Reversible And Irreversible Flashcards
Reversible plasma membrane alteration
blebs, loss of microvilli, loosing of intercellular attachment
Reversible Mitochondrial alteration
earliest manifestation of sublethal injury
swelling, appearance of phospholipid rich amorphous densities
Reversible dilation of endoplasmic reticulum
loss of the ribosomes
Reversible nuclear alteration
clumping of nuclear chromatin
Two patterns of morphologic change can be recognized under the light microscope
Cellular swelling
Fatty change
Cell swelling
Called hydropic changes or vacuolar degeneration
universal to all cell types
loss of ionic and fluid homoeostasis
cells show clear vacuoles in the cytoplasm
distended and pinched-off segments of ER
Fatty changes
Specific to cells dealing with fat metabolism, liver and heart
Lipid vacuoles in the cytoplasm
gross features of reversible injury:
increase in the weight of the organ
pallor of the organ
excessive damage to all membranes, cytosolic and organelles
Irreversible injury (lethal)
a potential mediator of irreversible cell death.
Calcium is a potential mediator of irreversible cell death. Increase intracellular Ca content from the extracellular compartments, with activation of the different enzymes
With the low pH,……… are activated.
Leakage of digestive enzymes from lysosomes.
With the low pH, hydrolases are activated. They begin to digest the cell components.
Autolysis: if the cells are digested by their own enzymes
Heterolysis: if the cells are digested by lysosomes from other cells
These processes require hours to develop, and so there are no detectable changes in cells if, e.g., a myocardial infarct causes sudden death.
Irreversible functional changes (which precede any morphologic change)
most necrotic cells and their debris disappear by
a combined process of extracellular enzyme digestion and leukocyte phagocytosis.
If necrotic cells and cellular debris are not promptly eliminated
They will attract calcium salts and other minerals and undergo dystrophic calcification
Two phenomena characterize irreversibility
Inability to reverse mitochondrial dysfunction
Development of severe membrane damage
this is the vital step to which no return
Cell membrane damage:
Progressive loss of membrane phospholipids.
By activation of phospholipases by Ca, and decrease synthesis of proteins
Cytoskeletal abnormalities.
Loss of the filaments between the cytoplasm and the cell membrane. So the cell membrane becomes loose and susceptible to rupture.
Toxic oxygen radicals.
This leads to peroxidation of the membranes.
Lipid breakdown products.
These act as detergents on the membranes.
mitochondrial dysfunction
One of the earliest manifestations of irreversible cell injury is the vacuolization of the mitochondria, and the accumulation of amorphous, calcium-rich densities in mitochondrial matrix
Affect the oxidative Phosphorylation, decrease ATP
The morphological correlations of irreversible cell injury
the sequence of morphological changes that follows cell death in living tissue
the sequence of morphological changes that follows cell death in living tissue
Necrosis
1- enzymatic digestion of the cell
* by lysosomal enzymes:
- autolysis. - heterolysis.
=>Leakage of proteins and cellular constituents e.g:
Cardiac muscle: creatine kinase & troponins.
Liver: alkaline phosphatase
Ultrastructural morphological changes: Necrosis
Defects in cell membrane
Mitochondrial swelling and large densities
Swelling of the ER and detachment of ribosomes
Appearance of myelin figures
Rupture of lysosomes
Necrosis: Light microscopic features
Changes in the cytoplasm in Necrosis:
acidophilia of the cytoplasm (pink staining)
binding of eosins to denatured proteins
loss of basophilia from the loss of RNA
glassy cytoplasm: loss of glycogen
vacuolated cytoplasm: degeneration of organelles
calcification of cells
Changes in the nucleus in Necrosis:
Pyknosis: increased basophilia due to shrinkage of the nucleus
Karyorrhexis: fragmentation of the pyknotic nucleus by nucleases
Karyolysis: loss of the basophilia of the chromatin, secondary to DNAase activity.
1-2 days following death, the nucleus disappears completely
nucleus disappears completely
1-2 days following death
