An acute obstruction in a coronary artery can cause myocardial cell death

An acute obstruction in a coronary artery can cause

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An acute obstruction in a coronary artery can cause myocardial cell death Apoptosis programmed cell death, normal Prevents abnormal cells from
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10 and needed process Normal physiologic death by apoptosis occurs during embryogenesis; involution of hormone-dependent tissue after hormone withdrawal, such as involution of the lactating breast after weaning; cell loss in proliferating cell populations, such as immature lymphocytes in the bone marrow or thymus that do not express appropriate receptors; and elimination of possibly harmful lymphocytes that may be self- reactive and cause death of cells after they perform useful functions (for example, neutrophils after an acute inflammatory reaction). Dysregulated – excessive or insufficient apoptosis - may not eliminate lymphocytes that react against host tissue being multiplied Death of lymphocytes after an inflammatory reaction. Involution of lactating breast after weaning (death of hormone- dependent tissue). Ex: Involution of lactating breast after weaning. Death by apoptosis causes loss of cells by -sever cell injury (injured cell exceeds repaired cell -accumulation of misfolded proteins create mutations or free radicals which cause endoplasmic reticulum stress -infection Cytotoxic T lymphocytes respond to viral infections by inducing apoptosis and, therefore, eliminating the infectious cells. -obstruction in tissue ducts pancreas, kidney, parotid gland. Increased apoptosis is known to occur in several neurodegenerative diseases Altered Cellular Metabolism 3. Examine the mechanisms and effects of altered cellular metabolism. a. Analyze the steps of ethanol metabolism and describe how it causes hepatocellular damage. · Ethanol is metabolized to acetaldehyde in the cytoplasm of the cell. · The major pathway involves alcohol dehydrogenase, an enzyme located in the cytosol of hepatocytes. The MEOS depends on cytochrome p-450 (CYP2E1) an enzyme for cell oxidation. Activating CYP2E1 is thought to accelerate ethanol metabolism. · After ingestion alcohol goes to stomach and small intestine to go to liver. · Is distributed to tissues and body.
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11 · Oxidative stress is associated with cell membrane phospholipid depletion, alters fluidity and functions of cell membrane. · Ethanol increases apoptotic cell death. - The initial liver changes are characterized by accumulation of inflammatory cells and matrix deposition around the portal vein. Reactive oxygen and nitrogen species and dysregulated redox signaling pathways are associated with alcohol consumption b. Analyze the main concepts of ketogenesis and describe the implications for clinical practice. Ketogenesis Concept Role Clinical implications Role of the hepatocytes Breaks down Acetul-CoA into three ketone bodies: Acetoacetate, Acetone, and B-hydroxybutyrate This is the basis of ketoacidosis.
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