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Chapter: Pathology: Cellular Injury and Adaptation

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Other Cellular Alterations During Injury

Lipids that can accumulate intracellularly include triglycerides (e.g., fattychange in liver cells), cholesterol (e.g., atherosclerosis, xanthomas), and com-plex lipids (e.g., sphingolipid accumulation).

OTHER CELLULAR ALTERATIONS DURING INJURY

Pathologic Accumulations

·            Lipids that can accumulate intracellularly include triglycerides (e.g., fattychange in liver cells), cholesterol (e.g., atherosclerosis, xanthomas), and com-plex lipids (e.g., sphingolipid accumulation).

·            Proteins can accumulate in proximal renal tubules in proteinuria and canform Russell bodies (intracytoplasmic accumulation of immunoglobulins) in plasma cells.

·            Glycogen storage diseases

·              Exogenous pigments include anthracotic pigmentation of the lung (secondaryto the inhalation of carbon dust), tattoos, and lead that has been ingested (e.g., gingival lead line, renal tubular lead deposits).

Endogenous pigments

·            Lipofuscin is a wear-and-tear pigment that is seen as perinuclear yellow-brownpigment. It is due to indigestible material within lysosomes and is common in the liver and heart.

 

·            Melanin is a black-brown pigment derived from tyrosine found in melanocytesand substantia nigra.

 

·            Hemosiderin is a golden yellow-brown granular pigment found in areas ofhemorrhage or bruises. Systemic iron overload can lead to hemosiderosis (increase in total body iron stores without tissue injury) or hemochromatosis (increase in total body iron stores with tissue injury). Prussian blue stain can identify the iron in the hemosiderin.

 

·            Bilirubin accumulates in newborns in the basal ganglia, causing permanentdamage (kernicterus).

 

Hyaline change is a nonspecific term used to describe any intracellular or extracel-lular alteration that has a pink homogenous appearance (proteins) on H&E stains.

·            Examples of intracellular hyaline include renal proximal tubule protein reab-sorption droplets, Russell bodies, and alcoholic hyaline.

 

·            Examples of extracellular hyaline include hyaline arteriolosclerosis, amyloid, and hyaline membrane disease of the newborn.

 

Pathologic forms of calcification

·            Dystrophic calcification is the precipitation of calcium phosphate in dying ornecrotic tissues. Examples include fat necrosis (saponification), psammoma bodies (laminated calcifications that occur in meningiomas and papillary car-cinomas of the thyroid and ovary), Mönckeberg medial calcific sclerosis in arterial walls, and atherosclerotic plaques.

 

·              Metastatic calcification is the precipitation of calcium phosphate in nor-mal tissue due to hypercalcemia (supersaturated solution). The many causes include hyperparathyroidism, parathyroid adenomas, renal failure, paraneo-plastic syndrome, vitamin D intoxication, milk-alkali syndrome, sarcoidosis, Paget disease, multiple myeloma, metastatic cancer to the bone. The calcifica-tions are located in the interstitial tissues of the stomach, kidneys, lungs, and blood vessels.

 

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