[PL2.3] CELL INJURY, CELL DEATH,& ADAPTATIONS

Most common type of necrosis seen in hypoxic death of cells except in the brain

coagulative necrosis

Coagulative necrosis results from

denaturation of proteins and enzymes

Effect of protein denaturation in coagulative necrosis

blocks proteolysis of dead cells

Early histologic feature of coagulative necrosis

preserved cellular outline with loss of nuclei

Late histologic change in coagulative necrosis

breakdown of necrotic cells by lysosomal enzymes

Localized area of coagulative necrosis

infarct

Type of necrosis where tissue is transformed into a viscous liquid

liquefactive necrosis

Liquefactive necrosis is dominated by

autolysis and heterolysis

Main cause of liquefactive necrosis

action of hydrolytic enzymes

Tissue types commonly affected by liquefactive necrosis

brain, bacterial infections, amoebic abscess

Necrotic material produced in liquefactive necrosis due to leukocytes

pus

Color and texture of pus

creamy yellow, viscous

Type of necrosis applied to a limb that has lost its blood supply

gangrenous necrosis

Type of gangrene involving bacterial infection and liquefactive necrosis

wet gangrene

Type of gangrene without infection, mostly coagulative

dry gangrene

Type of necrosis seen in tuberculosis

caseous necrosis

Visual appearance of caseous necrosis

friable, white, cheeselike

Granuloma is a structureless collection of what in caseous necrosis?

lysed cells and amorphous granular debris

Type of necrosis involving fat destruction due to pancreatic enzymes

fat necrosis

In fat necrosis, lipases break down triglycerides into fatty acids, which combine with calcium to form what?

chalky white areas (fat saponification)

Type of necrosis associated with immune complex deposition in blood vessels

fibrinoid necrosis

H&E appearance of fibrinoid necrosis

bright pink and amorphous

Cause of fibrinoid necrosis

deposition of antigen-antibody complexes

Type of programmed cell death regulated by intrinsic cellular mechanisms

apoptosis

In apoptosis, what do cells activate to degrade DNA and proteins?

intrinsic enzymes

Fragments produced during apoptosis containing parts of cytoplasm and nucleus

apoptotic bodies

Membrane condition of apoptotic cells

intact but structurally altered to signal phagocytes

Physiologic cause of apoptosis: removal of excess cells during

development

Physiologic cause of apoptosis: regression of hormone-dependent tissues

hormone withdrawal

Apoptosis is part of what process in rapidly renewing tissues?

cell turnover

Apoptosis eliminates potentially harmful what?

self-reactive lymphocytes

Apoptosis occurs after a cell has

served its useful purpose

Pathologic cause of apoptosis: genomic injury

DNA damage

Pathologic apoptosis due to disrupted protein processing

accumulation of misfolded proteins

Apoptosis in disease caused by organisms

cell death in certain infections

Apoptosis due to blockage of secretions or flow

pathologic atrophy in parenchymal organs after duct obstruction

Feature of apoptosis: reduction in cell volume

cell shrinkage

Most characteristic nuclear feature of apoptosis

chromatin condensation

Apoptotic cells show membrane protrusions called

cytoplasmic blebs

Apoptotic cells break into small membrane-bound pieces called

apoptotic bodies

Apoptotic cells are usually removed by

phagocytosis by macrophages

Microscopic appearance of apoptotic cells

intensely eosinophilic cytoplasm with dense nuclear chromatin fragments

Apoptosis is mediated by a family of enzymes called

caspases

First phase of apoptosis where initiator caspases are activated

initiation phase

Second phase of apoptosis involving cell fragmentation

execution phase

Two major pathways of apoptosis

mitochondrial (intrinsic) and death receptor (extrinsic)

Major mechanism of apoptosis

intrinsic (mitochondrial) pathway

Key event in mitochondrial apoptosis

increased mitochondrial permeability and cytochrome c release

Does intrinsic apoptosis require death receptors?

no

Pro-apoptotic mitochondrial membrane proteins

Bim, Bid, Bad, Bax, Bak

Pro-apoptotic cytoplasmic molecule

Smac/DIABLO

Anti-apoptotic proteins that block mitochondrial apoptosis

BCL-2, BCL-XL

Apoptotic pathway involving activation of plasma membrane receptors

extrinsic (death receptor) pathway

Key death receptors involved in extrinsic apoptosis

TNF and Fas