Parathyroid gland
Anatomy. The parathyroid glands, four in number, small, oval in shape, commonly about 0.5 cm in size, soft, mobile, yellowish brown in color and arranged in pairs — most often closely applied to the thyroid gland, either within or closely applied to its capsule. The upper pair : are more constant in position than the lower.80 percent is found in the posterolateral aspect of the thyroid, immediately above the termination of the inferior thyroid artery, close to the cricothyroid articulation. Most of the remaining 20 per cent is posterolateral to the upper pole of the thyroid lobe. The lower pair : are more variable in position: 40 percent are found at the lower pole of the thyroid .40 percent are within the thymic tongue .20 percent are variable in site, most often some distance lateral to the thyroid, Less often in the mediastinal thymus a few centimeters below the Sternal notch .Histology The stroma consists of a rich sinusoidal capillary network with islands of secretory cells interspersed with fat cells. The glandular cells are of two types: The ‘chief’ or ‘principal’ cells are small with vesicular nuclei and poorly staining cytoplasm. ‘Water clear’ cells, derived from the chief cells, are found in hyperplastic and neoplastic glands. The ‘oxyphil’ cells are less numerous and larger, with a granular cytoplasm and deeply staining nuclei.
Stimulate Osteoclastic activity
Parathyroid hormone : Is an 84-amino acid peptide which has a short half life before degradation into amino-terminal and carboxy terminal fragments, with the amino-terminal fragment having biological activity. Available assays measure either the intact hormone, the amino- or carboxy terminal or ‘mid-portion’ fragments.Thyrocalcitonin :Is secreted by the Para follicular cells of the thyroid (thvrocalcitonin). It lowers the serum calcium and affects calcium storage in bones, quite the opposite action from parathormone.Parathyroid hormone-related protein (PTH-rP) : Is a hypercalcemic factor with similar bioactivity to that of parathyroid hormone. Since its recent isolation from cancer cell lines and carcinoma of the breast, strong evidence has emerged that it is an important hormonal mediator of cancer-associated hypercalcemia in patients with solid tumors.Plasma let-RP 1-86 concentrations may be measured by a two-site immunoradiometrtc assay.The first symptoms are tingling and numbness in the face (circum oral numbness),fingers and toes. In extreme cases, cramps in the hands and feet are very painful; the extended fingers are flexed at their metacarpophalangeal joints, with the thumb strongly adducted the toes are plantarflexed and the ankle joints extended — the so-called carpopedal spasm. Spasm of the muscles of respiration not only results in pain and stridor, but dread of suffocation. In infancy, the symptoms of tetany’ may be mistaken for epilepsy, although there is no loss of consciousness.Latent tetany may be demonstrated by:Chvostek’s sign. Tapping over the branches of the facial nerve at the angle of the jaw will produce twitching at the corner of the mouth, the ala of the nose and the eyelids.Trousseau’s sign. A sphygmomanometer cuff applied to the arm and inflated above the systolic blood pressure for not more than 2 minutes will produce carpal spasm.
Treatment In acute cases :The symptoms may be relieved speedily by the slow intravenous injection of 10—20 ml of a 10 per cent solution of calcium gluconate in 10 minutes. This may be repeated until the patient’s circulating calcium level has been stabilized. For longer-term management, the absorption of calcium is enhanced by oral administration of the most active metabolite of vitamin D3 — 1,25 dihydroxycholecalciferol (1,25(OH)2D3). Its major action is on the gut, promoting active absorption of calcium and phosphorus, raising calcium levels to normal within a week. Magnesium supplements may occasionally be needed.
Hyperparathyroidism Hyperparathyroidism is associated with an increased secretion of parathyroid hormone. This occurs in:primary .Secondary Tertiary hyperparathyroidism.•
Clinical features. Hyperparathyroidism, rarely found in the first decade of life, most commonly found between the ages of (20 - 60 years).Is commoner in women than men, and the clinical features vary enormously, even when the biochemical changes are similar. Asymptomatic cases:The most common presentation is the detection of unsuspected and asymptomatic hypercalcaemia by routine biochemical screening.‘Bones, stones, abdominal groans and psychic moans.’ Only 50 per cent of patients suffer from any of these.Nonspecific symptoms include muscle weakness, thirst, polyuria, anorexia, and weight loss — a challenge to the clinician.
Bone diseaseThere may be generalized decalcification of the skeleton, as in osteitis fibrosa cystica (von Recklinghausen’s disease). single or multiple cysts, or pseudotumours of any bone & are particularly common in the jaw bones. Early radiological changes first appear in the skull and in the phalanges with loss of density and sub periosteal erosions. Many patients presenting with vague pains in the bones and joints are mistakenly diagnosed as rheumatic.
Renal stones. Hyperparathyroidism must be considered in every patient presenting with renal tract stone or nephrocalcinosis (Fig. 38.5), and even in those cases of renal colic where no stone can be demonstrated.Dyspeptic cases. Patients with nausea, vomiting and anorexia are relatively common. Peptic ulcer and pancreatitis are not infrequently found in association with hyperparathyroidism, but the relationship is not as yet fully understood.Psychiatric cases are not uncommon; women, complaining of tiredness, listlessness and with obvious personality changes, are often wrongly labelled ‘neuroFig. 38.5 Nephrocalcinosis. tic’ or ‘menopausal’. •elevation of serum parathormone concentration. Renal stones Hyperparathyroidism must be considered in every patient presenting with renal tract stone or nephrocalcinosis and even in those cases of renal colic where no stone can be demonstrated.Dyspeptic casesPatients with nausea, vomiting and anorexia are relatively common.Peptic ulcer and pancreatitis are not infrequently found in association with hyperparathyroidism, but the relationship is not as yet fully understood.Psychiatric cases are not uncommon; women, complaining of tiredness, listlessness and with obvious personality changes, are often wrongly labeled ‘’ or ‘menopausal’. Patients have been admitted to mental institutions because of irrational behavior.
Acute hyperparathyroidism. This diagnosis is difficult and only too often made after death. Nausea and abdominal pain is followed by severe vomiting, dehydration, oliguria, and finally coma. The serum calcium is very high. Treatment is urgent after rehydration, which is vital. Biphosphonates (disodium etidronate and pamidronate) are specific inhibitors of bone resorption. They are highly effective given parenterally and may also be used in the preoperative, short-term medical management of severe hypercalcemia in primary hyperparathyroidism.
Clinical examination and investigation Clinical examination :may be unrewarding but the cause of dehydration or confusion may be found in the eyes. Corneal calcification may be detected. It begins on the lateral and medial borders of the limbus (which distinguishes it from arcus senilis) and is best seen through a hand lens by the light of a bright torch reflected off the iris. Less common is band keratopathy in which a transverse band of calcification forms across the front of the cornea, and conjunctival calcification where redness of the eye also occurs. Hypertension may be present in up to 50 per cent of cases. There may be electrocardiographic changes with a shortened QT interval, primarily by an effect on the length of the S.—T segment. A parathyroid adenoma is very seldom palpable in the neck.
The diagnosis is confirmed with the following biochemical findings:Elevation of serum calcium (8.8-10.5 mg/dl). (2.2-2.6 mmol/l)Serum calcium occurs as calcium ions complexed to citrate and bound to albumin. Therefore the serum albumin concentration should be known in order to apply a correction factor: Corrected serum calcium (mmol/l) = measured Serum Ca (mg/dl) + 0.8 (40—A) . A = serum albumin (g/dl).Diminution of serum phosphorus (lower limit of normal 0.8 mmol/l).Increased excretion of calcium in the urine (upper limit of normal 62 mmol per 24 hours for females, 75 mmol for males).Elevation of the serum alkaline phosphatase in cases with bone disease.
Treatment The only corrective treatment is surgical removal of the overactive gland or glands. In symptomatic patients, the indications for operation are clear cut. Many patients, however, in whom hypercalcemia has been discovered incidentally, are not overtly symptomatic and a decision in favor of operation is more difficult. Preoperative treatment is not usually necessary except in acute cases, when rapid correction of dehydration and electrolyte imbalance is necessary, with a careful daily check on the serum calcium. Drugs might be used for correction of hypercalcemia.