Downloaded 122 times
Uploaded byForensic Pathology
Cellinjuryanddeath lecture-i-090515081023-phpapp01
This document discusses pathological calcification and summarizes its main types: 1) Dystrophic calcification refers to the local deposition of calcium salts in necrotic or degenerate tissues regardless of normal serum calcium levels. 2) Metastatic calcification reflects deranged calcium metabolism and systemic deposition of calcium salts associated with increased serum calcium levels. 3) Pigments that accumulate in tissues include exogenous pigments like carbon and tattoos, as well as endogenous pigments such as lipofuscin, melanin, hemosiderin, and bile.
More Related Content
Similar to Cellinjuryanddeath lecture-i-090515081023-phpapp01
![Prac excises 3[1].5](https://cdn.slidesharecdn.com/ss_thumbnails/pracexcises31-150331131154-conversion-gate01-thumbnail.jpg?width=640&height=640&fit=bounds)
Cellinjuryanddeath lecture-i-090515081023-phpapp01
- 1. PATHOLOGICAL CALCIFICATION Definition:- Abnormal deposition of calcium salts together with smaller amount of Mg++ ,Fe++ & other minerals in tissues other than osteoid or enamel
- 2. Pathologic calcification • Dystrophiccalcification • Metastatic calcification
- 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. Pathologic Calcification DystrophicCalcification - Area of tissue necrosis - Aging or damage heart valve - Atherosclerosis - Single necrotic cell “psammoma body”
- 5. Aortic valve ,gross , (calcified aortic stenosis). 5
- 6. Metastatic calcification reflects deranged calcium metabolism in contrast to dystrophic calcification and is associated with increase serum calcium level & systemic deposition of Ca++salts in interstitial tissue of gastric mucosa, kidney,lungs,systemic arteries& pulmonary veins.
- 7. Metastatic calcification Hypercalcimia • Increased secretion of parathyroid hormone • Destruction of bone tissue 2ndry to primary tumor of bone marrow ( multiple myeloma, leukemia), or diffuse skeletal metastasis. • Vitamin D-related intoxication • Renal failure •Excessive intake of calcium & absorbable antacids as milk or calcium carbonate.
- 8. This is dystrophiccalcification in the wall of the stomach. At the far left is an artery with calcification in its wall
- 9. “Metastatic calcification" inthe lung of a patient with a very high serum calcium level (hypercalcemia).
- 10. PIGMENTS EX-ogenous--- (tattoo, Anthracosis) END-ogenous---they all look the same, (e.g., hemosiderin, melanin, lipofucsin, bile), in that hey are all golden yellowish brown on “routine” Hematoxylin & Eosin (H&E) stains
- 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)
- 12.
- 13.
- 14. Pulmonary anathracosis (depositionof carbon particles)
- 15. Carbon- laden macrophages(black exogenous pigment)
- 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. Lipofuscin granules ina cardiac myocyte as shown by A, light microscope (deposits indicated by arrows) , and B,Electron microscopy (perinuclear ,intralysosomal location).
- 18. Lipofuscin (wear &tear) pigments in cardiac myocytes
- 20. Melanin • Melanin –melas= black • In melanocytes formed by oxidation of tyrosine to dihydroxyphenylalanine by tyyrosinase enzyme
- 21. Nevus ( melaninpigmentation)
- 22. :Hemosiderin – aggregatesof ferritin micelles (iron + apoferritin = ferritin) Hemosiderosis:- Excess of hemosiderin granules in mononuclear phagocytes without organ dysfunction Causes:- Local (bruise) Systemic as Hemolytic anemia, Increased absorption of dietary iron Repeated blood transfusion Hemochromatosis:- Excess of hemosiderin granules in mononuclear phagocystic system & paranchymal cells causing organ dysfunction ( liver fibrosis, DM, heart failure).
- 23. Hemosiderin granules inliver cells A, H&E section showing golden-brown,finely granular pigment. B, Prussian blue reaction, specific for iron.
- 24. Alveolar (hemosiderin-laden) macrophagesin patient with heart failure (heart failure cells)
- 25. Heart failure cells(hemosiderin-laden macrophages ),Prussian blue reaction
- 26. Jaundice Yellowish discoloration ofskin & sclera due to deposition of bilirubin pigment.
- 27. Bile pluges inliver of patient with obstructive jaundice
- 28.
- 29. The brown coarselygranular material in macrophages in this alveolus is hemosiderin
- 30. These renal tubulescontain large amounts of hemosiderin, as demonstrated by the Prussian blue iron stain
- 31.
- 32. Ageing: “Progressive time relatedloss of structural and functional capacity of cells leading to death” • Senescence, Senility, Senile changes. • Ageing of a person is intimately related to cellular ageing.
- 33. Factors affecting Ageing: • Genetic – Clock genes, (fibroblasts) • Diet – malnutrition, obesity etc. • Social conditions - • Diseases – Atherosclerosis, diabetes etc. • Werner’s syndrome.
- 34. Cellular mechanisms of ageing • Cross linking proteins & DNA. • Accumulation of toxic by-products. • Ageing genes. • Loss of repair mechanism. • Free radicle injury • Telomerase shortening.
- 35.
- 36. Ageing –changes: • Gradualatrophy 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.
- 37.
- 38. Factors affecting ageing: • Stress • Diminished stress • Infections response. • Diseases • Diminished immune • Malnutrition response. • Accidents • Good health.
- 39. 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
- 40.
Editor's Notes
- #3 74
- #8 77
- #11 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
- #13 This tiny amount of microscopic tattoo pigment can make white skin look quite black! Is this EXogenous or ENDogenous?
- #14 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?
- #29 Why would somebody order a prussian blue stain, or a S-100 immunoperoxidase stain or a HMB-45 stain?