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Pathoma > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

stable angina (reversible injury) at what level of stenosis?

A

> 70% stenosis of coronary arteries due to atherosclerosis

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2
Q

what is the hallmark of reversible injury?

A

cellular swelling

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3
Q

characteristics of stable angina?

A

<20 minutes
radiates to left arm/jaw
diaphoresis
SOB

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4
Q

stable angina tx?

A

rest

nitroglycerin

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5
Q

ST-segment depression represents?

A

subendocardial ischemia

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6
Q

unstable angina (reversible injury) pathogenesis?

A

rupture of plaque –>

thrombosis and incomplete occlusion

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7
Q

prinzmetal angina (reversible injury)?

A 
vasospasm of a coronary artery
ST elevation (transmural ischemia) due to complete occlusion via vasospasm clamp-down
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8
Q

episodic chest pain unrelated to exertion?

A

Prinzmetal angina

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9
Q

Prinzmetal angina tx?

A

NG

CCB

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10
Q

complete occlusion of coronary artery and necrosis of myocytes (>20min)

A

MI

ddx: vasospasm, emboli, vasculitis (Kawasaki)

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11
Q

characteristics of MI?

A 
crushing chest pain >20min
radiates to left arm/jaw
diaphoresis
dyspnea (pulm congestion)
no relief from NG
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12
Q

troponin levels:

starts/peaks/returns

A

2-4h post-MI
peaks at 24
normal by 7-10 days

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13
Q

CK-MB levels:

starts/peaks/returns

A

4-6h post-MI
peaks at 24h
returns by 72h
good for dx reinfarction

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14
Q

MI tx

A 
aspirin & heparin
supplemental O2
nitrates
B-blocker (slow HR)
ACE-i
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15
Q

contraction bands due to?

A

reperfusion of Ca2+ causing contraction

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16
Q

reperfusion injury would cause?

A

a continued rise in cardiac enzyme levels, and necrosis

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17
Q

coagulative necrosis sign?

A

removal of nucleus

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18
Q

post-MI:
1 day
1 week
1 month

A

1 day: coagulative necrosis
>1d: inflammation until 1 wk
>1wk: granulation tissue
1 month: scar

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19
Q

post-MI: 4-24h

A

dark discoloration
coagulative necrosis
arrhythmia

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20
Q

<4 hours post-MI

A

no gross/microscopic changes

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21
Q

post-MI: 1-3d

A

yellow pallor
neutrophils
friction rub (pericarditis due to neutrophil inflammation)

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22
Q

post-MI: 4-7d

A 
yellow pallor
macrophages (eat up debris)
free wall rupture (due to MP's)
tamponade
septal rupture --> shunt
pap muscle rupture (RCA)
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23
Q

post-MI: 1-3 wks

A

red border
granulation tissue
fibroblasts/collagen/vessels

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24
Q

post-MI: months

A 
white scar
fibrosis
aneurysm
mural thrombus
Dressler (pericardial antigen exposure --> autoimmune pericarditis)
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25
Q

what only happens with transmural infarcts?

A

fibrinous pericarditis

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26
Q

fatal ventricular arrhythmia without sx or <1h after sx onset

A

sudden cardiac death

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27
Q

causes of sudden cardiac death

A

atherosclerosis #1

MVP, cardiomyopathy, cocaine

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28
Q

special cells seen in pulmonary congestion

A

heart failure cells
due to capillary rupture
iron accum. in MP’s

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29
Q

CHF forward effects

A

RAAS activation
tx: ACE-i (do not want to up TPR)
prevent downward spiral

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30
Q

Features of R-heart failure

A

JVD
Painful HSM –> “cardiac cirrosis”
Nutmeg liver
Pitting edema

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31
Q

cardiac congenital defect sweet spot

A

weeks 3-8

most are sporadic

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32
Q

most common heart defect?

associated with?

A

VSD

fetal alcohol syndrome

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33
Q

what size defect to expect with early presentation? can lead to what syndrome?

A

large defect, greater extent
Eisenmenger
these require surgery

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34
Q

characteristics of Eisenmenger’s

A

RVH
polycythemia (hypoxemia)
clubbing

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35
Q

defect assoc. w/down syndrome

A

ostium primum

36
Q

most common type of ASD

A

ostium secundum

37
Q

sound assoc. w/ASD?

A

split S2

38
Q

PDA assoc. w/what disease?

A

congenital Rubella

39
Q

characteristics of PDA

A

distal to arch
holosystolic “machine-like” murmur
can lead to Eisenmenger –> reversal of shunt to R->L and since it is distal to the arch results in LE edema

40
Q

action of Indomethacin

A

decreases PGE

closes PDA

41
Q

Tetralogy of Fallot

A

Pulm. artery stenosis (prognosis)
RVH
Overriding aorta
VSD

leads to early cyanosis
tx: squatting

42
Q

Tetralogy on X-ray?

A

Boot shaped heart

43
Q

Transposition of the Vessels Tx?Assoc. w/what maternal disease?

A

Maintain PDA (give PGE)
Create ASD or VSD
*maternal diabetes

44
Q

Conditions that cause early cyanosis

A

Tetralogy
Transposition
Truncus persistant
Tricuspid atresia

45
Q

Tricuspid atresia

A

Tricuspid valve doesn’t form
RV doesn’t receive blood –> becomes hypoplastic
Compatible only if assoc. ASD

46
Q

Coarctation: infantile v. adult

A

Infantile: distal to arch, proximal to PDA; LE cyanosis b/c pulmonary circuit is low pressure due to PDA

Adult: no PDA, distal to arch; HTN of the upper extremities, hypotension of the LE

47
Q

Infantile coarctation assoc with?

A

Turner syndrome

48
Q

Adult coarctation assoc. with?

A

*Bicuspid aortic valve

Also notching of ribs

49
Q

acute rheumatic fever

A

group A B-strep
kids 2-3wks post-throat
bacterial M protein mimicry

50
Q

ARF: Jones criteria

A

Evidence of prior infection: ASO or anti-DNase B titer
Minor crit: fever, ESR
Major crit: JONES

51
Q

JONES criteria

A 
J: joint (migratory arthritis)
O: heart (pancarditis)
N: nodules in skin
E: erythema marginatum (annular rash)
S: sydenham chorea

JNES resolve with time, no sequelae; not so with O

52
Q

ARF pancarditis

A

Endocarditis: vegetations on MV (rarely AV) causing regurg.

*Myocarditis: Aschoff bodies (giant cells and fibrinoid/collagen material) *most common COD in ARF

Pericarditis: friction rub

53
Q

Anischkow cells

A

Histiocytes with “caterpillar nuclei” within Aschoff bodies

54
Q

Chronic re-exposure to GAS

A

Can lead to chronic rheumatic valvular disease: scarring –> fusion of commissures (“fish mouth appearance”) –> stenosis of MV, thickening of chordae

55
Q

distinguish rheumatic valve disease from “wear and tear”

A

coexisting mitral stenosis and fusion of aortic valve (because RHD always starts with mitral, so cannot have only aortic and RHD) also no fusion in normal wear/tear

56
Q

3 complications of aortic valve stenosis?

A

concentric LVH
angina/syncope w exercise
microangiopathic hemolytic anemia (due to blood flowing across calcified valves)

57
Q

most common cause of aortic regurg?

A

aortic root dilation
syphilitic aneurysm
infective endocarditis

58
Q

early blowing diastolic murmur
bounding pulses, pulsating nail bed
head bobbing (hyperdynamic circulation)

A

aortic regurgitation

59
Q

treatment of AR

A

valve replacement once LV dysfunction develops

60
Q

hallmark sound of MR

A

mid-systolic click followed by murmur

61
Q

MR murmur intensifies when?

A

squatting or expiration

62
Q

Acute rheumatic disease causes?

Chronic rheumatic disease causes?

A

Mitral regurg

Mitral stenosis

63
Q

MS complications

A

LA dilation
Pulmonary congestion/HTN
Atrial fibrillation
Mural thrombi

64
Q

most common overall cause of endocarditis

A

S. viridans
low virulence
only damaged valves
small vegetations that don’t destroy valve

65
Q

most common cause of endocarditis in IV drug users

A

S. aureus
high virulence
normal valves (tricuspid)
large vegetations that destroy valve

66
Q

endocarditis w prosthetic valves

endocarditis w colorectal carcinoma

A

S. epidermidis

S. bovis

67
Q

endocarditis w negative cultures

A

HACEK

68
Q

complications of septic emboli

A 
Janeway lesions (non-tender)
Osler nodes (painful on fingers/toes)
Splinter hemorrhages
69
Q

best way to detect valvular lesions

A

TEE

70
Q

2 causes of nonbacterial thrombotic endocarditis

A

sterile lesions on MV via:
hypercoag state
adenocarcinoma

71
Q

sterile vegetations on both sides of valve?

A

Libman-Sacks

Assoc w SLE –> MV regurg

72
Q

cardiomyopathy sequelae

A

dilated heart –> systolic dysfxn

MV/TV regurg and arrhythmia

73
Q

most common causes of cardiomyopathy

A 
idiopathic
genetic
myocarditis
alcohol
drugs (doxorubicin/cocaine)
pregnancy
74
Q

dilated cardiomyopathy tx?

A

transplant

75
Q

hypertrophic CM

A

dominant
sarcomere protein mutations
LVH
syncope w exercise

76
Q

hypertrophic CM biopsy

A

myofiber hypertrophy with disarray

77
Q

restrictive CM

causes (which one in kids?)

A

decreased compliance –> diastolic problem
Amyloidosis
sarcoidosis
hemochromatosis
endocardial fibroelastosis (kids)
Loeffler syndrome (eos inflammation –> fibrosis)

78
Q

restrictive CM presentation

A

low voltage EKG

diminished QRS amplitude

79
Q

benign mesenchymal proliferation w gelatinous appearance

A

myxoma
abundant GROUND SUBSTANCE
mesenchyme b/c this is only part of heart tissue that can grow

80
Q

most common primary cardiac tumor in adults?

A

myxoma

81
Q

pedunculated mass in left atrium, blocking the mitral valve

A

myxoma –> syncope via obstruction of MV

82
Q

most common cardiac tumor in children

benign hamartoma

A

rhabdomyoma

83
Q

rhabdomyoma associated w?

arises where?

A

tuberous sclerosis

ventricle

84
Q

heart is common site of met for which tumors?

A

melanoma
lymphoma
breast/lung carcinoma

85
Q

secondary cardiac tumors (metastases) involve what?

A

pericardium –> effusion

Pathoma (5 decks)

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