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Cards (U.W.) Flashcards

1
Q

which aortic arches don’t contribute to adult anatomy

A

1,2, and 5th

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2
Q

adult anatomy derived from 3rd aortic arch?

A

proximal internal and common carotid A

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3
Q

adult anatomy derived from 4th aortic arch?

A

true aortic arch and subclavian As

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4
Q

adult anatomy derived from 6th aortic arch?

A

pulmonary As and ductus arteriosus

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5
Q

explain Tetrology of Fallot?
cause?
4 associated defects

A
  • deviation of the infundibular septum during development, causes VSD (1) and an overriding aorta (2)
    other associated problems include RVOT obstruction (3) which causes (4) RVH
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6
Q

describe the location of the AV node

A

in the RA, near the septum of the tricuspid valve and coronary sinus orifice

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7
Q

low pitched holosystolic murmur at LLSB that increases with increased afterload

A

VSD

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8
Q

murmurs that are louder with increased handgrip

A

MR,AR, VSD

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9
Q

in a pacemaker where are the three leads placed and how?

A
  1. ) RA 2.) RV via the IVC and SVC

3. LV via coronary sinus which runs in the atrioventricular groove

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10
Q

describe the course of the saphenous V

A

starts at medial foot, runs anterior to medial malleolus and superficially on medial aspect of leg, reaches the femoral triangle inferolaterally to the PUBIC TUBERCLE

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11
Q

describe the blood supply of the retinal A (important in retinal artery occlusion)

A

ICA-> opthalmic A-> retinal A

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12
Q

lead 1, avL, and v5-v6 correlates to which part of the heart? which blood supply

A

lateral left ventricle,

supplied by L circumflex A

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13
Q

V1-V4 correlates to which part of the heart? which blood supply

A 
anterior LV and interventricular septum 
supplied LAD (note distal LAD spares septum, and is V3-V4)
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14
Q

II, III, AVF correlates to which part of the heart

A

RV and inferior LV

RCA

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15
Q

calculate True Positive

A

SENSITIVITY *( # of people WITH disease)

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16
Q

calculate False Negative

A

(1- SENSITIVITY) * (# of people WITH disease)

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17
Q

Aschoff Bodies

A

granulomas of plump macrophages in cardiac tissue

pathognomonic for ARF induced carditis

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18
Q

Wet Beri Beri

A

thiamine B1 deficiency

peripheral neuropathy + CHF

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19
Q

Stanford Type A dissection originates near

Stanford Type B dissection originates near

A

A- ascending- sinotubular junction

B- descending- near L subclavian A

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20
Q

progressive heart failure shortly following viral infection is suspicious for what kind of HF

A

DILATED cardiomyopathy

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21
Q

Nonbacterial thrombotic endocarditis (NBTE)

A

platelet rich, sterile thrombi on cardiac valves

can be related to an advanced malignancy or a chronic inflamm condition (Lupus, Antiphospholipid)

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22
Q

Turner’s Syndrome is associated with what valvular deficiency

A

Bicuspid Aortic Valve

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23
Q

ACUTE pericarditis is associate w

A

pericardial friction rub

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24
Q

Pulsus Paradoxicus

A

upon INSPIRATION, SBP drop by 10+ mmHG
seen in cardiac tamponade, constrictive pericarditis, severe asthma/COPD
reason? bc if expansion of heart is impaired or prevented, inspiration which causes increase in R atrial/ vent filling will cause bowing of septum, decreased LV vol and decreased SV

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25
Q

the collagenous scar formed in the heart, post MI, is what kind of collagen?

A

Collagen type I

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26
Q

collagen type I found in

A

bone, tendons, ligaments,

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27
Q

collagen type II found in

A

cartilage, nucleus pulposis, vitreous humor

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28
Q

collagen type III found in

A

granulation tissue, skin, lungs

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29
Q

collagen type IV found in

A

basement membrane

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30
Q

coronary steal syndrome

A

in response to ischemia, local vasodilators cause coronary arteries supplying ischemic regions to preferentially dilate.
giving this patient a synthetic coronary artery dilator like adenosine or dipyramidole can shunt blood AWAY from ischemic areas making ischemia worse. this is bc a’s to ischemic areas are already max dilated, now these drugs are dilating other coronary a’s too

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31
Q

loss of palpable pulse during inspiration is a physical finding of what

A

pulsus paradoxus

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32
Q

Beck’s Triad includes what? is consistent with which diagnosis

A

1.) hypotension
2.) JVD
3.) diminished heart sounds
acute cardiac tamponade

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33
Q

varicose veins? what causes it? what does it cause?

A

dilated tortuous superficial veins of LE, due to incompetent valves/loss of wall strength
can cause skin ulcers, edema, stasis dermatitis, poor wound healing (note: major thrombotic events are rare bc its superficial veins.)

34
Q

what is most susceptible to atherosclerosis

A

Lower abdominal aorta

coronary As

35
Q

which arteritis’s involve granulomatous formation

A

GCA, takayasu

36
Q

carcinoid heart disease

A

carcinoid syndrome( a neuroendocrine tumor producing excess 5HT, histamine, and VIP) can cause cardiac symptoms. the extra serotonin stimulates fibroblast growth, and fibrous plaque causing TR, pulmonic valvulopathy, and RHF

37
Q

holosystolic murmur that increases in intensity upon inspiration

A

TR

38
Q

Origin of middle meningeal A

A

ECA-> maxillary A->MM

39
Q

what prevents edema in moderate elevations of central venous pressure?

A

increased lymph drainage. even though CVP is increasing, therefore capillary hydrostatic P is increasing, causing more fluid to be filtered into interstitial space, this is offset by increased lymph clearance

40
Q

Osler- Weber- Rendu syndrome

A

autosomal dominant condition of hereditary hemorrhagic telengectasias
common presentation: nosebleeds+ pale pink spider like lesions

41
Q

occlusion of RCA causes what kind of HF

A

RHF bc while yes, RCA supplies inferior LV via PDA it is not the only source of LV blood supply. Meanwhile, the RV is mainly only supplied by the RCA so RV failure is seen first. ( double check xray findings, and if lungs are clear you know this is only the RHF)

42
Q

how to decrease LVOT HOCM murmur

A

increase the preload or afterload.

- ex: squat/passive leg raise and handgrip

43
Q

hyperplastic arteriosclerosis vs hyaline arteriosclerosis?
describe each
what is each associated with

A

hyperplastic- onion skin like concentric thickening–> hypertensive crisis
hyaline- homogenous acellular thickening–> lower levels of hypertension

44
Q

murmur at RSB (w/ radiation to carotids) cresecendo decrescendo

A

AS

45
Q

where is angiotensinogen made

A

liver

46
Q

where is ACE found

A

pulmonary endothelial cells

47
Q

how does squatting help in a tet spell

A

it increases SVR, making the blood want to flow through stenotic pulmonary circulation instead of going into systemic

48
Q

after how long of ischemia do the cardiac myocytes stop contracting

A

1 minute due to ATP depletion and cellular toxins

49
Q

till how long after ischemia is injury reversible for the cardiac myocytes

A

30 minutes- until the adenosine is depleted

50
Q

what is normal LA max pressure

A

10 mmhg

51
Q

increase in LA max pressure and peaked, early, tall “v” waves in pressure tracing of LA is

A

mitral regurg

52
Q

severe MR can be indicated by what heart sound

A

S3- S3 is an indicator of LV dilation or increased blood flow into LV

53
Q

irregularly irregular rhythm

A

a-fib

54
Q

AAA pathogenesis

A

chronic transmural inflammation leads to weakening and progressive expansion of aortic wall due to MMPs released by inflamm cells

55
Q

Concentric hypertrophy of LV

A
  • caused by chronic increase in afterload – like aortic stenosis and chronic HTT
56
Q

liofuscin

A

yellow brown perinuclear pigment seen in aging/cachetic pts due to lipid peroxidation and free radical buildup

57
Q

why is it advisable to give aspirin before Niacin t(x) for hyperlipidemia

A

niacin (aka nicotinic acid) decreases LDL and TGs and increases HDL. However it also releases prostaglandins which causes the unwanted side-effect of flushing and itching. Aspirin which ihibits PGE production can help

58
Q

DIFFERENTIAL clubbing/cyanosis of LE only, without any discrepency in pulse or BP is what disease?

A

large PDA that has reversed from L->r flow to r–>L flow (eisenmenger)

59
Q

Rheumatic heart disease causes what patholologically

A

chronic inflamm and scarring of valve

60
Q

Infective endocarditis pathology

A

disruption of endocardial surface–> sterile platelet and fibrin attaches (nidus)–> after bacterial infection, bacteria colonize nidus

61
Q

enterrococcus endocarditis is usually preceded by what procedures

A
  • GU related or GI related

cystoscopy, obstetrics, colonoscopy

62
Q

isoproterenol

A

non selective B agonist. B1- increased contractility; B2- decreased TPR

63
Q

claudication caused by

A

atherosclerosis

64
Q

loss of what can make systolic HF significantly worse??

A

loss of atrial kick

65
Q

what is INR

A

patient’s PT/ control PT
- we are measuring PT bc Warfarin inhibits carboxylation of vit K dependent coag factors like Factor VII and remember factor VII is in extrinsic pathway (measured by PT)

66
Q

myxomatous changes in media are found in

A

“cystic medial degeneration” aka aortic aneurysm (often seen in Marfan’s)

67
Q

what jvp waveform is missing in an a-fib pt

A

“a” wave, first wave, has to do with atrial contraction

68
Q

adenosine side effects

A

flsuhing, chest burning, hypotension, high grade AV block

69
Q

most serious complication of kawasaki

A

coronary artery aneurysm

70
Q

where is cardiac action potential speed the fastest

A

purkinje cells

71
Q

where is cardiac action potential speed the slowest

A

AV node

72
Q

from fastest to slowed name the cardiac action potential cells

A

park at venture ave

purkinje, atrial, ventricular, AV node

73
Q

how does a cardiac myocyte relax after excitation and contraction

A

well it has to get the Ca2+ out of the cytoplasm in one of two ways

(1) Na+/Ca2+ exchanger
(2) SERCA- Ca2+ ATPase - this one brings Ca2+ back into SR

74
Q

how do you best listen to S3/S4?

A
  • use bell at apex

- lateral decubitus & end expiration to bring heart closer to chest

75
Q

nitrates work by

A

primarily venodilation

causes decreased preload, so reduces myocardial work and therefore myocardial oxygen demand

76
Q

what predisposes to IE in developed countries

A

MVP

77
Q

Cilastazol

A
  • phosphodiesterase inhibitor

- inhibits platelet aggregation and acts as arterial vasodilator

78
Q

wide fixed splitting of S2

A

ASD

79
Q

S3 is what kind of dysfuntion? S4?

A

S3- systolic

S4- diastolic

80
Q

how do mineralocorticoid receptor antagonists (spironolactone, eplerone) improve survival/mortality in HF

A

the K+ sparing dieuretics are aldosterone inhibitors

81
Q

VSD sounds like

A

holosystolic murmur over LLSB

82
Q

when is peak intensity of AR

A

right after aortic valve closure

need to knows (31 decks)

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