heart pathology Flashcards
common changes in aging chambers
sigmoid shaped ventricular septum- as you get older heart shrinks -> squigly coronary aa and septum bends -> blocks outflow -> increased ventricular pressure -> hypertrophy
common changes in aging valves
aortic valve calcification
mitral vavle annular calcific deposits
common changes in aging epicardial coronary aa
tortuosity
diminished compliance
calcific deposits
atheroscleroitc plaque
common changes in aging myocardium
brown atrophy- lipofuscin deposition (aging pigment)
common changes in aging aorta
dilated asscending aorta w/rightward shift
5 basic causes of cardiac dysfunction
pump failure
obstruction to flow thru heart
regurgitnat flow
shunted flow
disorders of cardiac conduction
disruption of continuity of circulatory system
heart 300-600g
pulmonary HTN, IHD
heart 400-800g
systemic HTN, aortic stenosis, mitral regurg, dilated cardiomyopathy
heart 600-1000
aortic regurg, hypertrophic cardiomyopathy
characteristics of cardiac remodeling
increased heart size and mass
increased protein synthesis
induction of immediate-early genes
induction of fetal gene program
abnormal proteins
fibrosis
inadequate vasculature
characteristics of cardiac dysfunction
heart failure
arrhythmias
neurohumoral stimulation
pressure overload hypertrophy
concentric hypertrophy
increased thickness in wall due to increased workload
left ventricle- systemic HTN or aortic stenosis
right ventricle- cor pulmonale
volume overload hypertrophy
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
CHF
characterized by either or both:
diminished CO (systolic or diastolic dysfunction) aka forward failure
damning of blood in venous system aka backward failure
left sided heart failure
congestion in lungs and pleural cavity
commonly caused by ischemic heart disease, HTN heart disease, aortic mitral valvular disease, cadiomyopathy
pathologic findings of left sided heart failure
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
left sided heart failure extracardiac effects
lung- congestion, edema, long term- siderophages (heart failure cells), dypsnea, orthopnea
kidney- decreased CO -> renal hypoperfusion -> RAAS and/or prerenal azotemia
brain-hypoxic encephalopathy
right sided heart failure
commonly due to left sided heart failure
pure/isolated can uncommon, due to cor pulmonale
right sided heart failure extracardiac effects
pitting edema
liver and portal system- congestive hepatomegaly
spleen- congestive splenomegaly
pleural and pericardial cavity effusions
congestive hepatomegaly
chronic passive congestion in hepatic sinusoids
centrilobar necrosis
cardiac cirrhosis- increased fibrous tissue in centrilobular zone
BNP <100
unlikey to be CHF
BNP >100
most consistent w/CHF
most common congenital heart malformations
ventricular septal defects followed by atrial septal defects, however atrial more common in adults b/c ventricular resolve or surgically corrected before adulthood
NKX2-5
non syndromic mutated TF gene
ASD, VSD, conduction defects
TBX5
syndromic: Holt-Oram
TF gene
ASD, VSD, conduction defects
TBX1
deletion of 22q11.2
TF digeorge syndrome
cardiac outflow defects
fibrillin
structural protein mutated in marfans
increased TGFbeta signlaing -> aortic aneurysms, valve abnormalities
eisenmenger syndrome
late cyanotic congenital heart disease due to switch from left -> right shunt to right -> left shunt
usually months- years after birth
VSD
pressure hypertrophy in right ventrical
volume hypertrophy in left initially
90% membranous, 10% muscular
ASD
secundum- fossa ovalis, 90%
primum- adjacent to AV valve
sinus venosus- near SVC
PDA
tx- NSAIDS to close or porstaglandin E to keep open
AVSD
present in 40-60% of down syndrome kids
tetralogy of Fallot
VSD
Subpulmonic stenosis w/obstruction of R ventricular outflow tract
aorta overrises VSD
R ventricular hypertrophy
what is the arrow pointing at
membranous ventricular septal defect
view of left heart
what would you give an infant w/transpoition of the great vessels until they can have surgery
prostaglandin E
infantile coarctation of the aorta
hypoplasia of aorta prior to PDA
cyanosis of inferior body and wak femoral pulses
adult coarctation of aorta
ridge like fold opposite ligamentum arteriosis
HTN in UL, hypotension in LL
valvular aortic stenosis
have hypoplastic, dysplastic, or abnormal number of cusps
subaortic stenosis
ring or collar below cusps
supravalvular aortic stenosis
elastin gene mutation w/aortic dysplasia
william-beuren syndrome
deletion of 28genes from chrom 7 w/ELN gene (elastin) haploinsufficiency
hypercalcemia, glucose intolerance, facial, and cognative defects
conditions associated w/coarctation of the aorta
bicuspid aortic valve
circle of willis aneurysms
turner syndrome
IHD
imbalance btwn supply and demand of heart
90% due to atherosclerosclerotic coronary arterial obstruction
leading cause of death for males and females in US
4 clinical syndromes associated w/IHD
sudden cardiac death
anginia pectoris
chronic IHD w/heart failure
MI
common causes of IHD
fixed atherosclerotic narrowing of coronaries
thrombosis overlying a disrupted plaque
localaized platelet aggregation
vasospasm
emboli
hypotension
coronary artery vasculitis
stable angina
greater then 75% stenosed
no plaque disruption or plaque associated thrombus
unstable angina
variable stenosis
frequent plaque disruption
nonocclusive plaque associated thrombus, often w/thomboemboli
transmural myocardial infarction
variable stenosis
frequent plaque disruption
occlusive plaque associated thrombus
subendocardial infarction
variable stenosis and plaque disruption
widely variable plaque associated thrombus
sudden death
usually severe stenosis
freqent plaque disruption
often small platelet aggregaes or thrombi and/or thromboemboli
prinzmetal/varient angina
sustained vasospasm
cardiac raynaud
cold or emotion induced cardiac vasospasm
if greater then 20min can lead to MI
takotsubo cardiomyopathy
dilated cardiomyopathy secondary to emotional or physical stress w/normal coronary angiogram
channelopathies
usually autosomal dominant
chronic ischemic heart disease
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
transmural infarction
ischemic necrosis >50% of ventricular wall thickness
commonly associated w/acutre plaque change w/thrombosis
subendocardial infarction
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
MI sequence of events
sudden change in plaque
formation of inital platelet plug over plaque
vasospasm due to adhesion
propagation of plug -> stable clot
occlusion
onset of ATP depletion
seconds
decreases glycolysis
loss of contractility
<2min
ATP reduced to 50%
10min
ATP reduced to 10%
40min
irreversible cell injury
aka necrosis
20-40min
microvascular injury
>1hr
complete unsalvagable necrosis
6hours
1-30min
no gross or light microscopic findings
electron microscope- relaxation of myofibrils, glycogen loss, mito swelling
30min-4 hours
no gross features
light microscope usually nothing, sometimes can see variable waviness of fibers at border
electron microscope- sarcolemmal disruption, mito amorphous densities
4-12 hours
grossly usually no changes sometimes dark mottling
light microscope- early coagulation necrosis, edema, hemorrhage
12-24hrs
dark mottling grossly
early nuetrophillic infiltrate on light microscopy
1-3 days
grossly mottling w/yellow-tan infarct center
brisk interstitial infiltrate of neutrophils
3-7 dyas
early phagocytosis of dead cells seen on light microscopy
10-24 days
red-gray depressed infarct borders
well established granulation tissue
2-8wks
gray white scar
increased collagen deposition on light microscopy
>2months
dense collagenous scar
how old is this infarct
1 day
how old is this infarct
3-4 days
how old is this infarct
7-10 days
how old is this infarct
2-3wks
how old is this infarct
months
pathologic changes associated w/reperfusion
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
what is this
hemorrhagic infarct due to reperfusion injury
myoglobin
initial elevation 1-4hrs
peak 6hr
time to return to baseline 18-24hr
CK-MB
initial elevation 3-12 hrs
peak 10-24hr
time to return to baseline 48-72hr
MB isoforms
initial elevation 1-6hrs
peak 4-12hr
time to return to baseline 38hr
cTnI
initial elevation 3-12hrs
peak 10-24hr
time to return to baseline 5-10days
cTnT
initial elevation 3-12hrs
peak 12-24hr
time to return to baseline 5-14days
physiologic complications of AMI
contractile dysfunction
arrhythmias
papillary m dysfunction w/mitral regurg
pathologic complication of AMI
myocardial rupture
pericarditis
right ventricular infarction
infarct extension (enlargemenet) and expansion(thinning/dilation)
mural thrombosis
bentricular aneurysm
progressive late heart failure
identify
anterior mycoardial rupture
identify
rupture of ventricular septum
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complete rupture of necrotic papillary muscle
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fibrous pericarditis
identify
early expansion of anteroapical infarct and mural thrombus
indentify
aprical left ventrical aneurysm
aortic calcific aortic stenosis
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)
calcific stenosis of congenital bicuspid aortic valve
more susceptible to progressive degernative calcification
5th-6th decades
mitral annular calcification
occurs in: women >60, myxomatous mitral valves, elevated left ventricular pressure(HTN)
generally does not affect valve fnx
occasionally associated w/arrythmiaas
mycomatous degeneration of mitral valve
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
myxomatous degeneration of mitral valve primary pathologic changes
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)
myxomatous degeneration of mitral valve secondary pathologic changes
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
identify
myxomatous degereration of mitral valve
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ballooning and enlargement of valve leaflet in myxomatous degeneration of mitral valve
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Opened valve, showing pronounced hooding of the posterior mitral leaflet with thrombotic plaques at sites of leaflet-left atrium contact
identify
Opened valve with pronounced hooding (double arrows) in a patient who died suddenly. Note also mitral annular calcification
aschoff body
collection of large activated histiocytes
basically a granuloma
antischkow cells
mononuclear cells
aschoff cells
multinucleated form
caterpillar cells
unique linear chromatin pattern
identify
aschoff cell
identify
antischkow cell
identify
caterpillar cell
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aschoff body
jones criteris
group A strep infection
plus either 2 major findings
1 major plus 1 minor finding
major jones criteria
migratory polyarthritis of large joints
acute carditis w/cardiac enlargements and diminished fnx
subQ nodules
erythma marginatum of skin
sydenham chorea
minor jones criteria
elevated sed rate or elevated C-reactive protein
identify
Acute and chronic rheumatic heart disease. Acute rheumatic mitral valvulitis superimposed on chronic rheumatic heart disease.
identify
Chronic Rheumatic mitral stenosis with diffuse fibrous thickening and distortion of the valve leaflets and commissural fusion
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Chronic Rheumatic Valve D, Mitral stenosis with thickening of the chordae tendineae (D). Note neovascularization
identify
Chronic Rheumatic aortic stenosis, demonstrating thickening and distortion of the cusps with commissural fusion
infective endocarditis
serious destrucive infection of heart valves or mural endocardium by orangisms leading to
effects of infective endocarditis
bulky friable vegetations
destruction of underlying cardiac structures (especially vavles)
risk of systemic microemboli
usually left valves (except in IV drug abusers
common organisms in infective endocarditis
1 in artificial valves S. epidermis
S. viridan > S. aureus > HACEK
HACEK
haemophilus
actinobacilus
cardiobacertium
eikenella
kingella
acute bacterial endocarditis
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
subacute bacterial endocarditis
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
duke criteria
for diagnosing infective endocarditis
either pathologic or clinical criteria
if using clinical criteria must have 2 major or 1 major + 3minor or 5 minor
pathologic criteria for infective endocarditis
microorganisms demonstrated by culutre or histo exam in a vegetation, embolus from vegetation, or intracardial abscess
on autopsy only
major criteria for infective endocarditis
- 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
minor criteria for infective endocarditis
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
janeway lesions
small erythematous or hemorrhagic macular, nontender elsions on palms and soles
consequences of septic emboli
osler nodes
small tender subQ nodules that develop in pulp of digits or occasionally more proximal in fingers and persist for hours-days
Roth spots
are oval retinal hemorrhages w/pale centers
identify
Endocarditis of mitral valve (subacute, caused by Streptococcus viridans). The large, friable vegetations are denoted by arrows.
identify
Acute endocarditis of congenitally bicuspid aortic valve (caused by Staphylococcus aureus) with extensive cuspal destruction and ring abscess (arrow).
identify
Histologic appearance of vegetation of endocarditis with extensive acute inflammatory cells and fibrin. Bacterial organisms were demonstrated by tissue Gram stain.
identify
Healed endocarditis, demonstrating mitral valvular destruction but no active vegetations.
non-infected vegetations
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
identify
Nearly complete row of thrombotic vegetations along the line of closure of the mitral valve leaflets (arrows).
identify
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).
libman-sacks endocarditis
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
identify
Libman-Sacks Endocarditis of the mitral valve in SLE
small warty verrucae along lines of closure of valve leaflets
acute rheumatic heart disease
typically shows large irregular masses on valve cusps that may extend onto chordae
infective endocarditis
small balnd vegetations ususally attached at line of closure
1+ present
NBTE
small or medium sized vegetations on either or both sides of valve leafelts or wlesewhere on endocardial surface
LSE
carcinoid syndrome
caused by metastatic carcinoid tumor porducing serotonin, kallikrein, bradykinin, histamine, prostaglandin, tachykinins
carcinoid syndrome symptoms
diarrhea
flushing
skin rash
bronchoconstiction
carcinoid syndrome heart effects
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
chemicals that mimic carcinoid heart disease
fenfluarmine/phentermine
methysergide
ergotamine
identify
Characteristic endocardial fibrotic lesion involving the right ventricle and tricuspid valve.
identify
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.
complications of cardiac valve prostheses
thrombosis/thromboembolism
anticoagulant-related hemorrhage
prosthetic valve endocarditis
structural deterioration
inadequate or exhberant healing
hemolysis
identify
Thrombosis of a mechanical prosthetic valve
identify
Calcification with secondary tearing of a porcine bioprosthetic heart valve, viewed from the inflow aspect.
classifications of cardiomyopathies
dialted 90% (large flabby heart)
hypertrophic 6-8%
restrictive uncommon (mild increase in cardiac mass w/o increase in volume of left venticle)
endomyocardial biopsy
used to differentiate idiopathic dilated from myocarditis secondary to virus
biopsy taken from septum to prevent cardiac tampenade
major causes of myocardits in US
ocsackieviruses A and B and other enteroviruses
Lyme disease
hypersenstivity myocarditis (Eos)
trichinosis- undercooked meat
major causes of myocarditis in south america
Chagas disease (trypanosoma cruzi)
immune mediated causes of myocarditis
postviral
poststreptococcal
SLE
drug hypersensitivity
transplant rejection
random causes of myocarditis
sarcoidosis
giant cell myocarditis
dialated cadiomyopathy
LVEF <40%
impariment of contracticly (systolic dysfunction)
dialted cardiomyopathy causes
genetic, alcohol, myocarditis, hemochromatosis, chronic anemia, doxorubicin, arcoidosis, idopathic
dilated cardiomyopahty indirect myocardial dysfunction
IHD
valvular heart disease
HTN heart disease
congenital heart disease
hypertrophic cardiomyopathy
LVEF 50-80%
impairment of compliance (diastolic dysfunction)
causes of hypertrophic cardiomyopathy
genetic
friedreich ataxia
sotrage diseases
infants of diabetic mothers
hypertrophic cardiomyopathy indirect myocardial dynsfunction
HTN heart disease
aortic stenosis
restrictive cardiomyopathy
LVEF 45-90%
impairment of compliance (diastolic dysfunction)
causes of restricitive cardiomyopathy
amyloidosis
radiation induced fibrosis
idiopathic
restrictive cadiomyopaahty indirect myocardial dysfunction
pericardial constriction
