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USMLE Step 1 > Cardiovascular > Flashcards

Cardiovascular Flashcards

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USMLE® Step 1 flashcards
1
Q

The trabeculated parts of the heart arise from which embryonic structures?

A

The primitive atrium and primitive ventricle

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2
Q

The embryonic bulbus cordis gives rise to which part(s) of the mature heart?

A

The smooth parts of the L and R ventricles

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3
Q

The primitive pulmonary vein gives rise to which part(s) of the mature heart?

A

The smooth part of the L atrium

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4
Q

The right horn of the sinus venosus gives rise to which part(s) of the mature heart?

A

The smooth part of the R atrium

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5
Q

The superior vena cava arises form which structures of the embryonic heart?

A

R common cardinal vein and R anterior cardinal vein

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6
Q

Defect of which protein leads to dextrocardia via disruption of normal cardiac looping?

A

left-righ dynein

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7
Q

Kartagener syndrome

A

Individuals have situs inversus secondary to primary ciliary dyskinesia. Associated with reduced/absent ability to clear mucus from lungs and hearing loss.

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8
Q

What is a paradoxical embolus? With what condition(s) is it associated?

A

This is a clot formed in the venous circulation by usual mechanisms, but presents atypically (i.e. as a stroke) because it crosses over to the arterial side via a patent foramen ovale or an atrial septal defect.

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9
Q

A ventricular septal defect is most often due to problems with the formation of what structure?

A

The membranous (v. muscular) interventricular septum

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10
Q

Growth of which embryonic structure helps to separate the atria from the ventricles, contributes to atrial septations, AND forms part of the membranous IV septum?

A

Endocardial cushion

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11
Q

Failure of proper neural crest cell migration can lead to which cardiac defects?

A

Transposition of the great vessels
Tetralogy of Fallot
Persistent truncus arteriosus

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12
Q

What are the four defects seen in Tetralogy of Fallot?

A

Overriding aorta
Pulmonary stenosis
VSD
RVH

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13
Q

What is Ebstein anomaly?

A

When the tricuspid leaflets are tethered to the endocardium of the RV due to incomplete separation of the valve from endocardial cushion tissue.
Leads to an “atrialized R ventricle”

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14
Q

Three main shunts of the fetal circulation:

A

Ductus venosus
Foramen ovale
Ductus arteriosus

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15
Q

What are the three sites of erythropoiesis in a fetus prior to the bone marrow kicking in?

A

Yolk sac, liver, spleen

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16
Q

A doctor notes a new-onset murmur of mitral regurgitation 3 days after their patient was admitted for an MI. What complication did this patient experience, and what artery was likely involved in the MI?

A

Posteromedial papillary muscle rupture

Secondary to MI involving posterior descending artery

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17
Q

Why may an infarct involving the RCA lead to bradycardia or heart block?

A

The SA and AV nodes are usually supplied by the RCA, so infarct can cause nodal dysfunction.

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18
Q

How is mean arterial pressure calculated?

A

2/3DBP + 1/3SBP

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19
Q

Contractility is increased by what ion changes?

A

Increased intracellular calcium
Decreased extracellular sodium (2’ to decreased activity of the Na/Ca exchanger)
Increased intracellular sodium (as in digitalis, same mechanism)

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20
Q

Contractility is decreased with:

A 
B1 blockade
HF w/ systolic dysfunction
Acidosis
Hypoxia/hypercapnia
Non-dihydropyridine Ca channel blockers
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21
Q

What is physiologic splitting of S2?

A

Splitting of the S2 sound during inspiration
Drop in intrathoracic pressure causes increased venous return to the R hear and thus increased RV ejections time and delayed closure of the pulmonic valve.

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22
Q

What is wide splitting of S2 and in what condition(s) is it seen?

A

Exaggeration of normal splitting seen in conditions that delay RV emptying (pulmonic stenosis, RBBB)

23
Q

What is fixed splitting of S2 and in what condition(s) is it seen?

A

Seen in conditions that cause L to R shunt, overloading the pulmonary circulation so that pulmonic closure is greatly delayed regardless of breath due to the increased flow through the pulmonic valve.
i.e. ASD

24
Q

What is paradoxical splitting of S2 and in what conditions is it seen?

A

Delayed aortic valve closure reverses the normal order of valve closure, so splitting is actually heard on expiration because inspiration delays closure of P2, moving it closer to A2 and eliminating the split.
Seen in AS, LBBB.

25
Q

What ion channel(s) is/are responsible for phase 0 of the myocardial AP?

A

Voltage-gated sodium channels open (rapid influx depolarizes)

26
Q

What ion channel(s) is/are responsible for phase 1 of the myocardial AP?

A

Closure of Na channels.

Voltage-gated potassium channels begin opening.

27
Q

What ion channel(s) is/are responsible for phase 2 of the myocardial AP?

A

Voltage-gated Ca channels open and Ca influx balances K efflux.
Ca induced Ca release -> contraction

28
Q

What ion channel(s) is/are responsible for phase 3 of the myocardial AP?

A

Opening of voltage-gated slow K channels and closure of voltage-gated Ca channels -> massive K efflux.

29
Q

What ion channel(s) is/are responsible for phase 4 of the myocardial AP?

A

K channels. Membrane highly permeable to K at resting potential.

30
Q

What ion channel(s) is/are responsible for phase 0 of the pacemaker AP?

A

voltage-gated Ca channels

31
Q

What ion channel(s) is/are responsible for phase 3 of the myocardial AP?

A

Voltage gated K channels -> K efflux

32
Q

What ion channel(s) is/are responsible for phase 4 of the myocardial AP?

A

mixed Na and K f-type channels, which are activated by repolarization of the cell and enable automaticity.

33
Q

Causes of long QT syndrome:

A

Drugs (class IA and III antiarrhythmics, macrolide antibiotics, haloperidol, TCAs, ondansetron)
Hypokalemia
Hypomagnesemia
Congenital long QT syndrome

34
Q

Romano-Ward syndrome

A

AD congenital long QT syndrome with purely cardiac phenotype,

35
Q

Jervell and Lange-Nielsen Syndrome

A

AR congenital long QT syndrome with sensorineural deafness.

36
Q

Brugada Syndrome

A

AD mutation of cardiac Na channels seen in Asian males -> pseudo RBBB and ST elevation in V1-V3. Risk of Vtach, Vfib, SCD.

37
Q

What characteristics of WPW syndrome result in the delta wave with widened QRS seen on ECG?

A

Faster accessory conduction pathway from the atria to the ventricles allows the ventricles to begin depolarizing earlier.

38
Q

What bacterial infection may lead to development of third degree heart block?

A

Lyme disease, infection with Borrelia burgdorferi

39
Q

Actions of atrial natriuretic and B-type natriuretic peptides.

A

Causes vasodilation and decreased sodium reabsorption at the renal collecting tubule.

40
Q

How are signals from the baro- and chemoreceptors of the aortic arch transmitted to the brain?

A

Via vagus n. to solitary nucleus of the medulla

41
Q

How are signals from the baro- and chemoreceptors of the carotid sinus transmitted to the brain?

A

Via glossopharyngeal n. to the solitary nucleus of the medulla

42
Q

What chemical changes cause stimulation of the chemoreceptors in the carotid and aortic bodies?

A

Decreased PO2, Increased PCO2, Decreased pH

43
Q

What chemical changes cause stimulation of the central chemoreceptors in the brain?

A

Changes in PCO2 and pH, but NOT changes in PO2.

44
Q

Heart defects associated with fetal alcohol syndrome:

A

VSD, PDA, ASD, tetralogy of Fallot

45
Q

Early cyanosis is indicative of shunting in which direction?

A

Right to Left

46
Q

Late cyanosis is indicative of shunting in which direction?

A

Left to Right (which becomes R to L due to remodeling of pulmonary vasculature)

47
Q

What additional heart defects does a baby with tricuspid atresia need for survival?

A

ASD and VSD

48
Q

What determines prognosis in Tetralogy of Fallot?

A

The degree of pulmonary stenosis

49
Q

Exposure to what drug in utero is known to cause Ebstein anomaly?

A

Lithium

50
Q

Causes of late cyanosis (“blue kids”):

A

VSD > ASD > PDA

51
Q

Eisenmenger syndrome

A

When an uncorrected L to R shunt leads to pathologic remodeling of the pulmonary vasculature -> pulmonary HTN and RVH -> reversal of the shunt from R to L rusulting in cyanosis, clubbing, and polycythemia.

52
Q

What chromosomal syndrome is associated with coarctation of the aorta?

A

Turner syndrome (XO)

53
Q

Complication of surgical correction of CHD resulting in shortness of breath with physical exertion later in childhood.

A

Phrenic nerve injury -> hemi-diaphragmatic paralysis

USMLE Step 1 (1 decks)

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