Pathology - Primary Hypoparathyroidism
This can be acquired as a consequence of thyroid surgery, but in this instance, it is congenital or brought on by an autoimmune condition. Hypocalcemia is brought on by the incapacity of PTH loss to keep serum calcium (and, to a lesser degree, magnesium) levels within normal ranges. PTH typically raises serum calcium levels through boosting bone turnover, lowering calcium excretion in the kidneys, and promoting the production of vitamin D3 (1,25-dihydroxycholecalciferol) in the kidneys, which enhances calcium absorption in the intestines. Muscle cramps and tingling are signs of hypocalcemia-induced increased nerve and muscle excitability. The gating of voltage-sensitive sodium channels is impacted by low blood calcium, which causes the cell membrane potential to become hyperexcitable. The Trousseau phenomenon, in which the inflation of a sphygmomanometer cuff causes tetany in muscles distal to the cuff, or a positive Chvostek's sign serve as examples of this. PTH also suppresses proximal tubular phosphate reabsorption, which preserves renal phosphate excretion. Thus, hyperphosphatemia is also caused by PTH deficiency. Rare individuals with PTH resistance, or "pseudohypoparathyroidism," which results from PTH receptor mutations or related G-protein coupling, exhibit comparable clinical symptoms. The majority of the time, vitamin D supplements can be used to treat hypoparathyroidism in individuals by raising serum calcium levels.
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