Unit 5 - Parathyroids and Bone Flashcards Preview

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Flashcards in Unit 5 - Parathyroids and Bone Deck (26):

relationship between OPG/RANKL/RANK

RANKL = ligand that is related to TNF
RANK and OPG (osteoprotegerin) are key regulators of resorption, and receptors for RANKL and TNF
-OPG inhibits bone resorption (physiological and pathological)


what are bone turnover markers?

formation: bone-specific alkaline phosphatase and osteocalcin
resorption: serum TRAP, serum/urine NTx and CTx


control and actions of PTH

-when Ca++ level falls, PTH is stimulated (inverse relationship)
-mainfunction is to defend VS hypocalcemia (activates AC --> increase cAMP release)
--stimulate bone resorption by OC (indirectly thru OBs)
--stimulate renal tubular absorption of Ca and Mg
--inhibit renal tubular reabsorption of PO4 and bicarb
--stimulate synthesis of active vit D (calcitriol) from 25 form in kidney


how does Ca circulate in the plasma?

1. ionized (50%); active
2. protein-bound (40%); mostly to albumin
3. complexed to bicarb, citrate, PO4


what does acidosis and alkalosis do to Ca binding to albumin?

acidosis: decreases binding (increases active ionized Ca), enhances tubular reabsorption
alkalosis: increases binding (decreases active ionized Ca), increases tubular clearance


what is the main determinant of intestinal absorption of Ca and P?



who can get phosphorus deficiencies?

alcoholics and people taking antacids with Al (binds phosphate to prevent absorption; used to prevent hyperophosphatemia in renal failure)


how is Mg related to PTH?

it is necessary for its release, and for action of hormone on its target tissues
-if Mg low, PTH is stimulated and vice versa


what do furosemide and cisplatin do to Mg reabsorption?

inhibit reabsorption in LoH


what is "transient hypocalcemia" seen in?

postoperatively after hyperparathyroid treatment
-normal, but suppressed parathyroid glands are regaining sensitivity to Ca++, and usually mild
-if prolonged, it's rare and rapid deposition of Ca and PO4 into bone


what is routine medical followup for conservatively treated parathyroidism?

-yearly Ca and Cr levels
-BMD assessments at spine, hip, and wrist every one or two
-adequate hydration and ambuation
-moderate Ca intake despite hypercalcemia (prevent further stimulation of PTH secretion)


what is PTHrp (related peptide) associated with?

humoral factor secretion by squamous cell cancers and ovarian carcinomas
-PTH suppressed, PTHrP increased


what do skeletal metastases release?

cytokines and factors that stimulate OC-mediated bone resorption


what is familial hypocalcuric hypercalcemia? how does it differ from primary parathyroidism

AD mutation of Ca-sensing receptor
-mostly asymptomatic, with rarely elevated PTH
-urinary Ca collection is low in FHH, unlike primary hyperparathyroidism
-parathyroidectomies willbe unsuccessful


what is milk alkali syndrome?

consumption of large amounts of Ca (Tums)
-rare now


what medications can cause hypercalcemia?

-Li therapy (chronically increases set point for PTH --> mass)


what are the levels of hypercalcemia and specific treatments?

mild (14) - life-threatening malignancy with immediate treatment (poor prognosis)


what is the difference between secondary and tertiary hyperparathyroidism?

secondary: plasma Ca is normal/low
tertiary: plasma Ca is high


what needs to be checked if low Ca is detected?

-albumin (may be normal if correcting for albumin)
-PTH (if low, it's hypoparathyroidism; if high, it's secondary hyperthyroidism)


hormonally, what is renal failure caused by?

-limited excretion of phosphate and diminished hydroxylation of 25(OH)D to active calcitriol --> reduce absorption and resorption --> hypocalcemia --> stimulates PTH release


why do you limit Ca++ intake when treating hypoparathyroidism?

keep it low-normal to prevent hypercalcuria (renal Ca retaining effect from PTH is lost; if combined with vit D, will have increased absorption and filtered load cleared by kidney, causing stones)


what are causes for hypomagnesemia? clinical manifestations?

-loss of Mg from GIT, primary aldosteronism, hypercalcemia
-concomitant hypocalcemia, hypokalemia


treatment for acute VS persistent hypocalcemia

acute: depends on severity; if symptomatic, give Ca gluconate (slow injection or steady infusion)
persistent: supplemental Ca and vit D


what can hyperphosphatemia be caused by?

-increased intake of oral, phosphate enemas, or IV
-decreased renal excretion (failure, hypoparathyroidism)
-transcellular shift from intra to extracellular space (like hypophos)


what are short-term VS long-term consequences of hyperphosphatemia?

short: hypocalcemia, tetany
long: tissue calcification, secondary hyperparathyroidism


what are the abnormalities that cause hypophosphatemia

1. decreased intestinal absorption of phosphorus (starvation, malnutrition, vit D deficiency)
2. increased urinary losses (hyperparathyroidism, renal tubular defects, abnormal vit D metabolism, oncogenic osteomalacia, DKA, drugs)
3. transcellular shift from intra to extracellular space (like hyperphos)