Cell Adaptations

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LECTURE BY DR EJAZ WARIS

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Cell Adaptations

  1. 1. <ul><li>Small minds discuss people… </li></ul><ul><li>Average minds discuss events.. </li></ul><ul><li>Great minds discuss ideas.. </li></ul><ul><li>Genius silently acts. </li></ul>
  2. 2. Intracellular Acuumulations <ul><li>The stockpiled substances fall into three </li></ul><ul><li>categories: </li></ul><ul><li>(1) a normal cellular constituent accumulated in </li></ul><ul><li>excess, such as water, lipids, proteins, and carbohydrates </li></ul><ul><li>2) an abnormal substance , either exogenous, such as a mineral </li></ul><ul><li>or products of infectious agents, or endogenous, such as a </li></ul><ul><li>product of abnormal synthesis or metabolism; and </li></ul><ul><li>(3) a pigment . </li></ul>
  3. 3. Most accumulations are attributable to three types of abnormalities <ul><li>1) A normal endogenous substance is produced at a normaL or increased rate, but the rate of metabolism is inadequate to remove it . </li></ul><ul><li>2) A normal or abnormal endogenous substance accumulates because of genetic or acquired defects in the metabolism,packaging,transport, or secretion of these substances . </li></ul><ul><li>3) An abnormal exogenous substance is deposited and accumulates </li></ul>
  4. 4. LIPIDS <ul><li>Steatosis:The terms steatosis and fatty change describe abnormal accumulations of triglycerides within parenchymal cells </li></ul><ul><li>the most common cause of significant fatty change in the liver (fatty liver) is alcohol abuse </li></ul><ul><li>Mechanisms </li></ul><ul><li>Morphology: a)Liver b) Heart </li></ul>
  5. 5. Fatty Change,Liver
  6. 6. <ul><li>Cholesterol and Cholesterol Esters </li></ul><ul><li>a)Atherosclerosis </li></ul><ul><li>b)Xanthomas </li></ul><ul><li>c)Inflammation & necrosis </li></ul><ul><li>d)Cholesterolosis </li></ul><ul><li>e)Niemann Pick disease </li></ul>
  7. 7. Cholesterolosis,gall bladder
  8. 8. PROTEINS <ul><li>Reabsorption droplets in proximal renal tubules are seen in renal diseases associated with protein loss in the urine (proteinuria). </li></ul><ul><li>A second cause is synthesis of excessive amounts of normal secretory protein, as occurs in certain plasma cells engaged in active synthesis of immunoglobulins. </li></ul><ul><li>Defects in protein folding may underlie some of these depositions in a variety of unrelated diseases </li></ul>
  9. 9. Other Accumulations <ul><li>Hyaline Change </li></ul><ul><li>Glycogen: </li></ul><ul><li>Pigments: </li></ul><ul><li>Exogenous : Carbon </li></ul><ul><li>Endogenous: melanin,hemosiderin,lipfuscin </li></ul>
  10. 10. Lipofuscin
  11. 11. Hemosiderin
  12. 12. Melanin
  13. 13. Hemosiderosis
  14. 14. Billirubin Liver
  15. 15. Carbon,Lungs
  16. 16. Pathologic Calcification <ul><li>Pathologic calcification is the abnormal tissue deposition of calcium salts, together with smaller amounts of iron, magnesium,and other mineral salts. It is a common process occurring in a variety of pathologic conditions. </li></ul><ul><li>Two types: Dystrophic & Metastatic </li></ul>
  17. 17. DYSTROPHIC CALCIFICATION <ul><li>Dystrophic calcification is encountered in areas of necrosis,whether they are of coagulative, caseous, or liquefactive type,and in foci of enzymatic necrosis of fat. </li></ul><ul><li>Calcification is almost inevitable in the atheromas of advanced atherosclerosis. </li></ul><ul><li>Psamomma bodies </li></ul><ul><li>Pathogenesis </li></ul>
  18. 18. METASTATIC CALCIFICATION <ul><li>Metastatic calcification may occur in normal tissues whenever there is hypercalcemia. Hypercalcemia also accentuates dystrophic calcification. </li></ul><ul><li>4 causes of hypercalcemia: </li></ul><ul><li>i) increased secretion of parathyroid hormone (PTH) with subsequent bone resorption, </li></ul>
  19. 19. Continued… <ul><li>ii) destruction of bone tissue , occurring with primary tumors of bone marrow, </li></ul><ul><li>Iii) vitamin D–related disorders , </li></ul><ul><li>Iv) renal failure </li></ul>
  20. 20. Dystrophic Calcification
  21. 21. Metastatic Calcification
  22. 22. Cellular adaptations
  23. 23. Objectives: <ul><li>Understand Growth disorders. </li></ul><ul><li>Difference between Neoplastic & Non neoplastic growths. </li></ul><ul><li>Classification of growth disorders. </li></ul>
  24. 25. Non-Neoplastic Proliferation: <ul><li>*Controlled & Reversible </li></ul><ul><li>Hypertrophy – Size </li></ul><ul><li>Hyperplasia – Number </li></ul><ul><li>Metaplasia – Change </li></ul><ul><li>Dysplasia – Disordered </li></ul><ul><li>Atrophy - size </li></ul>
  25. 26. Neoplastic Proliferation:Tumors <ul><li>Uncontrolled & Irreversible* </li></ul><ul><li>Benign </li></ul><ul><ul><li>Localized, non-invasive. </li></ul></ul><ul><li>Malignant ( Cancer ) </li></ul><ul><ul><li>Spreading, Invasive. </li></ul></ul>
  26. 27. Metaplasia <ul><li>Reversible change in which one adult cell type (epithelial/mesenchymal) is replaced by another cell type </li></ul><ul><li>Adaptive substitution of cells that are sensitive to stress </li></ul>
  27. 28. Examples <ul><li>Squamous metaplasia </li></ul><ul><li>Intestinal metaplasia </li></ul><ul><li>Connective tissue metaplasia </li></ul><ul><li>Why is it two edged sword???? </li></ul>
  28. 29. Mechanisms of metaplasia <ul><li>Reprogramming of stem cells known to exist in normal tissues or of undifferentiated stem mesenchymal cells present in connective tissue </li></ul><ul><li>The precursor cells differentiate along a new pathway,signalled by cytokines,growth factors,and ECM components in the cell’s environment </li></ul>
  29. 30. Influences that predispose to metaplasia ,if persistent,may induce malignant transformation in metaplastic epithelium
  30. 34. Atrophy <ul><li>Shrinkage in the size of the cell by loss of cell substance </li></ul><ul><li>Physiologic or pathologic </li></ul><ul><li>Common causes are : </li></ul><ul><li>i)decreased work load </li></ul><ul><li>ii)loss of innervation </li></ul><ul><li>Iii)diminished blood supply </li></ul>
  31. 35. Atrophy <ul><li>iv)inadequate nutrition </li></ul><ul><li>v)loss of endocrine stimulation </li></ul><ul><li>vi)ageing </li></ul><ul><li>vii)pressure </li></ul><ul><li>ALTHOUGH ATROPHIC CELLS MAY HAVE DIMINISHED FUNCTION,THEY R NOT DEAD </li></ul><ul><li>Mechansims </li></ul>
  32. 38. Hyperplasia <ul><li>Increase in the number of cells in an organ or tissue ,usually resulting in increased volume of the organ or tissue </li></ul><ul><li>Physiologic hyperplasia: </li></ul><ul><li>i)hormonal ii)compensatory </li></ul><ul><li>Mechanisms </li></ul><ul><li>Pathologic hyperplasia </li></ul>
  33. 39. Pathologic hyperplasia constitutes a fertile soil in which cancerous proliferation may eventually arise
  34. 42. Goitre – Iodine Deficiency
  35. 43. Hypertrophy <ul><li>Increase in the size of the cells resulting in an increase in the size of the organ </li></ul><ul><li>No new cells,just larger cells </li></ul><ul><li>Physiologic </li></ul><ul><li>Pathologic </li></ul><ul><li>Mechanisms </li></ul>
  36. 44. LVH in Chronic Hypertension: Left Ventricular Hypertrophy
  37. 45. Dysplasia <ul><li>Disordered growth </li></ul><ul><li>Loss in the uniformity of the individual cells as well as loss in their architectural orientation </li></ul><ul><li>Cellular and nuclear changes </li></ul><ul><li>Is it reversible or irreversible ? </li></ul><ul><li>Carcinoma in situ </li></ul><ul><li>Does not necessarily progress to cancer </li></ul>
  38. 48. Pathogenesis – Smoke - Lung Dis.
  39. 49. Normal Adaptation Benign Malignant Polyclonal Monoclonal Mechanism of Growth Disorders
  40. 50. Take home messages <ul><li>Understanding of Growth disorders. </li></ul><ul><li>Difference between Neoplastic & Non neoplastic growths. </li></ul><ul><li>Classification of growth disorders </li></ul>
  41. 51. Watch your thoughts; they become words. Watch your words; they become actions. Watch your actions; they become habits. Watch your habits; they become character. Watch your character; it becomes your destiny
  42. 52. Thank you

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