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Cell injury, death and adaptation Yemen University Lectures 1 and 2

Cell injury, death and adaptation Yemen University Lectures 1 and 2. Dr H eyam Awad FRCPath. Coordinator : Dr Heyam Awad Email: h_awad@ju.edu.jo Lectures will be available on my university website www.ju.edu.jo Office hours: Monday and Wednesday 10-12 .. Office in hospital 3 rd floor.

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Cell injury, death and adaptation Yemen University Lectures 1 and 2

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  1. Cell injury, death and adaptationYemen UniversityLectures 1 and 2 Dr HeyamAwad FRCPath

  2. Coordinator : Dr HeyamAwad • Email: h_awad@ju.edu.jo • Lectures will be available on my university website www.ju.edu.jo • Office hours: Monday and Wednesday 10-12 .. Office in hospital 3rd floor.

  3. Lecture distribution • Cell injury 4+lab • Inflammation 6 +2labs • Repair 3 +lab • Haemodynamic diseases 5+lab • Neoplasia 8 +2 labs • Genetic diseases 8 + 2 labs

  4. EVALUATION • 1 EXAM • THEORY AND PRACTICAL. • mock

  5. What is pathology? • Patho… disease • Logy… study • Pathology = study of disease involves: causes of disease.. Etiology : mechanisms.. pathogenesis :morphological changes.

  6. Etiology: Origin of disease , underlying causes. • Pathogenesis: steps in the development of disease…… cellular and molecular changes . • Morphology: macroscopic and microscopic changes.

  7. Why to study pathology???

  8. Cellular adaptations and cell injury • Cells maintain a steady state.. Homeostasis. • Stresses .. Adaptation….. New homeostatic state with preservation of function. • Stress beyond capability of adaptation.. Cell injury. • Cell injury… reversible within certain limits • Then .. Irreversible…. Ends in cell death. • Two types of cell death: necrosis and apoptosis.

  9. Adaptation • Hyertrophy • Hyperplasia • Atrophy • metaplasia

  10. Adaptation • Adaptive changes are reversible. • Can be physiologic or pathologic.

  11. Hypertrophy: Increased cell size. • Hyperplasia: increased number of cells.. Cell division. • Metaplasia: change from one adult cell type to another • Atrophy: decreased size.

  12. Hypertrophy versus hyperplasia

  13. Hypertrophy • Increased cell size. • Due to increased organelles and proteins. • Increased intracellular synthesis.. Caused by: increased demands, hormones or growth factors.

  14. Physiologic hypertrophy • Uterus during pregnancy… due to estrogen • Skeletal muscle… due to increased demand

  15. Physiologic hypertrophy

  16. Pathologic hypertrophy • Cardiac.. Hypertensive heart disease • Pathogenesis.. Two types of signals: mechanical: stretch and trophic: growth factors and androgenic hormones

  17. Pathologic hypertrophy

  18. Pathologic hypertrophy

  19. hyperplasia • Only in tissues that can replicate. • Can be physiologic or pathologic.

  20. Physiologic hyperplasia • Hormonal: uterus, breast. • Compensatory: after removal or loss of part of tissue.

  21. Pathologic hyperplasia • Due to excess in hormones or growth factors. • E:g endometrial hyperplasia. • Controlled.. Responds to decreased stimulation. This differentiates it from cancer

  22. Normal endometrium

  23. Endometrial hyperplasia

  24. atrophy • Shrinkage in cell size due to loss of cell substance. Causes • decreased work load. • Loss of innervation • Loss of endocrine stimulation. • Aging

  25. Atrophy • Physiologic: endometrial atrophy during menopause • Pathologic: loss of innervation.

  26. atrophy Mechanisms: • Decreased protein synthesis. • Degradation of cellular proteins. • Autophagy…. Literally means self eating.

  27. Brain atrophy

  28. Muscle atrophy

  29. metaplasia • Adult cell type replaced by another adult cell type. • Arise in reprogrammed stem cells to differentiate along a new pathway.

  30. Epithelial metaplasia • Respiratory epithelium to squamous. • Barrett's mucosa.. Esophegeal squamous to columnar

  31. Barrett’s mucosa

  32. Normal esophegeal mucosa

  33. Metaplastic, Barrett’s mucosa

  34. Metaplasia in mesenchymal tissue • Usually pathologic • Ossification of soft tissue due to injury.

  35. Cell injury

  36. Causes of cell injury/ 1 • Chemical agents • Infections. • Immunologic • Genetic factors • Nutritional imbalances • Physical agents • Aging.

  37. Causes of cell injury/ 2 Oxygen deprivation.. Hypoxia and ischemia. Hypoxia= oxygen deficiency Ischemia = loss of blood supply due to impaired arterial flow or reduced venous return. -Ischemia is the most common cause of hypoxia. -Other causes of hypoxia: *reduced oxygen carrying capacity in anemia or carbon monoxide deficiency. *inadequate oxygenation of the blood as in pnumonia.

  38. Rules and principles/ 1 • Cell response to injurious stimuli depend on type, duration and severity of the injury. • Example: low dose of a toxin can cause reversible injury whereas larger dosed can cause cell death. • Short-lived ischemia.. Reversible • Ischemia of long duration… death

  39. Rules and principles/ 2 • Response to injury also depends on type, status, adaptability and genetic makeup of the injured cell. • Example: skeletal muscle cells can stand 2-3 hours of ischemia without irreversible injury but cardiac muscles die in 20-30 minutes . • Glycogen content in hepatocytes can determine their response to injury.. How? • Genetic polymorphism in cytochrome P-450 influences response to toxins.

  40. Rules and principles/ 3 Cell injury results from functional and biochemical changes in essential cellular components, mainly: • Mitochondrial function • Calcium homeostasis • Cell and organelle membranes • DNA • Protein synthesis and folding.

  41. Rules and principles/ 4 All injurious stimuli first affect the molecular or biochemical level. Cellular functions lost before cell death occurs. The morphologic changes of cell injury (or cell death) occur very late.

  42. Rules/4 example • Ischemia of the heart… coronary artery occlusion. • Myocardial cells loose function ( become non-contractile) after 1-2 minutes of ischemia. • They die 20-30 minutes after ischemia. • It takes 2-3 hours to recognise ultrastructural changes of death (EM) • 6-12 hours by light microscope to appear dead.

  43. Morphology of reversible cell injury • Cellular swelling : due to failure of energy-dependent ion pumps in the plasma membranecausing inability to maintain ion and fluid homeostasis. • Fatty change : small or large lipid vacuoles (hepatocytes and myocardial cells)

  44. Cell swelling • The first manifestation of almost all forms of cell injury. • Reversible. • Grossly: organ affected becomes pale and gains weight. • Micro: small clear cytoplasmic vacuoles … which are distended endoplasmic reticulum.

  45. Cell swelling

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