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CELL ADAPTATIONS CELL INJURY CELL DEATH DR.SAMINA QAMAR AP PATHOLOGY.

CELL ADAPTATIONS CELL INJURY CELL DEATH DR.SAMINA QAMAR AP PATHOLOGY. OBJECTIVES. Understand the concepts of cellular growth adaptations--- Hyperplasia, Hypertrophy, Atrophy, Metaplasia, Dysplasia Reversible, irreversible cell injury. OBJECTIVES.

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CELL ADAPTATIONS CELL INJURY CELL DEATH DR.SAMINA QAMAR AP PATHOLOGY.

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  1. CELL ADAPTATIONS CELL INJURY CELL DEATH DR.SAMINA QAMAR AP PATHOLOGY.

  2. OBJECTIVES Understand the concepts of cellular growth adaptations---Hyperplasia, Hypertrophy, Atrophy, Metaplasia, Dysplasia Reversible, irreversible cell injury

  3. OBJECTIVES Understand the pathologic mechanisms at the SUB-cellular level---ATP, Mitochondria, Ca++, Free Radicals, Membranes Understand and differentiate the concepts of APOPTOSIS and NECROSIS Understand SUB-cellular responses to injury---Lysosomes, Smooth endoplasmic reticulum, Mitochondria, Cytoskeleton

  4. OBJECTIVES Identify common patterns of cellular swelling and fatty change. Cell aging

  5. To maintain a steady state of structure and function is HOMEOSTASIS

  6. Cellular response to injury • Non-lethal injury: cell will adapt • Hypoxia, chemical injury, infection: Reversible injury will result in fatty change. Irreversible injury will result in death • Repeated Injury: cellular aging

  7. ADAPTATIONS: Non-lethal injury. • Altered/changed steady state in structure and function of cell. • WHY: In response to physical/ pathological stimuli. Increased or decreased stimulation or any irritation.

  8. The –plasia brothers • HYPER- • HYPO- (A-) • NORMO- • META- • DYS- • ANA- • “Frank” ANA-

  9. HYPER-PLASIA IN-CREASE IN NUMBER OF CELLS, if they can divide.

  10. Examples: Endometrium,breast,liver.

  11. The –trophy brothers • HYPER- • HYPO- (A-) • DYS-

  12. HYPER-TROPHY IN-CREASE IN SIZE OF CELLS

  13. Examples:Myocardium, Myometrium, Muscle

  14. Hypertrophy v/s Hyperplasia.

  15. Can both occur simultaneously?

  16. A-TROPHY*? DE-CREASE IN SIZE OF CELLS? YES SHRINKAGE IN CELL SIZE DUE TO LOSS OF CELL SUBSTANCE

  17. ATROPHY • DECREASED WORKLOAD • DENERVATION • DECREASED BLOOD FLOW • DECREASED NUTRITION • AGING (involution) • PRESSURE • “EXHAUSTION”

  18. Examples: Brain, Muscle.

  19. METAPLASIA • A SUBSTITUTION of one NORMAL CELL or TISSUE type, for ANOTHER • COLUMNAR SQUAMOUS (Cervix) • SQUAMOUS COLUMNAR (Esophagus) • FIBROUS BONE • WHY?

  20. Examples: Respiratory epithelium, Barrett’s, myositis ossificans.

  21. Dysplasia: disorganized epithelium.

  22. Dysplasia:

  23. Normal-hyperplasia-dysplasia-carcinoma.

  24. CELL DEATH

  25. CELL DEATH What is DEATH? • DEATH is IRREVERSIBLE • But in cell its either reversible or irreversible. • APOPTOSIS vs. NECROSIS

  26. REVERSIBLE CHANGES • REDUCED oxidative phosphorylation • ATP depletion • Cellular “SWELLING”

  27. IRREVERSIBLE CHANGES • MITOCHONDRIAL IRREVERSIBILITY • IRREVERSIBLE MEMBRANE DEFECTS • LYSOSOMAL DIGESTION

  28. REVERSIBLE = INJURY IRREVERSIBLE = DEATH SOME INJURIES CAN LEAD TO DEATH IF PROLONGED and/or SEVERE enough

  29. CELL DEATH • APOPTOSIS (“normal” death) programmed death. • NECROSIS (“premature” or “untimely” death

  30. Death is of two types

  31. INJURY CAUSES (REVERSIBLE) Hypoxia, (decreased O2) PHYSICAL Agents CHEMICAL Agents INFECTIOUS Agents Immunologic Genetic Nutritional

  32. CHEMICAL INJURY • “Toxic” Chemicals, e.g CCl4 • Drugs, e.g tylenol • Dose Relationship • Free radicals, organelle, DNA damage

  33. INJURY MECHANISMS (REVERSIBLE) DECREASED ATP MITOCHONDRIAL DAMAGE INCREASED INTRACELLULAR CALCIUM INCREASED FREE RADICALS INCREASED CELL MEMBRANE PERMEABILITY

  34. What is Death?What is Life? • DEATH is • IRREVERSIBLE MITOCHONDRIAL DYSFUNCTION • PROFOUND MEMBRANE DISTURBANCES LIFE is……..??? Till death hasn’t occurred.

  35. DEATH:ELECTRON MICROSCOPY B-Microvillus incorporated in cell, Blebs extruded from cell. C- Mitochondrial swelling.

  36. DEATH:PINK INLIGHT MICROSCOPY Nuclei

  37. LIQUEFACTIVE NECROSIS, BRAIN

  38. FIBRINOID NECROSIS

  39. APOPTOSIS: falling off. • NORMAL (preprogrammed) • PATHOLOGIC (associated with Necrosis)

  40. “NORMAL” APOPTOSIS • Embryogenesis • Hormonal “Involution” • Cell population control, e.g., “crypts” • Post Inflammatory “Clean-up” • Elimination of “HARMFUL” cells • Cytotoxic T-Cells cleaning up

  41. “PATHOLOGIC” APOPTOSIS • “Toxic” effect on cells, e.g., chemicals, pathogens • Duct obstruction • Tumor cells • Apoptosis/Necrosis spectrum

  42. APOPTOSIS MORPHOLOGY • DE-crease in cell size, i.e., shrinkage • IN-crease in chromatin concentration, i.e., hyperchromasia, pyknosis karyorhexis karyolysis • IN-crease in membrane “blebs” • Phagocytosis

  43. SHRINKAGE/HYPERCHROMASIA Karryorhexis, karryolysis.

  44. PHAGOCYTOSIS

  45. Damaged/necrotic cells can accumulate fat: Fatty change • Commonly occurs in Liver, heart. • Due to defective uptake, catabolism or secretion of lipid. • Severe fatty change can alter cellular structure and function. • Seen in diabetes, alcoholism, obesity.

  46. LIPID LAW • ALL Lipids are YELLOW grossly and WASHED out (CLEAR) microscopically

  47. FATTY LIVER

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