HYPERPARATHYROIDISM. The parathyroid glands are responsible for maintaining the extracellular calcium concentration . Hyperparathyroidism is a disease characterised by excessive secretion of parathyroid hormone,an 84 -amino acid polypeptide hormone. The main effects of parathyroid hormone are to increase the concentration of plasma calcium by *Increasing the release of calcium and phosphorus from the bone matrix. *Increasing calcium reabsorption by the kidneys. *Increasing renal production of 1,25-dihydroxy vitamin D3 (calcitriol ) which increases intestinal absorption of calcium. ANATOMY. Usually four parathyroids are situated posterior to the Thyroid gland.They are right and left superior and inferior glands. The inferior glands are derived from third pharyngeal pouch and migrate down. The superior glands are derived from fourth pharyngeal pouch and usually found just superior to the intersection of the inferior thyroid artery and recurrent laryngeal nerve. There are three types of hyperparathyroidism. Primary hyperparathyroidism. Secondary hyperparathyroidism. Tertiary hyperparathyroidism. PRIMARY HYPERPARATHYROIDISM. Primary hyperparathyroidism is unregulated overproduction of parathyroid hormone (PTH ) resulting in abnormal calcium homeostasis. The mean age at diagnosis is 52 -56 years. Female -to -male ratio is 3 :1. CAUSE. 85 % of cases -caused by single adenoma. 15 % of cases - caused by multiple adenomas or hyperplasia. Rarely,it is caused by parathyroid carcinoma. Familial cases can occur due to multiple endocrine neoplasia syndromes. , Hyperparathyroid - jaw tumour syndrome Familial isolated hyperparathyroidism (FIHPT ) PATHOPHYSIOLOGY. The chronic excessive resorption of calcium from bone due to excessive PTH can result in Osteopenia. Osteitis fibrosa cystica. Sub periosteal resorption of distal phalanges. Tapering of distal clavicles. Salt and pepper appearance of the skull. Brown tumours of the long bones. Other symptoms of hyperparathyroidism are. THE SYMPTOMATOLOGY OF HYPERPARATHYROIDISM ARE RENAL STONES. PAINFUL BONES. ABDOMINAL GROANS. PSYCHIC MOANS. OTHER SYMPTOMS OF HYPERPARATHYROIDISM. They are due to hypercalcemia.They are Muscle weakness. Fatigue. Volume depletion. Nausea and vomiting. Coma and death. Neuropsychiatric manifestations like depression and confusion. Peptic ulcer disease and pancreatitis. CLINICAL PRESENTATION. BONES,STONES,ABDOMINAL GROANS AND PSYCHIC MOANS. SKELETAL MANIFESTATIONS. Osteitis fibrosa cystica characterised by increased generalized bone resorption,particularly involving the phalanges causing subperiosteal resorption,and skull gives radiological appearance of salt and pepper skull. Renal manifestations are polyuria,kidney stones,hypercalcuria and nephrocalcinosis. Gastrointestinal manifestations are anorexia,nausea , vomiting,abdominal pain,constipation,peptic ulcer disease and pancreatitis. Neuromuscular and psychological manifestations are proximal myopathy,weakness,easy fatigability,depression,inability to concentrate and memory problems. Cardiovascular manifestations are hypertension,bradycardia,shortened QT interval,and left ventricular hypertrophy. PHYSICAL EXAMINATION FINDINGS ARE USUALLY NON CONTRIBUTORY. LABORATORY STUDIES. TESTING OF INTACT PARATHYROID HORMONE IS THE CORE OF THE DIAGNOSIS.AN ELEVATED INTACT PARATHYROID HORMONE WITH AN ELEVATED IONISED SERUM CALCIUM LEVEL IS DIAGNOSTIC OF PRIMARY HYPERPARATHYROIDISM. A 24 HOUR URINARY CALCIUM MEASUREMENT IS ESSENTIAL TO RULE OUT FAMILIAL HYPOCALCIURIC HYPERCALCEMIA. ULTRASOUND of the neck is a safe procedure for localization of abnormal parathyroid glands. NUCLEAR MEDICINE SCANNING WITH RADIOLABELLED SESTAMIBI is used to detect abnormal parathyroid tissues in which the radionuclide concentrates. 4D - CT SCAN AND MRI are also used to locate abnormal parathyroid glands. TREATMENT. SURGICAL EXCISION OF ABNORMAL PARATHYROID GLANDS IS THE ONLY PERMANENT,CURATIVE TREATMENT FOR PRIMARY HYPERPARATHYROIDISM. Surgical treatment is offered to all patients with symptomatic disease.The indications for surgery are *One mg /dl above the upper limit of reference range for serum calcium. *24 hour urinary calcium excretion is >> 400 mg. *A 30 %reduction in creatinine clearance. *Bone mineral density T score <<2.5. *Age << 50 years. Patients with asymptomatic hyperparathyroidism are monitored with serum calcium,serum creatinine and annual bone mineral density. Other management measures are. Moderate daily elemental calcium intake of 1000 mg Vitamin D intake. Maintain good hydration. Regular exercise. Avoidance of immobilisation. Avoid medications like thiazides,diuretics and lithium. Treatment with BIPHOSPHONATES - ALENDRONATE ,has been shown to improve BMD SECONDARY HYPERPARATHYROIDISM. Secondary hyperparathyroidism is the overproduction of parathyroid hormone secondary to a chronic abnormal stimulus for its production. Most common cause is CHRONIC RENAL FAILURE. Other causes are. Vitamin D deficiency. LABORATORY STUDIES. Serum level of parathyroid hormone,calcium,phosphorus and 25 - hydroxy vitamin D are measured. Parathyroid hormone -elevated. Calcium -low normal calcium. Phosphorus -high in renal insufficiency. - low in vitamin D deficiency. Vitamin D -Normal ->>> 30 ng /ml. - mild deficiency 21 - 29 ng /ml. -deficiency <<< 20 ng / ml. TREATMENT. Unlike primary hyperparathyroidism,MEDICAL MANAGEMENT IS THE MAINSTAY OF TREATMENT FOR SECONDARY HYPERPARATHYROIDISM. Correcting vitamin D deficiency. Dietary phosphate restricted. Phosphate binders are used. Calcium supplementation <<2 g/d TERTIARY HYPERPARATHYROIDISM. This is a state of excessive secretion of parathyroid hormone after long standing secondary hyperparathyroidism and resulting in hypercalcemia. Finally one word. Primary hyperparathyroidism. Calcium increased. PTH increased. Urine calcium increased. Phosphate reduced. Secondary hyperparathyroidism. Calcium reduced. PTH increased. Tertiary hyperparathyroidism. Calcium increased. PTH increased.


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