PATHO: CELLULAR INJURY

Cards (21)

  • Functional and morphologic changes are reversible if the damaging stimulus is removed
    REVERSIBLE CELL INJURY
  • Becomes irreversible with continuing damage and Cell cannot recover and dies
    Irreversible Cell Injury
  • Range from gross physical trauma of a motor vehicle accident to the single gene defect that results in a defective enzyme underlying a specific metabolic disease
    cause of cell injury
  • OXYGEN DEPRIVATION
    hypoxia
  • interferes with aerobic oxidative respiration“Oxygen Deficiency”
    hypoxia
  • Loss of blood supply in tissue due to impeded arterial flow or reduced venous drainage -“Hypoxemia”- and it is MOST common cause of hypoxia
    ISCHEMIA
  • A number of chemical substances can injure cells, Oxygen at sufficiently high partial pressures is toxic
    CHEMICAL AGENTS
  • Oxygen at sufficiently high partial pressures is toxic
    CORROSIVE CHEMICALS
  • vomited out of the body
    NON-CORROSIVE CHEMICALS
  • Could be bacteria, viruses, or fungi
    INFECTIOUS AGENT
  • Trauma, extremes of temperatures,radiation, electric shock, and sudden changes in atmospheric pressure all have wide-ranging effects on cells
    PHYSICAL AGENTS
  • Cellular Senescence leads to alterations in replicative and repairabilities of cells and tissues
    NUTRIENT DEFICIENCY
  • major pathway of cell death in many commonly encountered injuries
    NECROSIS
  • active, energy-dependent, tightly regulated types of cell death seen in some specific situations “Programmed Cell Death”
    APOPTOSIS
  • INFARCTS, IN ALL SOLIDS ORGANS EXCEPT THE BRAIN
    COAGULATIVE NECROSIS
  • BRAIN (LIQUEFY THE TISSUE)
    LIQUEFACTIVE NECROSIS
  • DIABETIC FOOD/USUALLY ONLIMB, GENERALLY ON LOWERLIMBLOWER LIMB
    GANGRENOUS NECROSIS
  • TUBERCULOSIS (CHEESE-LIKE)
    CASEOUS NECROSIS
  • PANCREATIC LIPASE/ ALCOHOL CAUSES PANCREATITIS
    FAT NECROSIS
  • SEEN IN IMMUNE REACTIONS INVOLVING BLOOD VESSELS/“FIBRINOID” (FIBRIN-LIKE)/ LUPUS
    FIBRINOID NECROSIS
  • it is defined as the paradoxical exacerbation of cellular dysfunction and death, following the restoration of blood flow to previously Ischaemic tissues.
    Reperfusion ischemic injury