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Cell injury

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Cell injury

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Cell injury

  1. 1. Cell Injury Dr Kamran Afzal MBBS, FCPS, PhD
  2. 2. Cell Morphology
  3. 3. Cell Physiology  Cell membrane: Semi-permeable membrane with pumps for ionic / osmotic homeostasis  Nucleus: Nucleolus (synthesis of ribosomal RNA)  Mitochondria: Oxidative phosphorylation (main source of ATP)  Endoplasmic reticulum (ER), Ribosomes and Golgi Apparatus: Protein synthesis and transport  Lysosome: Endocytosis, phagocytosis and pinocytosis followed by degradation  Peroxisome: Catalase and oxidase enzymes, metabolism of H2O2 fatty acid
  4. 4. Cellular Functions  Movement  Conductivity  Metabolic absorption  Secretion  Excretion  Respiration (oxidation)  Reproduction  Communication
  5. 5. Cell Injury  A change in cell structure, metabolism, physico-chemical properties and function which leads to impairment of its vital activity
  6. 6. Main Causes of Cell Injury  Internal stresses:  Metabolic imbalances, nutritional deficiencies or excesses  Genetic abnormalities  Hypoxia ˃ impairment in aerobic tissue respiration, ischemia ˃ decrease in blood supply  External stresses:  Physical agents (mechanical injury, high and low temp, radiation, electrical shock, sudden fluctuations of the barometric pressure, acceleration, etc)  Natural toxins, venoms, infections  Drugs and chemicals, abundant oxygen, increase in glucose, high doses of dietary salt, poisons, insecticides, carbon monoxide, asbestos, social stimulators, e.g. alcohol, narcotics
  7. 7. Stages in Cell Injury
  8. 8. Reversible Cell Injury  Occurs when environmental changes exceed the capacity of the cell to maintain normal homeostasis  But if the stress is removed or the cell withstands the assault the injury is reversible
  9. 9. Irreversible Cell Injury  If the stress remains severe, the cell injury becomes irreversible and leads to cell death
  10. 10. Reversible And Irreversible Cell Injury
  11. 11. Mechanisms of Cell Injury  Defects in membrane permeability  Mitochondrial damage ˃ Depletion of ATP  Accumulation of oxygen-derived free radical (Oxidative stress)  Influx of intracellular calcium and loss of calcium homeostasis
  12. 12. Mechanisms Of Cell Death  Physiological, as in cell life cycle  Necrosis: Morphologic changes seen in dead cells within living tissue  Autolysis: Dissolution of dead cells by the cells own digestive enzymes  Apoptosis: Programmed cell death  “Apoptosis is a pathway of cell death that is induced by a tightly-regulated suicide program in which cells destined to die activate enzymes that degrade the cell’s own nuclear DNA and nuclear and cytoplasmic proteins”
  13. 13. Cell Injury Signs  Morphological  Swelling  Dystrophy  Dysplasia  Necrosis  Autolysis  Functional  Decrease in function  Cellular  Increase in permeability  Cytoplasmic enzymes leakage to the blood  Metabolic derangements  Injury mediators  Synthesis impairments  Electrolyte balance disorders
  14. 14. Fatty Change  Occurs in:  Hypoxic injury  Toxic or metabolic injury  Appearance of lipid vacuoles in the cytoplasm  Swelling of cells is reversible  In cells involved in and dependent on fat metabolism  Hepatocytes  Myocardial cells
  15. 15. Pigmentation  Endogenous  Lipofuscin – ageing pigment  Melanin – in melanocyte  Hemosiderin – aggregates of ferritin  Accumulation of bilirubin Too much produced (e.g., hemolysis) Not processed (e.g., cirrhosis) Outflow blocked (e.g., choledocholithiasis)  Exogenous  Anthracosis (cigarette smoking; urban living)  Tattoo
  16. 16. Calcification  Abnormal tissue deposition of calcium salts  Dystrophic • Patients have a normal calcium level • Calcification affects previously damaged tissue (Ageing or damaged heart valve)  Metastatic • Patients have an elevated level of serum calcium Causes: Hyperparathyroidism, bony metastases, RF  Atherosclerosis (common)  Aortic stenosis (uncommon) - Calcification is not routinely reversible Tricuspid valve - Calcification
  17. 17. Amyloidosis  A group of diseases characterised by extracellular depostion of fibrillar proteinaceous substance called amyloid  Has morphological appearance, staining properties and physical structure but with variable protein or biochemical composition  Deposits intracellularly and extracellularly
  18. 18. Amyloidosis of Heart  Heart is involved in systemic amyloidosis  Advanced cases.. restrictive cardiomyopathy, arrhythmias  Gross: heart enlarged, surface pale, translucent and waxy Epicardium, endocardium and valves show tiny nodular deposits of amyloid  Microscopy: Amyloid deposits in and around coronaries  In primary amyloidosis, deposits of AL are seen around myocardial fibres in ring like formations (ring fibres)  In localised form, deposits are seen in left atrium and interatrial septum
  19. 19. Necrosis  Result of denaturation of intracellular proteins and enzymatic digestion of the lethally injured cell  Necrotic cells are unable to maintain membrane integrity  Lysosomal enzymes digest the necrotic cells  Dead cells may ultimately become calcified  Coagulative  Liquefactive  Caseous  Fat  Gangrenous  Fibrinoid
  20. 20. Coagulative Necrosis – Kidney A localized area of coagulative necrosis is called an infarct Gangrene - Coagulative necrosis involving multiple tissue planes
  21. 21. Caseous Necrosis – Tuberculosis collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border Fat Necrosis – Mesentry Focal areas of fat destruction, typically resulting from release of activated pancreatic lipases
  22. 22. Fibrinoid - Artery When complexes of antigens and antibodies are deposited in the walls of arteries Liquifactive Necrosis – Cerebrum Digestion of the dead cells, resulting In transformation of the tissue into a liquid viscous mass

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