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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
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 ## Footnote 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: ## Footnote 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

0. Step Ia (28 decks)

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