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Principles of cell injury and cellular adaptation .ppt

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Causes and pathogensis of cell injury and cellular adaptation

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Principles of cell injury and cellular adaptation .ppt

  1. 1. ChapterChapter :1:1 PrinciplesPrinciples ofof cellcell injuryinjury andand adaptationadaptation Presented by: Prof.Mirza Anwar BaigPresented by: Prof.Mirza Anwar Baig Anjuman-I-Islam's Kalsekar Technical CampusAnjuman-I-Islam's Kalsekar Technical Campus School of Pharmacy,New Pavel,NaviSchool of Pharmacy,New Pavel,Navi Mumbai,MaharashtraMumbai,Maharashtra 11
  2. 2. Contents: • Causes of cell injury • Pathogenesis and morphology of cell injury. • Cellular adaptation • Cellular atrophy and hypertrophy.
  3. 3. CELL INJURY • Cell injury results from a disruption of one or more of the cellular components that maintain cell viability. • Defined as variety of stresses a cell encounters as a result of internal or external environmental changes. • Cell injury is common to all pathologic processes. 3
  4. 4. CELL INJURY • Cellular adaptation • Reversible or irrversible cell injury • Subcellular changes and intracellular accumlation Injury at one point induces a cascade of effects. 4
  5. 5. Etiology: • Hypoxia and Ischamia: • Physical agents • Chemicals and drugs • Microbial agents • Immunologic agents • Nutritional derangemtns • Psychogenic diseases • Iatrogenic causes • Idiopathic diseases
  6. 6. HYPOXIC INJURY Cerebral infarction Myocardial infarction Renal atrophy 6
  7. 7. INFECTIOUS DISEASE Primary HerpesCandidiasis Tuberculosis Actinomycosis 7
  8. 8. PHYSICAL INJURY Thermal Burn Traumatic ulcer 8
  9. 9. CHEMICAL/DRUG INJURY Asprin Burn 9
  10. 10. Pathogenesis of cell injury • General principles of pathogenesis 1. Type, duration and severity of injurious agents 2. Type, status and adaptability of target cell 3. Underlying intracellular phenomena eg. Mitochondrial damage, cell wall damage, free radicals 4. Morphological consequences eg. Ultrastrucal changes, swelling 10
  11. 11. OUTCOMES OF CELL INJURY REVERSIBLE CELL DEATH CELL ADAPTATIONS NORMAL CELL CELL INJURY / CELL STRESS ACUTE CHRONIC 11
  12. 12. 1.Pathogenesis of ischemic and hypoxic injury Reversible cell injury: 1. Decreased generation of cellular ATP 2. Intracellualar lactic acidosis: Nuclear clumping 3. Damage to plasma membrane pump - ATP dependent Na /K pump, Ca pump 4. Reduced protein synthesis- Dispersed ribosomes Irreversible cell injury: 1. Mitochondrial damage- ↑ca influx 2. Activated phospholipase- membrane damage 3. Intracellular proteases- cytoskeleton damage 4. Activated endonucleases- nuclear damage 12
  13. 13. 1.1: Ischemia reperfusion injury and free radical mediated cell injury 3 different consequences: 1. from ischaemia to reversible injury 2. from ischaemia to reperfusion injury 3. from ischaemia to irreversible injury Mechanism: 1. Calcium overload: ↑lipid peroxidation of cell membrane 2. Generation of ROS: 3. Subsequent inflammatory reactions neutrophils utilize oxygen and gives free radicals 13
  14. 14. 2. Pathogenesis of chemical injury: • Direct cytotoxic effect – Direct cytotoxic effect: Hgcl2 poisoning, Anticancer agents Conversion to reactive toxic metabolites metabolites kills the cells eg, CCl4 affects liver Acetaminophen poisoning 3. Pathogenesis of physical injury: Ionizing radiations.- cell membrane & DNA damage 14
  15. 15. Cellular adaptation: Classifcation: a)Atrophy and Hypertrophy (↑or ↓in size) b)Hyperplesia (↑number of cells) c) Metaplasia (change from one type to another type) and dysplasia (changed phenotypic differentiation)
  16. 16. a. Atrophy 1.Physiologic atrophy: Brain,Gonads, 2.Pathologic atrophy a)Starvation atrophy b)Ischaemic atrophy eg, atropic kidney c)Disuse atrohy eg, atropy of pancreas d)Neuropathic atrophy eg. Motor neuron disease e)Endocrine atrophy eg, atropy of thyroid and adrenal 16
  17. 17. ATROPHY & ISCHEMIA Renal atrophy 17
  18. 18. ATROPHY & AGING Normal Brain Atrophic Brain 18
  19. 19. b. Hypertrophy – Physiologic hypertrophy eg uterus in pregnancy – Pathologic hypertrophy • Hypertrophy of cardiac muscle • Hypertrophy of smooth muscle – Cardiac achalasia – Pyloric stenosis – Intestinal strictures – Muscular arteries in hypertension • Hypertrophy of skeletal muscle • Compensatory hypertrophy eg, nephrectomy of one side, removal of one adrenal gland 19
  20. 20. HYPERTROPHY & INCREASED FUNCTIONAL DEMAND A A A = Normal heart B B B = Hypertensive heart C C C = Dilated heart 20
  21. 21. c. Hyperplasia: • Temporary Increase in the number of the parenchymal cells. • Resulting in enlargement of organ. • Often hypertrophy and hyperplasia occures simultaneously • Occures due to increased in mitosis of the resting cells. • Neoplasia causes change in the genetic composition of the cells. CAUSES: A. PHYSIOLOGICAL HYPERPLASIA: I) Hormonal hyperplasia eg: ↑in size of breast during pregnancy and lactation. Pregnant uterus ii) Compensatory hyperplasia: Eg: Regenration of liver cells after hepatectomy,epidermis after skin abrasion. B.PATHOLOGIC HYPERPLASIA: I) Endometrial hyperplasia in excess oestrogen ii) In wound healing: proliferation of fibroblasts cells iii) Formation of skin warts: papilloma viral infection
  22. 22. d. Metaplasia: • It is defined as a reversible change of one type of epithelial or mesenchymal cells to another type of adult epithelium or mesenchymal cells. • long time metaplasia may result in cancer. • Divided in 2 types: A. EPITHELIAL METAPLASIA: 1. Squamous metaplasia: Eg: In bronchus of chronic smokers Utreus of old age 2. Columnar metaplasia: Eg: Intestinal metaplasia in healed chronic gastric ulcer. B. MESENCHYMAL METAPLASIA: 1. Osseous metaplasia: Eg: arterial wall in old age 2. Cartilaginous metaplasia: Eg; healing of fractures
  23. 23. e. Dysplasia: • Means 'disordered cellular development'. • Often accompanied with metaplasia and hyperplasia. • Often occurs in epithelial cells. • Observed charactertics are – Increased number of layers of epithelial cells – Increased mitotic activity – Disorderly arrangement of cells from basel layer to surface layer. – Cellular and nuclear pleomorphism (variability in the size, shape and staining of cells and/or their nuclei.)
  24. 24. Morphology of Reversible cell injury 1.Hydropic change-swelling-kidney, liver,pancreas 2.Hyaline change- glass like 3.Mucoid change- mucus 4.Fatty change- fat accumlation eg fatty liver 24
  25. 25. Morphology of Irreversible cell injury a) Autolysis or self digestion b) Necrosis c) Apoptosis d) Gangrene e) Calcification 25
  26. 26. CONCEPTS - CELL DEATH • There is no singal biochemical event that equates with cell death. • Necrosis = “cell murder” • Apoptosis = “programmed cell death or cell suicide” 26
  27. 27. NECROSIS • Morphologic types of necrosis – Coagulative – Liquifactive – Caseous – Enzymatic (fat) • The type of necrosis is dependent upon patterns of enzymatic degradation of cells and extracellular matrix, the type of necrotic debris, and by bacterial products when present. 27
  28. 28. Coagulative necrosis: • Common type of necrosis • caused by irreversible focal injury,ischemia. • Foci are pale,firm and slightly swollen. • Hall mark is presence of tombstones. Liquefaction necrosis: Caused due to ischaemic injury or bacterial infection. Eg: infarct brain. Affected area is soft containing necrotic debris. Caseous necrosis: Found in foci of tuberclosis infection. have the features of coagulative and liquefaction necrosis. Appears like dry cheese,soft, granular and yellowish.
  29. 29. Fat necrosis: • Present at pancrease and breast. • Yellowish white firm deposits. • Fat cells have cloudy appearance and surrounded by inflammatory reactions. • Calcium soaps are present in the cells. Fibrinoid necrosis: • Deposition of fibrin like material. • Present in immunological tissue injuries. • Arterioles of hypertension,peptic ulcers. • Appears like brightly eosinophillic in vessel wall.
  30. 30. COAGULATIVE NECROSIS • Cell outline • Pink cytoplasm • Anucleated cells 30
  31. 31. COAGULATIVE NECROSIS 31
  32. 32. CASEOUS NECROSIS Tuberculosis 32
  33. 33. Apoptosis: In 2 process: A. Physiological process: 1. During development of embryo 2. Cells of hormone dependent tissues eg: endometrial sheeding, regression of lactating breast. 3. Involution of thymus gland in early age. B. Pathological process: 1. Cell death in tumour exposed to chemotherapeutic agents 2. Cell death by cytotoxic T cells in graft rejection. 3. Progressive depletion of CD4 cells in AIDS. 4. Cell death in viral infection 5. Pathological atropy 6. Cell death after exposure of radiations, hypoxia etc 7. Degenerative diseases of CNS eg: Alzheimers disease etc 8. Heart diseases
  34. 34. MORPHOLOGY OF APOPTOSIS Progressive cell shrinkage Chromatin condensation Plasma membrane blebbing Apoptotic bodies Phagocytosis - no inflammation 34
  35. 35. MECHANISMS OF APOPTOSIS 35
  36. 36. THANK YOU

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