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MID2163 TOPIC 2

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Notes about cell adaptations, the reversible injuries.

Notes about cell adaptations, the reversible injuries.

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  • 1. MID 2163PATHOLOGY
  • 2. TOPIC 2:CELL INJURY AND ADAPTATIONS
  • 3. CELL
  • 4. CellBasic structural and functional unit in human bodyHuman contain almost 100 trillion cellsDifferent cells in tissues constantly interact with each other = cell-cell and cell-matrix
  • 5. Cell3 principle components – Plasma membrane – Nucleus – Cytoplasm
  • 6. GOLGI CENTROSOME COMPLEX ENDOPLASMIC CYTOSKELETON RETICULUMCILIA & 10 RIBOSOMEFLAGELLA ORGANELLES PROTEASOME LYSOSOME MITOCHONDRIA PEROXISOME
  • 7. 3 MAIN GROUPS OF CELLS Labile cells Stable cells (unstable)Rapid proliferation Slow proliferation and cell turnover and cell turnovere.g: gut lining & e.g: hepatocytes epithelial cells Permanent cells Not able to proliferate e.g: neurons
  • 8. CELLINJURY
  • 9. Cell InjuryCells are active participants in their environment – constantly adjusting their structure & function to accommodate changing demands and extracellular stressesCells tend to maintain their normal condition = homeostasis
  • 10. Cell InjuryCells encounter physiologic stresses or pathologic stimuli = undergo adaptation – achieving a new steady state and preserving viability and functionUltimate fate of a cell (once exposed to a harmful stimulus) depends on the type, severity & duration of the stimulus and also the type of cells
  • 11. Cell InjuryExample: – Brain cells, heart cells susceptible to hypoxia and ischemia – liver cells susceptible to chemical injury – Calf muscle tolerates 2-3h of ischemia – Cardiac muscle dies in 20-30 min
  • 12. Cell InjuryCell exposed to injurious agents, the possible outcomes are: i. The cell may adapt to the situation ii. The cell may require reversible injury iii. The cell may obtained irreversible injury and may die
  • 13. CAUSES (internal) Deficiency of Ischaemia = vitamins, reduced blood hormones etc supplyEnzyme defects Immune-mediated(genetic) e.g. mechanismsglactosemia
  • 14. CAUSES (externally)Microbial agents: Chemical agentsbacteria, viruses, & toxins fungi e.g: paraquat Nutritional e.g: lead posoning Physicale.g: mechanical trauma, atmospheric pressure, thermal, U.V. light, Ionising radiation
  • 15. Cell InjuryInjury to a certain component in cell will lead to its dysfunctionThe cellular components that are prone to injury are: → Plasma membrane → Mitochondria → Nucleus → Lysosomes
  • 16. Plasma MembraneFunctions: – Maintain integrity of cell – Contact with extracellular environment = cell surface receptors – Passage of ions (through permeable channels) & complex molecule (pinocytosis or phagocytosis)
  • 17. Plasma Membrane If the cell injured, blebs of the cellular plasma membrane noted – Focal extrusion of the cytoplasm – Cell detach from the membrane Contact with extracellular environment = cell surface receptors Passage of ions (through permeable channels) & complex molecule (pinocytosis or phagocytosis)
  • 18. Plasma MembraneEffects of plasma membrane injury: – Loss of structural integrity - cause cell to rupture and die – Loss of function - water enters cells and cause cloudy swelling hence electrolyte imbalance within cell – Deposition of lipofuscin (brown atrophy) - brown pigments deposited within cytoplasm eg in myocardial cells and liver cells
  • 19. MitochondriaMain sites of energy production for cellular activitiesDisorder of energy production affects all cellular functions – Mitochondria swell, dissipation of energy gradient & impairment of mitochondrial volume – amorphous densities rich in phospholipid may appear = reversible
  • 20. NucleusContains DNA - controls all cellular activities – Action of at least 1000 genes – Each encodes a protein with structural, enzymatic or control functionsDamage to DNA (esp in dividing cells) – Effective repair mechanisms but severe damage usually leads to cell death by apoptosis GERM CELL SOMATIC CELL
  • 21. Germ Cell DNA Damage Spermatogonia / Oocytes Less severe damageSevere damage to to groups of geneschromosomal structure or single genes Prevention of conception  Develomental abnormalities Early abortion  Hereditary disease  Susceptibility to disease
  • 22. Somatic Cell DNA Damage All cells in our body  Acquired during life  Damage to stem cell Example: - development of cancer cells through activation of oncogens or loss of tumor supressor genes
  • 23. NucleusEffects of DNA abnormalities: – Failure of synthesis of structural proteins – Failure of mitosis – Failure of growth-regulating proteins – Failure of enzyme synthesis
  • 24. LysosomesMembrane bound organelles contain hydrolytic enzymes – Responsible for digestion and disposal of complex substancesDisorder may lead to escape of enzymes or to cellular overloading (storage disorders)
  • 25. Cell InjuryInjury may progress to: 1) Adaptation state • Mild/persistant injorious agents = recover to normal state 2) Reversible injury • Respond to injury but recover 3) Irreversible injury • Cell respond to injury and cannot recover (cell death)
  • 26. Cell InjuryIf the adaptive capability is exceeded or if the external stress is inherently harmful – cell injury develops!Severe or persistent stress results in irreversible injury and death of the affected cells
  • 27. Cell InjuryCells are stressed so severely – no longer able to adapt – exposed to inherently damaging agents – suffer from intrinsic abnormalitiesDifferent injurious stimuli affect many metabolic pathways and cellular organelles
  • 28. CELLADAPTATIONS
  • 29. CELL ADAPTATIONSChanges made by a cell in response to adverse environmental changes ➲REVERSIBLE CHANGES!
  • 30. Cell Adaptations 2 types of adaptations 1. Physiological adaptations:  usually response of cells to normal stimulation by hormones or endogenous chemical mediators  e.g: hormone-induced enlargement of the breast during pregnancy 1. Pathological adaptations:  responses to stress that allow cells to modulate their structure and function and thus escape injury
  • 31. Cell AdaptationsCells adapt by altering their pattern of growth – Hypertrophy – Hyperplasia – Atrophy – Metaplasia – Dysplasia*Within certain limits injury is reversible, and cells return to a stable baseline
  • 32. HypertrophyIncrease in the size of cells – Increased workload  increased protein synthesize and size & number of intracellular organells = increased organs size – Happen in cell that cannot be devide – Reaches limit  no longer able to compensate = failure & degeneration
  • 33. Hypertrophy Example: – Pathological: • enlargement of left ventricle in hypertensive heart disease – Physiological: • muscle increase in body builder
  • 34. HyperplasiaIncrease in the number of cells – Resulting from increase in cell division – happen in cell that can divide = mitosis – Compensatory (regeneration) & hormonal (occurs mainly at organs that depend on estrogen)
  • 35. Hyperplasia Example: – Physiological: • enlargement of breast during pregnancy – Pathological: • endometrial hyperplasia
  • 36. AtrophyDecrease in the size of cells – Reduced functional capacity, lead to decrease size of organ • Formation of autphagic vacuoles contain cellular debris from degraded organelles
  • 37. Atrophy Loss of cell substances due to  decrease workload  loss of innervation  diminished blood supply  inadequate nutrition  loss of endocrine stimulation
  • 38. AtrophyExamples: – Physiological: • reduced activity of old age = decrease in size of skeletal muscle, brain and testis • Thymus atrophy during early childhood – Pathological: • Trauma to a supply nerve root = skeletal muscle markedly riduced in size following loss of innervation
  • 39. Normal Adult 82 y.o = atrophy
  • 40. MetaplasiaReplacement of one differentiated tissues by another differentiated tissues – adaptive substitution - able to withstand the adverse environment = reversible! – Altered differentiation pathway of tissue stem cells May result in reduced functions or increased propensity for malignant transformation.
  • 41. MetaplasiaExample: – Squamous metaplasia – replacement of another type of epithelium with squamous epithelium – Osseus metaplasia – replacement of connective tissue by bone
  • 42. DysplasiaAbnormality of development – Morphological transformation – increased in rate of cell division & incomplete maturation of resultant cells – High nuclear to cutoplasmic ratioEarly neoplastic processExample: – Epithelial dysplasia of the cervix – detected by a pap smear