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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
Vitamin D effect on pi and calcium
increases the absorption of both and promotes mineralization of new bone
26
2 sources of Vitamin D
ingested in the diet | synthesized in skin from 7-dehydrocholesterol in presence of UV light
27
what positvely stimulates 1a hydroxylase to become active
decrease in Pi decrease in Calcium increase in PTH
28
1a hydroxylase and increased calcium txn level path
increased calcium binds receptor Gq/Gi stimulated-->IP3 and Ca++ stimulated inhibits CYP1a gene-->no 1a-hydroxylase
29
1a hydroxylase and increased PTH txn level path
PTH binds kidney cell receptor with Gs protein--->Gs pathway--->cAMP--> stimulates CYP1a gene to make 1a-hyrdoxylase
30
short term actions of PTH
bone formation via direct action on osteoblast
31
long term actions of PTH on bone
increased bone resorption (indirect action on osteoclasts)
32
Vitamin D and bone formation/resorption
Vitamin D acts synergistically with PTH to stimulate osteoclast activity and bone resorption
33
what increases RANKL and decreases OPG
PTH
34
what just increases RANKL
vitamin D
35
mechanism of PTH on the kidney
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
vitamin D effect on intestine
calcium comes down concentration gradient, calbindin binds it and shuttles it to Ca2+ ATPase into the blood
37
where in the kidney does Ca2+ reabsorption occur when stimulated by PTH
TAL and DCT
38
Vitamin D action on kidney
promotes Pi reabsoroption by proximal nephrons by stimulating NPT2a expression
39
calcitonin actions
decrease blood calcium and phosphate concentrations by inhibiting bone resorption -decreases activity and number of osteoclasts
40
estradiol stimulates what
intestinal Ca2+ absorption and renal tubular Ca2+ reabsorption -promotes survival of osteoblasts and apoptosis of osteoclasts
41
adrenal glucocorticoids (cortisol) and bones
promote bone resorption and renal Ca2+ wasting and inhibit intestinal ca2+ absorption -patinets treated with high levels of glucocorticoid can develop osteoporosis
42
hyperparathyroidism urine
increase in Pi, calcium, and cAMP
43
hyperparathyroidism: stone, bones, groans | - treatment
calcium stones, bone resorption, constipation treat with parathyroidectomy
44
secondary hyperparathyroidism
increase in PTH is secondary to hypocalcemia - renal failure - vitamin D defeciency
45
albright hereditary osteodystrophy (pseudohypoparathyroidism type 1a)
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
albright hereditary osteodystrophy phenotype
frank reynolds | -short stature, short neck, obesity, subcut calcifaction, shortened metatarsals and metacarpals
47
humoral hypercalcemia of malignancy
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
treatment for humoral hypercalcemia of malignancy
furosemide (inhibits Ca2+ reabsorption and increases calcium excretion) etidronate: inhibits bone resorption
49
familial hypocalciuric hypercalcemia
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
rickets
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
osteomalacia
in adults | new bone fails to mineralize
52
vitamin D dependent rickets type I
decrease 1a-hyrdoxylase
53
vitamin D-dependent rickets type II
decrease in vitamin D receptor
54
treatment for rickets-osteomalacia
- Vitamin D2 - Ca2+ - sunlight - calcitriol
55
osteoporosis treatment
-antiresoptive therapy -estrogens -SERMs -calcitonin -RANK inhibitors PTH

Endocrine (14 decks)

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