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Cell injury : Intracellular accumulations
Intracellular accumulations can occur through the buildup of various cellular constituents, including fat, proteins, carbohydrates, and pigments. Fatty change is the accumulation of triglycerides in cells, commonly seen in liver cells due to alcohol abuse, obesity, or other metabolic derangements. Proteins can accumulate intracellularly in conditions like myeloma or nephrotic syndrome. Glycogen storage diseases result in glycogen accumulation in cells. Pigment accumulations include lipofuscin, melanin, hemosiderin, and exogenous pigments like carbon. These accumulations can be transient or permanent and range from harmless to toxic.
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Cell injury : Intracellular accumulations
- 2. Learning objectives • Intracellularaccumulations – Fatty change – Proteins – Carbohydrates – pigments
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- 4. Intracellular accumulations • Manifestationof metabolic derangement • Accumulation may be transient & reversible or permanent. Effects: range from harmless to toxic • Three categories
- 5. Accumulations of Constituents of Normal Cellmetabolism Accumulations of Abnormal substances of abnormal Cell metabolism Accumulations of pigments Fats Proteins Carbohydrates Storage diseases Inborn errors of metabolism Endogenous pigments Exogenous pigments ACCUMULATIONS
- 6. Mechanisms of intracellularaccumulations Alpha 1 antitrypsin deficiency
- 8. FATTY CHANGE • Steatosis •Fatty metamorphosis • Intracellular accumulation of neutral fat(triglycerides) within the parenchymal cells. • Common in liver • Can occur in heart, skeletal muscle and kidneys.
- 9. • Causes offatty liver • - ALCHOL ABUSE • - DIABETES MELLITUS • - OBESITY • - PROTIEN MALNUTRION (starvation) • -DRUGS/TOXINS • -ANOXIA • -PREGNANCY
- 10. Excessive entry of lipidsinto the liver Enhanced fatty acid synthesis by hepatocytes Decreased oxidation of fatty acids by mitochondria Increased esterification of fatty acids to triglycerides Decreased apoprotein synthesis Impaired lipoprotein excretion
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- 18. Fat stains • Canbe demonstrated in fresh unfixed tissue by frozen section
- 23. Other Lipid Accumulations •Cholesterol and cholesterol esters – In atherosclerosis, cholesterol accumulates in smooth muscle cells and macrophages in the intima of arteries – In hereditary hyperlipemia, cholesterol accumulates in macrophages, usually under the skin, forming tumor-like structures known as xanthomas
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- 28. Excesses exceeding capacity of cell tometabolize Defects in protein folding, rendering them vulnerable to intracellular aggregation: Synthesis and secretion of excessive protein Nephrotic syndrome, defined by 24 hr. urine protein > 3.5 gms. manifested as cytoplasmic protein droplets in renal tubular epithelium Monoclonal immunoglobulins in serum and/or urine, due to bone marrow containing excess numbers of neoplastic plasma cells Eg: Myeloma Inherited metabolic disease, PiZZ genotype (1/7000 persons), resulting in < 10% normal plasma levels of alpha 1 - antitrypsin with accumulations of protein in hepatocytes
- 29. Intracellular Accumulation of Proteins •Primarily in epithelial cells of the proximal convoluted tubules of the kidney and in plasma cells • In the kidney, this excessive accumulation occurs subsequent to leakage of proteins from glomeruli into the glomerular filtrate • Plasma cells – RUSSEL BODIES • Alpha 1 antitrypsin deficiency • Mallory body or alcholic hyalin
- 32. Intracellular Accumulation of Glycogen •Glycogen Infiltration and Glycogen Storage • Glycogen appears as clear vacuoles in the cytoplasm of cells • Hyperglycemia • Epithelial cells of the distal portion of the proximal convoluted tubule and in the loop of Henle in the kidney • Leukocytes within inflamed or necrotic tissue • Liver • Cardiac muscle fibers
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- 34. • Pigments arecolored substances, some of which are normal constituents of cells (e.g., melanin), whereas others are abnormal and accumulate in cells only under special circumstances – Exogenous – Endogenous
- 35. EXOGENOUS ENDOGENOUS 1. Carbon– coal dust • Anthracosis • Coal workers pneumoconiosis 2. Tattooing • India ink, carbon 3. Ingested • Argyria : silver • Lead • carotenemia 1. Lipofuschin 2. Melanin 3. Hemosiderin
- 36. • Exogenous pigments Carbon(anthracosis) Coal dust (pneumoconiosis) Lung: pick up by alveolar macrophages regional lymph nods blackening the tissues of the lungs (anthracosis)
- 37. Here is anthracoticpigment in macrophages in a hilar lymph node The black streaks seen between lobules of lung beneath the pleural surface are due to accumulation of anthracotic pigment.
- 38. EXOGENOUS ENDOGENOUS 1. Carbon– coal dust • Anthracosis • Coal workers pneumoconiosis 2. Tattooing • India ink, carbon 3. Ingested • Argyria : silver • Lead • carotenemia Melanin Hemosiderin Lipofuschin
- 39. Lipofuschin • Insoluble pigment,also known as lipochrome or wear-and-tear pigment • Composed of polymers of lipids and phospholipids in complex with protein • Not injurious to the cell or its functions • Telltale sign of free radical injury and lipid peroxidation
- 40. • In sectionsit appears as a yellow-brown, finely granular cytoplasmic, often perinuclear, pigment • Seen in liver and heart of ageing patients • Patients with severe malnutrition • Cancer cachexia
- 46. EXOGENOUS ENDOGENOUS 1. Carbon– coal dust • Anthracosis • Coal workers pneumoconiosis 2. Tattooing • India ink, carbon 3. Ingested • Argyria : silver • Lead • carotenemia • Lipofuschin • Melanin • Hemosiderin
- 47. Melanin • Endogenous, non-hemoglobin-derived,brown-black pigment • Only endogenous brown-black pigment • Formed when the enzyme tyrosinase catalyzes the oxidation of tyrosine to dihydroxyphenylalanine in melanocytes and dendritic cells.
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- 49. HYPER PIGMENTATION GENERALISED LOCALISED 1. Addisonsdisease 2. Chloasma 1. Café au lait spots 2. Peutz jeghers syndrome 3. Melanosis coli 4. Nevi and tumors
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- 51. EXOGENOUS ENDOGENOUS 1. Carbon– coal dust • Anthracosis • Coal workers pneumoconiosis 2. Tattooing • India ink, carbon 3. Ingested • Argyria : silver • Lead • carotenemia • Lipofuschin • Melanin • Hemosiderin
- 53. Hemosiderin • Hemoglobin-derived, goldenyellow-to-brown, granular or crystalline pigment • Major storage forms of iron • Hemosiderin pigment represents aggregates of ferritin micelles • Small amounts of hemosiderin can be seen in the mononuclear phagocytes of the bone marrow, spleen, and liver, which are actively engaged in red cell breakdown.
- 54. Excess of iron LOCALSYSTEMIC Common bruise 1. Acquired Hemosiderosis • Hemolytic disorders • Blood transfusion • Iatrogenic 2. Heriditary hemochromatosis • Increased absorption 3. Excessive dietary intake.
- 56. Iron pigment appearsas a coarse, golden, granular pigment lying within the cell's cytoplasm
- 57. Perls prussian bluestain
- 59. The brown coarselygranular material in macrophages in this alveolus is hemosiderin that has accumulated as a result of the breakdown of RBC's and release of the iron in heme. The macrophages clear up this debris, which is eventually recycled.
- 61. EXOGENOUS ENDOGENOUS 1. Carbon– coal dust • Anthracosis • Coal workers pneumoconiosis 2. Tattooing • India ink, carbon 3. Ingested • Argyria : silver • Lead • carotenemia 1. Lipofuschin 2. Melanin 3. Hemosiderin
- 62. Summary • Intracellular accumulations –Fatty change – Proteins – Carbohydrates – pigments
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