Unit 5 - Parathyroids and Bone Flashcards Preview

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Flashcards in Unit 5 - Parathyroids and Bone Deck (26):
1

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)

2

what are bone turnover markers?

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

3

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

4

how does Ca circulate in the plasma?

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

5

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

6

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

1,25-(OH)2D

7

who can get phosphorus deficiencies?

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

8

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

9

what do furosemide and cisplatin do to Mg reabsorption?

inhibit reabsorption in LoH

10

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

11

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)

12

what is PTHrp (related peptide) associated with?

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

13

what do skeletal metastases release?

cytokines and factors that stimulate OC-mediated bone resorption

14

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

15

what is milk alkali syndrome?

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

16

what medications can cause hypercalcemia?

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

17

what are the levels of hypercalcemia and specific treatments?

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

18

what is the difference between secondary and tertiary hyperparathyroidism?

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

19

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)

20

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

21

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)

22

what are causes for hypomagnesemia? clinical manifestations?

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

23

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

24

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)

25

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

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

26

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)