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0. Step Ia > Cardiac Pharm from FA (and UWorld questions) > Flashcards

Cardiac Pharm from FA (and UWorld questions) Flashcards

1
Q

Digoxin: what does it directly inhibit?

what does this cause?

A

cardiac myocyte Na/K ATPase.

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

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2
Q

generally, what are the 2 effects of Digoxin?

A
  • increases intracellular Ca -> increases inotropy
  • stimulates vagus nerve -> decreases HR
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3
Q

2 clinical uses for digoxin?

A
  • 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.
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4
Q

digoxin - toxicity?

A

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

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5
Q

digoxin: changes to ECG?

A

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

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6
Q

Digoxin: what factors predispose patients to toxicity?

A
  • 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)
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7
Q

Digoxin: antidote?

what not to do?

A
  • 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
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8
Q

Digoxin: class?

A

cardiac glycoside

aka digitalis

found in Foxglove plant in so many suburban gardens.

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9
Q

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

A
  • 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)

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10
Q

Which classes of anti-arrhythmics cause QT prolongation?

A

IA (Na blockers)

III (K blockers)

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11
Q

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

Name the 4 K blocker anti-arrhythmics

A
  • 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?!?)

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12
Q

what do beta blockers do?

A

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

slow Phase 4 depolarization.

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13
Q

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

A

Verapamil is more cardioselective than Diltiazem.

(these are Ca blockers)

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

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14
Q

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?

A

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.

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15
Q

Aspirin and Clopidogrel: synergistic effect? why/not?

A

Yes

because they have different mechanisms.

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16
Q

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

A

Streptokinase

Thrombolytic agent

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17
Q

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

A
  • Primary/essential HTN
  • HTN with CHF
  • HTN with diabetes
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18
Q

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

A

diuretics, ACE inhibitors/ARBs, Ca channel blockers

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19
Q

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

A

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

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20
Q

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

A

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

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21
Q

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

A

for decompensated CHF use beta blockers cautiously

they are contraindicated with cardiogenic shock

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22
Q

what drugs are protective against diabetic nephropathy?

A

ACE inhibitors/ARBs

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23
Q

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

A

ACE inhibitors

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24
Q

MOA of Ca channel blockers? effect?

A

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

effect = reduce muscle contractility

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25
Q

name the 5 Ca channel blockers

which are dihydropyridines and which are not?

A

Amlodipine

Nimodipine

Nifedipine

Diltiazem

Verapamil

ANN = dihydropyridines

D/V = non-dihydropyridines

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26
Q

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

A

Amlodipine and Nifedepine

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27
Q

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

A

Verapamil, then Diltiazem (the non-dihydropyridines)

“Verapamil -> Ventricle”

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28
Q

Amlodipine and Nifedipine: Clinical use?

A

Ca channel blockers

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

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29
Q

Nimodipine: clinical use?

A

Ca channel blocker

Use = subarachnoid hemorrhage. Prevents cerebral vasospasm.

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30
Q

Diltiazem, Verapamil: clinical use?

A

Ca channel blockers

HTN, angina, afib/atrial flutter

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31
Q

Calcium channel blockers: tox?

A

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

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32
Q

Hydralazine: class?

A

anti-hypertensive

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33
Q

Hydralazine: clinical use?

A

severe HTN, CHF.

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

Coadministered with a beta blocker to prevent reflex tachycardia.

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34
Q

Hydralazine: tox?

A

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

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35
Q

Hydralazine: contraindication?

A

in angina/CAD

due to compensatory tachycardia.

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36
Q

commonly used drugs in a hypertensive emergency? (5)

A
  • nitroprusside
  • nicardipine
  • clevidipine
  • labetolol
  • fenoldopam
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37
Q

Nitroprusside: use?

mech? tox?

A

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)

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38
Q

Fenoldopam: use?

mech? tox?

A

used in hypertensive emergency.

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

Decr BP and incr naturiuresis.

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39
Q

Nitroglycerin, Isosorbide dinitrate

Mech?

A

Vasodilation

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

Dilates veins >>> arteries.

Decr preload.

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40
Q

Nitroglycerin, Isosorbide dinitrate

Use?

A

Angina, coronary artery syndrome, pulm edema

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41
Q

what is Monday Disease?

A

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
Q

Nitroglycerin/isosorbide dinitrate: tox?

A

Monday disease

Reflex tachy, hypotension, flushing, headache

43
Q

Revlex tachycardia due to Nitroglycerin/isosorbide dinitrate: treatment?

A

beta blockers

44
Q

what is the goal of antianginal therapy?

A

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

  • end-diastolic volume
  • blood pressure
  • HR
  • contractility
45
Q

Nitrates affect Preload or Afterload?

effect on:

EDV?

BP?

contractility?

HR?

Ejection time?

MVO2?

A

Nitrates affect Preload

EDV? DECR

BP? DECR

contractility? INCR (reflex)

HR? INCR (reflex)

Ejection time? DECR

MVO2? DECR

46
Q

Beta blockers affect Preload or Afterload?

EDV?

BP?

contractility?

HR?

Ejection time?

MVO2?

A

Beta blockers affect Afterload

EDV? INCR

BP? DECR

contractility? DECR

HR? DECR

Ejection time? INCR

MVO2? DECR

47
Q

Nitrates + beta blockers together - effect on:

EDV?

BP?

contractility?

HR?

Ejection time?

MVO2?

A

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
Q

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

A
  • Pindolol
  • Acebutolol
49
Q

Nifedipine

effect is more similar to nitrates or beta blockers?

A

Nitrates

50
Q

Verapamil

effect is more similar to nitrates or beta blockers?

A

Beta blockers

51
Q

5 categories of lipid-lowering agents?

A
  • HMG-CoA reductase inhibitors
  • Niacin
  • Bile acid resins
  • Cholesterol absorption blockers
  • Fibrates
52
Q

what are the 5 HMG-CoA reductase inhibitors listed?

A

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

Lovastatin

Pravastatin

Simpastatin

Atorvastatin

Rosuvastatin

53
Q

HMG-CoA reductase inhibitors: Mechanism of action?

A

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
Q

Statins: effect on LDL? HDL? TAGs?

A

LDL: decrease dramatically

HDL: increase

TAGs: decrease

55
Q

Niacin: effect on LDL? HDL? TAGs?

A

LDL: decr

HDL: incr (niacin = best for this)

TAGs: decr

56
Q

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

A

LDL: decr

HDL: incr (slight)

TAGs: incr (slight)

57
Q

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

A

LDL: decr

HDL: no effect

TAGs: no effect

58
Q

Fibrates: effect on LDL? HDL? TAGs?

A

LDL: decr

HDL: incr

TAGs: decrease A LOT (best for this)

59
Q

Statins: SEs?

A
  • Hepatotoxicity (increases LFTs)
  • Rhabdomyolysis (esp when used with fibrates and niacin)
60
Q

Niacin: Mech?

A

Inhibits lipolysis in adipose tissue

Reduces hepatic VLDL synthesis

61
Q

Niacin: SEs?

A
  • Red flushed face (will decrease with aspirin or long term use)
  • Hyperglycemia (acanthosis nigricans)
  • Hyperuricemia (exacerbates gout)
62
Q

Bile acid resins: Mech?

A

Prevent intestinal re-absorption of bile acids

->liver must use more cholesterol to make more

63
Q

Bile acid resins: SEs?

A

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

also decr absorption of fat-sol vitamins

64
Q

Ezetimibe: Mech?

A

Directly prevents chol absorption at the small intestine brush border

65
Q

Ezetimibe: SEs?

A
  • increased LFTs (rarely)
  • diarrhea
66
Q

Fibrates: mech?

A
  • Upregulate LPL to increase clearance of TAGs from bloodstream
  • Activates PPAR-alpha to induce HDL synthesis
67
Q

Fibrates: SEs?

A
  • Myositis (increased risk with concurrent statins)
  • Hepatotoxicity (increases LFTs)
  • Cholesterol gallstones (esp with concurrent bile acid resins)
68
Q

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

Mech?

A
  • 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
Q

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

what causes increased toxicity for all Class I drugs?

A

hyperkalemia

70
Q

Class IA drugs: name them (3)?

A

Quinidine

Procainamide

Disopyramide

“The Queen Proclaims Diso’s pyramid”

71
Q

Class IA drugs (Quinidine, Procainamide, Disopyramide)

Mech (specific to IA)?

A

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
Q

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

A

Atrial arrhythmia

Ventricular arrhythmia

Esp re-entrant and ectopic SVT and VT

73
Q

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

A

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

Procainamide: Reversible SLE-like syndrome

Disopyramide: heart failure

74
Q

Class IB drugs: name them (2)

A
  • Lidocaine
  • Mexiletine
  • Phenytoin can also fall into this category
75
Q

Class IB drugs (Lidocaine, Mexiletine): Mech?

A

Decr AP duraction

Preferentially affect ischemic or depol Purkinje and ventricular tissue.

76
Q

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

A
  • Acute ventricular arrhythmia, esp post-MI. (B is BEST post-MI)
  • Digitalis-induced arrhythmias
77
Q

Class IB drugs (Lidocaine, Mexiletine): Tox?

A

CNS stimulation/depression

CV depression

78
Q

Class IC drugs: name them (2)

A

Flecainide

Propafenone

“Can I have Fries Please”

79
Q

Class IC (Flecainide, Propafenone): Mech?

A
  • Significantly prolongs refractory period in AV node
  • Minimal effect on AP duration
80
Q

Class IC (Flecainide, Propafenone): Clinical Use?

A
  • SVTs, including afib.
  • Last resort in refractory VT
81
Q

Class IC (Flecainide, Propafenone): Tox?

Contraindications?

A
  • Pro-arrhythmic
  • Contraindicated Post-MI

“IC is Contraindicated in structural and ischemic heart disease”

82
Q

Class II (beta blockers) name them (6)

A
  • Metoprolol
  • Propranolol
  • Esmolol
  • Atenolol
  • Timolol
  • Carvedilol
  • Note labetalol is NOT a beta blocker (used for hypertensive emergency)
83
Q

Beta blockers: Mech?

A
  • 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
Q

Which beta blocker is very short acting?

A

Esmolol

85
Q

Beta blockers: Clinical Use?

A
  • SVT
  • Slowing ventricular rate during afib and atrial flutter
86
Q

Beta blockers: Tox?

A

Impotence

Exacerbation of COPD and asthma

CV effects (bradycardia, AV block, CHF)

CNS effects (sleep, sedation)

May mask signs of hypoglycemia

87
Q

Beta blockers: Contraindication?

Trmt for OD?

A

CI in cocaine users

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

OD: give glucagon.

88
Q

Toxicity specific to Metoprolol?

A

Dyslipidemia

89
Q

Toxicity specific to Propranolol?

A

Exacerbation of vasospasm in Prinzmetal angina

90
Q

Class III (K channel blockers) name 4

A
  • Amiodarone
  • Ibutilide
  • Dofetilide
  • Sotalol

“AIDS”

91
Q

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

A

Incr AP duration

Incr ERP

Incr QT interval

Used when other anti-arrhythmics fail!

92
Q

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

A

Afib

Atrial flutter

Amiodarone and Sotalol: ventricular tachycardia

93
Q

Sotalol: toxicity?

A

torsades de pointes

excessive beta blockade

94
Q

Ibutilide: tox?

A

torsades de points

95
Q

Amiodarone: tox?

what labs should we check when using amidarone?

A
  • 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
Q

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

A

Verapamil

Diltiazem

97
Q

Ca channel blockers (Verapamil, Diltiazem): mech?

A
  • Decr conduction velocity
  • Incr ERP
  • Incr PR interval
98
Q

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

A
  • Prevention of nodal arrhythmias (ie SVT)
  • rate control in afib
99
Q

Ca channel blockers (Verapamil, Diltiazem): tox?

A
  • constipation
  • flushing
  • edema
  • CV effects (CHF, AV block, sinus node depression)
100
Q

Adenosine: class? Mech?

A

Misc antiarrhythmic

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

101
Q

Adenosine: Use?

Tox?

what blocks its effects?

A

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
Q

Mg2+: class? Use?

A
  • Misc anti-arrhythmic
  • Used in torsades de pointes, digoxin toxocity

0. Step Ia (28 decks)

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