and breast pregnancy ovulation estrogen thickens grows endometrium Excessive

And breast pregnancy ovulation estrogen thickens

This preview shows page 3 - 5 out of 7 pages.

and breast; pregnancy, ovulation (estrogen) thickens & grows endometriumExcessive hormonal stimulation or effects of GF ontarget cellsEndometrium- imbalance of progesterone and estrogen (increase in estrogen); excessive menstrual bleeding, Benign prostatic hyperplasia- changes in hormone balanceCan be corrected with hormone imbalance correctedDysplasia Metaplasia N/AN/A Mechanisms of Cellular Injury 2. Analyze the mechanisms and outcomes of cellular injury. a. Differentiate between the etiology, clinical manifestations and pathophysiology of cellular injuries caused by hypoxia, reperfusion injury, free radicals, and ethanol. Cellular Injury Etiology Clinical Manifestations Pathophysiology Hypoxic Injury Ischemia- reduced blood supply Reduced amount of oxygen in air Loss of hgb, or hgb function Decreased RBCS, Respiratory and CV diseases Poisoning of oxidative enzymes within cells CK, LDH, ALT, AST, Troponin. Drowning, lack of oxygen WOB Sickle cell Anemia Inflammation Abrupt lack of contraction caused by mitochondrial phosphorylation =Lack of ATP production>increase in anerobic metabolism>generates ATP from glycogen when there is no oxygen>glycogen stores deplete & anaerobic metabolism ceases>reduction in ATP>plasma membrane NA K pump fails>intracellular accumulation of Na and Ca & diffusion od K out of the cell>cell membrane damage = more Ca into cell>cell swell>dilation of ER, ribosomes detatch from RER> reduced protein synthesis>cell swell, Na,
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4 water, and Cl> vaculation in cytoplasm, swelling of lysosomes and mitochondria>accumulation of intracellular Ca>activates some enzyme systems (proteases, nitic oxide synthease, phospholipases, and endonuclease> cytoskeleton disruption, membrane damage, inflammation DNA and chromatin degradation, ATP deletion = CELL DEATH BY APOPTOSIS Reperfusion Injury Restoration of oxygen, Regeneration of highly reactive oxygen intermediates(oxidativ e stress)- including hydroxyl radical, superoxide, hydrogen peroxide. Theses cause further membrane damage & mitochondrial calcium overload (esp neutrophils, WBCS) Tissue transplantations Ischemic syndromes of heart, kidney, liver, and cerebrum When oxygen is restored xanthine dehydrogenase is converted to xanthine oxide. During ischemic period excessive ATP consumption leads to accumulation of hypoxanthine and xanthine>reperfusion>metabolize d by xanthine oxidase = massive amounts of radicals (superoxide and hydrogen peroxide).
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