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.