病理课件变性汉魅hanmei—医学专区分享.ppt

Degeneration Morphology of fatty change Sudan III, Oil red O, Osmic acid Liver Heart Kidney Intracellular hyaline changes Hyaline degeneration of arterioles Hyaline degeneration of connective tissue Fig 2-13 Metastatic calcification Affecting Increased secretion of parathyroid hormone Destruction of bone tissue Vitamin D-related disorders: Sarcoidosis Renal failure Metastatic calcification Hypercalcimia Interstitial tissue of gastric mucosa Kidneys Lungs Pulmonary veins Systemic arteries 60 61 62 63 64 65 66 67 68 67 68 69 70 * * ACUTE CELLULAR SWELLING Excessive entry of free fatty acids into the liver (starvation, corticosteroid therapy). Enhanced fatty acid synthesis. Decreased fatty acid oxidation. Increased esterification of fatty acid to triglycerides (alcohol). Decreased apoprotein synthesis (CCl4). Impaired lipoprotein secretion from the liver (alcohol). FATTY CHANGE Hyaline changes (degeneration) Absorption of protein causing hyaline droplets in proximal epithelial cells in the kidney. Russel bodies in plasma cells. Viral inclusions in the cytoplasm or the nucleus. Masses of altered intermediate filaments (Mallory bodies). Intracellular hyaline changes A heterogeneous group of pathogenic fibrillar proteins accumulating in tissues and organs. Excess synthesis Resistance to catabolism AMYLOIDOSIS Chemical nature of amyloid fibrils Two major forms: AL (amyloid light chain protein) AA (amyloid-associated protein): Derived from serum AA (12kd) synthesized in liver and elevated in inflammatory states. Minor forms of amyloid fibrils: Transthyretin (TTR): A mutant form of a serum protein in familial amyloid polyneuropathy. A variant of TTR in aging. Beta-2-microglobulin (the component of class I MHC molecules) in long-term hemidialysis. Minor forms of amyloid fibrils: Beta-2-amyloid protein forms the core of cerebral plaques and deposits within cerebral vessel walls in Alzheimer