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Hyperparathyroidism: signs

Epidemiology: Primary hyperparathyroidism occurs in about 0.1% of the population, most commonly begins in the third to fifth decades of life, and occurs two to three times more frequently in women than men.

Etiology: Primary hyperparathyroidism usually results from enlargement of a single gland, commonly an adenoma and very rarely a carcinoma. Hypercalcemia almost always develops.

Important Facts: The normal total serum calcium level is 8.6 to 10.4 mg/dL, as measured in most laboratories. Fifty percent to 60% is bound to plasma proteins or is complexed with phosphate or citrate. The value is dependent on the albumin level, with a decline of 0.8 mg/dL for each 1-g/dL drop in albumin. Binding of calcium to albumin is dependent on pH: binding decreases with acidic pH and increases with alkaline pH. It should be noted that serum calcium and not ionized calcium decreases with decreases in albumin levels. PTH and vitamin D3 work to keep the level stable within 0.1 mg/dL in any individual.

Causes: To remember the causes, a useful mneumonic is CHIMPANZEE’s. Calcium excess (administration) Hyperparathyroidism Immobility / Iatrogenic Metastasis / Milk-alkali syndrome Paget’s disease Addison’s disease Neoplasms Zollinger Ellison syndrome Excess vit D Excess vit A Sarcoidosis

Symptoms: Many of the prominent symptoms of hyperparathyroidism are a result of the hypercalcemia that accompanies it. Regardless of the cause, hypercalcemia can produce any of a number of symptoms, the most prominent of which involve the renal, skeletal, neuromuscular, and GI systems —anorexia, vomiting, constipation, polyuria, polydipsia, lethargy, confusion, formation of renal calculi (in approximately 60-70% of patients with hyperparathyroidism), pancreatitis, bone pain, and psychiatric abnormalities. Peptic ulcer disease is more common in these patients due to increased production of gastrin and gastric acid. Mnemonic “Stones, Groans, Moans, Psychiatric Overtones”

Symptoms of Hyperparathyroidism

  • Neuro: confusion, lethargy, psychiatric abnormalities
  • GI: anorexia, vomiting, constipation, pancreatitis
  • GU: polyuria, polydipsia, formation of renal calculi (in approximately 60-70% of patients with hyperparathyroidism)
  • Other: bone pain

Anesthetic Considerations: 1/3 of patients will have hypertension, but the hypertension usually resolves with successful treatment of the primary disease. Can give intra-op PTH during thyroid surgery. ECG may show short PR or QT. Reduce Ca by increasing intravascular fluid volume and lasix.

For a more detailed explanation of why the symptoms listed above in bold occur, see below:

Sustained hypercalcemia can result in tubular and glomerular disorders, including proximal (type II) renal tubular acidosis. Polyuria and polydipsia are common complaints.

Skeletal disorders related to hyperparathyroidism are osteitis fibrosa cystica, simple diffuse osteopenia, and osteoporosis. The rate of bone turnover is five times higher in patients with hyperparathyroidism than in normal controls. Patients may have a history of frequent fractures or complain of bone pain, the latter especially in the anterior margin of the tibia.

Because free intracellular calcium initiates or regulates muscle contraction, neurotransmitter signaling, hormone secretion, enzyme action, and energy metabolism, abnormalities in these end organs are often symptoms of hyperparathyroidism. Patients may experience profound muscle weakness, especially in proximal muscle groups, as well as muscle atrophy. Depression, psychomotor retardation, and memory impairment may occur. Lethargy and confusion are frequent complaints.

Peptic ulcer disease is more common in these patients than in the rest of the population. Production of gastrin and gastric acid is increased. Anorexia, vomiting, and constipation may also be present.

Approximately a third of all hypercalcemic patients are hypertensive, but the hypertension usually resolves with successful treatment of the primary disease. Long-standing hypercalcemia can lead to calcifications in the myocardium, blood vessels, brain, and kidneys. Cerebral calcifications may cause seizures, whereas renal calcifications lead to polyuria that is unresponsive to vasopressin.