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N5315 Advanced Pathophysiology Endocrine System MODULE 8 verified document
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- University Of Texas - Arlington
N5315 Advanced Pathophysiology Endocrine System MODULE 8 verified document
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N5315 Advanced Pathophysiology Endocrine System MODULE 8 verified document Endocrine Anatomy and Physiology Analyze the anatomy and physiology of the endocrine system: 1. Examine the production and action of hormones produced by the thyroid, pancreas, and adrenal glands. Thyroid • regulated by TSH which is released from the anterior pituitary • T4 and T3 have the same functions;T3 is more potent, its actions are short -lived, and it is present in the blood in much smaller amounts • Prior to entering the nucleus of the cell, almost all of the T4 released by the thyroid gland is converted inside the cell to T3 • Bound to either albumin or thyroxine -binding globulin (TBG) in the blood: act as transport proteins for both hormones and release the hormones once they reach their target cells • Thyroxine is formed with iodine and it takes approximately 1mg per week to produce thyroxine • The iodides used in the making of thyroxine are trapped by the thyroid gland • The uptake of iodine is regulated by TSH. T3 and T4 are stored as thyroglobulin (TG) which is a precursor to both hormones • There is enough stored hormone to last for two-three months. This means that a person will have a failed thyroid for two-three months prior to manifesting any symptoms • A low level of thyroid hormone stimulates the release of thyroid - releasing factor, which in turn stimulates the release of TSH, which then stimulates the thyroid to release more T3 and T4 • Function: increase metabolism, maintenance of muscle tone; skeletal muscle maturation; antagonization of insulin; regulation of cellular metabolism; promotion of the production of heat; maintenance of cardiac output, contraction and rate; maintenance of GI secretion; assistance with calcium mobilization and stimulation of lipid metabolism; free fatty acid release; cholesterol synthesis; RBC production, regulates body heat production, and affects respiratory rate and oxygen utilization. Thyroid Hormone Effects on the Heart The production of the contractile protein α-myosin heavy chain is stimulated by T3 in the heart. T3 also stimulates the production of the sarcolemma ion pumps (Na+- K+ ATPase pump, Ca++ ATPase pump) and the β-adrenergic receptors. Understanding this will help you to understand that thyroid conditions may cause heart failure . For instance, hyperthyroidism may increase the heart rate, cardiac output and cause cardiomyopathy. Calcitonin is secreted by the C-cells of the thyroid. It functions to lower serum calcium by preventing the bone resorption effects of PTH, prostaglandins and calciferols by blocking osteoclastic activity. It is also responsible for lowering serum phosphate levels and decreasing GI absorption of calcium and phosphorus. Pancreas • digestive functions and is an organ of the endocrine system • contains islets of Langerhans o alpha cells secrete glucagon o beta cells secrete gastrin o delta cells secrete gastrin and somatostatin o F cells secrete pancreatic polypeptide that stimulates the secretion of gastric acid and inhibits cholecystokinin secretion Insulin is synthesized in the beta cells from proinsulin. Proinsulin is composed of an A peptide, B peptide and a C peptide. The C peptide is cleaved from the complex which leaves only the A and B peptides bonded which is insulin. C-peptide levels may be measured to determine the amount of insulin which is being secreted. Insulin secretion occurs when the beta cells are stimulated by the parasympathetic nervous system, typically before a meal. Insulin secretion may also be stimulated by elevated glucose levels, amino acids, and GI hormones such as glucagon, gastrin, secretin and cholecystokinin. Insulin levels drop because of sympathetic nervous stimulation of the beta cells, low glucose levels, high insulin levels and prostaglandins. Insulin binds with cell receptors and triggers the activation of glucose transporters (GLUT) to move the glucose into the cell. GLUT4 is the main transporter and it is associated with up to a 21-fold increase in glucose diffusion into the cell. This is especially true in skeletal muscle cells, cardiac muscle cells, liver and ad ipose cells. Age, weight, abdominal fat, and activity levels all impact insulin sensitivity. Insulin resistance is associated with HTN, heart disease and DM type 2. Amylin is a hormone secreted by the beta cells which helps to regulate glucose concentration by delaying gastric emptying and suppressing glucagon secretion. Glucagon is responsible for antagonizing insulin and increases blood glucose levels during times of fasting, exercise and hypoglycemia. It stimulates glycogenolysis in the liver. Low glucose levels stimulate the release of glucagon and vice versa. Amino acids such as alanine, glycine, and asparagine stimulate glucagon secretion. A protein rich meal will do the same. Glucagon initiates lipolysis. Pancreatic somatostatin regulates the alpha and beta cells of the pancreas by inhibiting insulin and glucagon. Incretin hormones are released by the endocrine cells of the GI system. The major hormone is glucagon -like peptide -1 (GLP-1) and glucose dependent insulinotropic polypeptide (GIP). They control the levels of glucose after one eats by stimulating glucose dependent insulin secretion, inhibiting glucagon synthesis, slowing gastric emptying, and stimulating hepatic glucose secretion. They help to incr ease the intracellular insulin stores. The GLP-1 peptide is a target for the diabetes drug class GLP-1 receptor agonists which help to enhance the function of this protein. The enzyme dipeptidyl peptidase 4 (DPP-4) break down incretins. Diabetes drugs work to inhibit this enzyme and are known as DDP4 inhibitors. Adrenal GlandThe benefits of buying summaries with Stuvia:
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