Parathyroid gland

. The parathyroid glands

develop from the third and fourth pharyngeal pouches The thymus also develops from the third pouch that’s why some time we call the inferior parathyroid gland as para thymus
However, the inferior parathyroid may be found anywhere along this line of descent which explains its variable location due its long journey
Parathormone
The parathyroid glands secrete the parathyroid hormone (PTH), which controls the level of serum calcium in extracellular fluid. PTH is released in response to a low serum calcium or high serum magnesium level. PTH activates osteoclasts to resorb bone, and increases calcium reabsorption from urine and renal activation of vitamin D with subsequent increased gut absorption of calcium. Renal excretion of phosphate is also increased
HYPERPARATHYROIDISM
Primary hyperparathyroidism
Primary hyperparathyroidism is commonly a sporadic rather than familial condition associated with hypercalcaemia and inappropriately raised serum PTH levels due to enlargement of one or more glands and hypersecretion of PTH .while The normal response to hypercalcaemia is PTH suppression.
Epidemiology
The prevalence of sporadic primary hyperparathyroidism increases with age and affects women more than men. Approximately 1 per cent of adults are hypercalcaemic on biochemical screening, Familial hyperparathyroidism occurs as part of the following.
genetically determined conditions:
• MEN1 (multiple endocrine neoplasia type 1: Werner’s
syndrome);
• MEN2A (Sipple syndrome), rarely in MEN2B;
• Familial hyperparathyroidism
Pathology
The majority (85 per cent) of patients with sporadic primary hyperparathyroidism have a single adenoma and approximately 13 per cent have hyperplasia affecting all four glands
A single enlarged gland with three small normal glands is characteristic of a single adenoma while Parathyroid hyperplasia by definition affects all four glands
Clinical presentation
The classic quartet of ‘stones, bones, abdominal groans and psychic moans’ is rarely observed in developed countries when the diagnosis is usually detected on serum calcium estimation well before the full picture of severe bone disease (von Recklinghausen’s disease), renal calculi and calcinosis, pancreatitis and psychiatric disorder


Diagnosis
elevated or normal PTH levels in the presence of high serum calcium is diagnostic of primary HPT. Other causes of hypercalcaemia must be considered and excluded Causes of hypercalcaemia.
Cusses of hypercalcemia
Endocrine
Primary hyperparathyroidism
Thyrotoxicosis
Phaeochromocytoma
Adrenal crisis
Renal failure
Secondary hyperparathyroidism
Tertiary hyperparathyroidism

Malignant disease

Skeletal secondaries
Myeloma
Nutritional
Milk alkali syndrome
Excess vitamin D intake
Granulomatous disease
Tuberculosis
Sarcoidosis
Immobilisation
Inherited disorders
Hypercalciuric hypercalcaemia

Treatment of primary hyperparathyroidism;
At present surgery is the only curative option and should be offered to all patients with significant hypercalcaemia provided they are otherwise fit for the procedure. Occasionally, patients present with a parathyroid crisis and severe hypercalcaemia (serum calcium greater than3.5 mmol/L). This results in confusion, nausea, abdominal pain, cardiac arrhythmias and hypotension with acute renal failure Intravenous saline and bisphosphonate therapy (pamidronate). are required to correct the dehydration and hypercalcaemia.
Indications for parathyroidectomy in primary hyperparathyroidism.
Urinary tract calculi
Reduced bone density
High serum calcium
Deteriorating renal function
Symptomatic hypercalcaemia


Secondary hyperparathyroidism
Chronic renal failure results in secondary hyperparathyroidism. The kidney cannot convert vitamin D into the physiologically active 1,25-cholecalciferol. Reduced intestinal absorption of calcium resulting in a low serum calcium and elevated phosphate resulting to increases secretion of parathyroid hormone Prolonged stimulation results in parathyroid hyperplasia. Initially this is reversible following renal transplantation but when autonomous hyperfunction progresses after transplantation this is termed tertiary hyperparathyroidism.
Clinical and biochemical features
These include bone pain, pruritus, muscle weakness, renal osteodystrophy
and soft-tissue calcification
Treatment
Medical treatment of secondary hyperparathyroidism includes dietary phosphate restriction, calcium and vitamin D supplementation. Surgery is indicated when there is an excessive rise in the calcium/phosphate product and serum PTH
Parathyroid carcinoma
Cancer of the parathyroid is rare accounting for 1 per cent of cases of hyperparathyroidism. Typical features are very high calcium and PTH levels often with a palpable neck swelling or occasionally lymphadenopathy. Scanning may support the diagnosis
The diagnosis is rarely known at the time of exploration but, if suspected, operation should include excision of the tumour mass with en bloc thyroid lobectomy and node dissection when indicated.

Recurrent hyperparathyroidism

Recurrent hyperparathyroidism is diagnosed when hypercalcaemia recurs more than 12 months after an initially curative operation
. This may occur due to:
• missed pathology at the first operation;
• (rarely) development of a second adenoma;
• hyperplasia in autotransplanted tissue;
• parathyromatosis (disseminated nodules of parathyroid tissue within the soft tissues of the neck and superior mediastinum caused by rupture of abnormal parathyroid tissue at initial surgery)
HYPOPARATHYROIDISM
Symptoms and signs
The symptoms and signs of acute hypoparathyroidism are related to the level of serum calcium and range through mild circumoral and digital numbness and paraesthesia, to tetanic symptoms with carpopedal or laryngeal spasms, cardiac arrhythmia and fits. Chronic hypoparathyroidism can lead to abnormal bone demineralisation, cataracts, calcification in basal ganglia and consequent extrapyramidal disorders.
Percussion of the facial nerve just below the zygoma causes contraction of the ipsilateral facial muscles (Chvostek’s sign).
Carpopedal spasm can be induced by occlusion of the arm with a blood pressure cuff for 3 minutes (Trousseau’s sign).
Electrocardiogram changes include prolonged QT intervals and QRS complex changes.


Management of postoperative hypocalcaemia
_ Check serum calcium within 24 hours of total thyroidectomy or earlier if symptomatic
_ Medical emergency if the level is <1.90 mmol/L: correct with 10 mL of 10 per cent calcium gluconate intravenously;
10 mL of 10 per cent magnesium sulphate intravenously may also be required
_ Give 1 g of oral calcium three or four times daily
_ Give 1–3 μg daily of oral 1-alpha-vitamin D if necessary