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USMLE Step 1 > Cardiology > Flashcards

Cardiology Flashcards

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USMLE® Step 1 flashcards
0
Q

Ostium secundum

A

Formed as tissue degenerates in superior septum primum

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1
Q

Septum secundum

A

Contains F ovale

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2
Q

Truncus arteriosus

A

Becomes ascending aorta and pulmonary trunk

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3
Q

Bulbus cordis

A

Becomes smooth parts ventricles

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4
Q

Left horn of sinus venosus

A

Becomes coronary sinus

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5
Q

Right horn of sinus venosus

A

Becomes smooth part RA

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6
Q

Right common and Right anterior cardinal veins

A

Becomes SVC

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7
Q

ASD

A

Most common type=ostium secundum type. Usu asymptomatic until adulthood.

Signs: wide fixed splitting S2, ESM in aortic area.

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8
Q

VSD

A

Most comm congenital heart malformation. Most commonly from incomplete fusion AV cushions. Most small and resolve spontaneously.

Sxs: easy fatiguability, harsh holosystolic murmur best heard at tricuspid area

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9
Q

Aorticopulmonary septum

A

Separates truncus arteriosus into aorta and pulmonary trunks.

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10
Q

Left to right shunts

A

VSD, ASD, PDA.

Late cyanosis.

If do not close and continued high flow in pulm circulation, can cause hypertrophy of pulm arterial system and even fibrosis.

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11
Q

Right to left shunts

A 
TOF
TGA
TAPVR
Tricuspid atresia
Truncus arteriosus

Early cyanosis and squatting

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12
Q

Eisenmenger syndrome

A

Initial L to R shunt but then continued high flow in pulm vasculature causes hypertrophy, RVH until shunt reverses. Late cyanosis.

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13
Q

Squatting-mechanism to alleviate sxs

A

Occurs in R-L shunts. Squatting increases systemic vascular resistance (L sided P) by compressing femorals. Decreases pressure gradient between R and L sides of heart so may alleviate sxs.

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14
Q

1st aortic arch

A

Becomes part of maxillary artery

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15
Q

2nd aortic arch

A

Becomes stapedial artery and hyoid artery

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16
Q

3rd aortic arch

A

Becomes common carotid and proximal internal carotid artery

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17
Q

4th aortic arch

A

Becomes aortic arch and proximal R subclavian artery

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18
Q

5th aortic arch

A

Regresses in humans

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19
Q

6th aortic arch

A

Becomes proximal pulmonary arteries and ductus arteriosus

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20
Q

Pre-ductal coarctation of aorta

A

Proximal to DA. DA typically remains patent

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21
Q

Post-ductal coarctation of aorta

A

Distal to DA. Increased BP in arms, decreased BP in legs, weak/absent femoral pulses, collateral circulation.
*Rib notching due to increased flow through intercostal arteries.

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22
Q

PDA

A

L-R shunt. Most common in premies. Does not result in early cyanosis. Give prostaglandin inhibitors-indomethacin, NSAIDs.

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23
Q

22q11 deletion

A

Assoc with truncus arteriosus, TOF

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24
Q

Down’s syndrome

A

Associated with ASD (especially), VSD, AV septal defect

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25
Q

Child of diabetic mother

A

Association with TGA

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26
Q

Congential rubella-cardiac defects

A

Septal defects, PDA, pulmonary artery stenosis

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27
Q

Marfans

A

Aortic insufficiency=late complication

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28
Q

Signs of tamponade

A

Decreased MAP, distended neck veins (inability SVC to drain), pulsus paradoxus, electrical alternans on ECG

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29
Q

Subendocardial infarct

A

Repeated episodes of temporary occlusion of coronary artery (unstable angina) or severe anemia/hypotension. ST depression.

*If flow through coronary artery compromised, subendocardial tissue most vulnerable to ischemic injury sicne farthest from either blood supply.

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30
Q

Causes pericarditis

A

SLE, RA, MI, TB, malignancy

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31
Q

Fastest conduction velocity in heart’s electrical system

A

His-Purkinje

32
Q

Slowest conduction velocity in heart’s electrical system

A

AV node

33
Q

Decreased contractility

A

Beta blockers, CCBs, HF, parasymp stimulation, acidosis, hypoxia, hypercapnia

34
Q

Venous O2

A

Can be measured at pulmonary artery

35
Q

Ficks CO equation

A

CO=O2 consumption/(arterial O2-venous O2)

36
Q

S2 splitting

A

Inspiration increases.

Wide-RV emptying delayed, e.g. RBBB, pulmonic stenosis

Fixed-ASD.

Paradoxical-delayed LV emptying (AS, LBBB). P2A2…when inspire, split eliminated since P2 delayed.

37
Q

Carotid baroreceptors

A

Tonically active
Increased activity indicates increase in BP.
Trasmitted by CN IX

38
Q

Aortic arch baroreceptors

A

Transmitted by CN X

39
Q

Arterioles

A

Largest resistance in CV system

40
Q

Serum

A

plasma-clotting factors

41
Q

Fastest to Slowest conduction velovity

A

His-Purkinje, Atrial, Ventricular, AVN

42
Q

Absolute refractory period

A

Phases 0-2

43
Q

Effective refractory period

A

Conducted AP cannot be generated.

44
Q

How cardiac muscle differs from skeletal

A

Has: plateau, spontaneous depolarization, gap junctions, more mitochindria, increased contractile force through changes in fiber contractility (vs #fibers recruited in skel muscle)

45
Q

Measure of contractility

A

EF

46
Q

Bowditch effect

A

Myocardial contractility increases with higher heart rates. Possibly due to inability of Na+/K+-ATPase to keep up with influx od Na so increased Ca within myocyte.
Aka Treppe phenomenon or staircase effect

47
Q

Frank Starling law

A

Force of systolic contraction proportional to initial length of cardiac muscle in diastole. (i.e. increased stretch or preload will increase FOC).

48
Q

S2-effect of inspiration

A

Increases splitting

49
Q

Wide splitting S2

A

Where RV emptying delayed, e.g. pulmonic stenosis, RBBB

50
Q

Carotid stretch receptors

A

Tonically active. Transmitted by CNIX

51
Q

Aortic arch stretch receptors

A

Transmitted by CNX

52
Q

Mediation of arteriolar dilation and venous constriction

A

Histamine and bradykinin

53
Q

TXA2

A

Vasoconstrictor

54
Q

Prostacyclin

A

vasodilator

55
Q

Capacitance

A

=V/P. Ability to store charge, i.e. how distensible a BV is. Inversely related to elastance

56
Q

Hypertension

A

> 140 and/or >90 on 3+ readings or single reading >170/110

57
Q

Prehypertension

A

120-139/80-89

58
Q

Stage 1 HTN

A

140-159/90-99

59
Q

Stage 2 HTN

A

> 160/>100

60
Q

Initial medication for primary HTN

A

Thiazides

61
Q

Secondary HTN-causes

A

Renal artery stenosis, renal parenchymal disease, OCP, glucocorticoids, phenylephrine, NSAIDS, pheo, Conns, hyperthyroidism, Cushings, coarctation, fibromuscular dysplasia

62
Q

Hypertensive retinopathy

A

AV nicking, pappiledema, loss venous pulsation, flame hemorrhages

63
Q

Malignant hypertension

A

Severe, rapid increase in BO, usu >240/120. Assoc with end organ damage (“flea bitten kidneys). Young African-Americans, LVH, papilledema, retinal hemorrhage

64
Q

Munckeberg arteriosclerosis

A

Benign medical calcification of medium sized muscular arteries. Elderly, those with DM, metabolic syndrome, HTN.

65
Q

Arteriolosclerosis

A

Affects INTIMA of small arterioles and arteries. most often in those with DM, metabolic syndrome, HTN

66
Q

Hyaline arteriolosclerosis

A

Protein deposits in essential HTN-pink arterial wall thickening with luminal narrowing. DM-due to advanced glycosylation end products being deposited in BM. HTN-increased pressure forces proteins into wall causing hardening of arteries.

67
Q

Hyperplastic arteriolosclerosis

A

In malignant HTN. Increase in smooth muscle cell proliferation and BM duplication-“onion skinning”. Esp prevalent in renal arterioles.

68
Q

Myocarditis-causes

A

Most common cause in developed world is viral–coxsackie B, rubella, CMV. Worldwide-Chagas disease. Bacterial in immunocompromised (S aureus, C diphtheriae, H influenzae). Others: toxoplasmosis, Kaposis, Lyme, ARF, RhF, lupus, doxorubicin

69
Q

Subacute Bacterial Endocarditis

A

Usually affects previously damaged valves. VIRIDANS. May see ring enhancing lesions in brain due to septic emboli. Staph epidermidis on prosthetic valves.

70
Q

Duke criteria for endocarditis

A

Positive serial cultures, prior endocardial involvement, IV drug use, fever, vasc/immune phenomenon, valvular lesions on echo

71
Q

Marantic Endocarditis

A

Non-Bacterial Thrombotic Endocarditis. Small sterile fibrin vegetations on heart valves of those with devastating disease. Paraneoplastic syndrome-mucin secreting tumors (usu colon or pancreatic)

72
Q

Libman-Sacks Endocarditis

A

Ab damage to valves from SLE/ Sterile vegetations on BOTH SIDES of heart valves. Oft asymptomatic but may have a heart murmur.

73
Q

DCM-causes

A

Idiopathic (most common), EtOH abuse, thiamine deficinecy, coxsackie B, Chagas, HIV, cocaine doxorubicin, Lyme, sarcoidois, hypothyroidism, Wegener granulomatosis, acromegaly, peripartum CM

74
Q

DCM-presentation

A

4 chamber enlargement. R or L HF. Decreased EF, JVD, edema, orthopnea, hepatomegaly, cardiomegaly.

75
Q

HCM-presentation

A

Syncope, dyspnea, S4, cardiomegaly, MR, pain releived by squatting and exacerbated by strenuous exercise

76
Q

Diastolic HF-causes

A

Impaired filling: MS, tamponade, pericardial contstriction.
Impaired relaxation: hypertrophy, CM, ischemia
Impaired compliance

77
Q

“Heart failure cells”

A

Intra-alveolar hemosiderin-laden macrophages

USMLE Step 1 (15 decks)

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