Cellinjuryanddeath lecture-i-090515081023-phpapp01


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  • If you see a golden brown, slightly refractile pigment on routing light H&E microscopy, it is either hemosiderin, melanin, or bile derived. A few other degenerative pigments, such as lipofucsin, are also possible. Special stains can prove it is one or the other, if it is not abundantly clear from its cellular or pathologic setting and/or location
  • This tiny amount of microscopic tattoo pigment can make white skin look quite black! Is this EXogenous or ENDogenous?
  • Why does anthracosis look worse along the pleural surface than on cut sections? Why are MANY extrathoracic lymph nodes also anthracotic? What in the body is black and NOT due to EXOGENOUS pigments?
  • Why would somebody order a prussian blue stain, or a S-100 immunoperoxidase stain or a HMB-45 stain?
  • Cellinjuryanddeath lecture-i-090515081023-phpapp01

    1. 1. PATHOLOGICAL CALCIFICATION Definition:- Abnormal deposition of calcium saltstogether with smaller amount of Mg++ ,Fe++ &other minerals in tissues other than osteoid orenamel
    2. 2. Pathologic calcification• Dystrophic calcification• Metastatic calcification
    3. 3. • Dystrophic calcification refers to local deposition of calcium salts in necrotic or degenerate tissues, whatever the type of necrosis, in spite of normal serum Ca++
    4. 4. Pathologic Calcification Dystrophic Calcification - Area of tissue necrosis - Aging or damage heart valve - Atherosclerosis - Single necrotic cell “psammoma body”
    5. 5. Aortic valve , gross , (calcified aortic stenosis). 5
    6. 6. Metastatic calcification reflects deranged calcium metabolismin contrast to dystrophic calcification andis associated with increase serum calciumlevel & systemic deposition of Ca++saltsin interstitial tissue of gastric mucosa,kidney,lungs,systemic arteries&pulmonary veins.
    7. 7. Metastatic calcification Hypercalcimia• Increased secretion of parathyroid hormone• Destruction of bone tissue 2ndry to primary tumor ofbone marrow ( multiple myeloma, leukemia), or diffuseskeletal metastasis.• Vitamin D-related intoxication• Renal failure•Excessive intake of calcium & absorbable antacids asmilk or calcium carbonate.
    8. 8. This is dystrophic calcification in the wall of the stomach. At the far left is an artery with calcification in its wall
    9. 9. “Metastatic calcification" in the lung of a patient with a very high serum calcium level (hypercalcemia).
    10. 10. PIGMENTSEX-ogenous--- (tattoo, Anthracosis)END-ogenous--- they all look thesame, (e.g., hemosiderin, melanin,lipofucsin, bile), in that hey are allgolden yellowish brown on “routine”Hematoxylin & Eosin (H&E) stains
    11. 11. Accumulation of Pigments• Exogenous pigments Carbon ( anthracosis) Coal dust ( pneumoconiosis) Lung: pick up by alveolar macrophages regional lymph nods blackening the tissues of the lungs (anthracosis)
    13. 13. ANTHRACOSIS
    14. 14. Pulmonary anathracosis (deposition of carbon particles)
    15. 15. Carbon- laden macrophages (black exogenous pigment)
    16. 16. Accumulation of Pigments• Endogenous pigment :Lipofuscin – aging pigment(fucus=brown) lipid, phospholipid-protein complex (lipid peroxidation) ,brown-yellow pigment accumulated as the atrophic and dying cells undergo autophagocytosis. Harmless,Sign of free radical injury & lipid perioxidation, seen in aging patients severe malnutrition & cancer cachexia.
    17. 17. Lipofuscin granules in a cardiac myocyte as shown by A, light microscope (deposits indicated byarrows) , and B,Electron microscopy (perinuclear ,intralysosomal location).
    18. 18. Lipofuscin (wear & tear) pigments in cardiac myocytes
    19. 19. Melanin• Melanin – melas= black• In melanocytes formed by oxidation of tyrosine to dihydroxyphenylalanine by tyyrosinase enzyme
    20. 20. Nevus ( melanin pigmentation)
    21. 21. :Hemosiderin – aggregates of ferritin micelles (iron + apoferritin =ferritin) Hemosiderosis:- Excess of hemosiderin granules inmononuclear phagocytes without organ dysfunction Causes:- Local (bruise) Systemic as Hemolytic anemia, Increased absorption of dietary iron Repeated blood transfusionHemochromatosis:- Excess of hemosiderin granules inmononuclear phagocystic system & paranchymal cells causingorgan dysfunction ( liver fibrosis, DM, heart failure).
    22. 22. Hemosiderin granules in liver cells A, H&E section showing golden-brown,finelygranular pigment. B, Prussian blue reaction, specific for iron.
    23. 23. Alveolar (hemosiderin-laden) macrophages in patient with heart failure(heart failure cells)
    24. 24. Heart failure cells (hemosiderin-laden macrophages ),Prussian blue reaction
    25. 25. JaundiceYellowish discoloration of skin &sclera due to deposition of bilirubinpigment.
    26. 26. Bile pluges in liver of patient with obstructive jaundice
    27. 27. Hemosiderin
    28. 28. The brown coarsely granular material in macrophages in this alveolus is hemosiderin
    29. 29. These renal tubules contain large amounts of hemosiderin, as demonstrated by the Prussian blue iron stain
    30. 30. • Fig 1-20
    31. 31. Ageing:“Progressive time related loss of structural and functional capacity of cells leading to death”• Senescence, Senility, Senile changes.• Ageing of a person is intimately related to cellular ageing.
    32. 32. Factors affecting Ageing:• Genetic – Clock genes, (fibroblasts)• Diet – malnutrition, obesity etc.• Social conditions -• Diseases – Atherosclerosis, diabetes etc.• Werner’s syndrome.
    33. 33. Cellular mechanisms of ageing• Cross linking proteins & DNA.• Accumulation of toxic by-products.• Ageing genes.• Loss of repair mechanism.• Free radicle injury• Telomerase shortening.
    34. 34. Telomerase in ageing:GermCellsSomaticCells
    35. 35. Ageing –changes:• Gradual atrophy of tissues and organs.• Dementia• Loss of skin elasticity• Greying and Loss of hair• BV damage – atherosclerosis/bruising.• Loss of Lens elasticity  opacity  vision• Lipofuscin pigment deposition – Brown atrophy in vital organs.
    36. 36. Pathologyof elderly
    37. 37. Factors affecting ageing:• Stress • Diminished stress• Infections response.• Diseases • Diminished immune• Malnutrition response.• Accidents • Good health.
    38. 38. Conclusions:• Cellular Injury - Various causes• Reversible Injury  Adaptations – Hypertrophy, Hyperplasia, Atrophy – Accumulations - Hydropic, hyaline, fat..• Irreversible Injury - Necrosis – Coagulative, Liquifactive, Caseous• Ageing - Causes, Changes, Factors
    39. 39. THE END