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Lecture 4

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McGill University
PHGY 210
Ann Wechsler

Lecture 4 Pathophysiology of Adrenal Cortex Addison’s Disease – hypofunction of adrenal cortex, due to atrophy of the cortex tissue. Most of unknown origin, but could be from advanced stage of tuberculosis. Reduced metabolism, lack of energy, lethargy due to lack of glucocorticoids. Mineralocorticoids shortage cause sodium level to go down, heart rate goes down, potassium goes up and pH goes down. Treated with administering more hormones. Cushing’s Disease – Hyperfunction, hyperplasia of the adrenal cortex increase circulating ACTH. Both glucocorticoids and mineralocorticoids go up. Lead to diabetes mellitus over time. Protein shortage in bones, lead to osteoporosis. Ion levels decrease (especially sodium), edema, puffy face. Treated by removing parts of the adrenal cortex. 1% of the Pancreas: Endocrine is scattered across the exocrine tissue. Most of the endocrine cells are called beta cells for insulin. The rest are alpha cells that produce glucagon. Insulin is more important since it is the only hormone that decreases blood sugar. Glucagon is replicable due to the presence of glucocorticoids. 5mM at normal concentration, 80mg%. Glucose is very hydrophilic. Not easily permeable at cell membrane. Insulin deficiency: beta cell decay lead to diabetes mellitus. High blood sugar, cells don’t get enough sugar. Denovoglucogenesis will produce glucose even with a glucose free diet. Fats are not burned efficiently, leave behind large amounts of residue. Produces acetones and other organic molecules that reduce pH. Eventually lead to diabetic coma, could result in death over long periods of time. At 180mg%. Dehydration, increased urination polyurea, polydipsia (thirst). Need insulin therapy. If patient is already in coma, require acidosis and electrolyte imbalance correction. Causes: type 1 due to autoimmune issues killing beta cells. Type 2 due to hyposensitivity. Both are in adults. In infants, it could be genetic. Rare cases of defective insulin release, also insulin independent. Need drugs to stimulate release. If blood sugar drops too much, patient slips into insulin shock, or sugar coma. TYPE 2 Diabetes: hyporesponsiveness due to overproduction of insulin + glucose or reduction of receptor to insulin. Can be treated by diet and exercise. Juvenile Diabetes: type 1, need insulin for life. Glucose Tolerance Test: Overnight fast followed by 0.75g to 1.5g of glucose per kg of body mass. Diabetic would respond with a far larger jump in insulin levels. Gastrin and vagal impulses (digestive nerves) cause insulin release. Glucagon (like insulin, a peptide hormone): opposite of insulin, raise
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