MID2163 TOPIC 2

527 views

Published on

Notes about cell adaptations, the reversible injuries.

Published in: Education
1 Comment
1 Like
Statistics
Notes
  • It is very good , Knowledge is to share thanks VS
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
No Downloads
Views
Total views
527
On SlideShare
0
From Embeds
0
Number of Embeds
2
Actions
Shares
0
Downloads
18
Comments
1
Likes
1
Embeds 0
No embeds

No notes for slide

MID2163 TOPIC 2

  1. 1. MID 2163PATHOLOGY
  2. 2. TOPIC 2:CELL INJURY AND ADAPTATIONS
  3. 3. CELL
  4. 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. 5. Cell3 principle components – Plasma membrane – Nucleus – Cytoplasm
  6. 6. GOLGI CENTROSOME COMPLEX ENDOPLASMIC CYTOSKELETON RETICULUMCILIA & 10 RIBOSOMEFLAGELLA ORGANELLES PROTEASOME LYSOSOME MITOCHONDRIA PEROXISOME
  7. 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. 8. CELLINJURY
  9. 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. 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. 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. 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. 13. CAUSES (internal) Deficiency of Ischaemia = vitamins, reduced blood hormones etc supplyEnzyme defects Immune-mediated(genetic) e.g. mechanismsglactosemia
  14. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 28. CELLADAPTATIONS
  29. 29. CELL ADAPTATIONSChanges made by a cell in response to adverse environmental changes ➲REVERSIBLE CHANGES!
  30. 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. 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. 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. 33. Hypertrophy Example: – Pathological: • enlargement of left ventricle in hypertensive heart disease – Physiological: • muscle increase in body builder
  34. 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. 35. Hyperplasia Example: – Physiological: • enlargement of breast during pregnancy – Pathological: • endometrial hyperplasia
  36. 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. 37. Atrophy Loss of cell substances due to  decrease workload  loss of innervation  diminished blood supply  inadequate nutrition  loss of endocrine stimulation
  38. 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. 39. Normal Adult 82 y.o = atrophy
  40. 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. 41. MetaplasiaExample: – Squamous metaplasia – replacement of another type of epithelium with squamous epithelium – Osseus metaplasia – replacement of connective tissue by bone
  42. 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

×