Hyper- and hypoparathyroidism. Etiology & pathogenesis. Organ-site alterations. Tumors of parathyroid glands
The Parathyroid glands sit posterior and superior to the thyroid, there being four glands. The most prevalent cell is the chief cells which secrete parathyroid hormone. The parathyroid hormone (PTH) is responsible for a number of things:
- Renal tubular reabsorption of calcium
- Urinary phosphate excretion (changing serum phosphate levels)
- Conversion of vitamin D to its active dihydroxy form in kidney which augments GI calcium absorption
- Alters osteoclastic activity
In all cases, increased PTH increases calcium level (so it increases calcium reabsorption, increases phosphate excretion, encourages vitamin D conversion and increases osteoclast activity).
Hyperparathyroidism
- Primary form
- Most commonly adenoma (95%) but can be primary hyperplasia and carcinoma - mostly genetic causes
- Causes hypercalcemia
- Morphologically adenomas are confined to a single gland, and are composed of chief cells. Primary hyperplasia is commonly multiglandular, and a pattern of hyperplasia is visible
- Most common clinical picture is that of silent hypercalcemia. Other symptoms are GI disturbances, depression, muscle weakness and polyuria.
- Note PTH will be high (this is how we identify the cause of hypercalcemia, in case of osteolytic malignancy or vitamin D toxicity, PTH is very low due to feedback loop).
- Secondary form
- Associated with chronic depression in serum calcium level causing parathyroid glands to go into overdrive. Most common cause is renal failure. Renal failure causes renal insufficiency, leading to decreased phosphate excretion causing hyperphosphatemia, this depresses calcium levels.
- In these cases the parathyroid glands are hyperplastic
- Clinical picture is dominated by that of renal failure. Calcium levels stay stable as parathyroid glands are able to compensate, PTH levels are however high
H&E, parathyroid adenoma (left): a solid mass of chief cells with no fat, separated by a thin capsule from the normal, fat-containing parathyroid tissue (right).
Image: “Parathyroid adenoma intermed mag” by Nephron, CC BY-SA 3.0, via Wikimedia Commons.
Mnemonic: symptomatic hyperparathyroidism is 'stones, bones, abdominal groans and psychic moans': kidney stones and nephrocalcinosis; bone resorption with osteitis fibrosa cystica and brown tumours; constipation, peptic ulcer and pancreatitis; depression, lethargy and confusion.
Hypoparathyroidism
- Far less common than hyperparathyroidism
- Causes
- Surgically induced - due to inadvertent removal of parathyroid glands
- Congenital absence (e.g. Digeorge syndrome)
- Autoimmune hypoparathyroidism
- Clinical picture is that of hypocalcemia
- Increased neuromuscular irritability (tingling, spasms, tetany)
- Cardiac arrhythmias
- Possible seizures