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FA CARDIO > Pathology > Flashcards

Pathology Flashcards

1
Q

L to R shunts

A

late cyanosis “ blue kids

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2
Q

what is the frequency of L to R shunts?

A

VSD>ASD>PDA

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3
Q

VSD

A

most common congenital cardiac defect

asymptomatic at birth, may manifest weeks later or remain asymptomatic throughout life

Most self resolve

larger lesions may lead to LV overload and HF

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4
Q

ASD

A

defect in interatrial septum

loud S1

wide, fixed split S2

Ostium secundum defects most common and usually occur as isolated findings

this is different than patent foramen ovale, in that it is not a problem in not fusing but rather the septa is missing tissue

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5
Q

PDA

A

in the fetal period, the shunt is R to L which is normal

in the neonatal period, you have a decrease in lung resistance so the shunt becomes L to R causing progressive RVH and/or LVH and HF

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6
Q

wide fixed split S2, loud S1

A

ASD

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7
Q

continuous machine like murmur

A

PDA

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8
Q

how do you keep a PDA open?

A

maintained by PGE synthesis and low O2 tension

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9
Q

how do you close a PDA?

A

indomethacin

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10
Q

Where is a PDA heard best?

A

left infraclaviular region with max intensity at S2 (inspiratory splitting ofS2)

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11
Q

PDA is associated with what maternal condition

A

Maternal Rubella (maculopapular rash begins in face and spreads down the body)

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12
Q

Eisenmenger syndrome

A

Uncorrected L to R shunt (VSD ASD PDA) –> increase in pulmonary blood flow –> pathologic remodeling of vasculature –> pulmonary arterial hypertension

RVH occurs to compensate, the shunt then becomes right to left

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13
Q

What do you see in Eisenmenger syndrome?

A

late cyanosis, clubbing, and polycythemia

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14
Q

COA

A

aortic narrowing near insertion of ductus arteriosus (“juxtaductal”)

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15
Q

COA

A

aortic narrowing near insertion of ductus arteriosus (“juxtaductal”)

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16
Q

COA is associated with

A

bicuspid aortic valve, other heart defect and Turner syndrome

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17
Q

what will you see in COA?

A

hypertension in upper extremities and weak, delayed pulse in lower extremities (brachial-femoral delay)

with age, collateral arteries erode ribs (notched appearance on CXR)

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18
Q

what are 2 consequences of COA

A

bacterial endocarditis, cerebral hemorrhage

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19
Q

what defect will you have from Alcohol exposure in utero (F.A.S)?

A

VSD, ASD, PDA, TOF

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20
Q

what defect will you have from congenital rubella?

A

septal defects, PDA, Pulmonary artery stenosis

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21
Q

what defect will you have from Down Syndrome

A

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

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22
Q

what defect will you have from infant of diabetic mother

A

Transposition of great vessels

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23
Q

what congenital defect will you have from Marfan Syndrome

A

MVP, thoracic aortic aneurysm and dissection, aortic regurgitation

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24
Q

what congenital defect will you have from Prenatal lithium exposure

A

Ebstein anomaly

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25
Q

what congenital defect will you have from Turner syndrome

A

Bicuspid aortic valve, COA

26
Q

what congenital defect will you have from Turner syndrome

A

Bicuspid aortic valve, COA

27
Q

what congenital defect will you have from Wlliams Syndrome

A

supravalvular aortic stenosis

28
Q

what congenital defect will you have from 22q11 syndromes

A

Truncus arteriosus, TOF

29
Q

hypertension

A

defined as persistent systolic BP > 140 mmHg and/or diastolic BP > 90 mmHg

30
Q

what are the risk factors of hypertension

A

increase age, obesity, diabetes, physical inactivity, excess salt intake, excess alcohol intake, family history; black> white>asian

31
Q

what are the risk factors of hypertension

A

increase age, obesity, diabetes, physical inactivity, excess salt intake, excess alcohol intake, family history; black> white>asian

32
Q

primary htn (essential) is related to an increase in

A

CO or TPR

33
Q

when is secondary HTN seen

A

renal/renovascular disease (fibromuscular dysplasia, usually found in younger women) and primary hyperaldosteronism

34
Q

hypertensive urgency

A

severe hypertension without acute end organ damage

35
Q

hypertensive urgency BP

A

> 180/>120

36
Q

hypertensive emergency

A

severe ht. with end organ damage

37
Q

what are some examples of hypertensive emergency

A

stroke, encephalopathy, papilledema, MI, HF, aortic dissection, kidney injury, microangiopathic hemolytic anemia, eclampsia, retinal hemorrhages and exudates

38
Q

hypertension predisposes to

A

CAD, LVH, HF, afib, aortic aneurysm, stoke, chronic kidney disease, retinopathy

39
Q

isolated systolic hypertension

A

systolic pressure is increased while diastolic is not; after age 50, caused by age related decrease in the compliance of aorta and its proximal major branches (ex:aortic stiffening)

40
Q

isolated systolic hypertension

A

systolic pressure is increased while diastolic is not; after age 50, caused by age related decrease in the compliance of aorta and its proximal major branches (ex:aortic stiffening)

41
Q

what are signs of hyperlipidemia

A

xanthomas, tendinous xanthoma, corneal arcus

42
Q

xanthomas

A

plaques or nodules composed of lipid-laden histiocytes in skin

43
Q

where do you normally find xanthomas, and what is a name for it?

A

on the eyelids, xanthelasma

44
Q

tendinous xanthoma

A

lipid deposit in tendon

45
Q

where do you normally find a tendinous xanthoma

A

achilles

46
Q

corneal arcus

A

lipid deposits in cornea

47
Q

corneal acrus is most common in

A

common in elderly! (arcus senilis), but appears earlier in life in hypercholesterolemia

48
Q

arteriosclerosis

A

hardening of the arteries, with arterial wall thickening and loss of elasticity

49
Q

arteriolosclerosis

A

affects the small arteries and arterioles

50
Q

what are the two types of arteriolosclerosis

A

hyaline (thickening of vessel walls in essential hypertension or diabetes mellitus)

hyperplastic (onion skinning in severe hypertension with proliferation of smooth muscle cells)

51
Q

hyaline arteriolosclerosis

A

(thickening of vessel walls in essential hypertension or diabetes mellitus)

52
Q

hyperplastic arteriolosclerosis

A

(onion skinning in severe hypertension with proliferation of smooth muscle cells)

53
Q

hyperplastic arteriolosclerosis

A

(onion skinning in severe hypertension with proliferation of smooth muscle cells)

54
Q

Monckeberg (medial calcific sclerosis)

A

affects medium sized arteries

calcification of elastic lamina of arteries –> vascular stiffening without obstruction

55
Q

what do you see on an X-ray of someone with Monckeberg

A

pipestem appearance

56
Q

which is common, arteriolosclerosis or Monckeberg

A

arteriolosclerosis

57
Q

do you see an obstruction in Monckeberg?

A

no! does not obstruct blood flow, and the intimate is not involved

58
Q

Atherosclerosis

A

disease of elastic arteries (large) and large and medium sized muscular arteries

caused by buildup of cholesterol plaques

59
Q

What are risk factors for atherosclerosis

A

modifiable: smoking, hypertension, hyperlipidemia, diabetes
nonmodifiable: age, sex (increase in men and postmenopausal women), family hx

60
Q

what is important in the pathogenesis of atherosclerosis

A

inflammation

61
Q

what is the pathogenesis of atherosclerosis?

A

endothelial cell dysfunction –> macrophage and LDL accumulation –> foam cell formation –>fatty streaks –> smooth muscle cell migration (involves PDGF and FGF) –>proliferation, and extracellular matrix deposition –> fibrous plaque –> complex atheromas

FA CARDIO (4 decks)

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