cardio

Question 1

Truncus arteriosus (TA) gives rise to?

Answer 1

Ascending aorta and pulmonary trunk

Question 2

Bulbus cordis gives rise to?

Answer 2

Smooth parts (outflow tract) of left and right ventricles

Question 3

Primitive atria gives rise to?

Answer 3

Trabeculated part of left and right atria

Question 4

Primitive ventricle gives rise to?

Answer 4

Trabeculated part of left and right ventricles

Question 5

Primitive pulmonary vein gives rise to?

Answer 5

Smooth part of left atrium

Question 6

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

Answer 6

Coronary sinus

Question 7

Right horn of SVgives rise to?

Answer 7

Smooth part of right atrium

Question 8

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

Answer 8

SVC

Question 9

Amlodipine, nimodipine, nifedipine

Answer 9

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

Question 10

diltiazem, verapamil.

Answer 10

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

Question 11

Hydralazine

Answer 11

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)

Question 12

drugs to use in hypertensive emergency

Answer 12

nicardipine nitroprusside labetalol fenoldpam clevidipine

Question 13

nitroprusside

Answer 13

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

Question 14

fenoldpam

Answer 14

D1 R agonist. VasoD decrease BP  increase natriuresis.

Question 15

nitroglycerin, isosorbide dinitrate

Answer 15

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

Question 16

Monday Disease

Answer 16

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).

Question 17

compare nitrates and b-blockers for anti-angina therapy

Answer 17

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.

Question 18

HTN + prego

Answer 18

methydopa hydralazine (ACEI are taratogens)

Question 19

HTM + diabetes

Answer 19

ACEI ARB

Question 20

HTN + HF

Answer 20

ACEI CCB (not B blocker)

Question 21

HTN + asthma/COPD

Answer 21

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

Question 22

HTN + CKD

Answer 22

ACEI ARB can give loop diuretic

Question 23

HTN + BPH

Answer 23

alpha blocker

Question 24

HTN + post -MI

Answer 24

b-blocker spironolactone non-dihydropyridine CCB

Question 25

HTN + recurrent stroke

Answer 25

diuretic ACEI

Question 26

statins

Answer 26

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

Question 27

niacin

Answer 27

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

Question 28

cholestyramine, colestipol, colesevelam

Answer 28

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)

Question 29

ezetimibe

Answer 29

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

Question 30

gemfibrozil, clofibrate, bezafibrate, fenofibrate

Answer 30

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)

Question 31

digoxin

Answer 31

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.

Question 32

Class IA antiarrhythmics

Answer 32

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. 

Question 33

class IB antiarrhythmics

Answer 33

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. 

Question 34

class IC antiarrhythmics

Answer 34

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**. 

Question 35

class II antiarrhythmcs

Answer 35

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. 

Question 36

class III antiarrhythmics

Answer 36

 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. ![Image result for class iiI antiarrhythmics]()

Question 37

class IV antiarrhythmics

Answer 37

(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). 

Question 38

adenosine

Answer 38

 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.

Question 39

Mg

Answer 39

Effective in torsades de pointes and digoxin toxicity.

Question 40

aortic stenosis

Answer 40

systolic ejection click. Crescendo- decrescendo