Download
cell adaptations cell injury cell death dr samina n.
Skip this Video
Loading SlideShow in 5 Seconds..
CELL ADAPTATIONS CELL INJURY CELL DEATH DR.SAMINA QAMAR AP PATHOLOGY. PowerPoint Presentation
Download Presentation
CELL ADAPTATIONS CELL INJURY CELL DEATH DR.SAMINA QAMAR AP PATHOLOGY.

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

8 Views Download Presentation
Download Presentation

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

- - - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

  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