Endocrine Diseases Dr/Abd Elghany Hefnawy

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

Diabetes Mellitus (DM) Dr/Abd Elghany Hefnawy

Pathophysiology

Sources & control of plasma glucose

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

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

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

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)

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

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

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.

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

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

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

Pathogenesis

Etiology and predisposing factors Clinical findings

Hyperglycemia DM Low insulin level Disturbances of entrance of glucose intracellular

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

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

Clinical signs

Polyphagia Polydepsia Polyueria Thirst Dehydration Weakness and emaciation

Polyphagia

Vomiting Corneal opacity Neuropathy

Emaciation Coma & Death Renal failure

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

Glucose Blood glucose Fasting ( mg/dl) Random (up to 150 mg/dl) Urine glucose (Glucoseueria) When Blood glucose more mg/dl GTT (Glucose Tolerant Test)

GTT (Glucose Tolerant Test)

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

Problems of diabetic dog

Treatment and control

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

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