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Thyroid and Parathyroid

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secretion is increased, but appropriately so. The effect of PTH in human beings is to<br />

increase serum calcium concentration (Fig. 36-45). Hypercalcemia occurs because the<br />

: principal actions of PTH involve the following<br />

. Increase of bone osteoclast <strong>and</strong> osteoblast activity<br />

Increase in rate of conversion of 25-hydroxycholecalciferol (25- hydroxyvitamin ( 2)<br />

D 3) to 1,25-dihydroxycholecalciferol (1,25- dihydroxyvitamin D 3) in the kidneys by<br />

. stimulation of 1 a-hydroxylase activity<br />

Increase of gastrointestinal absorption of calcium by enhancing vitamin D<br />

. synthesis<br />

. Increased excretion of bicarbonate by the kidney<br />

Decrease in serum phosphate level by increasing the excretion of urinary<br />

. phosphate<br />

PTH is a single-chain polypeptide of 84 amino acids. The entire polypeptide is<br />

referred to as intact PTH, a hormone that has a half-life of 2 to 5 min. The N-terminal<br />

PTH portion (1–34), also called the amino (N) terminal, is biologically active, with a<br />

half-life of 2 min. The C-terminal PTH portion (35–84) or carboxyl (C) terminal, is<br />

biologically inactive, with a half-life of approximately 30 min. Among other effects,<br />

PTH acts to promote bone resorption <strong>and</strong> to increase calcium absorption from filtered<br />

. urine in the renal tubule<br />

Calcium<br />

Calcium is the principal regulator of parathyroid hormone release. This regulation is<br />

mediated by calcium receptors or other receptors on the parathyroid cell surface. A<br />

membrane protein that has been proposed to constitute such receptors (calcium ion–<br />

sensing receptor [CaR]) demonstrates reduced expression in hyperparathyroidism <strong>and</strong><br />

seems causally related to the relative insensitivity of the secretion to external calcium<br />

in pathologic parathyroid cells. This protein consequently may be an important cause<br />

for the hypercalcemia of this disorder. Modulating the functions of such proteins<br />

comprises interesting means of future therapy in several disorders of mineral<br />

metabolism. Increased knowledge of these proteins <strong>and</strong> parathyroid pathophysiology<br />

may clarify the presence of relevant mutations, secretory derangements, <strong>and</strong><br />

propensity for cell growth, from which accurate classification of parathyroid diseases<br />

. <strong>and</strong> improved treatment strategies might evolve<br />

Calcium is the most abundant cation in human beings, <strong>and</strong> its distribution within cells<br />

is essential for virtually all physiologic functions. Calcium balance in a normal<br />

individual is tightly regulated. The body contains approximately 1000 g of calcium,<br />

with minimal variations from day to day in serum calcium concentration (Fig. 36-46).<br />

Total serum concentrations, as tested by routine laboratory analysis, are accurate as<br />

long as serum protein concentrations are normal. Total calcium level must always be<br />

considered in its relationship to plasma protein levels, especially serum albumin (for<br />

each gram per deciliter of alteration of serum albumin above or below 4.0 mg/dL,<br />

there is a 0.8 mg/dL increase or decrease in protein-bound calcium <strong>and</strong> thus in total<br />

.(<br />

serum calcium<br />

( 1)<br />

( 4)<br />

( 3)<br />

( 5)

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