Cellular injury, adaption, & death

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Cellular injury, adaption, & death by Mind Map: Cellular injury, adaption, & death

1. causes of cellular injury

1.1. reversible injury

1.1.1. hypoxia inadequate tissue oxygenation reduce blood flow reduced O2 saturation cell with high metabolic demand brain myocardium consequences decr. oxidative phosphorylation

1.1.2. cell membrane injury

1.1.3. hydrodynamics maintains homeostasis disrupted cause → apoptosis

1.2. oxidative stress ( free radicals)

1.2.1. damage by free radicals OH superoxide Anioin ( O2) H2O2

1.2.2. sources Endogenous metabolic enzymatioc rxn metal cations inflammatory dz. neoplastic dz. exogenous chemicals drugs toxins radiation tissue trauma

1.2.3. consequences image to lipids /proteins & DNA chronic tissue damage & dz. organ failure

1.2.4. defense mechanism superoxide (SOD) catalyzes superoxide radical → O2 or H2O2 Catalase conversion of H202 → O2 & H2O Glutathione perioxdase conversion of lipid hydroperoxides → Alcohols & reduce to H2O2→ H2O Vit. E neutralize free radicals Selenium cofactor for enzyme: glutathione peroxidase / ascorbate , ceuroloplasmin, transferrin, cysteine

1.2.5. oxidative injury chronic injury optimize cellular funct. acute injury Nutritional myopathy

1.3. physical agents

1.3.1. types trauma direct cell death & loss of blood supply extreme cold impair blood flow & cause ice formaton extreme heat denatures proteins & damages membranes electricity generative extreme heat & alters condition ionizing radiation free radical formation radiation DNA damage

1.4. irreversible

1.4.1. necrosis oncotic necrosis cell swelling beyond point of no return coagulative necrosis caused by ischemic injury caseation necrosis -TQ caused by chronic inflammation liquefactive necrosis encephlomalacia suppurative inflam. gangrenous necrosis dry gangrene moist gangrene gas gangrene Epithelium ulceration erosioni fat enzymatic necrosis of fat traumatic necrosis of fat abdominal fat necrosis of cattle sequences necrosis

1.4.2. apoptosis programmed cell death cellular shrinkage No iniflammtiion assoc. Morphology condensation of chromatin condensation of cytoplasm Apoptotic bodies

1.4.3. postmortem autolysis

1.4.4. chronic injury & cellular adaptation autophagocytosis changes in cell size number appearance

2. Hyperplasia- TQ

3. Metaplasia

4. Metaplasia

5. Hypertrophy a

6. ATrophy