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
2
Q
common changes in aging valves
A
aortic valve calcification
mitral vavle annular calcific deposits
3
Q
common changes in aging epicardial coronary aa
A
tortuosity
diminished compliance
calcific deposits
atheroscleroitc plaque
4
Q
common changes in aging myocardium
A
brown atrophy- lipofuscin deposition (aging pigment)
5
Q
common changes in aging aorta
A
dilated asscending aorta w/rightward shift
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
7
Q
heart 300-600g
A
pulmonary HTN, IHD
8
Q
heart 400-800g
A
systemic HTN, aortic stenosis, mitral regurg, dilated cardiomyopathy
9
Q
heart 600-1000
A
aortic regurg, hypertrophic cardiomyopathy
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
11
Q
characteristics of cardiac dysfunction
A
heart failure
arrhythmias
neurohumoral stimulation
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
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
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
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
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
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
18
Q
right sided heart failure
A
commonly due to left sided heart failure
pure/isolated can uncommon, due to cor pulmonale
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
20
Q
congestive hepatomegaly
A
chronic passive congestion in hepatic sinusoids
centrilobar necrosis
cardiac cirrhosis- increased fibrous tissue in centrilobular zone
21
Q
BNP <100
A
unlikey to be CHF
22
Q
BNP >100
A
most consistent w/CHF
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
24
Q
NKX2-5
A
non syndromic mutated TF gene
ASD, VSD, conduction defects
25
TBX5
syndromic: Holt-Oram
TF gene
ASD, VSD, conduction defects
26
TBX1
deletion of 22q11.2
TF digeorge syndrome
cardiac outflow defects
27
fibrillin
structural protein mutated in marfans
increased TGFbeta signlaing -\> aortic aneurysms, valve abnormalities
28
eisenmenger syndrome
late cyanotic congenital heart disease due to switch from left -\> right shunt to right -\> left shunt
usually months- years after birth
29
VSD
pressure hypertrophy in right ventrical
volume hypertrophy in left initially
90% membranous, 10% muscular
30
ASD
secundum- fossa ovalis, 90%
primum- adjacent to AV valve
sinus venosus- near SVC
31
PDA
tx- NSAIDS to close or porstaglandin E to keep open
32
AVSD
present in 40-60% of down syndrome kids
33
tetralogy of Fallot
VSD
Subpulmonic stenosis w/obstruction of R ventricular outflow tract
aorta overrises VSD
R ventricular hypertrophy
34
what is the arrow pointing at
membranous ventricular septal defect
view of left heart
35
what would you give an infant w/transpoition of the great vessels until they can have surgery
prostaglandin E
36
infantile coarctation of the aorta
hypoplasia of aorta prior to PDA
cyanosis of inferior body and wak femoral pulses
37
adult coarctation of aorta
ridge like fold opposite ligamentum arteriosis
HTN in UL, hypotension in LL
38
valvular aortic stenosis
have hypoplastic, dysplastic, or abnormal number of cusps
39
subaortic stenosis
ring or collar below cusps
40
supravalvular aortic stenosis
elastin gene mutation w/aortic dysplasia
41
william-beuren syndrome
deletion of 28genes from chrom 7 w/ELN gene (elastin) haploinsufficiency
hypercalcemia, glucose intolerance, facial, and cognative defects
42
conditions associated w/coarctation of the aorta
bicuspid aortic valve
circle of willis aneurysms
turner syndrome
43
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
44
4 clinical syndromes associated w/IHD
sudden cardiac death
anginia pectoris
chronic IHD w/heart failure
MI
45
common causes of IHD
fixed atherosclerotic narrowing of coronaries
thrombosis overlying a disrupted plaque
localaized platelet aggregation
vasospasm
emboli
hypotension
coronary artery vasculitis
46
stable angina
greater then 75% stenosed
no plaque disruption or plaque associated thrombus
47
unstable angina
variable stenosis
frequent plaque disruption
nonocclusive plaque associated thrombus, often w/thomboemboli
48
transmural myocardial infarction
variable stenosis
frequent plaque disruption
occlusive plaque associated thrombus
49
subendocardial infarction
variable stenosis and plaque disruption
widely variable plaque associated thrombus
50
sudden death
usually severe stenosis
freqent plaque disruption
often small platelet aggregaes or thrombi and/or thromboemboli
51
prinzmetal/varient angina
sustained vasospasm
52
cardiac raynaud
cold or emotion induced cardiac vasospasm
if greater then 20min can lead to MI
53
takotsubo cardiomyopathy
dilated cardiomyopathy secondary to emotional or physical stress w/normal coronary angiogram
54
channelopathies
usually autosomal dominant
55
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
56
transmural infarction
ischemic necrosis \>50% of ventricular wall thickness
commonly associated w/acutre plaque change w/thrombosis
57
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
58
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
59
onset of ATP depletion
seconds
decreases glycolysis
60
loss of contractility
\<2min
61
ATP reduced to 50%
10min
62
ATP reduced to 10%
40min
63
irreversible cell injury
aka necrosis
20-40min
64
microvascular injury
\>1hr
65
complete unsalvagable necrosis
6hours
66
1-30min
no gross or light microscopic findings
electron microscope- relaxation of myofibrils, glycogen loss, mito swelling
67
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
68
4-12 hours
grossly usually no changes sometimes dark mottling
light microscope- early coagulation necrosis, edema, hemorrhage
69
12-24hrs
dark mottling grossly
early nuetrophillic infiltrate on light microscopy
70
1-3 days
grossly mottling w/yellow-tan infarct center
brisk interstitial infiltrate of neutrophils
71
3-7 dyas
early phagocytosis of dead cells seen on light microscopy
72
10-24 days
red-gray depressed infarct borders
well established granulation tissue
73
2-8wks
gray white scar
increased collagen deposition on light microscopy
74
\>2months
dense collagenous scar
75
how old is this infarct
1 day
76
how old is this infarct
3-4 days
77
how old is this infarct
7-10 days
78
how old is this infarct
2-3wks
79
how old is this infarct
months
80
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
81
what is this
hemorrhagic infarct due to reperfusion injury
82
myoglobin
initial elevation 1-4hrs
peak 6hr
time to return to baseline 18-24hr
83
CK-MB
initial elevation 3-12 hrs
peak 10-24hr
time to return to baseline 48-72hr
84
MB isoforms
initial elevation 1-6hrs
peak 4-12hr
time to return to baseline 38hr
85
cTnI
initial elevation 3-12hrs
peak 10-24hr
time to return to baseline 5-10days
86
cTnT
initial elevation 3-12hrs
peak 12-24hr
time to return to baseline 5-14days
87
physiologic complications of AMI
contractile dysfunction
arrhythmias
papillary m dysfunction w/mitral regurg
88
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
89
identify
anterior mycoardial rupture
90
identify
rupture of ventricular septum
91
identify
complete rupture of necrotic papillary muscle
92
identify
fibrous pericarditis
93
identify
early expansion of anteroapical infarct and mural thrombus
94
indentify
aprical left ventrical aneurysm
95
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)
96
calcific stenosis of congenital bicuspid aortic valve
more susceptible to progressive degernative calcification
5th-6th decades
97
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
98
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
99
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)
100
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
101
identify
myxomatous degereration of mitral valve
102
identify
ballooning and enlargement of valve leaflet in myxomatous degeneration of mitral valve
103
identify
Opened valve, showing pronounced hooding of the posterior mitral leaflet with thrombotic plaques at sites of leaflet-left atrium contact
104
identify
Opened valve with pronounced hooding (double arrows) in a patient who died suddenly. Note also mitral annular calcification
105
aschoff body
collection of large activated histiocytes
basically a granuloma
106
antischkow cells
mononuclear cells
107
aschoff cells
multinucleated form
108
caterpillar cells
unique linear chromatin pattern
109
identify
aschoff cell
110
identify
antischkow cell
111
identify
caterpillar cell
112
identify
aschoff body
113
jones criteris
group A strep infection
plus either 2 major findings
1 major plus 1 minor finding
114
major jones criteria
migratory polyarthritis of large joints
acute carditis w/cardiac enlargements and diminished fnx
subQ nodules
erythma marginatum of skin
sydenham chorea
115
minor jones criteria
elevated sed rate or elevated C-reactive protein
116
identify
Acute and chronic rheumatic heart disease. Acute rheumatic mitral valvulitis superimposed on chronic rheumatic heart disease.
117
identify
Chronic Rheumatic mitral stenosis with diffuse fibrous thickening and distortion of the valve leaflets and commissural fusion
118
identify
Chronic Rheumatic Valve D, Mitral stenosis with thickening of the chordae tendineae (D). Note neovascularization
119
identify
Chronic Rheumatic aortic stenosis, demonstrating thickening and distortion of the cusps with commissural fusion
120
infective endocarditis
serious destrucive infection of heart valves or mural endocardium by orangisms leading to
121
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
122
common organisms in infective endocarditis
S. viridan \> S. aureus \> HACEK
#1 in artificial valves S. epidermis
123
HACEK
haemophilus
actinobacilus
cardiobacertium
eikenella
kingella
124
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
125
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
126
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
127
pathologic criteria for infective endocarditis
microorganisms demonstrated by culutre or histo exam in a vegetation, embolus from vegetation, or intracardial abscess
on autopsy only
128
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
129
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
130
janeway lesions
small erythematous or hemorrhagic macular, nontender elsions on palms and soles
consequences of septic emboli
131
osler nodes
small tender subQ nodules that develop in pulp of digits or occasionally more proximal in fingers and persist for hours-days
132
Roth spots
are oval retinal hemorrhages w/pale centers
133
identify
Endocarditis of mitral valve (subacute, caused by Streptococcus viridans). The large, friable vegetations are denoted by arrows.
134
identify
## Footnote
Acute endocarditis of congenitally bicuspid aortic valve (caused by Staphylococcus aureus) with extensive cuspal destruction and ring abscess (arrow).
135
identify
Histologic appearance of vegetation of endocarditis with extensive acute inflammatory cells and fibrin. Bacterial organisms were demonstrated by tissue Gram stain.
136
identify
## Footnote
Healed endocarditis, demonstrating mitral valvular destruction but no active vegetations.
137
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
138
identify
## Footnote
Nearly complete row of thrombotic vegetations along the line of closure of the mitral valve leaflets (arrows).
139
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).
140
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
141
identify
## Footnote
Libman-Sacks Endocarditis of the mitral valve in SLE
142
small warty verrucae along lines of closure of valve leaflets
acute rheumatic heart disease
143
typically shows large irregular masses on valve cusps that may extend onto chordae
infective endocarditis
144
small balnd vegetations ususally attached at line of closure
1+ present
NBTE
145
small or medium sized vegetations on either or both sides of valve leafelts or wlesewhere on endocardial surface
LSE
146
carcinoid syndrome
caused by metastatic carcinoid tumor porducing serotonin, kallikrein, bradykinin, histamine, prostaglandin, tachykinins
147
carcinoid syndrome symptoms
diarrhea
flushing
skin rash
bronchoconstiction
148
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
149
chemicals that mimic carcinoid heart disease
fenfluarmine/phentermine
methysergide
ergotamine
150
identify
Characteristic endocardial fibrotic lesion involving the right ventricle and tricuspid valve.
151
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.
152
complications of cardiac valve prostheses
thrombosis/thromboembolism
anticoagulant-related hemorrhage
prosthetic valve endocarditis
structural deterioration
inadequate or exhberant healing
hemolysis
153
identify
Thrombosis of a mechanical prosthetic valve
154
identify
Calcification with secondary tearing of a porcine bioprosthetic heart valve, viewed from the inflow aspect.
155
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)
156
endomyocardial biopsy
used to differentiate idiopathic dilated from myocarditis secondary to virus
biopsy taken from septum to prevent cardiac tampenade
157
major causes of myocardits in US
ocsackieviruses A and B and other enteroviruses
Lyme disease
hypersenstivity myocarditis (Eos)
trichinosis- undercooked meat
158
major causes of myocarditis in south america
Chagas disease (trypanosoma cruzi)
159
immune mediated causes of myocarditis
postviral
poststreptococcal
SLE
drug hypersensitivity
transplant rejection
160
random causes of myocarditis
sarcoidosis
giant cell myocarditis
161
dialated cadiomyopathy
LVEF \<40%
impariment of contracticly (systolic dysfunction)
162
dialted cardiomyopathy causes
genetic, alcohol, myocarditis, hemochromatosis, chronic anemia, doxorubicin, arcoidosis, idopathic
163
dilated cardiomyopahty indirect myocardial dysfunction
IHD
valvular heart disease
HTN heart disease
congenital heart disease
164
hypertrophic cardiomyopathy
LVEF 50-80%
impairment of compliance (diastolic dysfunction)
165
causes of hypertrophic cardiomyopathy
genetic
friedreich ataxia
sotrage diseases
infants of diabetic mothers
166
hypertrophic cardiomyopathy indirect myocardial dynsfunction
HTN heart disease
aortic stenosis
167
restrictive cardiomyopathy
LVEF 45-90%
impairment of compliance (diastolic dysfunction)
168
causes of restricitive cardiomyopathy
amyloidosis
radiation induced fibrosis
idiopathic
169
restrictive cadiomyopaahty indirect myocardial dysfunction
pericardial constriction
170
