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Endo Repro Midterm > Regulation of Calcium and Phosphate Metabolism > Flashcards

Regulation of Calcium and Phosphate Metabolism Flashcards

1
Q

How does the amount of calcium change during aging?

A
  • decreases in the amount of calcium absorbed from dietary intake and in dietary intake of calcium
  • existing bone cells are reabsorbed by the body faster than new bone is made
  • aging contributes to osteopenia or osteoporosis
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2
Q

Where is calcium predominantly located in the body?

A

bones and teeth 99%

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3
Q

What are the percentages of calcium in ECF, plasma, and ICF?

LO1

A

ECF- 0.1%
plasma - <0.5%
ICF - 1%

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4
Q

What is the biologically active form of calcium?

LO1

A

free, ionized calcium

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5
Q

What does ultrafilterable mean?

A

can cross membranes

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6
Q

What are the percentage of calcium in the blood?

LO1

A

protein bound 40%

ultrafilterable 60%

  • complexed to ions 10%
  • ionized calcium 50% *biologically active form
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7
Q

When is calcium higher than 10 normal for the patient’s age?

A

teenage years/puberty

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8
Q

What is the normal range for calcium?

A

9-10

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9
Q

What is hypocalcemia?

  • definition
  • symptoms
  • indicators
A
  • decreased plasma calcium concentration
  • symptoms: hyperflexia, spontaneous twitching, muscle cramp, tingling, numbness
  • indicators: Chvostek sign and Trousseau sign
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10
Q

What is Chvostek sign?

A

twitching of the facial muscles elicited by tapping on the facial nerve

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11
Q

What is Trousseau sign?

A

carpopedal spasm upon inflation of a blood pressure cuff

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12
Q

What is hypercalcemia?

  • definition
  • symptoms
A
  • increased plasma calcium concentration
  • symptoms: decreased QT interval, constipation, lack of appetite, polyuria, polydipsia, muscle weakness, hyporeflexia, lethargy, coma
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13
Q

How do changes in plasma calcium concentration influence membrane excitability?

LO2

A

decreased ECF calcium –> increased excitability of sensory and motor nerves and muscle by lowering threshold potential for Na channels –> less inward current required to depolarize to threshold and fire action potentials (hypocalcemic tetany)

  • sensory neurons: tingling and numbness
  • motor neurons: spontaneous muscle twitches
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14
Q

What can calcium levels in plasma be altered by?

A
  • changes in plasma protein concentration –> total Ca2+ same direction as plasma proteins (no change in ionized calcium)
  • changes in ion concentration –> change in fraction of calcium complexed with anions –> opposite directions
  • acid-base abnormalities –> change the fraction of calcium bound to albumin b/c H+ competes for binding spots
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15
Q

What organ systems are involved in calcium homeostasis?

LO4

A

bone, kidney, and intestine

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16
Q

What hormones are involved in calcium homeostasis?

LO4

A

parathyroid hormone, calcitonin, vitamin D

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17
Q

What hormone does not contribute to homeostasis of calcium, but still has a role?

A

calcitonin

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18
Q

What happens in bone remodeling?

LO4

A

bone deposition

bone resorption

  • stimulated by PTH and vit D
  • inhibited by calcitonin

-no net gain or loss of Ca2+

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19
Q

What happens in the SI regarding calcium?

LO4

A
  • absorption of Ca2+ stimulated by vit D
  • secretion of Ca2+

-net 200 mg absorbed

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20
Q

What happens in the kidneys regarding calcium?

LO4

A

filtration

resorption
-stimulated by PTH

200 mg excreted

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21
Q

What must occur to maintain Ca2+ balance?

LO4

A

amount Ca2+ absorbed in GI must equal amount excreted in urine

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22
Q

What is the relationship between Ca2+ and phosphate?
-normal range

LO5

A

phosphate

  • ECF concentration of Pi is inversely related to Ca2+
  • Normal range is 2.5-4.5 mg/dL
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23
Q

What is the distribution of Pi in the body?

A 
bone 85%
plasma <1%
-84% ionized
-`10% protein bound
-6% complexed to various cations, including K+ and Na+
ICF 15%
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24
Q

What cells secrete PTH?

LO5

A

chief cells of parathyroid glands

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25
Q

Describe PTH

  • type of hormone
  • structure
  • synthesis
  • storage
A
  • peptide hormone
  • single chain polypeptide with 84 aa
  • preproPTH (115 aa)
  • proPTH (90 aa)
  • packaged into secretory granules
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26
Q

Where is the biologically active part of PTH?

A

N-terminus 1-34 aa

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27
Q

Is the PTH secretion low or high with high calcium?

A

low

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28
Q

Is PTH secretion low or high with low calcium?

A

high

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29
Q

Explain the CaSR

LO6

A
  • receptor on parathyroid monitoring extracellular side

- calcium binds receptor –> inhibits PTH gene

30
Q

What is the effect of vit D on PTH?

LO6

A

PTH is needed for the active form of vit D, so active form of vit D inhibits PTH gene.

31
Q

What sensors are used by CaSR?

A

Gq and Gi

32
Q

Describe regulation of PTH in chronic hypercalcemia

A

causes decreased synthesis and storage of PTH, increases breakdown of stored PTH, and release of inactive PTH fragment into the circulation

33
Q

Describe regulation of PTH in chronic hypocalcemia

A

causes increased synthesis and storage of PTH and hyperplasia of parathyroid glands (secondary hyperparathyroidism)

34
Q

What is the effect of magnesium on regulation of PTH?

**future practice

A
  • parallel but less significant effects on PTH secretion
  • severe hypomagnesemia is exception: result of chronic Mg2+ deplesion as in alcoholism –> inhibition of PTH synthesis, storage, and secretion
35
Q

What is the receptor for PTH?

A

G alpha protein linked adenylyl cyclase –> cAMP

36
Q

What are the actions of PTH on bone?

LO7

A

increased bone resorption

37
Q

What are the actions of PTH on kidney?

LO7

A

decreased phosphate reabsorption (phosphaturia)
increased calcium reabsorption
increased urinary cAMP

38
Q

What are the actions of the PTH on the intestine?

LO7

A

increased calcium absorption (indirect via vit D)

39
Q

How does vitD affect calcium and phosphate homeostasis?

LO8

A

promotes mineralization of new bone through its coordinated actions in the regulation of both Ca2+ and Pi plasma concentrations

40
Q

Describe vit D/cholecalciferol

A
  • prohormone
  • physiologically inactive
  • must be successively hydroxylated to an active metabolite
41
Q

Describe vitamin D synthesis

LO9

A 
7-dehydrocholesterol
--UV light (skin)--> or diet-->
cholecalciferol
--liver (25-hydroxylase)-->
25-OH-cholecalciferol (main circulating form but low activity) --kidney 24-hydroxylase --> inactive 24,25-(OH)2-cholecalciferol OR --1alpha hydroxylase --> 1,25 (OH)2 cholecalciferol (active)
42
Q

What stimulates 1 alpha hydroxylase?

A

low calcium concentration
high PTH
low phosphate concentration

43
Q

What is the other name for 1 alpha hydroxylase?

LO10

A

CYP1alpha

44
Q

What is the negative feedback loop of PTH and 1,25-dihydroxycholecalciferol?

LO11

A

PTH stimulates Gs of epithelial cell of PT –> cAMP/PKA –> CYP1alpha gene –> 1 alpha hydroxylase

25(OH) vit D –1 alpha hydroxylase–> 1,25 (OH)2 vit D level sensed by parathyroid chief cells –> inhibit gene expression of PTH gene

45
Q

What are the actions of PTH on bone formation and resorption?

LO12

A
  • receptors on osteoblasts
  • short term: bone formation via direct action on osteoblasts
  • long term: increased bone resorption (indirect action on osteoclasts mediated by cytokines from osteoblasts)
46
Q

How does vit D interact with PTH on bone?

LO12

A

acts synergistically with PTH to stimulate osteoclast activity and bone resorption

47
Q

What are the actions of calcitonin in bone resorption?

LO13

A

decrease calcium and Pi concentrations by inhibiting bone resorption

  • calcitonin receptors expressed on osteoclasts
  • decreased activity and number of osteoclasts
  • major stimulus is increased Ca2+
48
Q

What is M-CSF?

A

macrophage colony-stimulating actors
-induce stem cells to differentiate into osteoclast precursors, mononuclear osteoclasts, and mature multinucleated osteoclasts

49
Q

What is RANKL?

A

receptor activator for NF-kappa B ligand

  • cell surface protein produced by osteoblasts, bone lining cells, and apoptotic osteocytes
  • primary mediator of osteoclast formation
50
Q

What is RANK?

A

cell surface protein receptor on osteoclastss and osteoclast precursors

51
Q

What is OPG?

A

osteoprotegerin: soluble protein produced by osteoblasts; decoy receptor for RANKL; inhibits RANKL/RANK interaction

52
Q

What is OPG?

A

osteoprotegerin: soluble protein produced by osteoblasts; decoy receptor for RANKL; inhibits RANKL/RANK interaction

53
Q

What does PTH do on bone agent/factors?

A

increases RANKL, decreases OPG

54
Q

What does vitamin D do on bone agent/factors?

A

increases RANKL

55
Q

What is the mechanism of PTH on the kidney?

A
  • binds receptor
  • Gs
  • AC
  • cAMP
  • PKA
  • phosphorylation
  • inhibits Na+/phosphate transporter –> phosphaturia
56
Q

What is the action of vit D on the kidney?

A

sitmulates BOTH Ca2+ and Pi reabsorption

57
Q

What is the mechanism of vit D on GI?

A

vit D –> mRNA –> protein synthesis –> calbindin –> Ca2+ calbindin –> basolateral side

**increases Ca2+ and Pi absorption

58
Q

What is the function of calbindin?

A

shuttle

buffer level of calcium intracellularly

59
Q

What is primary hyperparathyroidism?

  • mechanism
  • actions
  • labs

LO14

A
  • elevated PTH –> elevated resorption, activation of vit D, elevated Pi excretion and Ca2+ reabsorption
  • “stones, bones, and groans” - hypercalcuria stones, increased bone resorption - bones, constipation - groans
  • treatment requires parathyroidectomy

PTH high
Ca2+ high
Pi low
vit D high

60
Q

What is secondary hyperparathyroidism?

  • mechanism
  • actions
  • labs

LO14

A

-increased PTH due to low calcium levels (chronic kidney disease and vit D deficiency)

both
PTH high
Ca2+ low
vit D low

renal failure - high Pi
vit D deficiency - low Pi

61
Q

hypoparathyroidism

  • causes
  • symptoms
  • treatment

LO15

A

causes

  • thyroid surgery
  • parathyroid surgery
  • autoimmune or congenital (less common)

symptoms

  • muscle spasms or cramping
  • numbness, tingling, burning especially around mouth and fingers
  • seizures
  • kids: poor teeth development, mental deficiency

treatment
-oral calcium supplement and active form of vit D

62
Q

hypoparathyroidism
-labs

LO15

A

PTH low
Ca2+ low
Pi high
vit D low

63
Q

pseudohypoparathyroidism type 1a

  • pathophysiology
  • labs
A

PTH binds PTHR
defective Gs is unable to activate adenylyl cyclase

  • AD disorder
  • hypocalcemia and hyperphosphatemia
  • high PTH

ALBRIGHT HEREDITARY OSTEODYSTROPHY
-short stature, short neck, obesity, subcutaneous calcification, shortened metatarsal and metacarpals

PTH high
Ca2+ low
Pi high
vit D low

64
Q

humoral hypercalcemia of malignancy

  • pathophysiology
  • labs
A

PTH related peptide (PTHrP) produced in tumors with similar homology to PTH
-binds and activates same receptor as PTH

PTH low
Ca2+ high
Pi low
vit D low (paradoxally)

65
Q

familial hypocalciuric hypercalcemia

  • genetics
  • cause
  • labs
A
  • AD
  • mutations that inactivate CaSR in parathyroid glands and parallel calcium receptors in the kidney
PTH normal/high
Ca2+ high
urine Ca2+ low
Pi normal
vit D normal
66
Q

Rickets and osteomalacia
-cause

LO19

A

impaired vit D metabolism

  • dietary deficiency
  • vit D resistance (deficit in synthesis of active form from absence of 1 alpha hydroxylase or mutations affecting vit D receptor)
67
Q

Rickets

  • definition
  • characterizations
  • types

LO19

A

children

  • insufficient amount of calcium and phosphate are available to mineralize growing bone
  • characterized by growth failure and skeletal deformities
  • type I (low 1 alpha hydroxylase)
  • type II (low vit D receptor)
68
Q

osteomalacia

LO19

A
  • new bone fails to mineralize

- characterized by bending and softening of weight bearing bones

69
Q

labs of vit D deficiency

LO18

A 
PTH high (secondary)
Ca2+ normal/low
Pi low
Urine Pi high
Urine cAMP high
vit D low
bone osteomalacia high resorption
70
Q

risk factors for osteoporosis

LO20

A

decrease in bone mass increases with age

gender - female b/c loss of estrogen after menopause

71
Q

treatment of osteoporosis

A

-anabolic therapy short term PTH
-antiresorptive therapy
biophsophonates
estrogen
selective estrogen receptor modulators
calcitonin
RANKL inhibitors

Endo Repro Midterm (12 decks)

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