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Parathyroid gland Emberyology of Parathyroid The upper parathyroid has its origin in the fourth branchial pouch and moves to a position in adult life adjacent to the middle third of the lateral thyroid lobe. The lower parathyroid originates from the third branchial pouch to travel in a longer distance to the lower pole of thyroid. It has more frequent ectopic positions Historical background Since Von Ricklinghouse at 1891, who described fibro cystic disease of the bones produced by hyperparathyroidism But he did not define the nature of association , till the full, good description done by Albright 1932 describing the association between renal stones and parathyroid glands Many trials done in between Anatomy of parathyroid glands Number 4 in nearly 80% 3 in nearly 13% 5 in nearly 6% Very rare more or less Upper more stationary post above the inferior thyroid artery or behind or between branches Lower parathyroid: Highly variables 50% lateral or posterior to the lower pole 12.5% below the lower pole < > 1 cm May be inside the capsule but never under the tissue Weight: Average for opne = 35 mg Average for 4 = 120 - 140 mg Blood supply: Superior glands ---> Superior thyroid a. Inferior glands -----> Inferior thyroid a. Some ectopic ----> by other vessels Rare inferior by ----> superior thyroid Calcium metabolism Body contains 1,000,gm calcium Extracellular -- 1 gm calcium Average intake 0.5 - 1 gm / day Average urinary output 100 - 200 mg / day In plasma, about 47% ionized Phosphorus metabolism Body contains 500 gm of phosphorus Intracellular fluid 0.4 gm 15% are protien bound Serum value varies: 3 - 3.5 mg% in adult 5 - 6 mg% in children Parathyroid hormone Each hormone contains 84 amino acids with molicular weight about 9,500 C - terminal fragment is the easiest to measure N - terminal fragment is the biologically active Serum calcium homeostasis: Physiologically there. is feed back mechanism between S. calcium and the PTH. Also calcitonin has a rule to antoganize hypercalcaemia. PTH experimentally leads to hypercalcemia hypophosphataemia and phosphaturia mechanisms of action of PTH A. Direct action on bone - increased bone resorption B. Increased calcium absorption from intestine C. Decreased tubular absorption of phosphate D. Effect of PTH on kidney and bone through activation of cyclic AMP. Causes of hypercalcaemia Endocrine causes: A. Hyperparathyroidism B. Hyper or hypothyroidism C. Addison's disease D. VI Pomas and pheochromocytomas Malignancy: A. Solid tumours with or without bony metastasis Multiple myeloma B. Lymphoma and leukaemias Causes of hypercalcaemia Granulomatous disease: A. Sarcoidosis B. Tuberculosis Increased intake: A. Calcium B. Vit. D. and Vit. A intoxication Milk alkali syndrome Miscellaneous: A. Benign familial hypocalcuric hypercalcemia Paget's disease B. Immobilization C. Thiazides D. Lithium Medical treatment of hypercalcemia A. Parenteral solut. and diuretics B. Phosphate:either I.V. or oral side effect C. EDTA (Elhylene Diaminotetracetic Acid) D. Sulfate and citrate therapy E. Calcitonin:best in combination with phosphate prolonged use leads to CT escape F. Dialysis:especially in severe renal failure G. Corticosteroids:It's effect is by antagonizing the effects of Vit.D. H. Treatment of hypercalcaemic crises: Usually by haemodialysis I. Treatment of persisted or recurrent hyper-parathyroidism by trans catheter staining with contrast agent Through the feeding artery of the parathyroid either The internal mammary branch or the inferior thyroid branch, either by gelfoam or silicone or by radiographic contrasts best used in an ectopic parathyroid adenoma. Hypercalcaemic crises Rapid and sudden elevation to 14 mg% Symptoms: Many ending by coma. Etiology: A. Primary hyperthyroidism B. Other causes The second type responds adequately to steorids The first type responds to calcitonin, Mithramycin, intravenous phosphate with adequate hydration. Then parathyroidectomy Hyperparathyroidism with other diseases. First to treat the disease before the complications To avoid the hypercalcaemic crises Pathology of primary hyperparathyroidism Hyperplasia Multiglandular disease 15-20% Adenoma single in 80-85% Carcinoma less than 1% Ectopic hyperparathyroidism Now hyperplasia is chief cell and oxyphil cell hyperplasia The activity of the gland depends upon the fat either extracellular or intracellular. It is very difficult to differentiate between adenoma and hyperplastic gland and the normal one. Also microscopic differentiation between adenoma and hyperplasia is difficult. carcinoma of parathyroid there is high serum calcium above 14 mg% palpable neck mass in about 50% of cases. Carcinoma of parathyroid very difficult to diagnose histologically and to differentiate from benign adenoma local infiltration, recurrence, distant metastasis are the only acceptable criteria. Complications which are agressive i.e. pancreatitis, renal stones and renal failure, bone diseases more common. Adequate resection of the parathyroid with adjacent safety margin including the thyroid lobe in that side. Secondary hyperparathyroidism Defined as a state of compensatory hyper Secretion of PTH which could occur in any clinical condition in which there is a tendency to hypocalcaemia. Possible causes: A. Chronic renal failure B. Ricket's osteomalacia C. Intestinal malabsorption D. Fanconi's syndrome and renal tubular acidosis E. Some said that main causes of hypocalcaemia - mainly the ionic part is due to phosphate retention - which lowers free calcium. The most important indication of parathyroidectomy is severe bone pain unresponsive to Vit. D administration. Medical treatments: Dialysis, Vit. D. Phosphate binder Tertiary hyperparathyroidism: It is autonomous increase of the activity of chief cell hyperplastic gland in secondary hyperparathyroidism ending in Adenomatous change. The main trigger factor is the hypocalcaemia. Sometimes, this autonomous hyperactivity stopped after renal transplantation and the gland gradually involuted. In other conditions, the autonomous activity continues, and parathyroidectomy is recommended. Multiple endocrine neoplasia syndromes MEN. I Wermer's syndrome Pituitary + Pancreatic (Gastrinoma) hyperparathyroidism MEN . II A. Sipple's syndrome Pheochromocytoma + Medullary carcinoma of thyroid hyperparathyrodism MEN. II B. Medullary carcinoma of thyroid + Pheochromocytoma hyperparathyroidism Ganglion neuroma Neuroma of tongue Marfanoid habit All are inherited and autosomal dominant with variable percentage of each tumour. Clinical picture of hyperparathyroidism: Renal stones, nephrocalcinosis Bone disease pain, cysts, 'brown tumours, fractures Peptic ulcer Pancreatitis Fatigue Muscle weakness Hypertension usually renal Central nervous symptoms and signs Mental disturbance, till coma Other of MEN Neck swelling Hypercalcaemic crises Polyurea, Polydipsia, hypokalemia Asymptomatic The patient should be diagnosed before "Renal stones, painful hones, abdominal groans and psychic moans". Early symptoms Fatiguability, weakness, depression, polyurea, polydepsia, constipation. Diagnosis of Primary hyperparathyroidism: Hypercalcaemia with elevated PTH concentration is usually diagnostic of hyperparathyroidism. Estimation of the ionized fracture of CA++ usually help to exclude the so-called Normocalcaemic hyperparathyroidism. Estimation of serum protein is helpful. Serum phosphate is low in most cases Alakaline phosphatase in case of bone disease elevated Urinary calcium output above 200 mg/day, mainly to exclude familial hypocalcuric hypercalcaemia Plasmachloride: Usually elevated Cyclic AMP level: elevated in urine Bone biopsy mainly from iliac crest Localization studies Localization studies valuable mainly in tumours, but in hyperplasia highly misleading. Ultrasound could localize up to 80%, mainly in the neck, needle aspiration could he done also. Thallium - Technetium, subtraction technique, Technetium will be taken by both. Thallium by the thyroid only. Subtraction will give the parathyroid only. excellent for ectopic. Good number false positive results. CT, for mediastinal or substernal tumours highly valuable Venous catherization with blood sampling for PTH, difficult, but best to lateralize in difficult cases i.e. nodular goitre. For inexperienced Surgeon and single tumour, localization could be used. Surgical treatment of Primary hyperparathyroidism: Needs: Experiencedsurgeon Experienced Pathologist Requirements to improve neck exploration: Absolute haemostasis Complete exploration, extensive elevation of the flaps up and down An unhurried time schedule Knowledge of the anatomy of the parathyroid glands A systemic exploration in an attempt to identify all glands Possible sites of the glands: At site of crossing of recurrent laryngeal and interior thyroid artery Upper posterior capsular region of the superior pole of thyroid Subcapsular position In the superior mediastinum after cleaning the inferior poles of thyroid gland. In the thymus Paraeosopharyngeal, parapharyngeal, retrooesopharyngeal or retro-pharyngeal regions Incision of carotid sheath. Included in the glands? Mediastinotomy in other session How much excision Single adenoma 3 1/2 glands subtotal .Total with autograft Frozen section is better Complications of Surgery: A. Hypocalcaemia B. Recurrent laryngeal injury C. Haematoma D. Wound infection