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USMLE Step 1 > Cardio > Flashcards

Cardio Flashcards

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USMLE® Step 1 flashcards
1
Q

Essential HTN

Antihypertensive therapy

A

Drugs: diuretics, ACE inhibs, ARBs, CCBs

See Renal for more info about diuretics, ACE inhibs & ARBs

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2
Q

CHF

Antihypertensive therapy

A

Drugs: diuretics, ACE inhibs, ARBs, Beta blockers (compensated CHF), K+ sparing diuretics

Notes: Beta blockers must be used cautiously in decompensated CHF, and are contraindicated in cardiogenic shock

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3
Q

Diabetes mellitus

Antihypertensive therapy

A

Drugs: ACE inhibs, ARBs, CCBs, diuretics, Beta blockers, alpha blockers

Notes: ACE inhibs are protective against diabetic nephropathy. See pharm chapter for more details about alpha- blockers

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4
Q

Calcium Channel Blockers

A

Drugs: nifedipine, verapamil, diltiazem, amlodipine

MoA: block voltage-dependent L-type calcium channels of cardiac and smooth mm-> reduced mm contractility

Use: HTN, angina, arrhythmias (NOT nifedipine), Prinzmetal’s angina, Raynaud’s

Toxicity: cardiac depression, AV block, peripheral edema, flushing, dizziness, & constipation

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5
Q

Hydralazine

A

MoA: increases cGMP-> smooth mm relaxation. Vasodilates arterioles more than veins; after load reduction.

Use: severe HTN, CHF. 1st line therapy for HTN in pregnancy, w/ methyldopa. Frequently coadministered w/ a Beta-blocker to prevent reflex tachycardia.

Toxicity: compensatory tachycardia (contraindicated in angina/ CAD), fluid retention, nausea, headache, angina. SLE-like syndrome

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6
Q

Malignant HTN Tx

A

Commonly used drugs include nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam

Nitroprusside: short acting; increases cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide).

Fenoldopam: Dopamine D1 receptor agonist- coronary, peripheral, renal, and splanchnic vasodiln. Decreases blood pressure and increases natiriuresis.

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7
Q

Nitroglycerin, isosorbide dinitrate

A

MoA: vasodilator by releasing nitric oxide in smooth mm, causing increased cGMP and smooth mm relaxation. Dilates veins»> arteries. Decreases preload

Use: angina, pulmonary edema

Toxicity: reflex tachycardia, hypotension, flushing, headache, “Monday disease” in industrial exposure: development of tolerance for vasodilating axn during work week and loss of tolerance over weekend results in tachycardia, dizziness, and headache upon reexposure.

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8
Q

Antianginal therapy

A

Goal: reduction of myocardial O2 consumpn (MVO2) by decreasing 1 or more of the determinants of MVO2: end-diastolic volume, blood pressure, heart rate, contractility, ejection time

Notes:

  • CCBs: Nifedipine is similar to Nitrates in effect; verapamil is similar to Beta blockers in effect
  • Pindolol & acebutolol: partial Beta- agonists contraindicated in angina
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9
Q

Nitrates

antianginal therapy affecting preload

A 
EDV: decreased
BP: decreased
Contractility: Increased (reflex response)
HR: increased (reflex response)
Ejection time: decreased
MVO2: decreased
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10
Q

Beta blockers

antianginal therapy affecting after load

A 
EDV: increased
BP: decreased
Contractility: decreased
HR: decreased
Ejection time: increased
MVO2: decreased
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11
Q

Nitrates + Beta blockers

antianginal therapy

A 
EDV: no effect or decreased
BP: decreased
Contractility: little/ no effect
HR: decreased
Ejection time: little/ no effect
MVO2: greatly decreased
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12
Q

HMG- CoA reductase inhibitors

lipid-lowering agents

A

Drugs: lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin)

LDL: greatly decreases
HDL: mildly increases
TGs: mildly decreases

MoA: inhibit conversion of HMG-CoA to mevalonate (cholesterol precursor)

Side effects: hepatotoxicity (increased LFTs), rhabdomyolysis

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13
Q

Niacin (vit B3)

lipid-lowering agent

A

LDL: moderately decreases
HDL: moderately increases
TGs: mildly decreases

MoA: inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation

Side effects:

  • red, flushed face (decreased by aspirin or long-term use)
  • hyperglycemia (acanthosis nigricans)
  • hyperuricemia (exacerbates gout)
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14
Q

Bile acid resins

lipid-lowering agent

A

Drugs: cholestyramine, colestipol, colesevelam

LDL: moderately decreases
HDL: slightly increases
TGs: slightly increases

MoA: prevent intestinal reabsorpn of bile acids; liver must use cholest to make more

Side effects:

  • pts hate it- tastes bad & causes GI discomfort
  • decreased absorpn of ADEK
  • Cholest gallstones
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15
Q

Cholesterol absorpn blockers

lipid-lowering agents

A

Drugs: ezetimibe

LDL: moderately decreases
HDL: none
TGs: none

MoA: prevent cholest reabsorpn at SI brush border

Side effects: rare increased LFTs, diarrhea

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16
Q

Fibrates

lipid-lowering agents

A

Drugs: gemfibrozil, clofibrate, bezafibrate, fenofibrate

LDL: Mildly decreases
HDL: mildly increases
TGs: greatly decreases

MoA: upregulate LPL-> TG clearance

Side effects: myositis hepatotoxicity (increased LFTs), cholest gallstones

17
Q

Cardiac glycosides

A

Drugs: digoxin (75% bioavailability, 20-40% bound, half life= 40 hrs, urinary excretion)

MoA: direct inhibn of Na+/ K+ ATPase leads to indirect inhibn of Na+/ Ca+2 exchanger/ antiport. Increases intracellular Ca+2-> positive isotropy. Stimulates vagus nerve-> decreased HR

Use: CHF (increases contractility); A fib (decreases conduction at AV node and depression of SA node).
Toxicity:
continued on next card

18
Q

Cardiac glycosides (cont.)

A

Toxicity:

  • cholinergic: nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh)
  • ECG: increased PR, decreased QT, ST scooping, T wave inversion, arrhythmia, AV block
  • Can lead to hyperkalemia (poor prognostic indicator)
  • Factors predisposing to toxicity- renal failure (decreased excretion), hypokalemia (permissive for digoxin binding at K+ binding site on Na+/ K+ ATPase), quinidine (decreased digoxin clearance; displaces digoxin from tissue-binding sites).

Antidote: slowly normalize K+, lidocaine, cardiac pacer, anti-digoxin Fab fragments, Mg+2

19
Q

Antiarryhmthmics
Na+ channel blockers (class I)
(good diagram pg 283 FA)

A
  • Local anesthetics. Slow or block conduction (esp in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells. Are state dependent (selectively depress tissue that is frequently depolarized (e.g. tachycardia))
  • Hyperkalemia causes increased toxicity for ALL class I drugs
20
Q

Class IA antiarryhthmics

A

Drugs: Quinidine, procainamide, disopyramide
Mnemonic: Queen Proclaims Diso’s Pyramid

MoA: increases AP duration, increases effective refractory pd (ERP), increases QT interval. Affect both atrial and vent arrhythmias, esp reentrant and ectopic supra ventricular and ventricular tachycardia

Toxicity: quinidine (cinchonism- headache, tinnitus); procainamide (reversible SLE-like syndrome); disopyramide (heart failure); thrombocytopenia; torsades de points due to increased QT interval

21
Q

Class IB antiarrhythmics

A

Drugs: Lidocaine, Mexiletine, Tocainide

MoA: decreases AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue. Useful in acute ventricular arrythmias (esp post-MI) and in digitalis- induced arrhythmias.

Toxicity: local anesthetic. CNS stimulation/ depression, cardio depression

22
Q

Class IC antiarrhythmics

A

Drugs: flecainide, propafenone

  • No effect on AP duration. Useful in vent tachycardias that progress to VF and in intractable SVT. Usually used only as last resort in refractory tachyarrythmias. For pts w out structural abnormalities
  • Toxicity: proarrhythmic, esp post-MI (contraindicated). Significantly prolongs refractory pd in AV node
23
Q

Class II antiarryhtmics (Beta blockers)

Mechanism

A

Drugs: metoprolol, propranolol, esmolol, atenolol, timolol

MoA: decreases SA & AV nodal activity by decreasing cAMP, decreases Ca currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node= particularly sensitive; increases PR interval

  • Esmolol= very short acting
24
Q

Class II antiarryhtmics (Beta blockers)

Use & Toxicity

A

Use: vent tachycardia, SVT, slowing ben rate during A fib and A flutter

Toxicity: impotence, exacerbation of asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask signs of hypoglycemia. Metoprolol can cause dyslipidemia. Tx overdose w glucagon. Propranolol can exacerbate vasospasm in Prinzmetal’s angina

25
Q

Antiarrhytmics- K+ channel blockers (class III)

drugs & mechanism

A

Drugs: Amiodarone, Ibutilide, Dofetilide, Sotalol
Mnemonic : AIDS

MoA: increases AP duration, increases ERP. Used when other antiarrhythmics fail. Increases QT interval

25
Q

Antiarrhytmics- K+ channel blockers (class III)

drugs & mechanism

A

Drugs: Amiodarone, Ibutilide, Dofetilide, Sotalol
Mnemonic : AIDS

MoA: increases AP duration, increases ERP. Used when other antiarrhythmics fail. Increases QT interval

26
Q

Antiarrhytmics- K+ channel blockers (class III)

Toxicity

A
  • Sotalol: torsades de pointes, excessive Beta block
  • Ibutilide: torsades
  • amiodarone: pulm fibrosis, hypo/ hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits (blue/ gray) resulting in photo dermatitis, neuro effects, constipation, cardio effects (bradycardia, heart block, CHF)
  • *amiodarone has class I, II, III, and IV effects b/c it alters lipid membrane
  • *Remember to check PFTs, LFTs, and TFTs, when
26
Q

Antiarrhytmics- K+ channel blockers (class III)

Toxicity

A
  • Sotalol: torsades de pointes, excessive Beta block
  • Ibutilide: torsades
  • amiodarone: pulm fibrosis, hypo/ hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits (blue/ gray) resulting in photo dermatitis, neuro effects, constipation, cardio effects (bradycardia, heart block, CHF)
  • *amiodarone has class I, II, III, and IV effects b/c it alters lipid membrane
  • *Remember to check PFTs, LFTs, and TFTs, when using amiodarone
27
Q

Class IV antiarrhythmics (CCBs)

A

Drugs: verapamil, diltiazem

MoA: decreases conduction velocity, increases ERP, increases PR interval. Used in prevention of nodal arrhythmias (e.g. SVT)

Toxicity: constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

28
Q

Other antiarrhythmics

A

Adenosine: increases K+ out of cells-> hyper polarizing the cell and decreases intracellular Ca. Drug of choice in Dx/ abolishing supraventricular tachycardia. Very short acting (~ 15 sec). Toxicity includes flushing, hypotension, chest pain. Effects blocked by theophylline and caffeine.

Mg+2: effective in torsades de pointes & digoxin toxicity

USMLE Step 1 (5 decks)

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