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Cardio Flashcards

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USMLE® Step 1 flashcards
1
Q

Four cardiac defects associated with maternal alcohol consumption

A

ASD, VSD, PDA, tetrology of Fallot

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2
Q

3 Cardiac defects associated with congenital rubella

A

PDA, pulmonary artery stenosis, septal defects

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3
Q

3 cardiac defects associated with Down Syndrome

A

AV septal defect, ASD, VSD

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4
Q

Cardiac defect associated with diabetic mother

A

Transposition of great vessels (failure of aorticopulmonary septum to rotate)

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5
Q

Cardiac defects associated with marfan syndrome

A

MVP, aortic dissection, aortic regurg

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6
Q

Cardiac defect associated with prenatal lithium exposure (bipolar mother)

A

Ebstein anomaly

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7
Q

2 cardiac defects associated with 22q11 syndromes

A

Truncus arteriosis, tetrology of Fallot

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8
Q

2 cardiac defects associated with Turner Syndrome

A

Coarctation of Aorta, bicuspid aortic valve

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9
Q

List 3 nitrates used in angina

A

Nitroglycerin, Isosorbide dinitrate, isosorbide mononitrate

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10
Q

What is the mechanism of Nitrates

A

increase NO in smooth muscle cells, increase cGMP to vasodilate blood vessels (veins > arteries)

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11
Q

What are 3 conditions Nitrates are used to treat?

A

Angina, acute coronary syndrome, pulmonary edema

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12
Q

What effect do nitrates have on EDV, BP, contractility, HR, ejection time and myocardial oxygen demand, respectively?

A

decrease, decrease, none, increase (reflex), decrease and decrease

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13
Q

What are the side effects of nitrates?

A

reflex tachycardia, throbbing headache, hypotension, flushing; “Monday disease” (tolerance during weekdays but not weekend)

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14
Q

Which beta blockers are contraindicated in treating angina?

A

Pindolol and Acebutolol

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15
Q

Which therapy is used when standard angina medications are not effective?

A

Ranolazine

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16
Q

What is Ranolazine’s mechanism?

A

Blocks late-phase inward sodium flow of cardiomyocyte–> decreases inward flow of Ca+2 and decreases diastolic wall tension, thus decreasing myocardial oxygen demand

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17
Q

How does Ranolazine prolong the QT interval?

A

Inhibits outward flow of K+ in phase 3 of cardiomyocyte potential

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18
Q

What adverse effects associated with Ranolazine use?

A

constipation, headache, nausea, dizziness and prolonged QT (risk of Vfib)

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19
Q

Which enzyme do statins inhibit?

A

HMG CoA reductase

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20
Q

What is the mechanism of statin function?

A

Decrease cholesterol production by inhibiting HMG CoA reductase, increase LDLR expression, decrease overall cholesterol

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21
Q

which medication is most potent in reducing cardiac related mortality?

A

Statins

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22
Q

How do Statins influence LDL, HDL and TG levels?

A

Decrease a lot, increase and decrease

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23
Q

Adverse effects of statins

A

Slight increase in LFTs, myopathy (especially when used with fibrates and niacin)

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24
Q

Name 3 bile acid resins

A

Cholestyramine, colestipol, colesevelam

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25
Q

How do bile acid resins function?

A

Inhibit bile acid reabsorption in terminal ileum and dietary cholesterol absorption; causes increase in LDLR on hepatocytes and causes liver to use more of body’s cholesterol

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26
Q

How do bile acid resins affect LDL, HDL and TG levels?

A

Decrease, slightly increase and slightly increase

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27
Q

What are the side effects of bile acid resins (cholestyramine, colestipol, colesevelam)

A

GI upset, hypertriglyceridemia, decrease absorption of ADEK vitamins (contraindicated in pts with diverticulitis or blood thinners), gallstones

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28
Q

How does ezetimibe function?

A

Binds dietary cholesterol in GI and prevents its absorption, increases liver production of endogenous cholesterol and LDLR to decrease LDL

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29
Q

Side effects of Ezetimibe

A

rare increase in LFT, diarrhea

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30
Q

How does Ezetimibe affect LDL, HDL and TG levels?

A

Decrease, no effect, no effect

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31
Q

Name 3 Fibrates

A

Gemfibrozill, Bezafibrate, Fenofibrate

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32
Q

How do fibrates function?

A

Target VLDL, decrease VLDL by activating PPAR alpha and increasing activity of LPL to increase TG clearance

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33
Q

How do fibrates increase HDL levels?

A

Induce increase in APOA1 and APOA2 to bind HDL

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34
Q

How do fibrates affect LDL, HDL and TG levels?

A

Decrease, increase, substantially decrease

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35
Q

Adverse effects of fibrates?

A

Myopathy (esp with statins), gallstones

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36
Q

How does Niacin (B3) influence LDL, HDL and TG levels?

A

Decrease, increase, decrease

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37
Q

How does niacin function in controlling cholesterol?

A

At liver, decrease VLDL secretion, in tissues, decrease TG release; inhibit lipolysis and increase HDL

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38
Q

Side effects of niacin?

A

Red, flushed face (decrease with NSAID use), Hyperglycemia, Hyperuricemia, can cause increased LFT (monitor liver)

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39
Q

How do omega 3 fatty acids (fish oil) decrease TGs?

A

decrease production of ApoB and VLDL

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40
Q

Name a common cardiac glycoside

A

Digoxin

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41
Q

From where is digoxin derived?

A

Foxglove plant

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42
Q

What is Digoxin’s inotropic mechanism?

A

Directly inhibit cardiomyocyte Na+/K+ ATPase, indirectly inhibit Na+/Ca+2 pump, leading to increased intracellular Ca+2 and stimulating contraction

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43
Q

What is Digoxin’s antiarrhythmic mechanism?

A

Stimulate vagus nerve, acts on muscarinic receptor of AV node, decrease AV node conduction

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44
Q

What are two major uses for Digoxin?

A

Heart Failure and Atrial Fibrillation

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45
Q

What are the cholinergic adverse effects of Digoxin?

A

nausea, vomiting, diarrhea, blurry yellow vision, arrhythmia, AV block, bradycardia

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46
Q

What are the ionic adverse effects of Digoxin?

A

Can lead to hypekalemia

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47
Q

How do verapaimil, amiodarone and quinidine worse digoxin toxicity?

A

Displace digoxin from tissue-binding sites and decrease its clearance

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48
Q

How does hypokalemia worsen digoxin toxicity?

A

Allows Digoxin to bind more avidly to Na+/K+ ATPase

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49
Q

What EKG changes do you see in chronic Digoxin use?

A

T wave changes, QT shortening, ST scooping

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50
Q

Antidote for Digoxin toxicity?

A

Slowly normalize K+, anti-digoxin Fab, Mg+2, cardiac pacer

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51
Q

Which antiarrhythmics act primarily on cardiomyocyte potentials?

A

Class I and III

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52
Q

Which antiarrhythmics primarily act on SA/AV Node potentials?

A

Class II and IV

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53
Q

Which antiarrhythmics are primarily important for rate control?

A

II and IV (act on AV and SA nodes)

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54
Q

Which anitarrhythmics are important for rhythm control?

A

Class I and III

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55
Q

List the Class IA antiarrhythmics

A

Quinidine, Procainamide, Disopyramide

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56
Q

What is the mechanism of Class IA antiarrhythmics?

A

Bind and inhibit depolarized (open or inactive) Na+ channels, slow AP conduction by slowing phase 0

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57
Q

What does it mean when Class I drugs are state dependent

A

Selectively bind to receptors that are frequently depolarized (like in tachycardia)

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58
Q

How do Class IA drugs affect the effective refractory period of an action potential?

A

Prolong it (prolong QT), increase risk of Torsades des pointes

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59
Q

What is the clinical use for Class IA drugs?

A

Atrial and ventricular arrhythmias, especially re-entrant, ectopic SVTs and VTs (like WPW)

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60
Q

Describe the side effects of quinidine

A

cinchonism (tinnitus, headache)

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61
Q

Describe the adverse effects of procainamide

A

SLE-like syndrome due to production of ANA

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62
Q

Describe the adverse effects of disopyramide

A

Heart failure

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63
Q

How avidly do class IA, IB, and IC antiarrhythmics bind Na+ channels? (decrease slope)

A

IC > IA > IB

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64
Q

List three major Class IB antiarrhythmics

A

Lidocaine, Phenytoin, Mexiletine

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65
Q

What is the primary clinical use of Class IB antiarrhythmics?

A

Treatment of post-MI ventricular arrhythmias (best for ischemic tissue) and digitalis-induced arrhythmias

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66
Q

How do Class IB drugs affects AP duration?

A

Decrease it

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67
Q

Adverse effects of Class IB drugs?

A

CNS effects (slurred speech, tremors, parasthesias), CV depression

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68
Q

List 2 Class IC drugs

A

Flecainide, Propafenone

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69
Q

Mechanism of Class IC drugs?

A

Bind INa+ channels. Prolong ERP in AV node and bypass tracts. No effect on ERP in purkinje and ventricular tissue. Minimal effect on AP duration

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70
Q

Clinical use of Class IC drugs?

A

SVTs, Atrial fibrillation rhythm control

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71
Q

Adverse effects of Class IC drugs

A

Pro-arrhythmic, especially post-MI (contraindicated in structural and ischemic heart disease)

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72
Q

Structural and ischemic heart disease is a contraindication for which antiarrhythmic?

A

IC

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73
Q

Which antiarrhythmic class are beta blockers?

A

Class II

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74
Q

Which beta blockers are nonselective beta2 antagonists?

A

Propanolol and timolol

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75
Q

Which beta blocker has partial alpha antagonist properties?

A

Carvedilol

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76
Q

What is the mechanism of beta blockers?

A

Decrease SA and AV nodal activity by decreasing cAMP, decreasing Ca+2 currents and thus suppress abnormal pacemakers

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77
Q

Which slope of nodal conduction do beta blockers affect?

A

Phase 4 (decrease slope– prolong it)

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78
Q

How do beta blockers prolong PR interval?

A

AV node is more sensitive, delay conduction from SA to AV nodee

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79
Q

What are class II antiarrhythmics (beta blockers) clinically used for?

A

Rate control of SVTs, atrial fibrillation and flutter

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80
Q

Adverse effects of beta blockers?

A

Impotence, worsens COPD/asthma, bradycardia, AV block, CNS effects; may mask hypoglycemic signs

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81
Q

What is an adverse effect of metoprolol?

A

Dyslipidemia

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82
Q

What is an adverse effect of Propanolol?

A

can exacerbate vasospam in Prinzmetal angina

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83
Q

Antidote for beta blocker overdose?

A

Saline, atropin, glucagon

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84
Q

Why are carvedilol and labetalol okay to use for pheochromocytomas or cocaine toxicity?

A

Do not cause unopposed alpha1-agoonism (bc block both alpha and beta receptors)

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85
Q

List four Class III antiarrhythmics

A

Amiodarone, Ibutilide, Dofetilide, Sotalol

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86
Q

What is the mechanism of Class III antiarrhythhnmics?

A

Block K+ channels in cardiomyocytes, prolong phase 2 and 3 (effective refractory period, QT interval, AP duration)

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87
Q

What are Class III drugs primarily used to treat?

A

Rhythm control in atrial fibrillation and flutter. Amiodarone and sotalol for ventricular tachycardia

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88
Q

Adverse effects of sotalol

A

torsades des points, excessive beta blockade

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89
Q

Adverse effects of amiodarone

A

pulmonary fibrosis, corneal deposits, hyper and hypothyroidism (40% iodine by weight), neurologic effects, constipation, bradycardia, heart block, heart failure

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90
Q

Adverse effects of ibutilide

A

Torsades des pointes

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91
Q

What affect does Amiodorone have on CYP450?

A

Inhibits it

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92
Q

How is Amiodarone different from other Class III antiarrhythmics?

A

Has Class I, II, III and IV effects

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93
Q

What should be monitored while using amiodarone?

A

LFTs, PFTs, TFTs

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94
Q

List two major Class IV antiarrhythmics

A

Verapamil and Dilitiazem

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95
Q

What class of antiarrhythmics are calcium channel blockers?

A

Class IV

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96
Q

Which Ca+2 channels are Class IV antiarrhythmics specific for?

A

L-Type (phase 4 and 0)

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97
Q

Which part of the heart do class IV antiarrhythmics primarily work on?

A

SA and AV nodes

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98
Q

What is the mechanism of Class IV antiarrhythmics?

A

Decrease conduction velocity, prolong effective refractory period and increase PR interval by blocking Ca+2 channels

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99
Q

What are the two main clinical functions of Class IV antiarrhythmics?

A

Rate control for atrial fibrillation and prevential of nodal arrhythmias (SVTs)

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100
Q

What are the adverse effects of Class IV antiarrhythmics?

A

Constipation, flushing, edema, AV block (prolong PR interval), sinus node depression, heart failure

101
Q

List three Class V antiarrhythmics

A

Digoxin, Mg+2, Adenosine

102
Q

What is the clinical use of Magnesium?

A

Torsades des pointes and digoxin toxicity

103
Q

What is the clinical use of Adenosine?

A

Diagnose/terminate certain SVTs

104
Q

Which substances blunt effects of Adenosine?

A

Caffeine, Theophylline, methylxanthines

105
Q

Adverse effects of adenosine?

A

Flushing, hypotension, chest pain, “sense of doom,” bronchospasm

106
Q

How does Digoxin function as an antiarrhythmic?

A

Stimulates vagus nerve, suppresses SA and especially AV node to dampen AP conduction

107
Q

Which receptor does Dobutamine bind to?

A

Beta1, minimally on beta2 and alpha1

108
Q

What is dobutamine used for?

A

Management of refractory heart failure associated with severe LV systolic dysfunction and cardiogenic shock

109
Q

What affects on inotropy, chronotropy and vasodilation does dobutamine have?

A

positive inotrope (increase contractility), weakly positive chronotrope (increase heart rate a bit and thus oxygen consumption), mild vasodilation (decreased filling time)

110
Q

Define myocardial hibernation

A

State of chronic ischemia in which both myocardial metabolism and function are reduced to match the reduction in coronary blood flow– prevents myocardial necrosis
Function is restored upon restoration of blood flow

111
Q

What type of heart failure can restrictive cardiomyopathy lead to/

A

Diastolic heart failure

112
Q

Describe the presentation of diastolic heart failure

A

progressive exertional dyspnea, ascites, edema, elevated JVP, LV hypertrophy with LA enlargement

113
Q

What is the histological appearance of cardiac amyloidosis?

A

Acellular and amorphous pink material in cardiac muscle tissue

114
Q

What is the histologic appearance of cardiac sarcoidosis?

A

Noncaseating granulomas containing giant cells in myocardium

115
Q

Signs of embolism following an invasive vascular procedure in a pt with atheroembolic disease?

A

Blue toe, livedo reticularis with normal peripheral pulses

116
Q

Histo findings in pt with atheroembolic disease would show

A

Cholesterol clefts in arterial lumen

117
Q

Kidney biopsy of pts with poorly controlled hypertension would show

A

Hyperplastic arteriola changes (intimal fibroelastosis)

118
Q

What are the signs of left heart failure?

A

Bibasilar crackles, dyspnea on exertion, progressive fatigue

119
Q

Signs of right heart failure

A

Jugular venous distention , peripheral edema

120
Q

Viral myocarditis can lead to which cardiac condition

A

Dilated cardiomyopathy

121
Q

6 Causes of dilated cardiomyopathy

A

Viral infection, genetics, toxicity, alcholism, pregnancy, hemochromatosis

122
Q

Causes of concentric LVH

A

Long-standing hypertension, aortic stenosis

123
Q

Two characteristics of hypertrophic cardiomyopathy

A

Asymmetric septal hypertrophy and systolic anterior motion of mitral valve

124
Q

Which two conditions can cause cryptogenic stroke

A

PFO and ASD

125
Q

What causes a PFO

A

Incomplete fusion of septum primum and septum secundum

126
Q

What devo defect causes ASD

A

Aplasia of septum primum or secundum

127
Q

Holosystolic murmur at lower left sternal border is significant for

A

Ventricular septal defect

128
Q

Which coronary artery supplies posterior 1/3 of IV septum and most of inferior wall of left ventricle?

A

Posterior descending artery (branch of right coronary artery)

129
Q

Which coronary artery supplies anterior 2/3 of IV septum and anterior wall of left ventricle and part of anterior papillary muscle?

A

LAD

130
Q

Which part of the heart does the left circumflex coronary artery supply

A

Lateral and posterior superior walls of left ventricle

131
Q

Which coronary artery supplies wall of right ventricle and provides collateral circulation for LAD occlusion?

A

Right marginal branch of RCA

132
Q

Which anticoagulant drug targets GpIIb/IIIa?

A

Abciximab

133
Q

What condition does Abciximab treat?

A

Unstable angina, acute coronary syndrome (pts undergoing percutaneous coronary interventions)

134
Q

Which condition does Argatroban treat?

A

Heparin-induced thrombocytopenia

135
Q

What condition does Dabigatran treat

A

Afib and venous thromboembolism

136
Q

How do argatroban and dabigatran work?

A

Direct thrombin inhibitors

137
Q

How does heparin work?

A

Potentiates antithrombin III activity to inactivate thrombin (II) and Xa

138
Q

How does Clopidogrel inhibit platelet aggregation?

A

Blocks P2Y12 on platelet ADP receptors

139
Q

Severe coarctation of the aorta with a closed ductus arteriosis can present in a neonate as

A

signs of heart failure (dyspnea, fatigue) and shock

140
Q

Which cardiac condition is associated with Friedrich ataxia?

A

Hypertrophic cardiomyopathy

141
Q

Which proteins are deposited in cardiomyocytes in AL amyloidosis?

A

Monoclonal light chains

142
Q

Which proteins are deposited in cardiomyocytes in senile systemic amyloidosis?

A

wild-type transthyretin

143
Q

Which part of the heart are most cardaiac myxomas found?

A

Left atrium

144
Q

What is a common cause of dilated cardiomyopathy in Latin America?

A

Chagas disease (Trypanosoma cruzi infection)

145
Q

Abnormal electrical impulses in which part of the heart usually leads to AF?

A

Pulmonary veins

146
Q

How does AF beget AF?

A

Abnormal conduction causes remodeling of heart with shortened refractory periods and heightened excitability, forming ectopic foci and re-entrant impusles in atria

147
Q

In AF, which factor determines the ventricular contraction rate?

A

AV node refractory period

148
Q

In which cases does the Purkinje system assume pacemaker activity?

A

severe bradycardia (<40bmp)

149
Q

What is the mechanism of Alteplase?

A

Activates plasminogen to plasmin to cause clot lysis

150
Q

What is the most common adverse effect of fibrinolytic therapy and what are symptoms?

A

Intracerebral hemorrhage (abrupt onset decreased consciousness, asymmetric pupils, irregular breathing)

151
Q

Transesophageal echocardiography probe lies within closest proximity to which part of heart?

A

left atrium

152
Q

Which part of heart comprises most of posterior surface of heart?

A

Left atrium

153
Q

Which part of the heart comprises apex and left border of heart on frontal CXR?

A

Left ventricle

154
Q

Which part of the heart forms the right lateral cardiac border on CXR?

A

right atrium and SVC

155
Q

Which part of heart forms anterior surface and majority of inferior border?

A

Right ventricle

156
Q

Which part of the heart lies posterior and to the right of the main pulmonary artery?

A

Ascending aorta

157
Q

Which part of the heart travels above the right pulmonary artery and left bronchus?

A

Aortic arch

158
Q

Which structures originate from aortich arch?

A

Braciocephaic, left common carotid and left subclavian

159
Q

Which part of the heart lies posterior to esophagus and left atrium?

A

Descending aorta

160
Q

The combination of which two lipid-lowering agents increases myopathy?

A

Fibrates and statins

161
Q

Which 3 hypertensive medications cause vasodilation and reflex tachycardia

A

ACE inhibitors, nitrates, and peripheral alpha-1 selective adrenergic blockers (prazosin)

162
Q

Which 5 medications have negative chronotropic effects?

A

beta blockers, non-dihydropyridine CCBs (diltiazem, verapamil), cardiac glycosides (digoxin), amiodarone and sotalol and cholinergic agonists (pilocarpine, rivastigmine)

163
Q

Combined use of which drugs can lead to negative chronotropic effects with severe bradycardia and hypotension?

A

Beta blockers and non-dihydropyridine CCBs

164
Q

In cardiac catheterization, an excessive rise in left atrial systolic pressure is indicative of

A

Mitral regurgitation

165
Q

In cardiac catheterization, elevated LV diastolic pressure and decreased aortic diastolic pressure indicates

A

Aortic regurge

166
Q

In cardiac catheterization, a large pressure difference between LV and aorta indicates

A

Aortic stenosis

167
Q

In cardiac catheterization, increased LAP during diastole indicates

A

Mitral stenosis

168
Q

Patients with benign prostatic hyperplasia and hypertension would benefit with treatment from

A

allpha-1 blockers (prazosin, Doxazosin, Terazosin)

169
Q

Patients with coronary artery disease and heart failure with hypertension will benefit from therapy with

A

cardioselective beta blockers

170
Q

Patients with essential hypertension first-line therapy

A

HCTZ

171
Q

Patients with evidence of vasospasm like Raynaud or Prinzmetal angina benefit with therapy from

A

CCBs

172
Q

Difference between dihydropyridine (-dipines) CCB and non-dihydropyridine CCB (verapamil, dilitiazem)

A

-Dipines are selective for vascular smooth muscle (vasodilation) and do not affect heart as much as non-DPs

173
Q

Endocardial thickening and fibrosis of tricuspid and pulmonary valves is a characteristic finding of

A

Carcinoid heart disease (elevated 5-HIAA)

174
Q

Which two antiarrhythmics lead to QT prolongation?

A

Class IA and Class III

175
Q

Mechanism of Class IB antiarrhythmicss

A

block Na+ channels and inhibit phase 0; does not prolong QT

176
Q

Mechanism of Class III antiarrhythmics

A

Block K+ channel (phase 3)

177
Q

Which two vascular beds are particularly susceptible to atherosclerosis?

A

Lower abdominal aorta and coronary arteries

178
Q

What is the primary risk factor for aortic dissection/?

A

Hypertension

179
Q

What is Monckeberg sclerosis

A

Sclerosis of medial layer of muscular arteries. Seen in >50 yos, generlaly leads to systolic hypertension

180
Q

Aortitis characterized by obliterative endarteritis of vasa vasorum signifies

A

Tertiary syphilis

181
Q

4 signs of a normal aging heart

A

Decreased LV chamber size, sigmoid-shaped ventricular septum, increased interstitial connective tissue with amyloid deposition; accumulation of lipofuscin in myocardiocytes (brownish pigment)

182
Q

Prussian blue stain on cardiomyocytes used to identify

A

Hemosiderosis due to chronic hemolytic anemia or hemochromatosis

183
Q

Asymmetric septal hypertrophy with disproportionate thickening of ventricular septum compared to LV free wall signifies

A

Hypertrophic cardiomyopathy

184
Q

Subendocardial vacuolization and fibrosis signify

A

Chronic ischemic heart disease

185
Q

What is Kussmaul sign and what does it signify

A

Paradoxical increase in JVP during inspiration,

chronic constrictive pericarditis, RHF, cardiac tamponade and restrictive cardiomyopathy

186
Q

Three conditions that can cause pulsus paradoxus

A

Cardiac tamponade, constrictive pericardial disease, cor pulmonale

187
Q

What does a pericardial knock (after S2) signify

A

Cosntrictive (chronic) pericarditis

188
Q

What is the EKG WPW triad?

A

Delta wave, shortened PR interval, widened QRS

189
Q

Describe the vagal maneuver pathway

A

Baroreceptors on carotid sinus stimulated by massage –> afferent limb via CN IX carries signal to vagal nucleus and medullary centers–> efferent limb via CN X synapses on SA and AV nodes to slow conduction through AV node and prolong AV refractory period

190
Q

Vagal maneuver is useful for which arryhtmia

A

Paroxysmal supraventricular tachycardia

191
Q

Why is the liver not that vulnerable to infarcts?

A

Has dual blood supply from portal vein and hepatic artery

192
Q

Explain reflex bradycardia upon administration of alpha1-receptor agonists (phenylephrine, methoxamine)

A

Increased SVR causes increased pressure on baroreceptors in carotid sinus–> stimulation of vagal response–> decreased AV nodal conduction velocity

193
Q

Kussmaul sign, increased JVP, pulsus paradoxus and pericardial knock are findings consistent with

A

Constrictive pericarditis

194
Q

What is the morphological finding of constrictive pericarditis?

A

Thick fibrous tissue in pericardial space between visceral and parietal pericardium

195
Q

first-line and second-line tx for ventricular arrhythmia during MI

A

Amiodarone, Lidocaine

196
Q

Why is Lidocaine preferred for tx of MI ventricular arrhythmias

A

Ischemic tissue has higher RMP, so more inactivated Na+ channels. Lidocaine preferentially binds to inactivated Na+ channels and has negligible effect on QRS due to short duration of action

197
Q

Acute kidney injury, hyperuricemia and acute gout, hyponatremia, hypokalemia and hyperglycemia and high cholesterol are side effects of

A

Thiazide diuretics

198
Q

Cough, angioedema and hyperkalemia are side effects of

A

ACE inhibitors

199
Q

Peripheral edema, dizziness or light headedness are side effects of

A

CCBs (amlodipine, nifedipine)

200
Q

Bronchospasm, bradycardia, fatigue and sexual dysfunction are side effects of

A

beta blockers

201
Q

Patients with bicuspid aortic valve have increased risk of which condition in their 50s?

A

Aortic stenosis (accelerated atherosclerosis and calcification of valve)

202
Q

Harsh, holosystolic murmur at mid to lower left sternal border that may not be detectable at birth but becomes audible 4-10 days of age suggests

A

Small VSD

203
Q

Why do large VSDs not have murmur and how do they present

A

Large VSD leads to relatively equal pressure between right and left ventricles, so no murmur. Present as heart failure, failure to thrive and diaphoresis with feeding; can result in cyanosis and pulm hypertension later in life

204
Q

Cyanosis and heart failure with Tricuspid regurg is suggestive of

A

Ebstein’s anomaly

205
Q

Immediate treatment/antidote for heparin overdose

A

Protamine sulfate (binds heparin and inactivates it)

206
Q

Immediate treatment/antidote for Warfarin overdose

A

Fresh frozen plasma

207
Q

Why is FFP not useful for heparin overdose?

A

contains ATIII, which can exacerbate effects of heparin

208
Q

Long term treatment for warfarin overdose

A

Vitamin K (takes days)

209
Q

All types of necrosis have which type of hallmark of cell injury? (seen in aging, stiffened aortic valves)

A

Dystrophic calcification

210
Q

Best spot to hear S3?

A

Cardiac apex with patient in left lateral decubitus position

211
Q

Which murmur is commonly associated with hypertrophic cardiomyopathy?

A

Mitral regurgitation

212
Q

How does phenylephrine (/NE) increase total peripheral resistance and decrease heart rate

A

selective alpha-1 agonist causes systemic vascular constriction and induces baroreceptor response to decrease SV and slow heart rate

213
Q

Which agent is a beta-receptor agonist that decreases TPR and diastolic pressure and increases cardiac rate, CO and pulse pressure?

A

Isoproterenol

214
Q

How does clonidine decrease blood pressure

A

alpha-2 receptor agonist that decreases central sympathetic outflow

215
Q

Single most important risk factor for developing aortic dissection

A

Hypertension

216
Q

Which anti-inflammatory irreversibly inhibits COX1 and COX2 via acetylation?

A

Aspiriin

217
Q

Which anti-inflammmatory reversibly inhibits COX enzymes

A

Acetaminophen

218
Q

Best alternative for patients with aspirin allergy

A

Clopidogrel

219
Q

Blocks P2Y12 component of ADP receptors on platelet surface and prevents aggregation

A

Clopidogrel

220
Q

Name two arteriolar vasodilators

A

Hydralazine and Minoxidil

221
Q

Side effect of arteriolar dilators

A

reflex SNS activation and RAAS response (increased HR, CO, Na+ and fluid retention)

222
Q

Persistent cough and angioedema are side effects of which medications

A

ACE inhibitors

223
Q

Peripheral vasoconstriction and cold extremities are side effects of which medication

A

Beta blockers

224
Q

How do cardiac myxomas produce constitutional symptoms (weight loss, fever) and hemorrhage?

A

Produce IL-6 and VEGF

225
Q

Histology of this condition shows scattered cells within mucopolysaccharide stroma, abnormal blood vessels and hemorrhaging. Typically found in left atria (80%)

A

Myxoma

226
Q

Which subunits between hemoglobin and myoglobin are nearly identical?

A

beta subunits

227
Q

Is myoglobin left-shifted or right-shifted?

A

Left-shifted (holds onto oxygen more tightly in muscle)

228
Q

Monomeric protein that binds oxygen in muscle

A

Myoglobin

229
Q

Two most common causes of death after lightning injury

A

Cardiac arrhythmias, respiratory arrest

230
Q

Drug of choice for treating paroxysmal supraventricular tachyardia (PSVTS)

A

ADENOSINE

231
Q

What causes wide and fixed splitting

A

Atrial septal defects

232
Q

A cerebrovascular event in the setting of a known venous thromboembolic disease raises suspicions for

A

paradoxical embolism and septal defects (ASD, PFO, VSD)

233
Q

Portal system is a derivative of which embryological structure?

A

Vitteline veins

234
Q

SVC is derived from which embryologic structure?

A

Common cardinal veins

235
Q

Fastest to slowest cardiac tissue conduction velocity

A

Purkinje system –> Atrial muscle –> ventricular muscle –> AV node (PAVA)

236
Q

Intracytoplasmic granules that are tinged yellowish-brown in myocardial cells represent (sign of aging or “wear and tear”)

A

Lipofuscin (product of free radical injury and lipid peroxidation)

237
Q

Virchow’s triad for developing venous thrombosis

A

Endothelial injury, venous stasis, and hypercoagulable state

238
Q

Risk factor for arterial thromboembolism

A

Atherosclerosis

239
Q

Which arteries are spared in polyarteritis nodosa (medium vessel vasculitis)?

A

Pulmonary (and bronchial sometimes)

240
Q

PDE-3 inhibitor that causes systemic vasodilation, increases cAMP and thus inotropy

A

Milrinone

241
Q

How does Digoxin primarily lower ventricular heart rate in afib?

A

Enhances efferent parasympathetic ganglionic transmission and potentiates end-organ responses to acetylcholine, leading to increased vagal output

242
Q

Most common cause of sudden cardiac death

A

Malignant ventricular arrhythmias (fibrillation)

243
Q

Claudication is due to

A

Atherosclerosis of large arteries

244
Q

Which venous vessel is the most deoxygenate?

A

Coronary

245
Q

Why is Heparin safer to use in pregnant women than Warfarin?

A

Heparin is hydrophilic and cannot cross the placenta while Warfarin is lipophilic and can cross placenta

246
Q

Wide fixed split S2 is suggestive of

A

Atrial septal defect

247
Q

This murmur presents with dyspnea, pulmonary congestion and right sided heart failure

A

Mitral stenosis

248
Q

Do not treat patients with hypertrophic cadriomyopathy, RV infarction, and those on phosphodiesterase inhibitors with

A

Nitrates

USMLE (36 decks)

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