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1
Q

heart originates from the

A

mesoderm

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2
Q

coronary arteries originate from

A

epicardium

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3
Q

neural crest cells forms the

A

AV valves, outflow tract and arch development

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4
Q

mesenchymal tissues forms the

A

valve tissue

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5
Q

cardiogenesis time

A

week 3- 6

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6
Q

rubella virus causes

A

supravalvular PS, asD and PDA

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7
Q

etiology of congenital heart disease

A

90% unknown

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8
Q

pulm. circulation is a low flow and high resistance

A

in utero

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9
Q

post-natal pulm. circulation (2)

A
  1. reduction of the pulmonary vascular resistance

2. higher partial pressure of oxygen

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10
Q

AV junction tissue (2)

A
  1. AV valves

2. atrial and ventricular septum

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11
Q

trisomy 21

A

endocardial tissue: ASD, VSD and PDA

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12
Q

turner

A

coarctation of aorta

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13
Q

tri 18

A

VSD

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14
Q

septum secundum

A

PFO

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15
Q

left ventricular hypoplasia

A

aortic stenosis

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16
Q

situs inversus

A

polysplenia

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17
Q

systolic split S2 murmur

A

ASD

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18
Q

holosystolic murmur- pansystolic

A

VSD

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19
Q

most common VSD

A
  1. paramembranous
  2. muscular
  3. AV canal
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20
Q

TOF (4)

A
  1. VSD
  2. pulm. stenosis
  3. overriding aorta
  4. right ventricular hypertrophy
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21
Q

failure of the conal septum to fuse with the septal band

A

TOF

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22
Q

DTGA needs a

A

VSD or ASD to survive

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23
Q

DTGA can be given

A

prostaglandin to improve mixing of blood by keeping the ductus arteriousus open

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24
Q

polygonal cells with clear cytoplasms

A

rhabdomyomas

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25
Q

associated with tuberous sclerosis

A

rhabdomyomas

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26
Q

tuberous sclerosis mutation

A

TSC1 and TSC2- hamartin and tuberin

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27
Q

there is myofiber disarray especially in the interventricular septum

A

hypertrophic cardiomyopathy

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28
Q

Myocardium is flabby and pale, with subendocardial scars.

A

dilated cardiomyopathy

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29
Q

On histopathology there is a patchy or diffuse interstitial infiltrate of T lymphocytes, macrophages and rare giant cells, with focal myocyte necrosis

A

viral myocarditis

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30
Q

causes of fibrinous pericarditis

A 
MI
post MI
uremia
chest radiation
Rheumatic fever
lupus
trauma
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31
Q

MI: pallor or red-blue hue (dark mottling)

A

<24 hr MI

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32
Q

MI: mottling with yellow tan infarct center

A

2-4 days

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33
Q

MI: risk for arrhythmia

A

2-4 days

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34
Q

MI: risk for free wall rupture

A

5-10 days

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35
Q

MI: hyperemic border, central yellow-tan softening

A

5-10 days

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36
Q

MI: depressed, soft, infarct borders, gelatinous appearance

A

10 days to 2 weeks

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37
Q

MI: gray white scar, progressive from border to center of infarct

A

2-8 weeks

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38
Q

MI: risk for ventricular anuerysm

39
Q

MI: wavy fibers , coagulative necrosis, myocyte eosinophilia, edema hemorrhage, contraction band

40
Q

MI: coagulation necrosis with loss of nuclei and striations, interstitial infiltrate of PMNs

41
Q

MI: beginning disintegration of dead myofibers with dying PMNs, macrophages with phagocytosis dead cells

42
Q

MI: well developed phagocytosis of dead cells, early formation of fibrovascular granulation tissue at margins

43
Q

MI: well established granulation tissue with new blood vessels and increased collagen deposition with decreased cellularity

44
Q

MI: dense collagenous scar

A

> 2 months

45
Q

bulky friable vegetations in the valves

A

infective endocarditis

46
Q

viridians

A

infective endocarditis

47
Q

rheumatic fever can cause what type of pericarditis

48
Q

pyrogens

A

rheumatic fever

49
Q

mydssytolic click

50
Q

cavo-tricuspid isthmus ablation

A

treatment for atrial flutter

51
Q

treatment for atrial fibrillation (course of 4)

A
  1. anti-coagulants
  2. rate control- BB or CCB (prevents rapid ventricular beating by blocking AV node)
  3. rhythm control- Ic or III
  4. ablation
52
Q

p waves in SVT or PSVT?

53
Q

SVT with narrow QRS

54
Q

treatment for Monomorphic VT

55
Q

ablation causing pulmonary vein isolation

A

atrial fib

56
Q

hemodynamically stable Vtach treatment

A

-amiodarone (Class III) or lidocaine (class IB)

57
Q

anti-arrhythmia medical therapy in Vtach with a ICD

A

prevent or reduce frequency of ICD firing

58
Q

use dependent effects thus effects of medication is greater on faster heart rates

A

sodium channel blocker

59
Q

Medication for WPW

60
Q

soidum channel block effect AP phases and ekg

A
  1. slope of phase 0 decreases
  2. prolongation of phase 3 (if class Ia)
  3. QRS widen
61
Q

when do you not want to give a sodium channel block (2)

A
  1. abn. heart structure

2. RBB or lBB because the QRS is already wide

62
Q

reverse use dependent effect thus medication is great on the heart rate is slow

A

potassium channel blocker

63
Q

effect of potassium channel blockers (2)

A
  1. prolong phase 3

2. QT lengthens

64
Q

medication tat exacerbate bradycardia

A

AV node blockers such as BB and CCB

65
Q

natural compensation for reduced blood flow

A

collateral artery formation

66
Q

resistance is too high leading to inadequate flow to downstream tissues

A
  1. decreased lumen radius
67
Q

statins for secondary prevention? primary prevention?

A

yes for secondary and maybe for primary if the pt. has a ASCVD score above > 7.5%

68
Q

main effects of nitrates

A

venodilation lowering preload and there is a lower afterload due to arterial dilation

69
Q

bad effects of nitrates (2)

A
  1. tachycardia

2. increased inotropy

70
Q

negative effect of Beta blockers

A

can increase wall tension in patients with left ventricular dysfunction

71
Q

negative effects of CCB

A
  1. reduce contractility

2. AV block

72
Q

acute thrombotic coronary artery occlusion

73
Q

may be demand-ischemia or sub-occlusive coronary thrombus

74
Q

inferior stemi associated with (4)

A
  1. GI symptoms
  2. NG induced hypotension
  3. AV nodal block if AV node is ischemic
  4. proximal RCA occlusion
75
Q

pletal

A

phosphodiesterase inhibitor for chronic claudication due to its ability to dilate vascular smooth muscle

76
Q

infrainguinal occlusion si often

77
Q

greater distal vascular disease

A

Diabetes and PVD

78
Q

Type B treatment for aortic dissection

A

medical therapy

79
Q

Type A treatment for aortic dissection

A

urgent surgical repair

80
Q

with a symptomatic carotid blockage of >50

% what can we do?

A

endarterectomy

81
Q

aortic valve stenosis

  • what type of overload?
  • murmur?
  • type of hypertrophy
A
  • pressure overload
  • systolic murmur: cresecendo-decrescendo
  • concentric
82
Q

aortic valve regurg

  • what type of overload?
  • murmur?
  • type of hypertrophy
A
  • volume overload
  • diastolic murmur- asutin flint
  • eccentric
83
Q

mitral stenosis murmur

A

diastolic murmur

84
Q

mutral regurg. murmur

A

holosystolic; pansystolic

85
Q

dilated LV cavity with a reduced left ventricular EF

86
Q

is there a loss of contractility in HFrEF?

87
Q

harsh systolic murmur and palpable thrill

88
Q

continuous murmur during systole and diastole

89
Q

TOF has what type of murmu

90
Q

in coarctation of the aorta what has higher BP the leg or arm?

91
Q

friction rub noise

A

pericarditis

92
Q

diffuse ST segment elevation and PR segment depression

A

pericarditis

93
Q

Y descent refers to

A

earliest stage of passive ventricular filling

Cardio (26 decks)

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