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USMLE 1 > Cardiovascular- Pharmacology > Flashcards

Cardiovascular- Pharmacology Flashcards

1
Q

Hypertension treatment

- Primary (essential) hypertension

A

Thiazide diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), dihydropyridine Ca2+ channel blockers.

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2
Q

Hypertension treatment

- Hypertension with heart failure

A

Diuretics, ACE inhibitors/ARBs, β-blockers
(compensated HF), aldosterone antagonists.

*In HF, ARBs may be combined with the neprilysin inhibitor sacubitril.

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3
Q

Hypertension treatment

- Hypertension with diabetes mellitus

A

ACE inhibitors/ARBs, Ca2+ channel blockers, thiazide diuretics, β-blockers.

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4
Q

Hypertension treatment

- Hypertension in asthma

A

ARBs, Ca2+ channel blockers, thiazide diuretics, selective β-blockers.

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5
Q

Hypertension treatment

- Hypertension in pregnancy

A

“He likes my neonate.”

Hydralazine, labetalol, methyldopa, nifedipine

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6
Q

Calcium channel blockers

  • dihydropyridines
  • non-dihydropyridines
A

Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine

diltiazem, verapamil

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7
Q

Calcium channel blockers (CLINICAL USE)

  • Dihydropyridines (except nimodipine):
  • Nimodipine:
  • Nicardipine, clevidipine:
  • Non-dihydropyridines:
A

hypertension, angina (including Prinzmetal), Raynaud
phenomenon

subarachnoid hemorrhage (prevents cerebral vasospasm).

hypertensive urgency or emergency.

hypertension, angina, atrial fibrillation/flutter

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8
Q

Calcium channel blockers (Adverse effect)

  • dihydropyridines
  • non-dihydropyridines
A

cardiac depression, AV block, hyperprolactinemia, constipation, gingival hyperplasia.

peripheral edema, flushing, dizziness.

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9
Q

Hydralazine

  • Mechanism
  • Clinical use
  • Adverse effects
A

Increase cGMP Ž smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction.

Severe hypertension (particularly acute), HF (with organic nitrate). Safe to use during pregnancy.

Compensatory tachycardia (contraindicated inangina/CAD), fluid retention, headache, angina.
 SLE-like syndrome.
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10
Q

Hypertensive emergency

A

Treat with clevidipine, fenoldopam, labetalol, nicardipine, or nitroprusside.

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11
Q

Fenoldopam

A

Dopamine D1 receptor agonist—coronary, peripheral, renal, and splanchnic vasodilation. Also used postoperatively as an antihypertensive. Can cause hypotension and tachycardia.

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12
Q

Nitrates

  • Names
  • Clinical use
  • Adverse effects
A

Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate.

Angina, acute coronary syndrome, pulmonary edema.

Reflex tachycardia (treat with β-blockers), hypotension, flushing, headache, “Monday disease” in industrial exposure. Contraindicated in right ventricular infarction.

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13
Q

Antianginal therapy

A

Goal is reduction of myocardial O2 consumption (MVO2) by decreasing 1 or more of the determinants of
MVO2: end-diastolic volume, BP, HR, contractility.

Nitrates, B-blockers, Verapamil is similar to β-blockers in effect, Pindolol and acebutolol are partial β-agonists that should be used with caution in angina.

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14
Q

Ranolazine

  • Mechanism
  • Clinical use
  • Adverse effects
A

Inhibits the late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption. Does not affect heart rate or contractility.

Angina refractory to other medical therapies

Constipation, dizziness, headache, nausea, QT prolongation

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15
Q

Milrinone

  • Mechanism
  • Clinical use
  • Adverse effects
A

Selective PDE-3 inhibitor.
- In cardiomyocytes: increase cAMP accumulation Ž high Ca2+ influx Ž increase inotropy and chronotropy.

  • In vascular smooth muscle: Increase cAMP accumulation Ž inhibition of MLCK activity Ž general vasodilation.

Short-term use in acute decompensated HF.

Arrhythmias, hypotension.

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16
Q

Lipid-lowering agents (mechanism and adverse effects)

- HMG-CoA reductase inhibitors

A

Inhibit conversion of HMGCoA to mevalonate;
decrease mortality in CAD patients.

Hepatotoxicity (Increase LFTs), myopathy (esp. when used with fibrates or niacin)

Low LDL, high HDL, Low tryglicerides

17
Q

Lipid-lowering agents (mechanism and adverse effects)

- Ezetimibe

A

Prevent cholesterol absorption at small intestine brush border.

Rare increase LFTs, diarrhea

Low LDL, high/normal HDL, low/normal Tryglicerides

18
Q

Lipid-lowering agents (mechanism and adverse effects)

- Bile acid resins (Cholestyramine, colestipol, colesevelam)

A

Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more.

GI upset, decrease absorption of other drugs and fat-soluble vitamins.

Low LDL, high HDL, high Tryglicerides

19
Q

Lipid-lowering agents (mechanism and adverse effects)

- Fibrate (Gemfibrozil, bezafibrate, fenofibrate)

A

Upregulate LPL Ž increase TG clearance. Activates PPAR-α to induce HDL synthesis.

Myopathy (risk with statins), cholesterol gallstones (via inhibition of cholesterol 7α-hydroxylase).

Low LDL, high HDL, low Tryglicerides

20
Q

Lipid-lowering agents (mechanism and adverse effects)

- Niacin (vitamin B3)

A 
Inhibits lipolysis (hormonesensitive lipase) in adipose
tissue; reduces hepatic VLDL synthesis.

Red, flushed face, which is decreased by NSAIDs or long-term use. Hyperglycemia, Hyperuricemia.

Low LDL, high HDL, low Tryglicerides

21
Q

Lipid-lowering agents (mechanism and adverse effects)

- PCSK9 inhibitors (Alirocumab, evolocumab)

A

Inactivation of LDL-receptor degradation, increasing
amount of LDL removed from bloodstream.

Myalgias, delirium, dementia, other neurocognitive effects.

22
Q

Cardiac glycosides (digoxin)

  • Mechanism
  • Clinical use
A

Direct inhibition of Na+/K+ ATPase Ž indirect inhibition of Na+/Ca2+ exchanger. higher [Ca2+]i Ž positive inotropy.

HF (increase contractility); atrial fibrillation (decrease conduction at AV node and depression of SA node).

23
Q

Cardiac glycosides (digoxin)

  • Adverse effects
  • Factors predisposing to toxicity
  • Antidote
A
  • Cholinergic—nausea, vomiting, diarrhea, blurry yellow vision (think van Gogh), arrhythmias, AV block. Can lead to hyperkalemia, which indicates poor prognosis.
  • Renal failure, hypokalemia, drugs that displace digoxin from tissue-binding sites, and decrease clearance (eg, verapamil, amiodarone, quinidine).
  • Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+.
24
Q

Antiarrhythmics— sodium channel blockers (class I)

A 
Slow or block conduction (especially in depolarized cells). decrease slope of phase 0 depolarization. Are
state dependent (selectively depress tissue that is frequently depolarized [eg, tachycardia]).
25
Q

Antiarrhythmics- Class IA

  • Names
  • Mechanism
A

“The Queen Proclaims Diso’s pyramid”.
Quinidine, Procainamide, Disopyramide.

increase AP duration, increase effective refractory period (ERP) in ventricular action potential, higher QT
interval, some potassium channel blocking effects.

26
Q

Antiarrhythmics- Class IA

  • Clinical use
  • Adverse effects
A

Both atrial and ventricular arrhythmias, especially reentrant and ectopic SVT and VT.

Cinchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), HF (disopyramide), thrombocytopenia, torsades de pointes due to High QT interval.

27
Q

Antiarrhythmics- Class IB

  • Names
  • Mechanism
A

“I’d Buy Liddy’s Mexican Tacos.”
Lidocaine, MexileTine.

Increase AP duration. Preferentially affect ischemic or
depolarized Purkinje and ventricular tissue. Phenytoin can also fall into the IB category.

28
Q

Antiarrhythmics- Class IB

  • Clinical use
  • Adverse effects
A

“IB is Best post-MI.”
Acute ventricular arrhythmias (especially post-
MI), digitalis-induced arrhythmias.

CNS stimulation/depression, cardiovascular depression.

29
Q

Antiarrhythmics- Class IC

  • Names
  • Mechanism
A

“Can I have Fries, Please.”
Flecainide, Propafenone.

Significantly prolongs ERP in AV node and accessory bypass tracts. No effect on ERP in Purkinje and ventricular tissue. Minimal effect on AP duration.

30
Q

Antiarrhythmics- Class IC

  • Clinical use
  • Adverse effects
A

SVTs, including atrial fibrillation. Only as a last resort in refractory VT.

Proarrhythmic, especially post-MI (contraindicated). IC is Contraindicated in structural and ischemic heart disease.

31
Q

Antiarrhythmics— β-blockers (class II)

  • Mechanism
  • Clinical use
A

Decrease SA and AV nodal activity. Suppress abnormal pacemakers by decreasing slope of phase 4.

SVT, ventricular rate control for atrial fibrillation and atrial flutter.

32
Q 
Antiarrhythmics— β-blockers (class II)
- Adverse effects
A

Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, HF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia.

Metoprolol can cause dyslipidemia. Propranolol can exacerbate vasospasm in Prinzmetal angina. β-blockers (except the nonselective α- and β-antagonists carvedilol and labetalol) cause unopposed α1-agonism if given alone for pheochromocytoma or cocaine toxicity.

Treat β-blocker overdose with saline, atropine, glucagon

33
Q

Antiarrhythmics— potassium channel blockers (class III)

  • Names
  • Mechanism
  • Clinical use
A

AIDS
Amiodarone, Ibutilide, Dofetilide, Sotalol.

Increase: AP duration, ERP, QT interval.

Atrial fibrillation, atrial flutter; ventricular tachycardia (amiodarone, sotalol).

*Amiodarone is lipophilic and has class I, II, III, and IV effects.

34
Q 
Antiarrhythmics— potassium channel blockers (class III)
- Adverse effects
A

Sotalol—torsades de pointes, excessive β blockade.

Ibutilide—torsades de pointes.

Amiodarone—pulmonary fibrosis, hepatotoxicity, hypothyroidism or hyperthyroidism (amiodarone is 40% iodine by weight), acts as hapten (corneal deposits, blue/ gray skin deposits resulting in photodermatitis),
neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, HF).

*Remember to check PFTs, LFTs, and TFTs when
using amiodarone

35
Q

Antiarrhythmics— calcium channel blockers (class IV)

  • names
  • mechanism
  • clinical use
  • adverse effects
A

Diltiazem, Verapamil

Decrease conduction velocity, increase ERP, increase PR interval.

Prevention of nodal arrhythmias (eg, SVT), rate control in atrial fibrillation.

Constipation, flushing, edema, cardiovascular effects (HF, AV block, sinus node depression).

36
Q

Other antiarrhythmics (adenosine)

  • Mechanism
  • Clinical use
  • Adverse effects
A

Increase K+ out of cells Ž hyperpolarizing the cell and decreasing ICa, decreasing AV node conduction.

Drug of choice in diagnosing/terminating certain forms of SVT. Very short acting (~ 15 sec). Effects blunted by theophylline and caffeine (antagonists).

flushing, hypotension, chest pain, sense of impending doom, bronchospasm.

37
Q 
Other antiarrhythmics (Mg)
- clinical use
A

Effective in torsades de pointes and digoxin toxicity.

38
Q

Ivabradine

  • Mechanism
  • Clinical use
  • Adverse effects
A

Selective inhibition of funny sodium channels (If), prolonging slow depolarization phase (phase 4).
Decrease SA node firing; negative chronotropic effect without inotropy. Reduces cardiac O2 requirement

Chronic stable angina in patients who cannot take β-blockers. Chronic HF with reduced ejection fraction.

Luminous phenomena/visual brightness, hypertension, bradycardia.

USMLE 1 (73 decks)

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