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Endocrine > Regulation of Calcium and Phosphate > Flashcards

Regulation of Calcium and Phosphate Flashcards

1
Q

calcium is in the body in 3 ways

A

protein-bound (albumin)
complexed to anions (phosphate, sulfate, citrate)
ionized free Ca2+

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2
Q

which is the active form of calcium

A

ionized Ca2+

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3
Q

symptoms of hypocalcemia

A

hyperrelexia, spontaneous twitching, muscle cramp, tingling and numness

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4
Q

chvostek sign

A

indicator of hypocalcemia: twitching of facial muscles eliicted by tapping on facial nerve

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5
Q

Trousseau sign

A

hypocalcemia: carpopedal spasm upon inflation of BP cuff

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6
Q

hypercalcemia symptoms

A

decreased QT, constipation, decrease appetite, hyporelexia, lethargy, coma

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7
Q

low extracellular Ca2+ and excitability

A

reduces activation threshold for Na+ channels, easier to evoke AP

  • increase in membrane excitability
  • generation of spontaneous AP is basis for hypocalcemic tetany
  • produces tingling and numbness and spontaneous muscle twitches
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8
Q

high extracellular Ca2+ and membrane excitability

A

decreases excitability

NS becomes depressed and reflex responses are slowed

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9
Q

increase in plasma protein concentration ____ total Ca2+ concentration
-ionized effect?

A

increases

no change in Ca2+ ionized

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10
Q

change in anion concentration: if increase phosphate concentration the ___ inoized Ca2+ concentration

A

decrease

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11
Q

in acedemia there is a __ of free ionized Ca2+

A

increase

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12
Q

in alkalemia there is a ___ in free ionized Ca2+ concentration

A

decrease

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13
Q

calcium homeostasis: GI tract and kidney

A

kidneys must excrete the same amount of Ca2+ that is absorbed in GI tract

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14
Q

what positively stimulates bone resorption

A

PTH and Vitamine D

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15
Q

distribution of Pi

A

bone-85%
ICF- 15%
Plasma-

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16
Q

extracellular concentration of Pi is ____ related to that of calcium

A

inversely

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17
Q

what cells of the parathyroid glands secrete PTH

A

chief cells synthesize and secrete

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18
Q

regulation of PTH gene expression Ca2+ high

A

calcium binds to receptor linked to Gq and Gi activates IP3 and DAG which inhibits PTH

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19
Q

chronic hypercalcemia and PTH

A

causes decreased synthesis and storage of PTH
increased breakdown of stored PTH
release of inactive PTH fragment into circulation

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20
Q

chronic hypocalcemia and PTH

A

causes increased synthesis and storage of PTH

hyperplasia of parathyroid glands (2ndary hyperparathyroidism)

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21
Q

magnesium and PTH

A

hypomagnesemia, elicits PTH
hypermagnesemia, inhibits PTH

severe hypomagnesemia inhibits PTH synthesis, storage, and secretion

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22
Q

effect of PTH on kidney

A

increased calcium reab
increased urinary cAMP and Pi
-decreased Pi reabsorption

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23
Q

how does PTH inhibit reabsorption of Pi and enhance its secretion

A

blocks Na+/Pi cotransporter from lumen into cell
(phosphaturic effect)
-important so that phoshpate does not combine with calcium and decrease free calcium ion levels

24
Q

PTH effect on intestine

A

PTH stimulates kidney to make 1a-hydroxylase which is an enzyme that makes active form of Vitamin D which stimulates intestinal Ca2+ absorption

25
Q

Vitamin D effect on pi and calcium

A

increases the absorption of both and promotes mineralization of new bone

26
Q

2 sources of Vitamin D

A

ingested in the diet

synthesized in skin from 7-dehydrocholesterol in presence of UV light

27
Q

what positvely stimulates 1a hydroxylase to become active

A

decrease in Pi
decrease in Calcium
increase in PTH

28
Q

1a hydroxylase and increased calcium txn level path

A

increased calcium binds receptor
Gq/Gi stimulated–>IP3 and Ca++ stimulated
inhibits CYP1a gene–>no 1a-hydroxylase

29
Q

1a hydroxylase and increased PTH txn level path

A

PTH binds kidney cell receptor with Gs protein—>Gs pathway—>cAMP–> stimulates CYP1a gene to make 1a-hyrdoxylase

30
Q

short term actions of PTH

A

bone formation via direct action on osteoblast

31
Q

long term actions of PTH on bone

A

increased bone resorption (indirect action on osteoclasts)

32
Q

Vitamin D and bone formation/resorption

A

Vitamin D acts synergistically with PTH to stimulate osteoclast activity and bone resorption

33
Q

what increases RANKL and decreases OPG

A

PTH

34
Q

what just increases RANKL

A

vitamin D

35
Q

mechanism of PTH on the kidney

A

PTH binds receptor and creates cAMP (excreted in urine) activates PK which phosphorylates Na+/Pi+ transporter and turns off.

-second renal action is on DCT to reabsorb calcium

36
Q

vitamin D effect on intestine

A

calcium comes down concentration gradient, calbindin binds it and shuttles it to Ca2+ ATPase into the blood

37
Q

where in the kidney does Ca2+ reabsorption occur when stimulated by PTH

A

TAL and DCT

38
Q

Vitamin D action on kidney

A

promotes Pi reabsoroption by proximal nephrons by stimulating NPT2a expression

39
Q

calcitonin actions

A

decrease blood calcium and phosphate concentrations by inhibiting bone resorption

-decreases activity and number of osteoclasts

40
Q

estradiol stimulates what

A

intestinal Ca2+ absorption and renal tubular Ca2+ reabsorption

-promotes survival of osteoblasts and apoptosis of osteoclasts

41
Q

adrenal glucocorticoids (cortisol) and bones

A

promote bone resorption and renal Ca2+ wasting and inhibit intestinal ca2+ absorption

-patinets treated with high levels of glucocorticoid can develop osteoporosis

42
Q

hyperparathyroidism urine

A

increase in Pi, calcium, and cAMP

43
Q

hyperparathyroidism: stone, bones, groans

- treatment

A

calcium stones, bone resorption, constipation

treat with parathyroidectomy

44
Q

secondary hyperparathyroidism

A

increase in PTH is secondary to hypocalcemia

  • renal failure
  • vitamin D defeciency
45
Q

albright hereditary osteodystrophy (pseudohypoparathyroidism type 1a)

A

inherited autosomal dominant disorder, Gs for PTH in BONE and KIDNEY is defective

  • hypocalcemia, and hyperphophatemia
  • Increased PTH
  • administration of exogenous PTH produces no phosphaturic response and no increase in urinary cAMP
46
Q

albright hereditary osteodystrophy phenotype

A

frank reynolds

-short stature, short neck, obesity, subcut calcifaction, shortened metatarsals and metacarpals

47
Q

humoral hypercalcemia of malignancy

A

PTHrP is produced by tumors with close homology to PTH
-increase urinary Ca2+, Pi, and cAMP
-increase in blood calcium
decrease in blood Pi
-decrease in PTH
-decrease in vitamin D (vitamin D levels are normally suppressed in cancer)

48
Q

treatment for humoral hypercalcemia of malignancy

A

furosemide (inhibits Ca2+ reabsorption and increases calcium excretion)

etidronate: inhibits bone resorption

49
Q

familial hypocalciuric hypercalcemia

A

autosomal dominant disorder
mutation inactivates CaSR in parathyroid glands
-decrease in urinary calcium
-increase in serum calcium

senstivity is lost in renal and parathyroid receptors

50
Q

rickets

A

insufficient amount of Ca2+ and Pi available to mineralize growing bone

  • dietary deficiency of vitamin D
  • vitamin D resistance (defecient 1a-hydroxylase)
  • mutations in vitamin D receptor
51
Q

osteomalacia

A

in adults

new bone fails to mineralize

52
Q

vitamin D dependent rickets type I

A

decrease 1a-hyrdoxylase

53
Q

vitamin D-dependent rickets type II

A

decrease in vitamin D receptor

54
Q

treatment for rickets-osteomalacia

A
  • Vitamin D2
  • Ca2+
  • sunlight
  • calcitriol
55
Q

osteoporosis treatment

A

-antiresoptive therapy
-estrogens
-SERMs
-calcitonin
-RANK inhibitors
PTH

Endocrine (14 decks)

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