Parathyroid glands/Ca2+/PO4 (Wong)
Terms in this set (74)
how much calcium does the human body possess?
where does most of the calcium reside?
in the bone (99%)
where does the rest of calcium reside?
what is the primary form of calcium in the bone?
hydroxyapatite crystals = Ca10(PO4)6(OH)2
what are the functions of bone?
primarily to maintain skeletal structure
but also a Ca2+ reservoir that is stored (bone synthesis) or mobilized (bone resorption) in response to deviations in extracellular and intracellular Ca2+ levels
what forms of Ca2+ exist in the extracellular fluid?
interstitial fluid calcium = ionized and complexed
plasma calcium = ionized and complexed + some bound, which accounts for the higher concentration in plasma
what is extracellular fluid Ca2+ vital for?
maintanence of normal electrochemical membrane potential
where is intracellular Ca2+ mostly sequestered?
within mitochondria and microsomes
what calcium concentrations are hormonal control mechanisms primarily sensitive to?
extracellular [Ca2+] = primarily plasma calcium concentrations
fluctuations in intracellular and bone calcium pools are regulated indirectly through their equilibrium with the regulated ECF Ca2+ pool
how is calcium equilibrium maintained?
through hormonal regulation of intestinal absorption, kidney reabsorption, and bone reabsorption and synthesis
what is an important principle related to calcium homeostasis?
bone calcium will always be sacrificed to maintain ICF and ECF [Ca2+]
what 3 hormones are involved in the regulation of calcium and phosphorus?
Parathyroid hormone (PTH)
Vitamin D, calcitriol
what are the affects of PTH on calcium and phosphorus?
Increases plasma [Ca2+]
Decreases plasma [PO3-]
what are the affects of calcitriol/vitamin D on calcium and phosphorus?
increases plasma [Ca2+]
increases plasma [PO3-]
what are the affects of calcitonin?
decreases plasma [Ca2+]
secreted by parathyroid gland
acts directly on bone and renal tubules and indirectly on the GI tract
mainly on the GI tract
protein hormone secreted by parafollicular C-cells in the thyroid gland
acts mainly on bone
what cells in the parathyroid gland secrete PTH?
metabolism of PTH
proteolysis = half life: minutes
storage of PTH
secretion of PTH
transport of PTH
mechanism of PTH
membrane receptor: G-protein
what is the role of the kidneys in response to PTH?
to changes in PTH levels and are primarily responsible for
minute-minute regulation of ECF [Ca2+]
what is the role of PTH in calcium reabsorption from distal nephron?
this segment of the nephron is
90% of the total calcium reabsorbed by the kidneys occurs in the
what part of calcium reabsorption in the kidney nephron is PTH dependent?
only ~10% of filtered Ca2+ reaches the distal tubule, and only about 10% of that Ca2+ can be reabsorbed even at max PTH =
what is the role of PTH in phosphate excretion in the kidney?
tubular reabsorption of PO4 and
this is exerted mainly at the
PTH decreases the abundance of Na+/PO4 Co transporters
what is the role of PTH and vitamin D?
PTH stimulates the renal activation of Vitamin D, which is essential for the absorption of ingested Ca2+ and PO4
where is the site of action of PTH on the bone?
the osteon = functional unit of compact bone
what is the rapidly responsive mechanism of Ca2+ mobilization?
lacunae and canaliculi are filled with ECF (bone fluid Ca2+) that is in equilibrium with soluble bone-salts
acute hypocalcemia (decreased ECF [Ca2+]) causes the equilibrium to shif tin the direction of Ca2+ mobilization via bone salt ionization
what is the slowly responding mechanism that maintains ECF calcium homeostasis?
bone remodeling via ostoblasts, osteocytes, and osteoclasts
how does PTH increase ECF [Ca2+] through the rapidly responding mechanism?
increases Ca2+ permeability of the osteocyte membrane that separates the bone fluid (ECF) from the soluble bone salt compartment => increase Ca2+ flux into osteocytes, which lowers bone fluid [Ca2+], which shifts equilibrium toward soluble bone salt ionization and Ca2+ mobilization into bone fluid =
Ca2+ taken up by osteocytes is then transported via canaliculi leading to osteoblasts where it diffuses into the ECF to normalize plasma [Ca2+]
how does PTH increase ECF [Ca2+] through the slow responding mechanism?
causes a net
increase in bone resoprtion
through suppression of osteoblast (decrease) and increase osteoclast activity => increased ECF [Ca2+]
what is the timing of the slow responding mechanism?
activation occurs after many hours or days and weeks-months may be required for full development
what are the PTH actions on the GI tract?
direct effects, just stimulates Vitamin D activation in the kidneys
what is the most common cause of primary hyperparathyroidism?
parathyroid adenoma (80-85%)
what is the hallmark of primary hyperparathyroidism? what are the effects of this problem?
- muscle weakness, fatigue
- constipation, nausea
- CNS depression
what are the bone effects of primary hyperparathyroidism?
net bone resorption => weakened bone and bone pain
- increased risk for bone fracture
what are the renal effects of primary hyperparathyroidism?
what is the most common cause of hypoparathyroidism?
what are the clinical features of hypocalcemia?
what are the lab values of primary hyperparathyroidism?
increased alkaline phosphatase
what is the hallmark of severe hypoparathyroidism (hypocalcemia)?
=> spontaneous tonic muscular contraction caused by
increased Na+ membrane permeability
due to the decreased Ca2+ binding to Na+ channels
what is the principle manifestation of hypoparathyroidism?
= adduction of the thumb and flexion of the wrist
what are the lab findings of hypoparathyroidism?
decreased serum Ca2+
increased serum PO4
Vitamin D secretion
Vitamin D metabolism
modification = long half-life: hours-days
Vitamin D mechanism
intracellular membrane receptor
Vitamin D actions
GI calcium and phosphate absorption
Vitamin D regulation
activation (Plasma Ca2+)
what are the net effects of 1,25(OH)2D3?
increase [Ca2+] and [PO4] in ECF
the major site of action is the intestinal lumen
how does vitamin D increase calcium absorption?
increase Ca2+ permeability
of the apical brush border membrane and also stimulates the synthesis of
, which may function to bind Ca2+ after diffusing into enterocytes from the lumen, keeping the [Ca2+] LOW, maintaining a gradient for Ca2+ to diffuse down from the lumen
what are the actions of Vitamin D on the bone?
increase bone synthesis =
increase bone resorption =
what is the precursor to vitamin D3, where is it found?
7-dehydroxycholesterol in the
how does the precursor form of vitamin D3 leave the skin?
converts 7-dehydroxycholesterol to cholecalciferol
where does cholecalciferol go after being converted by sunlight?
to the liver where it is oxidized to form 25-hydroxycholecalciferol
what are the actions of vitamin D on the kidney?
increase Ca2+ reabsorption
increase PO4 reabsorption
what are the actions of vitamin D on parathyroid gland?
decrease PTH synthesis
what is essential for acquiring adequate amounts of calcium and phosphate from the diet?
vitamin D = 1,25dihydroxycholecalcirferol
what form of vitamin D is secreted from the kidneys?
form => 1,25dihydroxycholecalcirferol (
what disorders commonly cause impaired vitamin D synthesis?
liver and kidney disease
what is the major step in vitamin D production?
hydroxylation of 25(OH)-D3 by the enzyme
found in the
proximal tubule cells, which forms
what are the stimulatory factors of Vitamin D biosynthesis?
low ECF [Ca2+] indirectly
stimulates vitamin D biosynthesis by inducing PTH, the direct stimulator of vitamin D biosynthesis (1alpha hydroxylase)
low [PO4] also probably due to increase in PTH because PTH causes increase in excretion of [PO4]
what are the inhibitory factors of Vitamin D biosynthesis?
increased 1,25(OH)2D3, both directly and indirectly (by inhibiting PTH)
what causes Rickets?
deficiency in vitamin D production and activation, availability in the diet, or action at target cells
what is osteomalacia?
development of rickets in adults, can occur as a result of chronic steatorrhea (fat malabsorption)
what are the bone effects of Rickets?
bone loss (osteoporosis) and bone weakness
the situation is aggravated by the increase in PTH due to hypocalcemia => increase in osteoclast activity causing uncalcified and weak osteoid =>
is tetany observed in the early stages of rickets?
because the increased osteoclast activity maintains ECF [Ca2+]
what are the lab findings of Rickets?
Decreased serum [PO4]
(due to the increased PTH; contrast this with hypoparathyroidism)
normal or decreased serum [Ca2+]
increased alkaline phosphatase due to increased bone absorption and turnover
what is the treatment of rickets?
adequate amounts of calcium, phosphate AND vitamin D must be administered
what is the primary role of calcitonin?
lowering blood calcium by inhibiting osteoclast activity and stimulating osteoblast activity
what is the role of calcitonin on the GI tract?
decrease intestinal Ca2+ absorption and renal tubule Ca2+ reabsorption
what are the net effects of calcitonin?
decrease plasma [Ca2+] and [PO4]
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