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USMLE® Step 1 flashcards
1
Q

Patient with TIA/stroke in setting of thromboembolic disease (DVT) should be suspicious for what?

A

Paradoxical embolism

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2
Q

VSD most commonly occurs where?

A

membranous septum

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3
Q

3 main conotruncal abnormalities

A

Transposition of great vessels, TOF, persistent truncus arteriosus

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4
Q

Valves are formed from what structures?

A

Endocardial cushions

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5
Q

Anlantois–>Urachus

A

Median umbilical ligament

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6
Q

Ductus arteriosus

A

Ligamentum arteriousm

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7
Q

Ductus venosus

A

Ligamentum venosum

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8
Q

Foramen ovale

A

Fossa ovalis

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9
Q

Notochord

A

Nucleus pulposus

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10
Q

Umbilical arteries

A

Medial umbilical ligaments

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11
Q

Umbilical vein

A

Ligamentum teres hepatis (contained in falicform ligament)

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12
Q

What closes PDA?

A

Indomethacin (decrease prostaglandin)

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13
Q

Supplies posterior 1/3 of interventricular septum, posterior walls of ventricles, and posteromedial papillary muscle

A

Posterior descending/interventricular artery (PDA)

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14
Q

Supplies anterior 2/3 of interventricular septum, anterolateral papillary muscle, and anterior surface of left ventricle. Inferior wall of LV forms diaphragmatic heart surface

A

Left anterior descending (LAD)

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15
Q

Supplies lateral and posterior walls of left ventricle, anterolateral papillary muscle

A

Left circumflex coronary artery (LCX)

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16
Q

supplies right ventricle

A

Right (acute) marginal artery

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17
Q

What usually supplies SA/ AV node

A

Ricght coronary artery

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18
Q

Right dominant circulation

A

85% of individuals (PDA arises from RCA)

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19
Q

Left dominant ciruclation

A

8% individuals (PDA arises from LCX)

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20
Q

Codominant circulation

A

7% individuals (PDA arises from both LCX and RCA)

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21
Q

Where does coronary artery occlusion most commonly occur?

A

LAD

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22
Q

Two most important factors involved in coronary blood flow autoregulation and what do they regulate

A

NO-regulates large coronary artery + Pre-arteriolar vessels

Adenosine-regulates small coronary arteriolar vessels

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23
Q

Enlargement of what part of the heart can cause dysphagia/hoarseness?

A

Left atrium

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24
Q

Most coronary venous blood drains into

A

Coronary sinus of right atrium

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25
Q

Where does desceining aorta lie in regard to esophagus and left atrium?

A

Posterior to both allowing visualization of descending aorta via transesophageal echocardiography

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26
Q

3 specific factors differentiating heart ciruclation from blood flow provided to skeletal muscle and viscera

A

1) Heart muscle perfused during diastole consuming only 5% of CO
2) Myocardial oxygen req is very high (resting 75-80% and while at work around 90% and this extraction does not occur at this level anywhere else in body)
3) coronary flow regulated by metabolic factors (adenosine causes vasodilation and decreased vascular resistance)

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27
Q

Most common cause of early cyanosis

A

TOF

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28
Q

What other congenital heart anomaly do patients with persistent truncus arteriosus have?

A

VSD

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29
Q

Most common congenital cardiac defect?

A

VSD

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30
Q

How is ASD different than patent foramen ovale?

A

ASD has septae missing tissue while PDA has tissue that is unfused

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31
Q

What does tricuspid atresia require for viability?

A

Both ASD and VSD

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32
Q

Most important prognostic factor in TOF?

A

Pulmonic stenosis

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33
Q

What is the consequence of PDA?

A

Late cyanosis in lower extremities (differential cyanosis) and not upper extremities because PDA after major branches of aorta that feed the upper extremities. Due to late on set reversal of shunt flow from left to right to right to left.

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34
Q

Alcohol rexposure in utero (fetal alcohol syndrome)

A

VSD (important cause), PDA, ASD , TOF

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35
Q

Congenital rubella

A

PDA

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36
Q

Down syndrome

A

AV septal defect (endocardial cushion defect), VSD ASD (ostium primum ASD)

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37
Q

Infant of diabetic mother

A

Trasposition of great vessels

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38
Q

Marfan syndrome

A

MVP, thoracic aortic aneurysm and dissection

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39
Q

Prenatal lithium exposure

A

Ebstein anomaly

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40
Q

Turner syndrome

A

Bicuspid aortic valve, coarctation of aorta

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41
Q

Williams syndrome

A

Supravalvular aortic stenosis

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42
Q

22q 11 syndromes

A

Truncus arteriosus, TOF

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43
Q

Fredreich ataxia

A

Hypertrophic cardiomyopathy

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44
Q

Tuberous sclerosus

A

Valvular obstruction due to cardiac rhabdomyomas

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45
Q

Most common heart tumor

A

Metastasis from breast, lung, melanoma, lymphoma

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46
Q

Most frequent cardiac tumor in children

A

Rhabdomyomas (associated with tuberous sclerosis)

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47
Q

Most frequent cardiac tumor in adults

A

Myxomas

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48
Q

Growth factor avidly produced by myxomas?

A

VEGF

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49
Q

Fick principle

A

CO=rate of O2 consumption/arterial O2-venous O2 content

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50
Q

Mean arterial pressure

A

COTPR or 2/3 SBP1/3DBP

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51
Q

Pulse pressure

A

Systolic pressure-diastolic pressure

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52
Q

2 variables pulse pressure is related to

A

Directly related to SV and inversely related to capacitance

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53
Q

Contractility is a function of what?

A

intracellular calcium

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54
Q

La place law

A

radiuspressure/2wall thickness

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55
Q

4 factors that require increase myocardial oxygen demand

A

Increase contractility, increase afterload, increase heart rate, increase diameter of ventricle

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56
Q

What accounts for most TPR an what accounts for most blood storage capacity?

A

TPR, Veins

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57
Q

Resistance equation

A

Driving pressure(delta p)/flow (q)–>8nl/pir^4

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58
Q

Volumetric flow rate (Q)

A

flow velocity (v) * cross-sectional area (A)

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59
Q

What period of cardiac cycle is the period of highest O2 consumption

A

Isovolumetric contraction

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60
Q

JVP absent in atrial fibrillation

A

a wave

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61
Q

JVP absent in tricuspid regurgitation

A

x descent

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62
Q

a wave

A

right atrial contraction

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63
Q

c wave

A

RV contraction (closed tricuspid valve bulging into atrium)

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64
Q

x descent

A

right atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction

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65
Q

v wave

A

increase right atrial pressure due to filling agains closed tricuspid valve

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66
Q

y descent

A

RA emptying into RV

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67
Q

murmur best heard at aortic area

A

systolic murmur (aortic stenosis, flow murmur, aortic valve sclerosis)

68
Q

murmur best heard at left sternal border

A

diastolic murmur (AR/PR) systolic murmur (hypertrophic cardiomyopathy)

69
Q

murmur best heard at left infraclavicular region

A

Continuous murmur (patent ductus arteriosus)

70
Q

murmur best heard at pulmonic area

A

systolic ejection murmur (pulmonic stenosis, flow murmur (eg. physiologic murmur))

71
Q

murmur best heard at tricuspid area

A

pansystolic murmur (triscuspid regurgitation, VSD) diastolic murmur (tricuspid stenosis, ASD)

72
Q

murmur best heard at mitral area

A

systolic murmur (mitral regurg) diastolic murmur (mitral stenosis)

73
Q

Bedside maneuver: Inspiration

Effect:

A

Increase intensity of right heart sounds

74
Q

Hand grip

A

Increase afterload
Increase intensity of MR, AR, VSD
Decrease intensity of HOCM
MVP: later onset of click/murmur

75
Q

Valsalva, standing up

A

(decrease preload)
decrease intensity of most murmurs (including AS)
increase intensity of HOCM
MVP” earlier onset of click/murmur

76
Q

Rapid squatting

A

increase preload
increase intensity of AS murmur
decrease intensity of HOCM
MVP: later onset of click/murmur

77
Q

Speed of conduction

A

Purkinje>atria>ventricles>AV node

78
Q

Pacemeakers

A

SA>AV>Bundle of his/purkinje/ventricles

79
Q

Normal length of PR interval

A
80
Q

Normal length of QRS complex

A
81
Q

QT interval

A

ventricular depolarization, mechanical contraction of ventricles, ventricular repolarization

82
Q

PR interval

A

From start of atrial depolarization to start of ventricular depolarization

83
Q

T wave

A

ventricular repolarization. inversion may indicate recent mi

84
Q

J point

A

Point in between QRS complex and start of ST segment

85
Q

ST segment

A

isoelectric, ventricles depolarized

86
Q

presence of U wave is caused by what?

A

hypokalemia, bradycardia

87
Q

Drug induced causes of Torsades

A 
AntiArrhythmics
AntiBiotics
AntiCychotics
AntiDepressants
AntiEmetics
88
Q

Inheritance of Romano ward an jervell lange nielsen and brugada syndrome

A

Auto dominant and auto recessive and auto dominant

89
Q

Triad of WPW

A

Prolonged QRS, Shorter PR interval, Delta wave

90
Q

What regulates number of atrial impulses that can reach ventricle and determines ventricular contraction rate in afib?

A

AV node refractory period

91
Q

Afib treatment for chronic Afib (>48 hours)

A

Antithrombotic therapy (eg warfarin), rate control (b blocker, non-dihydropyridine Ca2+ channel blocker, digoxin), rhythm control (class IC or III antiarrhythmics)

92
Q

AFib treatment for new afib (

A

Cardioversion (used for new and not old afibb becuase cardioverision can dislodge possible clot)

93
Q

Where to right/left leads in pacemakers get in the heart

A

Right is simple from left subclavian to SVC while left is more difficult because it goes through coronary sinus on atrioventricular groove of right atrium

94
Q

1st degree AV block

A

PR interval >200 msec. Each PR interval is equal

95
Q

Difference btwn 2nd degree Type I and Type II av block

A

Type I- progressive lengthening of PR interval until beat is “dropped” (P wave not followed by QRS complex)
Type II-Dropped beats are not preceeded by change in PR interal (P wave not followed by QRS complex)

96
Q

Treatment of 1st, 2nd, 3rd AV block

A

1st-none
2nd type I-none type II-pacemaker
3rd degee-pacemaker

97
Q

Disease that can cause 3rd degree av block

A

lyme disease

98
Q

What is recombinant form of BNP for heart failure?

A

Nesiritide

99
Q

Aortic arch receptor transmits through what?

A

Vagus nerve to solitary nucleus of medulla (responds to increase in BP)

100
Q

Carotid sinus transmits through what?

A

Glossopharyngeal nerve to solitary nucleus of medulla (responds to decrease and increase in BP)

101
Q

Method by which carotid massage decreases HR

A

Increase AV node refractory period

102
Q

Triad of cushing reaction

A

hypertension, bradycardia, and respiratory depression

103
Q

Describe cushing rxn.

A

Increase in ICP–>arteriole constriction–>cerebral ischemia–>increased pCO2+decrease pH–>increased perfusion pressure (hypertension)–>increased stretch of carotid sinus–>peripheral reflex baroreceptor induced bradycardia

104
Q

Central vs peripheral chemoreceptor response

A

Central-Paco2, hypercapnia

Peripheral-PaO2, hypoxemia

105
Q

What can be used to treat paroxysmal supraventricular tachycardia in patients with no other history of heart disease?

A

Carotid massage (slows conduction through AV node and increase node refractory period sotpping reentrant tachycardia)

106
Q

What is unique about vasculature in lungs compared to other organs in setting of hypoxia

A

Lung hypoxia causes vasoconstriction so that only well ventilated areas are perfused. In other organs, hypoxia causes vasodilation

107
Q

Autoregulation of skeletal muscle

A

Exercise: lactate, adenosine, H+, K+, CO2

At rest: Sympathetic tone (alpha1 vasoconstriction, b2 vasodilation)

108
Q

Autoregulation of heart

A

local metabolites: adenosine, NO, CO2, decreased o2

109
Q

Autoregulation of brain

A

CO2( decrease pH)–>potent cerebral vasodilator

110
Q

equation for net fluix movement Jv

A

Kf[(Pc-Pi)-c(pi(c)-piIi)]

111
Q

4 factors causing edema with excess fluid outflow into interstitium commonly caused by:

A

Increase capillary pressure (increase Pc)
Decreased plasma proteins (decrease pi(C))
Increased capillary permeability (increased kf)
increased interstitial fluid colloid osmotic pressure (increase pi (i).)

112
Q

4 types of xanthomas?

A

Eruptive xanthoma-abruptly with plasma triglyceride or lipid increase
Tendinous xanthoma
Xanthalesma-eyelid or periorbital
Plane anthomas-appear as linear lesions in skin folds associated with primary biliary cirrhosis

113
Q

In what conditions is hyaline arteriolosclerosis found?

A

Essential hypertension or diabetes mellitus

114
Q

In what conditions is hyperplastic arteriolosclerosis found?

A

Severe hypertension

115
Q

Differentse bewtween arteriolosclerosis and monckeberg (medial calcific sclerosis)

A

Arteriolosclerosis decreases vessel caliber and produce end organ ischemia. Monckeberg is not clinically significant because does not affect luminal caliber and blood flow

116
Q

Vessels that arteriolosclerosis and monckeberg calcific sclerosis affect

A

Arteriolosclerosis-small arteries and arterioles

Monckeberg-medium sized arteries

117
Q

Pathophys of monckeberg (medial calcific sclerosis)

A

Calcification of internal elastic lamina (ie media of arteries). INTIMA NOT INVOLVED

118
Q

Varicose veins blood flow

A

From deep veins to superficial veins due to increased pressure in superificial veins causing them to dilate restricting venous outflow

119
Q

What is more common in varicose veins? thromboembolism or venous stasis?

A

Venous stasis that can cause ulcers common in the medial malleolus

120
Q

What can happen to skin in chronic venous insufficiency?

A

Stasis dermatitis with erythema and scaling and perogressive dermal fibrosis and hyperpigmentation.

121
Q

4 modifiable risk factors for atherosclerosis

A

HTN, diabetes, hyperlipidemia, smoking

122
Q

What is most responsible for producing intimal response in atherosclerosis?

A

SMC

123
Q

SMC migration involves what growth factors

A

FGF, PDGF, TGFB

124
Q

Main determinant onf whether or not a coronary artery plaque will cause ischemic myocardial injury?

A

RAT at which it occludes involved artery

125
Q

AAA is associated with what risk factor?

A

Atherosclerosis

126
Q

TAA associated with what risk factor?

A

Cystic medial degeneration

127
Q

What changes are seen with cystic medial degeneration?

A

Myxomatous changes

128
Q

Most common site of injury in blunt aortic rupture (traumatic aortic rupture most commonly in MVC)

A

Aortic isthmus

129
Q

Single most important risk foctor for development of intimal tears

A

HTN

130
Q

Common location of atheroscleorisis?

A

AA>coronary>popliteal>carotid

131
Q

EKG for stable, unstable, prinzmetal angina

A

ST sement depression, st segment depression, st segment elevation

132
Q

What test is most sensitive for coronary artery vasospasm?

A

Ergonovine test by stimulating alpha-adrenergic/serotonergic receptors

133
Q

What is the mechanism behind pharmacologic stress tests?

A

coronary steal syndrome

134
Q

What determines likelinhood of plaque rupture?

A

plaque stability rather than size where activated macrophages in the atheroma contribute to collagen degradation by secreting metalloproteinases contributing to collagen degradation

135
Q

Most common cause of sudden cardiac death

A

v fib

136
Q

Explain CAD induced SCD

A

Acute plaque–>acute myocardial ischemia–>electrical instability in heart–>potentially lead to vfib

137
Q

Leads with st elevations or Q waves

V1-V2

A

Anteroseptal (LAD)

138
Q

V3-V4

A

anteroapical (disatl LAD)

139
Q

V5-V6

A

Anterolateral (LAD or LCX)

140
Q

I, aVL

A

Lateral (LCX)

141
Q

InFerior (RCA)

A

II, III, aVF

142
Q

Gold standard for MI in first 6 hours

A

ECG

143
Q

Most sensitive and specific marker for MI (gold standard)

A

Troponin I (rise after 4 hours after infarction and increased for 7-10 days)

144
Q

Useful marker for detecting reinfarction that occurs days afterinitial MI

A

CKMB (because rises 6-12 hours after and levels return to normal within 48 hours)

145
Q

Risk of complications and time frame

0-4 hours, 4-24 hours, 1-3 days, 3-14 days, 2weeks- 2 months

A

0-24 hours (arrhythmia, cardiogenic shock , heart failure)
1-3 days (Fibrinous pericarditis)
3-14 days (Ventricular pseudoaneurysm (risk of rupture), free wall rupture–>tamponade, papillary muscle rupture–>mitral regur, iv septal rupture–>VSD)
2 weeks-2 months (Dressler syntrome, HF, arrhythmias, true ventricular aneurysm)

146
Q

valvular disorder in HOCM

A

May see mitral regurg due to impaired mitral valve closure

147
Q

Cause of LV outflow obstruction in obstructive HOCM

A

anterior displacement of mitral valve leaflet toward hypertrophied interventricular septum

148
Q

3 places where you see eccentric hypertrophy

A

1) aortic/mitral regurg
2) MI
3) dilated cardiomyopathy

149
Q

3 places where you see concentric hypertrophy

A

1) chronic htn
2) aortic stenosis
3) HOCM

150
Q

Mainstay treatment of CHF

A

ACE inhibitor

151
Q

drugs that decrease mortality in CHF

A

ACE inhibitors or ARBs, b blockers, and spironolactone

152
Q

drugs that are used for symptomatic relief in CHF

A

thiazide or loop diuretics

153
Q

drugs that improve both symptoms and mortality in select patients

A

Hydralazine with nitrate therapy

154
Q

Difference in EF, EDV and contractility and compliance in systolic vs diastolic dysfunction

A

Systolic-decreased contractility, decreased EF, increased EF

Diastolic-decreased compliance, same EF, same EDV, increased LV EDP

155
Q

First sign of shock

A

tachycardia

156
Q

CVP, CO, SVR or Hypovolemic, cardiogenic, obstructive, and distributive shock

A

Hypovolemic: decreased CVP, decreased CO, increased SVR
Cardiogenic/obstructive: increased cvp, decreased co, increased SVR
Distributive: decreased CVP, increased CO, decreased SVR

157
Q

tricuspid valve endocarditis associated with what 3 bugs in IV drug abuse

A

candida, s auereus, pseudomonas

158
Q

Negative culture and bacterial endocarditits

A

Coxiella burnetii, bartonella, HACEK

159
Q

2 manifestations of syphillitic heart disease

A

Aneurysm of ascending aorta or aortic arch, or aortic insufficiency (aortic regurg)

160
Q

Does verapamil work on skeletal muscle?

A

no. no significant flux of calcium across l-type calcium channels in skeletal muscle, but significant flux in cardiac and smc.

161
Q

How is ca2+ efflux established prior to myocyte relaxation?

A

ca2+ atpase (active transport to sequester calcium within sr to reistablish ion gradient) and Na+/ca2+ exchanger.

162
Q

what type of channels cause automaticity in cardiac nodal cells?

A

If channels

163
Q

What increases slope of phase 4 in SA node and determines HR

A

Catecholamines

164
Q

What decreases slope of phase 4 in SA node and decreases HR

A

Ach/adenosine

165
Q

Bacillary angiomatosis vs Kaposi sarcoma differnces

A

Mistaken for each other frequently but bacillary angiomatosis has neutrophils infiltrate while kaposi sarcoma has lympocytic infiltrate

USMLE Step 1-2015 (18 decks)

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