*Infarct - cellular effect area of necrosis which results from a sudden insufficiency of arterial blood flow clinical implications * Apoptosis- is programmed cell death and is a normal process . cellular effect mitochondrial damage can result in changes in membrane permeability, loss of membrane potential, and decreased ATP. Between the outer and inner membranes of the mitochondria are proteins that can activate the cells suicide pathways by this process apoptosis. (thought to be caused by oxidative stress ROS levels at high levels -box 2-1) - shrinakage of cell size, nucleus fragmentation, plasma membrane intact (but with altered structure), cellular contents intact, NO inflammation, often physiologic to eliminate unwanted cells clinical implications neutrophils after an acute inflammatory reaction, cell death of tumors, and rejection of tissue transplants the patho Between the outer and inner membranes of the mitochondria are proteins that can activate the cells suicide pathways by this process apoptosis. -Analyze the mechanisms and outcomes of cellular injury. -Differentiate between the etiology, clinical manifestations and pathophysiology of cellular injuries caused by hypoxia, free radicals, and ethanol. -Evaluate the process of necrosis, and apoptosis and describe the implications for clinical practice.
CELLULAR METABOLISM * Ethanol Metabolism -ethanol is metabolized to acetaldehyde in the cytoplasm of the cell, the enzyme alcohol dehydrogenase (ADH) helps with the conversion, causing oxidized niacin (NAD) to reduce to NADH. In the mito acetaldehyde is further converted by acetaldehyde dehydrogenase to acetate and further oxidized niacin (NAD) is reduced to NADH. Increasing the NADH/NAD ratio in the liver which causes (see clinical manifestations * Ketogenesis Formation of ketone bodies and occurs mostly in the mitochondria of the hepatocytes. Occurs as a result of the unavailability of glucose (this process is triggered by lack of glucose. The cell is unable to use glucose but the individual is hyperglycemic(this is what happens in DM type 2) (In liver with alcohol use) Decrease the citric acid cycle production of NADH leading to utilization of Acetyl-CoA for ketogenesis (causing ketoacidosis ) and lipogenesis (causing hepatosteatosis ) Role of Hepatocyte liver cell, ketogenesis occurs in the mitochondria of the hepatocyte; result of unavailability of glucose ;processes the acetyl Co-A Role of Mitochondria ketogenesis is the formation of the ketone bodies and occurs mostly in the mitochondria of the hepatocyte (liver cells). Role of Acetyl-Co A the end of the B-oxidation cycle results in the formation; In states of starvation or uncontrolled DM the cells do not receive enough glucose to produce energy, accelerating the B oxidation cycle and increase in the oxidation of fatty acids for energy and increased amounts of acetyl-Co A, it is then processed by hepatocytes and undergoes transformation to 3 ketone bodies: Acetoacetate, Acetone, and B-hydroxybutyrate-The basis of Ketoacidosis
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- Fall '15