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step 1 flashcards > cardio > Flashcards

cardio Flashcards

1
Q

Truncus arteriosus (TA) gives rise to?

A

Ascending aorta and pulmonary trunk

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2
Q

Bulbus cordis gives rise to?

A

Smooth parts (outflow tract) of left and right ventricles

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3
Q

Primitive atria gives rise to?

A

Trabeculated part of left and right atria

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4
Q

Primitive ventricle gives rise to?

A

Trabeculated part of left and right ventricles

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5
Q

Primitive pulmonary vein gives rise to?

A

Smooth part of left atrium

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6
Q

Left horn of sinus venosus (SV) gives rise to?

A

Coronary sinus

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7
Q

Right horn of SVgives rise to?

A

Smooth part of right atrium

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8
Q

Right common cardinal vein and right anterior cardinal vein gives rise to?

A

SVC

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9
Q

Amlodipine, nimodipine, nifedipine

A

(dihydropyridine); Block voltage-dependent L-type calcium channels Vascular smooth muscle se: AV block, hyperprolactinemia, and constipation

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10
Q

diltiazem, verapamil.

A

(non-dihydropyridine); Block voltage-dependent L-type calcium channels cardiac muscle se: AV block, hyperprolactinemia, constipation.

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11
Q

Hydralazine

A

increase cGMP–> smooth muscle cell relaxation. decrease AFTERLOAD use in prego with methy-dopa co-adminster with b-blocker to prevent reflex-tachyC Se: complensatory tachyC, Lupus like syndrome (anti-histone antibodies)

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12
Q

drugs to use in hypertensive emergency

A

nicardipine nitroprusside labetalol fenoldpam clevidipine

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13
Q

nitroprusside

A

release NO–> increase cGMP. *** Cyanide toxicity: give thiosulfate

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14
Q

fenoldpam

A

D1 R agonist. VasoD decrease BP  increase natriuresis.

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15
Q

nitroglycerin, isosorbide dinitrate

A

release NO–> increase cGMP. vasoD veins>>arteries. decrease PRELOAD Se: reflex tachyC (treat with B-blocker). hypoT, flushing contraindications: sidenafil (PDE inhibitor, viagra)

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16
Q

Monday Disease

A

industrial exposure to nitroglycerin, where you devo tolerance to vasoD effect during the week. over the weekend, you have loss of tolerance. On monday, you have s/s of of tachyC, dizziness, headache on reexposure (overexposure to nitro).

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17
Q

compare nitrates and b-blockers for anti-angina therapy

A

nitrates reduce PRELOAD decrease: EDV, BP, Ejection time, MVO2. increase: HR, Contractility (reflex response)- give a B-blocker with to stop this effect. CCB like nifedipine, have the same effect as nitrates, so they can also cause the reflex tachyC. b-blockers reduce AFTERLOAD: decrease: HR, contractility, MVO2 increase: EDV, Ejection time. CCB like verapamil have the same effect as b-blockers for angina DO NOT give: pindolol or acebutolol for angina because they are only partial agonist of the b receptor.

18
Q

HTN + prego

A

methydopa hydralazine (ACEI are taratogens)

19
Q

HTM + diabetes

A

ACEI ARB

20
Q

HTN + HF

A

ACEI CCB (not B blocker)

21
Q

HTN + asthma/COPD

A

CCB (not B blocker b/c broncospasm, or ACEI b/c of cough)

22
Q

HTN + CKD

A

ACEI ARB can give loop diuretic

23
Q

HTN + BPH

A

alpha blocker

24
Q

HTN + post -MI

A

b-blocker spironolactone non-dihydropyridine CCB

25
Q

HTN + recurrent stroke

A

diuretic ACEI

26
Q

statins

A

inhibit HMB-CoA synthase. increase LDL R exp decrease LDL se: rhabdomyolysis (check CK levels)

27
Q

niacin

A

vit B3. inhibits lypolysis in adipose. increases HDL Se: flushed face. hyperglycemia, hyper uricemia

28
Q

cholestyramine, colestipol, colesevelam

A

bile acid resins. increase LDL R exp *** can increase TGs se: bad taste, cholestrol Gallstones, GI discomfort. deceased absorption of fat soluble vitamins (D,E,A,K)

29
Q

ezetimibe

A

cholesterol absorption blocker. increase LDL R exp competes with NPC1L1 at small intestine brush border. se: Rare  LFTs, diarrhea

30
Q

gemfibrozil, clofibrate, bezafibrate, fenofibrate

A

most effective for hyperTGs. used in metabolic syndrome. activates PPAR-alpha to induce HDL synthesis. se: Myositis ( risk with concurrent statins), hepatotoxicity ( LFTs), cholesterol gallstones (esp. with concurrent bile acid resins)

31
Q

digoxin

A

inhibit Na/K ATPase use: CHF, AFib (decrease conductance at AV node) se: delirium, n+v+d, blurry vision, yellow vision. junctional escape rhythm, if bradyC- give atropine to increase the HR. vent tachyC arrhythmia hyperK factors that predispose to toxicity: renal failure, hypoK (digoxin can bind to K site in Na/K pump) tx for toxicity: Mg, normalize K. anti-digoxin Fab fragments.

32
Q

Class IA antiarrhythmics

A

Quinidine, Procainamide, Disopyramide.

MECHANISM  incrasase AP duratione, ERP, QT interval.
CLINICAL USE Both atrial and ventricular arrhythmias,
especially re-entrant and ectopic SVT and VT.
TOXICITY Cinchonism (headache, tinnitus with
quinidine), reversible SLE-like syndrome
(procainamide), heart failure (disopyramide),
thrombocytopenia, torsades de pointes due to
 QT interval.

33
Q

class IB antiarrhythmics

A

Lidocaine, Mexiletine.

MECHANISM  decrease AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue.
Phenytoin can also fall into the IB category.
CLINICAL USE Acute ventricular arrhythmias (especially post- MI), digitalis-induced arrhythmias. IB is Best
post-MI.
TOXICITY CNS stimulation/depression, cardiovascular
depression.

34
Q

class IC antiarrhythmics

A

Flecainide, Propafenone.

MECHANISM Significantly prolongs refractory period in AV
node. Minimal effect on AP duration.
CLINICAL USE SVTs, including atrial fibrillation. Only as a last resort in refractory VT.
TOXICITY Proarrhythmic, especially post-MI
(contraindicated).IC is Contraindicated in
structural and ischemic heart disease.

35
Q

class II antiarrhythmcs

A

Metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol

MECH: Decrease SA and AV nodal activity by decreasing  cAMP and Ca2+ currents. Suppress abnormal pacemakers by slope of phase 4.
AV node particularly sensitive— increase PR interval. Esmolol very short acting.
CLINICAL USE SVT, slowing ventricular rate during atrial fibrillation and atrial flutter.
TOXICITY Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block,
CHF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia.
Metoprolol can cause dyslipidemia. Propranolol can exacerbate vasospasm in Prinzmetal angina.
Contraindicated in cocaine users (risk of unopposed α-adrenergic receptor agonist activity). Treat
overdose with glucago

n.

36
Q

class III antiarrhythmics

A

 Amiodarone, Ibutilide, Dofetilide, Sotalol.

Mech: K channel blockers. increaseAP duration,  ERP. Used when other antiarrhythmics fail.  increase QT interval.
CLINICAL USE Atrial fibrillation, atrial flutter; ventricular
tachycardia (amiodarone, sotalol).
TOXICITY

Sotalol—torsades de pointes, excessive β
blockade.
Ibutilide—torsades de pointes.
Amiodarone—pulmonary fibrosis,
hepatotoxicity, hypothyroidism/
hyperthyroidism (amiodarone is 40% iodine
by weight), corneal deposits, skin deposits
(blue/gray) resulting in photodermatitis,
neurologic effects, constipation, cardiovascular
effects (bradycardia, heart block, CHF). remmeber to check PFT, LFTss, TFTs wehn using amiodarone.

37
Q

class IV antiarrhythmics

A

(class IV): CCBs
Verapamil, diltiazem.
MECHANISM  decrease conduction velocity, increase ERP,  increase PR interval.
CLINICAL USE Prevention of nodal arrhythmias (e.g., SVT), rate control in atrial fibrillation.
TOXICITY Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression).

38
Q

adenosine

A

 K+ out of cells Ž hyperpolarizing the cell and  ICa. Drug of choice in diagnosing/abolishing
supraventricular tachycardia. Very short acting (~ 15 sec). Adverse effects include flushing,
hypotension, chest pain. Effects blocked by theophylline and caffeine.

39
Q

Mg

A

Effective in torsades de pointes and digoxin toxicity.

40
Q

aortic stenosis

A

systolic ejection click.

Crescendo- decrescendo

step 1 flashcards (13 decks)

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