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Cardio 2 > heart pathology > Flashcards

heart pathology Flashcards

1
Q

common changes in aging chambers

A

sigmoid shaped ventricular septum- as you get older heart shrinks -> squigly coronary aa and septum bends -> blocks outflow -> increased ventricular pressure -> hypertrophy

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2
Q

common changes in aging valves

A

aortic valve calcification

mitral vavle annular calcific deposits

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3
Q

common changes in aging epicardial coronary aa

A

tortuosity

diminished compliance

calcific deposits

atheroscleroitc plaque

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4
Q

common changes in aging myocardium

A

brown atrophy- lipofuscin deposition (aging pigment)

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5
Q

common changes in aging aorta

A

dilated asscending aorta w/rightward shift

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6
Q

5 basic causes of cardiac dysfunction

A

pump failure

obstruction to flow thru heart

regurgitnat flow

shunted flow

disorders of cardiac conduction

disruption of continuity of circulatory system

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7
Q

heart 300-600g

A

pulmonary HTN, IHD

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8
Q

heart 400-800g

A

systemic HTN, aortic stenosis, mitral regurg, dilated cardiomyopathy

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9
Q

heart 600-1000

A

aortic regurg, hypertrophic cardiomyopathy

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10
Q

characteristics of cardiac remodeling

A

increased heart size and mass

increased protein synthesis

induction of immediate-early genes

induction of fetal gene program

abnormal proteins

fibrosis

inadequate vasculature

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11
Q

characteristics of cardiac dysfunction

A

heart failure

arrhythmias

neurohumoral stimulation

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12
Q

pressure overload hypertrophy

A

concentric hypertrophy

increased thickness in wall due to increased workload

left ventricle- systemic HTN or aortic stenosis

right ventricle- cor pulmonale

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13
Q

volume overload hypertrophy

A

eccentric hypertrophy

chamber dilation w/increased ventricular diameter caused by volume overload stimulus

ventricular wall thickness normal-minimally thickened

overall cardiac m mass increased

can be seen w/valve disorder and congential heart disease

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14
Q

CHF

A

characterized by either or both:

diminished CO (systolic or diastolic dysfunction) aka forward failure

damning of blood in venous system aka backward failure

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15
Q

left sided heart failure

A

congestion in lungs and pleural cavity

commonly caused by ischemic heart disease, HTN heart disease, aortic mitral valvular disease, cadiomyopathy

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16
Q

pathologic findings of left sided heart failure

A

cadiomegaly (hypertrophy, dilation or both)

secondary enlargement of left atrium, highly associated w/atrial fibrilation and mural thrombus

tachycardia

S3 gallop

mitral regurg -> systolic murmur

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17
Q

left sided heart failure extracardiac effects

A

lung- congestion, edema, long term- siderophages (heart failure cells), dypsnea, orthopnea

kidney- decreased CO -> renal hypoperfusion -> RAAS and/or prerenal azotemia

brain-hypoxic encephalopathy

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18
Q

right sided heart failure

A

commonly due to left sided heart failure

pure/isolated can uncommon, due to cor pulmonale

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19
Q

right sided heart failure extracardiac effects

A

pitting edema

liver and portal system- congestive hepatomegaly

spleen- congestive splenomegaly

pleural and pericardial cavity effusions

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20
Q

congestive hepatomegaly

A

chronic passive congestion in hepatic sinusoids

centrilobar necrosis

cardiac cirrhosis- increased fibrous tissue in centrilobular zone

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21
Q

BNP <100

A

unlikey to be CHF

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22
Q

BNP >100

A

most consistent w/CHF

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23
Q

most common congenital heart malformations

A

ventricular septal defects followed by atrial septal defects, however atrial more common in adults b/c ventricular resolve or surgically corrected before adulthood

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24
Q

NKX2-5

A

non syndromic mutated TF gene

ASD, VSD, conduction defects

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25
Q

TBX5

A

syndromic: Holt-Oram

TF gene

ASD, VSD, conduction defects

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26
Q

TBX1

A

deletion of 22q11.2

TF digeorge syndrome

cardiac outflow defects

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27
Q

fibrillin

A

structural protein mutated in marfans

increased TGFbeta signlaing -> aortic aneurysms, valve abnormalities

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28
Q

eisenmenger syndrome

A

late cyanotic congenital heart disease due to switch from left -> right shunt to right -> left shunt

usually months- years after birth

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29
Q

VSD

A

pressure hypertrophy in right ventrical

volume hypertrophy in left initially

90% membranous, 10% muscular

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30
Q

ASD

A

secundum- fossa ovalis, 90%

primum- adjacent to AV valve

sinus venosus- near SVC

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31
Q

PDA

A

tx- NSAIDS to close or porstaglandin E to keep open

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32
Q

AVSD

A

present in 40-60% of down syndrome kids

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33
Q

tetralogy of Fallot

A

VSD

Subpulmonic stenosis w/obstruction of R ventricular outflow tract

aorta overrises VSD

R ventricular hypertrophy

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34
Q

what is the arrow pointing at

A

membranous ventricular septal defect

view of left heart

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35
Q

what would you give an infant w/transpoition of the great vessels until they can have surgery

A

prostaglandin E

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36
Q

infantile coarctation of the aorta

A

hypoplasia of aorta prior to PDA

cyanosis of inferior body and wak femoral pulses

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37
Q

adult coarctation of aorta

A

ridge like fold opposite ligamentum arteriosis

HTN in UL, hypotension in LL

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38
Q

valvular aortic stenosis

A

have hypoplastic, dysplastic, or abnormal number of cusps

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39
Q

subaortic stenosis

A

ring or collar below cusps

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40
Q

supravalvular aortic stenosis

A

elastin gene mutation w/aortic dysplasia

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41
Q

william-beuren syndrome

A

deletion of 28genes from chrom 7 w/ELN gene (elastin) haploinsufficiency

hypercalcemia, glucose intolerance, facial, and cognative defects

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42
Q

conditions associated w/coarctation of the aorta

A

bicuspid aortic valve

circle of willis aneurysms

turner syndrome

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43
Q

IHD

A

imbalance btwn supply and demand of heart

90% due to atherosclerosclerotic coronary arterial obstruction

leading cause of death for males and females in US

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44
Q

4 clinical syndromes associated w/IHD

A

sudden cardiac death

anginia pectoris

chronic IHD w/heart failure

MI

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45
Q

common causes of IHD

A

fixed atherosclerotic narrowing of coronaries

thrombosis overlying a disrupted plaque

localaized platelet aggregation

vasospasm

emboli

hypotension

coronary artery vasculitis

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46
Q

stable angina

A

greater then 75% stenosed

no plaque disruption or plaque associated thrombus

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47
Q

unstable angina

A

variable stenosis

frequent plaque disruption

nonocclusive plaque associated thrombus, often w/thomboemboli

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48
Q

transmural myocardial infarction

A

variable stenosis

frequent plaque disruption

occlusive plaque associated thrombus

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49
Q

subendocardial infarction

A

variable stenosis and plaque disruption

widely variable plaque associated thrombus

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50
Q

sudden death

A

usually severe stenosis

freqent plaque disruption

often small platelet aggregaes or thrombi and/or thromboemboli

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51
Q

prinzmetal/varient angina

A

sustained vasospasm

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52
Q

cardiac raynaud

A

cold or emotion induced cardiac vasospasm

if greater then 20min can lead to MI

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53
Q

takotsubo cardiomyopathy

A

dilated cardiomyopathy secondary to emotional or physical stress w/normal coronary angiogram

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54
Q

channelopathies

A

usually autosomal dominant

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55
Q

chronic ischemic heart disease

A

insidious onset of CHF in patients with past MIs or angina

cadiomegaly w/left ventricular hypertrophy or dilation

evidence of previous healed MIs or ischemias

develop arythmias, CHF, and MIs

chronic ischemia that does not cause necrosis can lead to hypokinetic myocardium

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56
Q

transmural infarction

A

ischemic necrosis >50% of ventricular wall thickness

commonly associated w/acutre plaque change w/thrombosis

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57
Q

subendocardial infarction

A

area of ischemic necrosis <50% wall thickness

may occur as a result of acute plawue change and thrombosis

may result from prolonged and sever reduction in systemic blood pressure as encountered in shock

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58
Q

MI sequence of events

A

sudden change in plaque

formation of inital platelet plug over plaque

vasospasm due to adhesion

propagation of plug -> stable clot

occlusion

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59
Q

onset of ATP depletion

A

seconds

decreases glycolysis

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60
Q

loss of contractility

A

<2min

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61
Q

ATP reduced to 50%

A

10min

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62
Q

ATP reduced to 10%

A

40min

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63
Q

irreversible cell injury

A

aka necrosis

20-40min

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64
Q

microvascular injury

A

>1hr

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65
Q

complete unsalvagable necrosis

A

6hours

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66
Q

1-30min

A

no gross or light microscopic findings

electron microscope- relaxation of myofibrils, glycogen loss, mito swelling

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67
Q

30min-4 hours

A

no gross features

light microscope usually nothing, sometimes can see variable waviness of fibers at border

electron microscope- sarcolemmal disruption, mito amorphous densities

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68
Q

4-12 hours

A

grossly usually no changes sometimes dark mottling

light microscope- early coagulation necrosis, edema, hemorrhage

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69
Q

12-24hrs

A

dark mottling grossly

early nuetrophillic infiltrate on light microscopy

70
Q

1-3 days

A

grossly mottling w/yellow-tan infarct center

brisk interstitial infiltrate of neutrophils

71
Q

3-7 dyas

A

early phagocytosis of dead cells seen on light microscopy

72
Q

10-24 days

A

red-gray depressed infarct borders

well established granulation tissue

73
Q

2-8wks

A

gray white scar

increased collagen deposition on light microscopy

74
Q

>2months

A

dense collagenous scar

75
Q

how old is this infarct

A

1 day

76
Q

how old is this infarct

A

3-4 days

77
Q

how old is this infarct

A

7-10 days

78
Q

how old is this infarct

A

2-3wks

79
Q

how old is this infarct

A

months

80
Q

pathologic changes associated w/reperfusion

A

arrhythmias

myocardial hemorrhage w/contraction bands

irreversible myocardial damage in addition to that caused by initial episode

microvascular injury w/endothelial swelling -> no reflow

reversible myocardial stunning, can last for days

81
Q

what is this

A

hemorrhagic infarct due to reperfusion injury

82
Q

myoglobin

A

initial elevation 1-4hrs

peak 6hr

time to return to baseline 18-24hr

83
Q

CK-MB

A

initial elevation 3-12 hrs

peak 10-24hr

time to return to baseline 48-72hr

84
Q

MB isoforms

A

initial elevation 1-6hrs

peak 4-12hr

time to return to baseline 38hr

85
Q

cTnI

A

initial elevation 3-12hrs

peak 10-24hr

time to return to baseline 5-10days

86
Q

cTnT

A

initial elevation 3-12hrs

peak 12-24hr

time to return to baseline 5-14days

87
Q

physiologic complications of AMI

A

contractile dysfunction

arrhythmias

papillary m dysfunction w/mitral regurg

88
Q

pathologic complication of AMI

A

myocardial rupture

pericarditis

right ventricular infarction

infarct extension (enlargemenet) and expansion(thinning/dilation)

mural thrombosis

bentricular aneurysm

progressive late heart failure

89
Q

identify

A

anterior mycoardial rupture

90
Q

identify

A

rupture of ventricular septum

91
Q

identify

A

complete rupture of necrotic papillary muscle

92
Q

identify

A

fibrous pericarditis

93
Q

identify

A

early expansion of anteroapical infarct and mural thrombus

94
Q

indentify

A

aprical left ventrical aneurysm

95
Q

aortic calcific aortic stenosis

A

most common of all valvular abnormalities

clincial symptoms do not occur until 7th-9th decades

pressure hypertrophy results from obstruction and patient develops significant left ventricular concentric hypertrophy

left ventricular cardiac mass tend to be ischemic -> CHF (die w/in2yrs), Syncope (die w/in 3 yrs), angina (die w/in 5yrs)

96
Q

calcific stenosis of congenital bicuspid aortic valve

A

more susceptible to progressive degernative calcification

5th-6th decades

97
Q

mitral annular calcification

A

occurs in: women >60, myxomatous mitral valves, elevated left ventricular pressure(HTN)

generally does not affect valve fnx

occasionally associated w/arrythmiaas

98
Q

mycomatous degeneration of mitral valve

A

aka mitral valve prolapse

midsytolic click +/- regurgitant murmur

marfans

usually asymptomatic, but can cause: infective endocarditis, mitral insufficiency, stoke, arrythmias, atypical chest pain

diagnosed via echo

99
Q

myxomatous degeneration of mitral valve primary pathologic changes

A

intercordal ballooning of mitral valve leaflets

affected leaflets are enlarged, thick, and rubbery

concomitatn involvement of tircuspid vavle in 20-40%

mircorscopic changes in valve leaflet (thinned fibrosa, thickened spngiosa, deposition of mucoid/myxoid material)

100
Q

myxomatous degeneration of mitral valve secondary pathologic changes

A

dilation of annulus, fibrosis of valve leaflets and endocardial surfaces of atrium and ventircal - jet lesions

thrombi on atrial surfaces of mitral leaflets and focal calcification

101
Q

identify

A

myxomatous degereration of mitral valve

102
Q

identify

A

ballooning and enlargement of valve leaflet in myxomatous degeneration of mitral valve

103
Q

identify

A

Opened valve, showing pronounced hooding of the posterior mitral leaflet with thrombotic plaques at sites of leaflet-left atrium contact

104
Q

identify

A

Opened valve with pronounced hooding (double arrows) in a patient who died suddenly. Note also mitral annular calcification

105
Q

aschoff body

A

collection of large activated histiocytes

basically a granuloma

106
Q

antischkow cells

A

mononuclear cells

107
Q

aschoff cells

A

multinucleated form

108
Q

caterpillar cells

A

unique linear chromatin pattern

109
Q

identify

A

aschoff cell

110
Q

identify

A

antischkow cell

111
Q

identify

A

caterpillar cell

112
Q

identify

A

aschoff body

113
Q

jones criteris

A

group A strep infection

plus either 2 major findings

1 major plus 1 minor finding

114
Q

major jones criteria

A

migratory polyarthritis of large joints

acute carditis w/cardiac enlargements and diminished fnx

subQ nodules

erythma marginatum of skin

sydenham chorea

115
Q

minor jones criteria

A

elevated sed rate or elevated C-reactive protein

116
Q

identify

A

Acute and chronic rheumatic heart disease. Acute rheumatic mitral valvulitis superimposed on chronic rheumatic heart disease.

117
Q

identify

A

Chronic Rheumatic mitral stenosis with diffuse fibrous thickening and distortion of the valve leaflets and commissural fusion

118
Q

identify

A

Chronic Rheumatic Valve D, Mitral stenosis with thickening of the chordae tendineae (D). Note neovascularization

119
Q

identify

A

Chronic Rheumatic aortic stenosis, demonstrating thickening and distortion of the cusps with commissural fusion

120
Q

infective endocarditis

A

serious destrucive infection of heart valves or mural endocardium by orangisms leading to

121
Q

effects of infective endocarditis

A

bulky friable vegetations

destruction of underlying cardiac structures (especially vavles)

risk of systemic microemboli

usually left valves (except in IV drug abusers

122
Q

common organisms in infective endocarditis

A

1 in artificial valves S. epidermis

S. viridan > S. aureus > HACEK

123
Q

HACEK

A

haemophilus

actinobacilus

cardiobacertium

eikenella

kingella

124
Q

acute bacterial endocarditis

A

rapidly porgressive destruction of infected cardiac valve

infe tion by hightly virulent bacteria (S. aureus) commonly seen in IV drug abusers

even w/aggressive antibiotic therapy 50% die

125
Q

subacute bacterial endocarditis

A

insideous onset and protracted clinical course

involoved vavle usually deforemed or abnormal (historically RHD, no mitral valve prolapse most common)

infection by low virulence bacteria such as S. viridans

most patients recover

126
Q

duke criteria

A

for diagnosing infective endocarditis

either pathologic or clinical criteria

if using clinical criteria must have 2 major or 1 major + 3minor or 5 minor

127
Q

pathologic criteria for infective endocarditis

A

microorganisms demonstrated by culutre or histo exam in a vegetation, embolus from vegetation, or intracardial abscess

on autopsy only

128
Q

major criteria for infective endocarditis

A
  • blood cultures + for characteristic organisms or persistencly + for an unusulal organism
  • echocardiographic findings including valve-related or implant-related mass or abcess or partial seperation of artifical valve
  • new vavlualr regurg
129
Q

minor criteria for infective endocarditis

A

predisposing heart lesion of IV drug use

fever

vascular lesions, including arterial petchiae, hemorrhages, emboli, spetic infarcts, mycotic aneurysm, intracranial hemorrhage, janeway lesions

immunologic phenomena: glomerulonephritis, osler nodes, roth spots, RF

microbioloogic evidence, including sinlge culutre showing uncharacteristic organism

echocardiographic findings consisten w/but not diagnostic of endocarditis including changing murmur

130
Q

janeway lesions

A

small erythematous or hemorrhagic macular, nontender elsions on palms and soles

consequences of septic emboli

131
Q

osler nodes

A

small tender subQ nodules that develop in pulp of digits or occasionally more proximal in fingers and persist for hours-days

132
Q

Roth spots

A

are oval retinal hemorrhages w/pale centers

133
Q

identify

A

Endocarditis of mitral valve (subacute, caused by Streptococcus viridans). The large, friable vegetations are denoted by arrows.

134
Q

identify

A

Acute endocarditis of congenitally bicuspid aortic valve (caused by Staphylococcus aureus) with extensive cuspal destruction and ring abscess (arrow).

135
Q

identify

A

Histologic appearance of vegetation of endocarditis with extensive acute inflammatory cells and fibrin. Bacterial organisms were demonstrated by tissue Gram stain.

136
Q

identify

A

Healed endocarditis, demonstrating mitral valvular destruction but no active vegetations.

137
Q

non-infected vegetations

A

nonbacterial thrombotic endocarditis (NBTE)

small 1-5 mm along lines of closure

sterile lesions

risk factor is hypercoaguable state

fragment -> embolism

used to be called marantic endocarditis

138
Q

identify

A

Nearly complete row of thrombotic vegetations along the line of closure of the mitral valve leaflets (arrows).

139
Q

identify

A

Photomicrograph of NBTE, showing bland thrombus, with virtually no inflammation in the valve cusp (c) or the thrombotic deposit (t). The thrombus is only loosely attached to the cusp (arrow).

140
Q

libman-sacks endocarditis

A

endocarditis of SLE

samll sterile verrucous vegetations on any surface of: leaflets, valvular endocardium, chordae tendinae, ventricle or atrium subadjacent to AV valves

may be due to IC deposistion

141
Q

identify

A

Libman-Sacks Endocarditis of the mitral valve in SLE

142
Q

small warty verrucae along lines of closure of valve leaflets

A

acute rheumatic heart disease

143
Q

typically shows large irregular masses on valve cusps that may extend onto chordae

A

infective endocarditis

144
Q

small balnd vegetations ususally attached at line of closure

1+ present

A

NBTE

145
Q

small or medium sized vegetations on either or both sides of valve leafelts or wlesewhere on endocardial surface

A

LSE

146
Q

carcinoid syndrome

A

caused by metastatic carcinoid tumor porducing serotonin, kallikrein, bradykinin, histamine, prostaglandin, tachykinins

147
Q

carcinoid syndrome symptoms

A

diarrhea

flushing

skin rash

bronchoconstiction

148
Q

carcinoid syndrome heart effects

A

fibrous intimal thickening of endocardial surfaces of R side of heart, particularly right ventircle, and tricuspid and pulmonic valves

endocardial thickening is composed of predominately of smooth m proliferation and increased acid mucopolysaccharide matrix

149
Q

chemicals that mimic carcinoid heart disease

A

fenfluarmine/phentermine

methysergide

ergotamine

150
Q

identify

A

Characteristic endocardial fibrotic lesion involving the right ventricle and tricuspid valve.

151
Q

identify

A

Microscopic appearance of carcinoid heart disease with intimal thickening. Movat stain shows myocardial elastic tissue (black) underlying the acid mucopolysaccharide-rich lesion (blue-green). The underlying myocardium is unaffected.

152
Q

complications of cardiac valve prostheses

A

thrombosis/thromboembolism

anticoagulant-related hemorrhage

prosthetic valve endocarditis

structural deterioration

inadequate or exhberant healing

hemolysis

153
Q

identify

A

Thrombosis of a mechanical prosthetic valve

154
Q

identify

A

Calcification with secondary tearing of a porcine bioprosthetic heart valve, viewed from the inflow aspect.

155
Q

classifications of cardiomyopathies

A

dialted 90% (large flabby heart)

hypertrophic 6-8%

restrictive uncommon (mild increase in cardiac mass w/o increase in volume of left venticle)

156
Q

endomyocardial biopsy

A

used to differentiate idiopathic dilated from myocarditis secondary to virus

biopsy taken from septum to prevent cardiac tampenade

157
Q

major causes of myocardits in US

A

ocsackieviruses A and B and other enteroviruses

Lyme disease

hypersenstivity myocarditis (Eos)

trichinosis- undercooked meat

158
Q

major causes of myocarditis in south america

A

Chagas disease (trypanosoma cruzi)

159
Q

immune mediated causes of myocarditis

A

postviral

poststreptococcal

SLE

drug hypersensitivity

transplant rejection

160
Q

random causes of myocarditis

A

sarcoidosis

giant cell myocarditis

161
Q

dialated cadiomyopathy

A

LVEF <40%

impariment of contracticly (systolic dysfunction)

162
Q

dialted cardiomyopathy causes

A

genetic, alcohol, myocarditis, hemochromatosis, chronic anemia, doxorubicin, arcoidosis, idopathic

163
Q

dilated cardiomyopahty indirect myocardial dysfunction

A

IHD

valvular heart disease

HTN heart disease

congenital heart disease

164
Q

hypertrophic cardiomyopathy

A

LVEF 50-80%

impairment of compliance (diastolic dysfunction)

165
Q

causes of hypertrophic cardiomyopathy

A

genetic

friedreich ataxia

sotrage diseases

infants of diabetic mothers

166
Q

hypertrophic cardiomyopathy indirect myocardial dynsfunction

A

HTN heart disease

aortic stenosis

167
Q

restrictive cardiomyopathy

A

LVEF 45-90%

impairment of compliance (diastolic dysfunction)

168
Q

causes of restricitive cardiomyopathy

A

amyloidosis

radiation induced fibrosis

idiopathic

169
Q

restrictive cadiomyopaahty indirect myocardial dysfunction

A

pericardial constriction

170
Q
A

Cardio 2 (17 decks)

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