flat yellow lesion

leck necrosis

potentially reversible

seen in childhood

predominantly intracellular lipid composed of esterified cholesterol and foam cell

no significant focal thickening of intima.

gross: raised lesion above intimal surface, can form fissury plaque or laminated thrombi.

lipid core of foam cell composed of extracellular free cholesterol forming cholesterol cleft

oxid. LDL in macrophage + endothelial cell from media

ahterosclerotic plaque

cholesterol cleft: angulated, crystal-like

3 types of thrombi

composed of fibrin due to inflammation, injury, or diffuse intravascular coagulation

composed of erythrocyte, leukocyte, platelete

formed by agglutination of platelet and leukocyte followed by coagulation

coagulation thrombi

agglutination thrombi

combination thrombi: greastest majority

change in pattern of blood flow

changes in intimal surface of vessel

change in constituent of blood

virchow's triad

venous thrombi: statis of blood flow

arterial thrombi: damage to arterial wall with endothelial injury

hypercoagulability: for DIC

delicate, elevated, white net-like or rib-like markings on white and mixed parts of thrombus

alternating layer of RBC and fibrin + WBC

line of zahn

platelets aggregate

release substance to trigger coagulation

fibrin layer form to attract RBC

form lamellated thrombi

composition of white part of thrombi

composition of red part of thrombi

platelet-leukocyte lamellae

clotted blood

pulmonary artery with thrombi superimposed.

thrombi attached to non-atherosclerotic artery wall

thrombi has granulation with fibroblast and macrophage, calcification, canalization of thrombi

is thrombi originated from the artery?

no.

its deep vein thrombosis embolizing to pulmonary artery.

degeneration of constitutent within 24-48 hr, necrosis provoke inflammation in wall of vessel.

fibrinolysis  and liquefaction from 7-10 days.

red thrombi begins to retract, becoming firm, dry, and friable.

ingrowth of granulation tissue result in canalization of thrombus and recanalization of vessel lumen.

thrombi in vessel and attaches to it, overfills vessel, dry friable, lines of zahn, current jelly.

what kind of thrombi

thrombi in vessel doesn't adhere very well to vessel, fills part of vessel lumen, soft and mushy, coagulation of blood and lipids

chicken fat

what kind of thrombi

glomerular capillary loops filled with fibrin thrombi, homogenous, eosinophilic material.

fibrin stain show darker area in glomeruli

DIC, glomerular thrombosis.

in obstetric ccompensation

sepsis

trauma

malignancy

amniotic emboli

50% narrowing

75% area reduction

type of atherosclerosis plaque

dystrophic calcification

fibrous cap

lines of zahn

endothelial denudation

ulceration

fissuring of lesion as well as intraplaque hemorrhage

compliccated atherosclerosis plaque

small hemorrhage from vasa vasorum

major from disruption of plaque surface.

type of atherosclerosis plaque

variable mixture of lipid and fibrous tissue with intact fibrous capsule and endothelial surface

week of MI

gross: pale, dry, bulge slightly, surrounded by thin red line of congestion and hemorrhage

discrete yellow line

microscopic: early coagulation necrosis with neutrophil

week of MI

gross: thickness of cardiac wall reduced, red-purple, depressed band of granulation extending

gelatinous gray appearance .

micrscopic: granulation at edges with increase collagen indicating fibrosis

week of MI

white fibrous scar, wall thinned forming aneurysm.

% of transmural MI by coronary thrombi

subendocardial?

90%

1/3. most by transient platelet aggregation.

leading cause for in-hospital death from acute MI

mortality rate?

key determinant of it?

cardiogenic shock

90%

net loss of 40$ of myocardium

dense white acellular scar lacking pink color bundle of collagen

island of myocardium after granulation tissue producing fibrous tissue

surrounding myocyte is hypertrophied

form mural thrombi, aneurysm, or cardiac tympani

old infarct

hypertrophy to compensate for loss.

gross: enlarged, heavy, red, increased blood, increased central venous pressure, lower extremity edema

acute passive congestion of liver

decrease O2 supply from hypotension result in atrophy

increase central venous pressure result in dilatation and congestation of sinusoid

hepatic artery, portal vein, bile duct form portal triad to central vein to hepatic vein to IVC

hepatic+portal vein perfuse in sinusoid to space of disse to centrilobular region (last, most volurable to ischemia)

incrased amount of collagen

hemosiderin-laden macrophage

dusty red and sunken

maximum congestion in centrilobular section

yellow at periphery

atrophy of centrilobular hepatocyte

dilitation of centrilobular sinusoid

congestion of sinusoid w/ RBC

chronic congestion of liver

nutmeg liver

yellow periphery = fatty change.

atrophy due to hypotension, ischemia

dilitation due to increased central venous pressure

gross: brown induration of hemosiderin

diffuse thickening of alveolar septae (4 cell thick)

fibrosis in alveolar septae

distended capillary engorged with einsinophilic

macrophage with hemosiderin

gross: very red.

distended capilllary filled with RBC in alveolar septae

hemorrhage by diapedesis into alveoli

frothy fluid in alveoli

diffuse coagulation necrosis in centrilobular area

eosinophilicc hepatocyte

erythrocyte accumulate in sinusoid and space of disse

macrophage with pigment

normal hepatocyte with vaculoes of fatty metamorphosis near portal tract

acute centrilobular hemorrhagic necrosis

due to severe, rapid hypoxic injury

due to shock.

not concentric necrosis around central vein and sparing around portal track b/c hepatic artery + portal vein drain into sinusoid then to central vein

gross: flea bitten, sandy appearance.

interlobular artery, afferent, but not efferent artery  show thickened wall with amorphous pink smooth eosinophilic acellular material

glomeruli show replacement by collagenous CT.

tubule is atrophied

interstitial fibrosis with lymphocyte

cause?

hyaline arteriosclerosis caused by benign hypertension and slow progression

mild renal dysfunction

rapidly progressive pressure injury

onion-skin pattern in afferent artery with marked narrowing of lumen, not in efferent artery.

concentric lamellar proliferation of intimal cecll

fibrinoid necrosis when pressure elevate

hyperplastic arteriolosclerosis

severe renal ischemia and renal dysfunction

round acellular mesangial nodulesurrounded by cells from capillary loops

Kimmelstiel-wilson nodule in glomerulus

sclerotic in both afferent and efferent arteriole

loss of tubule and tubular atrophy

nodular diabetic glomerular hyaline arteriolosclerosis due to diffuse degenerative process

k-w nodule: increased in basement membrane related to increased cellular turnover and glycosylation of protein.

nephrotic syndrome with prominent proteinuria, hypertension and renal failure.

gross: cortical necrosis

coagulation necrosis

decrease urine b/c ischemia in damage to epithelium + tubular kidney blood flow

increase urine in regenerating proximal tubule

shock with acute cortical necrosis of kidney

glomeruli situated in cortex.

lymphocyte in whole heart

vs.

neutrophil in local region

suppurative by pyogenic bac.

interstitial by viral: usually self limiting.

parenchymatous by chaga's disease

mischellaneous such as fiedler's myocarditis in young adult

granulomatous myocarditis by sarcoidosis

differential for

dilated cardiomyopathy

hypertrophic

restrictive

viral

alcohol

hemochromatosis

idiopathic

cobalt

peripartum cardiomyopathy

adriamycin

sarcomere formation

fredreich's ataxia

infants of diabetic mother

amyloid, eosinophilic

radiation fibrosis

grainy, fibrin strands

adhesion between heart surface and pericardial sac

coagulation necrosis

PMN

epicardium thickened from amorphous eosinophilic stringy material

differential

serous pericardial effusion

fibrinous/serofibrinous effusion, pink effusion, high protein

purulent/suppurative effusion

hemorrhagic

very low protein, serous effusion = transudate

viral, AI, resolve spont.

uremia and rheumatic pericarditis, MI

bacterial

TB, neoplasm

heart failure

focal necrosis on valve, vegetation with granulation tissue and neutrophil,

elongated pseudohyphae in bimorphic form

new blood vessel at base of valve

fibroblast.

IE by candida

sterile thrombi, then bacteremia then toxin damage valve.

2 chronic pericarditis:

dense fibrous scar form following organization of purulent or hemorrhagic pericarditis, interfere with diastole, from staph, TB

organization of fibrinous exudate, visceral and parietal layer is fused causing obliteration of cavity

constrictive pericarditis

chronic obstructive/adhesive pericarditis