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General Pathology Exam Study Guide.

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General Pathology Exam Study Guide. Causes of cellular injury - answerhypoxia, chemical and physical injury, infections, immunologic reactions, genetic disorders, nutritional or vitamin deficiencies, aging Hypoxia - answer- lack of oxygen - can result from loss of blood supply, decrease in oxygen-carrying capacity of the blood due to anemia or carbon monoxide poisoning and poisoning of the enzymes of oxidative phosphorylation by toxins Infections - answer- viruses invade the cells, commander synthetic machinery and may release proteins that are toxic to the host - bacteria release exotoxins (phospholipase) or produce endotoxins (lipopolysaccharides) from their cell walls Cellular changes during injury - answer- cloudy swelling from cell membrane disruption, membrane damage, endoplasmic reticulum swelling, mitochondrial swelling, lysosomal swelling, nuclear changes, apoptosis coagulation necrosis - answer- most common form of necrosis in cells without large numbers of lysosomes - occurs after sudden ischemia, thermal injury, or toxin injury - heart is most common example Liquefactive necrosis - answer- results from cellular destruction by hydrolytic enzymes involved in autolysis and heterolysis - occurs in brain infarcts and pancreatic necrosis - called suppuration and resulting fluid is pus Caseous necrosis - answer- combination of liquefactive and coagulation necrosis - produces issue hat is grossly soft, friable, and cheese like - characteristic of TB, some granulomas and fungal infections Enzymatic fat necrosis - answercaused by the action of lipase on fatty tissue Gummatous necrosis - answer- seen in the late stage of syphilis - has a gelatinous appearance Apoptosis - answer-programmed cell death characterized by chromatin condensation, breakdown of DNA into nucleosome sized fragments, RNA and protein synthesis, minimal inflammatory response Calcification - answer- dystrophic calcification appears in areas of necrosis due to precipitation of calcium phosphate in low pH - metastatic calcification caused by hypercalcemia is due to precipitate of supersaturated solutions of calcium phosphate Cell types that cannot exhibit hyperplasia - answernerve, cardiac, skeletal and muscle cells transudate - answer- comparatively protein free fluid into extravascular space that leaks into the extravascular space - usually due to pressure differences between the vasculature and intracellular space exudate - answer- fluid containing proteins, cells and plasma that leads into the extravascular space - usually due to increased permeability of endothelial cell barriers and chemotactic factors attracting WBC Vascular changes in inflammation - answer-transient vasoconstriction followed by vasodilation - increased vascular permeability as the result of endothelial cell, transiently affecting venues - chemical mediators of increased vascular permeability include the vasoactive amines, histamine and serotonin - complement component C3a and C5a are anaphylatoxins and cause the release of more vasoactive amines - slowing of circulation due to increased blood viscosity from extravasation of fluid allows the leukocytes to migrate, roll and then adhere to endothelium Chemotaxis - answer- attracting of cells toward a chemical mediator that is released in the area of inflammation - two most important chemotactic factors for neutrophils are IL-8 and C5a Phagocytosis - answer- neutrophils and macrophages engulf and destroy foreign material - particle to be phagocytosed can be coated with serum opsonins, such as IgG and C3b - facilitate phagocytosis by allowing the particle to bind to complement receptor 1 (CR1) and the Fc receptor on the surface of the cell - phagocytic vacuole fuses with a lysosome


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