mech (specific to IA)?

General Class I mech: slows/blocks conduction, decr slope of Phase 0 depol, incr threshold for firing in abnl pacemaker cells.

Class IA:

-Incr AP duration

-Incr effective refractory period (ERP)

-Incr QT interval

72

Class IA (Quinidine, Procainamide, Disopyramide): clinical use?

Atrial arrhythmia

Ventricular arrhythmia

Esp re-entrant and ectopic SVT and VT

73

Class IA (Quinidine, Procainamide, Disopyramide): Tox?

Cinchonism (HA, tinnitus with quinidine), thrombocytopenia, torsades de pointes due to incr QT interval

Procainamide: Reversible SLE-like syndrome

Disopyramide: heart failure

74

Class IB drugs: name them (2)

-Lidocaine

-Mexiletine

-Phenytoin can also fall into this category

75

Class IB drugs (Lidocaine, Mexiletine): Mech?

Decr AP duraction

Preferentially affect ischemic or depol Purkinje and ventricular tissue.

76

Class IB drugs (Lidocaine, Mexiletine): Clinical Use?

-Acute ventricular arrhythmia, esp post-MI. (B is BEST post-MI)

-Digitalis-induced arrhythmias

77

Class IB drugs (Lidocaine, Mexiletine): Tox?

CNS stimulation/depression

CV depression

78

Class IC drugs: name them (2)

Flecainide

Propafenone

"Can I have Fries Please"

79

Class IC (Flecainide, Propafenone): Mech?

-Significantly prolongs refractory period in AV node

-Minimal effect on AP duration

80

Class IC (Flecainide, Propafenone): Clinical Use?

-SVTs, including afib.

-Last resort in refractory VT

81

Class IC (Flecainide, Propafenone): Tox?

Contraindications?

-Pro-arrhythmic

-Contraindicated Post-MI

"IC is Contraindicated in structural and ischemic heart disease"

82

Class II (beta blockers) name them (6)

-Metoprolol

-Propranolol

-Esmolol

-Atenolol

-Timolol

-Carvedilol

-Note labetalol is NOT a beta blocker (used for hypertensive emergency)

83

Beta blockers: Mech?

-Decrease SA and AV nodal activity by decr cAMP, decr Ca currents

-Suppress abnormal pacemaker cells by decr slope of Phase 4 depolarization

-AV node is particularly sensitive -> increased PR interval

84

Which beta blocker is very short acting?

Esmolol

85

Beta blockers: Clinical Use?

-SVT

-Slowing ventricular rate during afib and atrial flutter

86

Beta blockers: Tox?

Impotence

Exacerbation of COPD and asthma

CV effects (bradycardia, AV block, CHF)

CNS effects (sleep, sedation)

May mask signs of hypoglycemia

87

Beta blockers: Contraindication?

Trmt for OD?

CI in cocaine users

because of risk of unopposed alpha-adrenergic receptor agonist activity.

OD: give glucagon.

88

Toxicity specific to Metoprolol?

Dyslipidemia

89

Toxicity specific to Propranolol?

Exacerbation of vasospasm in Prinzmetal angina

90

Class III (K channel blockers) name 4

-Amiodarone

-Ibutilide

-Dofetilide

-Sotalol

"AIDS"

91

Class III K channel blockers (Amiodarone, Ibutilide, Dofetilide, Sotalol): mech?

Incr AP duration

Incr ERP

Incr QT interval

Used when other anti-arrhythmics fail!

92

Class III K channel blockers (Amiodarone, Ibutilide, Dofetilide, Sotalol): Use?

Afib

Atrial flutter

Amiodarone and Sotalol: ventricular tachycardia

93

Sotalol: toxicity?

torsades de pointes

excessive beta blockade

94

Ibutilide: tox?

torsades de points

95

Amiodarone: tox?

what labs should we check when using amidarone?

-pulmonary fibrosis

-hepatotoxicity

-hypothyroidism/hyperthyroidism (amiodarone is 40% iodine)

-corneal deposits

-skin deposits (blue/gray) --> photodermatitis

-neuro effects

-constipation

-CV effects (bradycardia, heart block, CHF)

-LABS: check PFTs, LFTs, TFTs

-Amiodarone has Class I, II, III, IV effects and alters the lipid membrane

96

Class IV antiarrhythmics (Ca channel blockers) name them (2)

Verapamil

Diltiazem

97

Ca channel blockers (Verapamil, Diltiazem): mech?

-Decr conduction velocity

-Incr ERP

-Incr PR interval

98

Ca channel blockers (Verapamil, Diltiazem): Clinical Use?

-Prevention of nodal arrhythmias (ie SVT)

-rate control in afib

99

Ca channel blockers (Verapamil, Diltiazem): tox?

-constipation

-flushing

-edema

-CV effects (CHF, AV block, sinus node depression)

100

Adenosine: class? Mech?

Misc antiarrhythmic

Increases K+ outflow -> cell hyperpolarizes -> intracellular Ca decreases

101

Adenosine: Use?

Tox?

what blocks its effects?

Use: drug of choice in diagnosing/aboloshing superventricular tachycardia. Very short acting (15 sec)

Tox: flusing, hypotension, chest pain

Blocked by theophylline (bronchodilator) and caffeine

102

Mg2+: class? Use?

-Misc anti-arrhythmic

-Used in torsades de pointes, digoxin toxocity