Rr 01 Cell Injury Part 4

Front 1

Describe necrosis

Back 1

Death of groups of cells, often accompanied by an inflammatory infiltrate

Front 2

Describe coagulative necrosis

Back 2

Preservation of the structural outline of dead cells

Front 3

Describe the mechanism of coagulation necrosis

Back 3

1. Denaturation of enzymes nad strucutral proteins
a. Intracellular accumulation of lactate and heavy metals
b. Exposure of cells to ionizing radiation
2. Inactivation of intracellular enzymes prevents dissolution (autolysis) of the cell

Front 4

Describe the microscopic features of coagulation necrosis

Back 4

1. Indistinct outlines of cells within dead tissue
2. Absent nuclei or karyolysis (fading of nuclear chromatin)

Front 5

Describe the infarction in coagulative necrosis

Back 5

1. Gross manifestation of coagulation necrosis secondary to the sudden occlusion of a vessel
2. Usually wedge-shaped if dichotomously branching vessels are occluded
3. Pale (ischemic type)
-Increased density of tissue (heart, kidney, spleen) prevents RBCs from diffusing through necrotic tissue
4. Hemorrhagic (red type)
-Loose-textured tissue (lungs, small bowel) allows RBCs to diffuse through necrotic tissue

Front 6

Describe dry gangrene

Back 6

Dry gangrene of the toes in individuals with DM is a form of infarction that results from ischemia. Coagulation necrosis is the primary type of necrosis that is present in the dead tissue

Front 7

Describe the factors influencing whether an infarction will occur in tissue

Back 7

1. Size of vessel that is occluded
2. State of development of collateral circulaton
3. Presence of dual blood supply
4. Sudden onset of ischemia in an organ with preexisting disease will more likely produce an infarction
5. Tissues iwth high O2 requirements are more likely to infarct than other less sensitive tissues
6. Rapidity with which vessel is occluded often determines whether an infarction will occur

Front 8

Describe liquefactive necrosis

Back 8

1. Necrotic degradation of tissue that softens and becomes liquefied
2. Mechanisms
-Lysosomal enzymes released by necrotic cells or neutrophiles cause liquefaction of tissue
3. Examples- CNS infarction, abscess in a bacterial infection

Front 9

Describe caseous necrosis

Back 9

1. Variant of coagulation necrosis
-Associated with acellular, cheese-like material
2. Mechanism
a. Caseous material is formed by the release of lipid from the cell walls of Mycobacterium tuberculosis and systemic fungi (eg. Histoplasma) after immune destruction by macrophages
b. Other diseases associated with granuloma formation do not exhibit caseation

Front 10

Describe the microscopic features of a granuloma

Back 10

A cellular material in the center surrounded by activates macrophages, CD4 helper T cells, and multinucleated giant cells

Front 11

Describe enzymatic fat necrosis

Back 11

Peculiar to adipose tissue located around an acutely inflamated pancreas

Front 12

Describe the mechanisms of enzymatic fat necrosis

Back 12

1. Activation of pancreatic lipase (eg alcohol excess) causing hydrolysis of triglyceride in fat cells with release of fatty acids
2. Conversion of fatty acids into soap (saponification)
-Combination of fatty acids and Ca

Front 13

Describe the gross appearance of enzymatic fat necrosis

Back 13

Chalky yellow-white deposits are primarily located in peripancreatic and omental adipose tissue

Front 14

Describe the microscopic appearance of enzymatic fat necrosis

Back 14

Pale outlines of fat cells filled with basophilic-staining calcified areas

Front 15

Describe traumatic fat necrosis

Back 15

1. Occurs in fatty tissue (eg. female breast tissue) as a result of trauma
2. Not enzyme mediated

Front 16

Describe fibrinoid necrosis

Back 16

1. Limited to small muscular arteries, arterioles, venules, and glomerular capillaries
2. Mechanism: Deposition of pink staining proteinaceous material in damaged vessel walls due to damaged basement membranes
3. Associated conditions: Immune vasculites (eg Henock-Schonlein purpura), malignant hypertension

Front 17

Describe apoptosis

Back 17

Programmed, enzyme-mediated cell death

Front 18

Describe the normal and pathologic processes associated with apoptosis

Back 18

1. Destruction of cells during embryogenesis
2. Hormone-dependent atrophy of tissue
3. Death of tumor cells and virus infected cells by CD8 cells
4. Corticosteroid destruction of lymphocytes (B and T cells)
5. Removal of acute inflammatory cells from healing sites
6. Damage to DNA by radiation, FRs, and toxins
7. Removal of misfolded proteins

Front 19

Describe the extrinsic pathway of apoptosis

Back 19

1. Binding of TNF to its receptor
2. Eventual activation of caspases

Front 20

Describe the intrinsic pathway of apoptosis

Back 20

1. Mitochondrial leakage of cytochrome c into the cytosol
2. Eventual activation of caspases

Front 21

What genes regulate apoptosis via the intrinsic pathway?

Back 21

-BCL2 gene family
-TP53 suppressor gene

Front 22

Describe the BCL2 gene family

Back 22

1. Located on chromosome 18
2. Manufactures gene products that inhibit apoptosis
3. Gene products prevent mitochondrial leakage of cytochrome c into the cytosol

Front 23

Describe the TP53 suppressor gene

Back 23

1. Temporarily arrests the cell cycle in the G1 phase to repair DNA damage (aborts apoptosis)
2. Promotes apoptosis if DNA damage is too great by activating the BAX apoptosis gene
-BAX gene products inactivate the BCL2 antiapoptosis gene

Front 24

Describe capsases

Back 24

1. Group of inactive proenzymes (proteases, endonucleases)
-Must be activated by the extrinsic or intrinsic system to produce apoptosis
2. Changes in the cell
3. Activation of endonuclease leads to nuclear pyknosis and fragmentation
4. Activation of protease leads to breakdown of the cytoskeleton
5. Formation of cytoplasmic buds on the cell membrane
-Buds contain nuclear fragments, mitochondria, and condensed protein fragments
6. Formation of apoptotic bodies by the breaking off of cytoplasmic buds
7. Phagocytosis of apoptotic bodies by neighboring cells or macropages

Front 25

Describe the microscopic appearance of apoptosis

Back 25

1. Cell detachment from neighboring cells
2. Deeply eosinophilic-staining cytoplasm
3. Pyknotic, fragmented, or absent nucleus
4. Minimal or no inflammatory infiltrate surrounding the cell