condensation, shrinkage of nucleus + cytoplasm

scattered single cell

shrinkage and condensation of nuclear chromatin

disolution of nuclear membrane and chromatin

multiple fragment of condensed nuclear chromatin + cytoplasm

apoptotic body

cleaved doublestranded DNA

more eosinophilic cytoplasm

apoptosis

pyknosis

karyolysis

karyorrhexis

progressive membrane damage

multifocal single cell death

well initially in inflammatory response, neutrophil and phagocytosis, decreased ATP, disregulation of ATPase, all membrane breakdown

always pathological

Tg accumulate in cytoplasm

reversible

nuclei is preserved

adaptation or sublethal injury

fatty change in liver:

heart and kidney

adaptation or fatty degeneration(reversible sublethal injury)

sublethal injury

multiple small nonmembrane-bound lipid droplet

clear, well defined, punched-out, vacuoles

increased in cell size with irregular, less well defined vacuolated cytoplasm due to increased water accumulation w/o displacement or alteration to nucleus

separation of organelle due to impaired oxidated meta lead to insufficient energy to maintain membrane pump indicate intracellular edema

most common form of injury with ischemia and toxic injury

wedge shaped, pale yellow to gray tissue with reddish border dur to hyperemia at border

hemosiderin b/c RBC trapped in infarct broke down by macrophage

unmasking of structural lipid give yellowish color

bilirubin diffuse into dead tissue.

irreversible cell injury

2 process:

ccoagulation: in protein rich region, breakdown of protein first.

liquifaction: in protein poor region where neutrophilic inflammation hydrolyzes cell rapidly

coagulation necrosis superimposed infection and neutrophilic inflammation in internal organ

edematous and weepy

soft semisolid, gray to pale yellow tissue

amorphous mass of granular eosinophilic material with no cell outline and no identifiable nuclei, no cavity, giant cell

caseous necrosis

pure coagulation: well preserved cell outline

pure liquefaction: disillusion and liquefaction of tissue

break down of neutral TG into FFA

amorphous pink stain to previously clear cytoplasm of adipocyte

bluish coloration

enzymatic fat necrosis

influx of Ca complex with FFA to form calcium soaps stain for hematoxylin

acute pancreatitis

ruptured gastric ulcer

blunt trauma

infection of subcutis

necrosis of parenchyma of pancreas

brain infarct

abscess formaton from neutrophilic inflamamtion.

gastric ulcer

normal cell is stressed, 2 phases

reversible/sublethal/degernation phase has 5 adaptive change

irreversible/lethal phase has 2 cell death

atrophy

hypertrophy

hyperplasia

metaplasia

dysplasia

apoptosis

oncosis

kidney bulging out

increase vacuolation,

bigger cell

fatty change: intracellular accumulation of neutral fat

stromal infiltration: replacement of parenchyma by adipocyte/fatty ingrowth/fatty invasion, no accumulation of neutral lipid.

adaptive changes: increase load, alcohol

sublethal injury/fatty degeneration: hypoxic injury, CCL4

obesity

corticosteroid

necrosis or fat in gross speciment

mottled yellow and brown area in myocyte

accumulation of fat

non-membrane bound lipid vacuole

epicardial fat, fatty tissue replacement

myocyte pushed aside by fat

separation of organelle

condesation of chromatin

intracellular fluid accumulation

reversible vs. irreversible?

amorphous swelling of flocculent density in mitochondria

destruction of sarcolemma

clumpy chromatin

necrosis of blood vessel wall

no outline of somooth muscle

hemogenous bright red

epithelium very leaky: leakage of plasma fluid into vessel wall

necrosis of wall

fibrin lay down

regeneration: single cell necrosis, labile cell

scar: collagen replacement

ulcer: excavation or defect on surface of tissue

cyst

sequestrum: in bone.

extracellular hyalin

intracellular hyalin

white shiny gross appearance of tissue or homogeneous eosinophilic histologic appearance

amyloid deposit seen on congo red stain.

sclerotic blood vessel

old collagenous fibrous tissue

brown  atrophy of heart

see wrinkled coronary artery

severe sustained starvation

see what pigment

lipofuscin:

breakdown of organelle of atrophied organ.

brown rusty discoloration granular,

liver

blue on prussian blue stain

hypereiosinophilic stain in liver cell

cause jaundice

yellow green pigment.

Hb breakdown, but contain no Fe.

white shiny gross appearance of tissue or homogeneous eosinophilic histologic appearance

hyaline droplets

russell body: plasma cell secrete actively , overloaded with protein inclusion.

alcoholicc injury to liver: alcohol hyalin

dystrophic calcification

metastatic calcification

nodular clump of Ca on aortic valve

common w/ aging

Ca, Po4 meta and serum level normal

Ca salt deposition on previously undamaged tissue

abnormal Ca meta.