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Physiopathology of pancreas

Physiopathology of pancreas. PANCREAS. INSULIN GLUCAGON SOMATOSTATIN. INSULIN – STRUCTURE. peptide low species variability (ie. Porcine and human insulin – 1 AA is different) half life 5-8 minutes degradation in liver and kidneys. BLOOD GLUCOSE REGULATION INSULIN AND GLUCAGON.

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Physiopathology of pancreas

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  1. Physiopathology of pancreas

  2. PANCREAS • INSULIN • GLUCAGON • SOMATOSTATIN

  3. INSULIN – STRUCTURE • peptide • low species variability (ie. Porcine and human insulin – 1 AA is different) • half life 5-8 minutes • degradation in liver and kidneys

  4. BLOOD GLUCOSE REGULATION INSULIN AND GLUCAGON

  5. STIMULATION Increased glucose Increased AA Increased fatty acids Gastrin Cholecystokinin Glucagon Epinephrine Parasympathetic system INHIBITION Decreased glucose Decreased AA Decreased fatty acids somatostatin INSULIN –REGULATION OF SECRETION

  6. INSULIN - LIVER • Increased glucose uptake • Stimulation of glycogenogenesis • Stimulation of glycolysis • Inhibition of gluconeogenesis • Increased fatty acids and very low density lipopoteins (VLDL) synthesis

  7. INSULIN - MUSCLES • Increased glucose uptake • Stimulation of glycogenogenesis • Stimulation of glycolysis • Stimulation of aminoacids transport • Stimulation of protein synthesis

  8. INSULIN - ADIPOCYTES • Increased glucose uptake • Stimulation of glycolysis • Stimulation of α-glycerol phosphate synthesis • Inhibition of lipolysis

  9. STIMULATION Decreased glucose Decreased AA Exercise Stress Sympathetic system INHIBITION Insulin Increased glucose Somatostatin GLUCAGON –REGULATION OF SECRETION

  10. GLUCAGON – METABOLIC EFFECTS • LIPIDS • Oxidation of fat in hepatocytes => ketones => alternate to glucose fuel • Release of FA from adipocytes • CARBOHYDRATES • Stimulation of glycogenolysis • Stimulation of gluconeogenesis • Increased FA => inhibition of glucose uptake by muscles and adipocytes • PROTEINS • AA uptake into liver => gluconeogenesis • Activation of liver urea cycle

  11.  Metabolic Effects of Insulin and Glucagon

  12. SOMATOSTATIN • 14-aminoacid peptide • produced in delta cells of pancreas (also in GI tract, hypothalamus) Releasestimulated by: • glucose • aminoacids • fattyacids • secretin • cholecystokinin Actions: • decreasesgutmotility • inhibitsrelease of gastrin, secretin, cholecystokinin • decreasesgastricacidsecretion • decreasesgastricemptying • decreasesgallbladercontraction • suppresses insulin and glucagonrelease • suppressesgrowthhormonerelease

  13. Control of eating behavior. CCK, cholecystokinin.

  14. Insulin and glucagon

  15. Pathogenesis of hyperglycemia. 1, Glycogenolysis. 2, Gluconeogenesis. 3, Reduced uptake of glucose-contributing hyperglycemia. 4, Glucosuria. 5, Lipolysis. 6, Proteolysis. 7, Fatty acid metabolism. Acetyl CoA, acetyl coenzyme A; glucose-6-P, glucose-6-phosphate; TCA, tricarboxylic acid; TG, triglycerides.

  16. Causes of Hyperglycemia • Diabetesmellitus • Endocrinehyperfunctionsyndromes • Glucagonoma • Cushing’ssyndrome • Growthhormonehypersecretion • Thyrotoxicosis • Pheochromocytoma • Acutepancreatitis • Drugs • Thiazidediuretics • Phenytoin • Hormones (e.g., cortisone, thyroxin)

  17. Signs and Symptoms of Hyperglycemia • Glucose increased in blood, urine, and body fluids • Polyuria—nocturia • Dehydration—dry mouth, skin, and mucosae • Polydipsia and increased thirst • Polyphagia and feeling of hunger • Weight loss/gain • Fatigue, nausea • Blurry vision and headaches • Pruritus vulvae or balanitis due to Candida albicans • Mood change, irritability, apathy

  18. Causes of Hypoglycemia Major organ failure Liver failure Kidney failure Heart failure Systemic diseases Multiple organ failure Sepsis Malnutrition Alcoholism Childhood inborn errors of metabolism • Diabetes therapy related • Insulin • Sulfonylurea • Tumors secreting insulin or IGF • Insulinoma • Sarcomas • Carcinoma of liver, kidneys, adrenal glands • Drugs • Pentamidine • Sulfonamides • Salicylates

  19. DIABETES MELLITUS 2000 – 2030number of cases[miliions]

  20. Classification of Diabetes Mellitus (DM) • Type 1 DM (absolute insulin deficiency due to beta cell destruction) • Type 2 DM (insulin resistance and relative insulin deficiency) • Other types of DM • Genetic defects involving islet cells, insulin receptors, etc. • Genetic and chromosomal syndromes (e.g., Down, Turner’s, and Klinefelter’s) • Pancreatic diseases and pancreatectomy • Systemic diseases (e.g., hemochromatosis, autoimmune endocrine insufficiency) • Excess of insulin antagonizing hormones (e.g., glucagons, corticosteroids, growth hormone, thyroid hormones) • Drug-induced DM (e.g., thiazide diuretics)

  21. Comparison of Types 1 and 2 Diabetes Mellitus (DM)

  22.  Clinical Findings in Diabetic Acidosis

  23. Comparison of Coma due to Diabetic Ketoacidosis and Hyperosmolar Nonketotic Diabetes Mellitus (DM)

  24. DIABETES MELLITUS - COMPLICATIONS • ACUTE • Ketoacidosis • Polyuria • Dehydration • Hyperosmolar coma • CHRONIC • Microangiopathy • Macroangiopathy • Neuropathy • Nephropathy • Ulcerations • Hyperlipidemia • Protein wasting

  25. Diabetic foot

  26. DIABETIC RETINOPATHY

  27. DIABETIC NEPHROPATHY

  28. HYPERFILTRATION => GLOMERULOSCLEROSIS

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