Thyroid gland Goiter Hypothyrodism Dr Abd Elghany Hefnawy

Thyroid gland (Goiter & Hypothyrodism) Dr/ Abd Elghany Hefnawy

Diet Iodine Tyrosin Iodothyronin Diiodothyronin(T 2) Tetraiodothyronin(T 4 ) (Inactive form) Iodine (Deiodination) Triiodothyronin(T 3) (Active from)

Increase BMR Increase Oxygen consumption Thermogensis(He at production ) specially in new born animals from BAT (Brown Adipose tissue) Thyroid H. Glucose absorption Gluconeogenesis Libido and estrous (Sexual activity) Decrease cholesterol Growth in young animals Milk production Metabolism of carotene into vit-A in the liver

Low BMR Cold weather intolerance (Hypothermia) Hypercholestr olemia Dwarfism Decrease Oxygen consumption Lipemia Obesity Hypothyrodism Testicular atrophy anestrum Low Milk production Yellowish skin Except sclera (Jaundice only)

Hypothyroidism Primary (Thyroid G) Secondary (TSH) Congenital Iodine deficiency Simple Goiter Iodine deficiency Thyrodidtis Tumor

Simple Goiter Clinical Signs Treatment Enlarged thyroid gland in the throat area Addition of food containing iodine (Fish) Dysphagia and dyspnoea Lugoles solution drop/5 kg oral Weakness and alopecia Surgical removal of tumor

Goiter

Hypothyroidism Clinical Signs Dwarfism A L O P E C I A Obesity

Low BMR Cold weather intolerance (Hypothermia) Hypercholestr olemia Dwarfism Decrease Oxygen consumption Lipemia Obesity Hypothyrodism Testicular atrophy anestrum Low Milk production Yellowish skin Except sclera (Jaundice only)

Diagnosis Treatment Clinical Signs Thyroxin 0. 1 mg/5 kg oral daily Hypercholestrolemia Anemia Low T 3 and T 4 (Thyroxine) Increase the dose after 2 -3 weeks Response of treatment appeared in the form of low cholesterol level

Parathyroid gland (Hyperparathyrodism) Dr/ Abd Elghany Hefnawy

Increase formation of 1, 25 DHCC causing increase Ca absorption from intestine Kidney -Decrease P reabsorption from PCT -Increase Ca reabsorption from DCT causing increase plasma Ca level PTH Bone Increase Ca resorption from bone causing increase plasma Ca level Intestine

Pseudo-HPT Primary-HPT Autonomous Hyperparathyrodism Secondary Nutritional. HPT Renal-HPT

Autonomous HPT Secretion of PTH is autonomous i. e. not related to the existing Ca level Primary-HPT Pseudo-HPT -Parathyroid neoplasm -Hyperplasia -Ectopic parathyroid neoplasm Excessive production of other bone resorbing substances (Nonparathyroid tissues) as mammary glands Hypercalcemia including Primary HPT Pseudo HPT Hypervitaminosis-D

Clinical Signs Anorexia and general depression Rubber jaw(softness of mandible bone) Constipation and vomiting Cardiac arrhythmia Easily fractured bone Polyueria and polydepsia Loss teeth Muscular weakness Calcium urolithiasis

Diagnosis History and clinical signs Lab diagnosis Radiography -Decrease bone density and increase bone cysts -High level of calcium and PTH -Low level of phosphorous -Ultrasonography -Surgical diagnosis

Steroid suppression test To differentiate between PHPT and Ps. HPT By injection of Dexamethazon (0. 5 -1 mg/kg IM) Calcium level decreased Ps. HPT If Calcium level remain high PHPT

Treatment Surgical interference

Renal Hyperparathyroidism

Renal failure Low production of vit-D (Active form 1. 25 DHCCF) Excessive Execretion of calcium Protein catabolism with excess release of phosphorous Hypocalcemia Hypertrophy of parathyroid gland Renal hyperparathyrodism

Diagnosis Treatment High PTH Calcium borogluconate Low calcium Vitamin-D IM Abnormal kidney function tests Treatment of renal failure

Nutritional Hyperparathyroidism Calcium Diet Phosphorous Young animal with signs of rickets

Diagnosis Treatment High PTH Calcium borogluconate Low calcium Reduction of using os corticosteroid because it reduces serum calcium High phosphorous (In rickets the P is low) Correction of the dietary supplementation Almunium hydroxide gel To inhibit P++ absorption

Hypoparathyroidism Congenital Autoimmune reaction in lymphatic parathyroditis Destruction of parathyroid gland by neoplasm Atrophy of parathyroid gland In case of prolonged hypercalcemia High number of puppies Usually in lactating bitch or queen

Increase the neuromuscular excitability -Tetany -Convulsion -Muscular spasm Clinical Signs Hyperesthesia (Hypersensitivity against external stimuli) Ataxia and weakness

Treatment Calcium borogluconat 10% (0. 5 -1 ml/kg) Admisteration of vitamin-D 50, 000 -100, 000 IU /Day

QUESTIONS

ﻭﺳﺎﺋﻞ ﺍﻟﺘﻮﺍﺻﻞ Email: abdelghani 72@yahoo. com Abdelghany. hefnawy@bu. edu. eg Facebook abdelghany hefnawy ﻋﺒﺪ ﺍﻟﻐﻨﻲ ﺣﻔﻨﺎﻭﻱ. ﺩ Web site to download lectures www. bu. edu. eg/staff/abdelghanyhefnawy (Courses) Tel 01011676482