NUR 0020 Study Guide - Quiz Guide: Benign Prostatic Hyperplasia, Robertsonian Translocation, Programmed Cell Death
Document Summary
Hypoxic injury: (lack of o2) rise in need for glucose in cells to maintain atp production anaerobic respiration: etiology: Ischemia: lack of blood flow to an area. Decreased delivery o2 due to low cardiac output (heart is too weak/blockage) Poisoning of cytochromes (cyanide: manifestations: increasing membrane permeability cannot maintain (extracellular) sodium and (intracellular) potassium pumps due to lack of. Atp cell death due to influx of calcium (membrane potentials cannot be maintained) Reperfusion injury: more damage than hypoxia, due to production of reactive o2 species (ros). Ros bind with nucleic acids, proteins, and membrane lipids and destroy the membrane: injury can include small burst of tachycardia, ros: cell with an extra electron, etiology of ros: Hyperoxemia: want to see after the hypoxic injury was treated especially with the heart: antioxidant therapies: bind with reactive oxygen species so they cant cause harm (vitamin e, mannitol, surfactant, methylene blue) Exotoxins: metabolic products released that damage cells ex.
