Liquefactive necrosis
Accumulation of leucocytes
Release of enzymes
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Types of necrosis
Caseous necrosis
Fat necrosis
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Morphological changes in necrosis
Reversible injury
Plasma membrane-Blebings
Mitochondria-Swelling and amorphous densities
Endoplasmic reticulum-Dilation, detachment of ribosomes and
myelin figures
Nucleus-start of disintegration
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Morphological changes in necrosis
Irreversible injury
Two M’s of irreversibility- Membrane damage & Mitochondrial
damage
Plasma membrane-Discontinuities
Cellular contents-Enzymatic digestion with leak
Nuclear changes-Pyknosis-karyorrhexis-karyolysis
Associated inflammation
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Morphological changes in necrosis
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Increased eosinophilia-loss of cytoplasmic RNA (which binds
the blue dye, hematoxylin)
Glassy homogeneous appearance-loss of glycogen particles
Cytoplasm-vacuolated and appears moth-eaten
whorled phospholipid masses called myelin figures that are
derived from damaged cell membranes.
Phospholipid precipitates
•phagocytosed by other cells or further degraded into fatty
acids- Calcification of such fatty acid residues results in the
generation of calcium soaps.
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Karyolysis- basophilia of the chromatin fade - loss of DNA
because of enzymatic degradation by endonucleases.
Pyknosis, characterized by nuclear shrinkage and increased
basophilia-Chromatin condenses into a solid, shrunken
basophilic mass.
Karyorrhexis, the pyknotic nucleus undergoes fragmentation.
With the passage of time (a day or two), the nucleus in the
necrotic cell totally disappears.
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Morphological changes in necrosis
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Normal Reversible injury Irreversible injury
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Frame of a skyscraper
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Apoptosis
Definition
Cell suicide
Physiological or pathological
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Causes of apoptosis
Physiological-Programmed cell death
Embryogenesis and developmental involution
Hormone withdrawal
Ovarian atresia-menopause
Immature cells-Bone marrow and thymus
WBC-End of inflammatory response
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Causes of Apoptosis
Pathologic causes of apoptosis
DNA damage-Cytotoxic drugs, radiation and hypoxia
Accumulation of misfolded proteins
Infections: mainly viral by inducing Tcell response
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Pathogenesis
caspase is based on two properties
“c” refers to a cysteine protease (i.e., an enzyme with cysteine in its
active site)
“aspase” refers to the unique ability of these enzymes to cleave
after aspartic acid residues
More than 10 members
Two groups—initiator and executioner
Initiator - caspase-8 and caspase-9
Executioners-caspase-3 and caspase-6
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Apoptotic proteins
Antiapoptotic-Bcl2 and Bcl-x
Proapoptotic – bad, bak, bid and bim
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Dysregulated apoptosis
1.Excessive apoptosis
2.Neurodegenerative disease, stroke and MI
Reduced apoptosis
1.Cancer
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Differences between
Necrosis and Apoptosis
Rotten apple
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Dried apple
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Soaked grains
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Dried grains
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Differences
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Take home message
Necrosis-Pathological
Associated with inflammation
Apoptosis-Physiological or pathological
Associated with phagocytosis
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