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Endocrine Diseases Dr/Abd Elghany Hefnawy T3&T4 PTH Anterior Posterior PAO Insulin Glucagon Adrenalin,Noradrenalin Corticosteriods.

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Presentation on theme: "Endocrine Diseases Dr/Abd Elghany Hefnawy T3&T4 PTH Anterior Posterior PAO Insulin Glucagon Adrenalin,Noradrenalin Corticosteriods."— Presentation transcript:

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2 Endocrine Diseases Dr/Abd Elghany Hefnawy

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

4 Diabetes Mellitus (DM) Dr/Abd Elghany Hefnawy

5 Pathophysiology

6 Sources & control of plasma glucose

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

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

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

10 Glucagon 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) (A cells)

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

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

14 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.

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

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

17 Old age (8 years) Sex (more in females) Adrenalin and nor adrenalin Obese animal

18 Pathogenesis

19 Etiology and predisposing factors Clinical findings

20 Hyperglycemia DM Low insulin level Disturbances of entrance of glucose intracellular

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

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

23 Clinical signs

24 Polyphagia Polydepsia Polyueria Thirst Dehydration Weakness and emaciation

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26 Polyphagia

27 Vomiting Corneal opacity Neuropathy

28 Emaciation Coma & Death Renal failure

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

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

31 GTT (Glucose Tolerant Test)

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

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34 Problems of diabetic dog

35 Treatment and control

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

37 كفااااااااااااااايه

38 QUESTIONS

39 وسائل التواصل Email: abdelghani72@yahoo.comabdelghani72@yahoo.com Abdelghany.hefnawy@bu.edu.eg Facebook abdelghany hefnawy د. عبد الغني حفناوي Web site to download lectures www.bu.edu.eg/staff/abdelghanyhefnawy www.bu.edu.eg/staff/abdelghanyhefnawy (Courses) Tel 01011676482


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