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Endocrine Diseases

Endocrine Diseases. Dr/Abd Elghany Hefnawy. Anterior. Posterior PAO. PTH. Adrenalin,Noradrenalin. Corticosteriods. T3&T4. Insulin Glucagon. Diabetes Mellitus (DM). Dr/Abd Elghany Hefnawy. Pathophysiology. Sources & control of plasma glucose. Sources. Fat. Glycerol. Glycogen.

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Endocrine Diseases

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  1. Endocrine Diseases Dr/Abd Elghany Hefnawy

  2. Anterior Posterior PAO PTH Adrenalin,Noradrenalin Corticosteriods T3&T4 Insulin Glucagon

  3. Diabetes Mellitus (DM) Dr/Abd Elghany Hefnawy

  4. Pathophysiology

  5. Sources & control of plasma glucose

  6. Sources Fat Glycerol Glycogen Gluconeogenesis Alanin (AA) Glycogen Glycogenolysis Glucose Intestine

  7. Control Hormonal control of blood glucose Promotes glycogenesis (formation of glycogen) Insulin (Beta cells) Activation of Acetyl carboxylase enzyme Essential for FFA (Free fatty acids) Triglycerides + Fat (Lipogenesis)

  8. Insulin Activation of hexokinase enzyme Essential for Phosphorylation Essential for Glucose entrance and metabolism inside the cells

  9. Glucagon (A cells) Stimulates the process of glycogenolysis for formation of glucose Promotes the mobilization of the hepatic storage of glucose to the blood (i.e it has hyperglycemic action)

  10. Brain tissue is very sensitive to low glucose level causing secretion of ACTH Growth Hormone Cortisol Lipolysis Increase mobilization of amino acids From the muscles to be converted into Glucose in the liver (Gluconeogenesis) Antagonism of Insulin actions

  11. Lipolysis Production of keton bodies Acetone Adour of the breath (Ketoacidotic stage)

  12. Definition It is a chronic complex disorder of carbohydrates, lipid and protein metabolism as a result of Inability to produce or utilization of an adequate amount of insulin.

  13. Etiology Damage or destruction of pancreatic β-cells due to Trauma or neoplasm Pancreatitis Hereditary Depletion or aplasia Of β-cells (Idiopathic) (I) Insulin dependent DM

  14. Overeating causing obesity Excess of growth hormone Excess of Glucagon hormone Excess of Glucocorticoides or cortisol therapy Hyperthyroidism (II) Insulin independent DM

  15. Predisposing factors Sex (more in females) Old age (8 years) Adrenalin and nor adrenalin Obese animal

  16. Pathogenesis

  17. Etiology and predisposing factors Pathogenesis Clinical findings

  18. Etiology and predisposing factors Disturbances of entrance of glucose intracellular Low insulin level Hyperglycemia DM

  19. When Glucose level more than 180-220 mg/dl Kidney cannot reabsorb glucose Loss of glucose (Energy) Glucosueria Glucose in urine increases the osmotic pressure Dehydration and Thirst Polyueria

  20. Polyphagia Loss of glucose (Energy) Glucosueria Dehydration and Thirst Polyueria Polydepsia

  21. Clinical signs

  22. Polyueria Polyphagia Polydepsia Thirst Dehydration Weakness and emaciation

  23. Polyphagia

  24. Vomiting Neuropathy Corneal opacity

  25. Renal failure Coma & Death Emaciation

  26. Diagnosis Case history (Etiology and predisposing factors) Clinical signs Laboratory diagnosis

  27. Laboratory diagnosis Glucose GTT (Glucose Tolerant Test) Blood glucose Urine glucose (Glucoseueria) Fasting (60-100 mg/dl) Random (up to 150 mg/dl) When Blood glucose more 180-220 mg/dl

  28. GTT (Glucose Tolerant Test)

  29. Laboratory diagnosis High Keton bodies High GOT GPT Lipase & Amylase High urine Sp Gravity (N= 1.025) Low Insulin

  30. Problems of diabetic dog

  31. Treatment and control

  32. Mild Moderate Sever Dangerous Restricted Feeding System 80% protein 20% carbohydrate Mild + Oral insulin Or Hypoglycemic drug as chloropamide Mild + S/C Insulin 2IU/Kg Sever + Fluid therapy

  33. كفااااااااااااااايه

  34. QUESTIONS

  35. وسائل التواصل Email: abdelghani72@yahoo.com Abdelghany.hefnawy@bu.edu.eg Facebookabdelghanyhefnawy د.عبد الغني حفناوي Web site to download lectures www.bu.edu.eg/staff/abdelghanyhefnawy (Courses) Tel 01011676482

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