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Events that lead to cell injury (Lethal (severe) injury (Myocardial…

- - - - Histological necrosis (≈ 8 hours) Cellular proteins are coagulated Visible with the naked eye and under the microscope as different from normal tissue
        
        Diagnosis: Coagulative necrosis of myocardium due to ischaemia (ie myocardial infarction)
      - Biochemical necrosis (point of irreversibility) Depleted glycogen & ATP; toxic metabolites Intracellular biochemistry grossly disrupted
        
        Intracellular membrane rupture
        7(a). Autolysis: cytoplasm dissolves (cell components degraded by lytic enzymes)
        7(b). Coagulation: cytoplasm solidifies (cell proteins denature)
      - 4. Membrane ion pumps start to fail, influx of H2O & electrolytes, cell swells Cell demonstrates sublethal/reactive changes (reversible) Toxic metabolites (e.g. lactic acid) start to accumulate If O2 is readmitted during this “period of grace”, tissue recovers
      - Anaerobic glycolysis generates ATP Time that cells survive this way varies: Myocardium ~45-60 minutes Neurones ~3-4 minutes Collagenous tissue ~2 hours
      - Acute anoxia to tissue
        
        Oxidative phosphorylation stops within cells (no O2, pyruvate cannot convert to acetyl coA, no Kreb’s cycle)
  - - - NUCLEAR CHANGES SEEN IN PROCESS OF NECROSIS Damage to nucleus
        Nucleus shrinks and condenses: PYKNOSIS Nucleus fragments: KARYORRHEXIS Nuclear fragments dissolve away: KARYOLYSIS
      - Types of necrosis
        
        g) Fibrinoid Necrosis Occurs in connective tissue, blood vessel walls in hypertension & autoimmune diseases Collagen degenerates, resembles fibrin Fibrinoid nodule seen in rheumatoid arthritis
        h) Gangrenous Necrosis Dark, discoloured, foul smelling tissue Result of ischaemia & infection of necrotic tissue with anaerobic bacteria , especially Clostridium spp
        
        f)Fat Necrosis i) Enzymatic type: Occurs only around the pancreas Associated with adipose tissue injury and release of pancreatic lipases (e.g. in alcoholics) Fat necrosis of pancreas
        Fat Necrosis ii) Traumatic type: Occurs when adipose tissue in any site is injured by trauma e.g. injury to breast tissue following surgery
        
        e) Gummatous Necrosis Due to infection with Treponema pallidum Occurs in tertiary syphilis (esp. in CVS & CNS)
        
        d) Haemorrhagic Necrosis Result of ischaemia leading to necrotic tissue infiltrated with extravasated red blood cells e.g. Lung infarct or torsion of the testis
        
        c) Caseous Necrosis Occurs in tuberculosis (infection with Mycobacterium tuberculosis) Due to hypersensitivity reaction and nature of the bacterium caseous necrosis of lung
        
        b) Colliquative (Liquefactive) Necrosis i) Occurs in the BRAIN Due to autolysis progressing almost to completion with little coagulation ischaemia autolysis of cells (cerebral infarct)
        
        b) Colliquative (Liquefactive) Necrosis ii) Occurs in SUPPURATION Due to neutrophils lysing pyogenic bacteria and tissue, i.e. heterolysis (not autolysis) heterolysis of cells (abscess)on ischaemia autolysis of cells (cerebral infarct)
        
        a)Coagulative Necrosis Most common, occurs in solid organs e.g. heart, kidney, spleen, liver ischaemia coagulation of proteins (myocardial infarct)
      - Reaction to necrotic tissue if patient survives:
        
        a) Inflammation seen around necrotic region b) Necrotic tissue removed by phagocytic cells c) Necrotic tissue replaced by scar tissue (fibrosis, except in the brain where gliosis occurs) d) Calcium may deposit in necrotic tissues