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35 Cards in this Set

  • Front
  • Back
necrosis
gross and microscopic manifestations that indicate cell death in living tissue -

enzyme degradation mainly -


always pathological

apoptosis
programmed cell death -

genetically controlled -


eliminates unwanted cells -


physiological and pathological

autolysis
degradation of cell and contents caused by own enzymes
heterolysis
degradation of cell and contents by extrinsic enzymes
putrefaction
lysis of dead tissue by bacterial enzymes
necrotic changes
hypereosinophilic cytoplasm (RNA loss + coagulated proteins),

glycogen loss (smaller cell, more pink),


nuclear changes

morphologic necrotic types
coagulative,

liquefactive,


caseous,


fat,


fibrinoid,


gangrenous,


gummatous

coagulative necrosis

microscopic:

cell outline and tissue architecture preserved,

nucleus loss,


increased eosinophilia;


macroscopic:


dense and dry appearance,


white-grey when cut

liquefactive necrosis

microscopic:

complete loss of cell and tissue structure,

no cell outlines,


neutrophils;


macroscopic:


soft and filled with fluid

caseous necrosis
no cell outlines or tissue architecture but firm consistency;

macroscopic:


yellowish-white, cheese-like from lipid release from cell walls;


microscopic:


eosinophilic material surrounded by inflammatory cells

enzymatic fat necrosis
focal areas of fat destruction, due to pancreatic enzyme actions;

pale outlines, hematoxylin stains calcium blue; pancreatitis --> fatty acids + Ca = saponification and chalky white calcium deposits

traumatic fat necrosis
trauma --> healing by fibrous tissue and calcification
fibrinoid necrosis
immunologic injury;

smudgy pink staining of fibrin-like protein material

gangrenous necrosis
loss of blood supply = form of infarction;

dry (coagulative)


wet (with infection and liquefactive);


in lower limbs and bowels

infarction
localized area of tissue necrosis from loss of or reduced blood supply;

coagulative in most tissues,


liquefactive in brain

Physiologic apoptosis
embyrogenesis,

hormone-dependent involution,


thymus involution in adults,


cells programmed to die (epidermis, gut), inflammatory cell destruction

Pathologic apoptosis
toxin induced,

councilman bodies,


psammoma bodies,


tumor cell death by cyt T cells,


neuronal loss in Alzheimer's,


HIV+ T-lymphocyte death

councilman bodies
dead hepatocytes in viral hepatitis
psammoma bodies
apoptosis of neoplastic cell with subsequent calcification
neoplastic
abnormally growing cell
apoptosis initiation
extrinsic or intrinsic caspase activation,

gene regulation

apoptosis execution
cell death caused by activated enzymes
removal of cells in apoptosis
cytoplasmic buds form on membrane that contain nuclear fragments,

mitochondria and protein fragments

extrinsic pathway
receptor-ligand interactions:

TNF + TNF1, Fas + Fas ligand --> caspase activation

intrinsic pathway
withdrawal of hormones or growth factors, damage to DNA --> release of cyt c --> caspase activation
Bcl-2
inhibits apoptosis by preventing release of cyt c from mitochondria
p53
tumor suppressor gene = stimulates apoptosis; elevated by DNA injury and pauses cell cycle to repair; activates Bax if repair is impossible
Bax
stimulates apoptosis
caspases
group of proteases that mediates execution phase
executioner caspases
activate endonucleases (DNA degradation) and proteases (cytoskeleton breakdown)
apoptotic bodies
broken off cytoplasmic buds
phagocytosis
absorbtion of apoptotic bodies by adjacent cells or macrophages
apoptotic morphology
eosinophilic cytoplasm,

pyknotic nucleus,


small cells,


apoptotic bodies,


phagocytosis,


lack of inflammatory response

dysregulated apoptosis
too much or too little apoptosis;

decreased = cancers, autoimmunity;


increased = neurodegenerative, death of infected cells (AIDS)

enzyme markers of cell death
AST aspartate aminotransferase (liver necrosis),

ALT alanine aminotransferase (liver necrosis),


CK-MB creatine kinase MB (AMI, myocarditis),


amylase and lipase (pancreatitis)