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Met2 > Calcium > Flashcards

Calcium Flashcards

1
Q

What changes occur when serum calcium is low?

A
  • PTH is released by chief cells in the parathyroid gland
  • reduces the reabsorption/increases excretion of phosphate in the kidney while decreasing calcium excretion
  • increases calcium and phosphate excretion in the bone
  • increases the absorption of calcium and phosphate in the intestines
  • causes vitamin D activation int he kidneys
  • inhibits sodium/water/bicarbonate reabsorption via effects on Na/H exchanger and Na/K ATPase
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2
Q

Where did the superior and inferior parathyroid glands originate from?

A

Develop from endodermal outpouchings
Inferior parathyroid: III out pouching
Superior parathyroid: IV out pouching

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3
Q

What type of receptor is the calcium sensing receptor?

A

GPCR

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4
Q

What is the effect of calcium binding to the calcium sensing receptor?

A
  • Reduces PTH secretion
  • Increases breakdown of stored PTH
  • Suppresses transcription of PTH gene
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5
Q

What is the result of inactivating mutations to the calcium sensing receptor?

A

Familial hypocalciuric hypercalcaemia (autosomal dominant)

- CaSR can’t sense high calcium –> PTH not suppressed by high calcium –> Ca2+ reabsorption not stopped

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6
Q

What is the effect of activated vitamin/calcitriol on PTH?

A

Suppresses PTH gene transcription

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7
Q

What is the effect of activated phosphate on PTH?

A

Stimulates PTH gene transcription

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8
Q

Where is most Ca2+ reabsorbed in the renal system?

A

Proximal tubule

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9
Q

How is Ca2+ reabsorbed at the:

  • Proximal tubule
  • Loop of henle
  • Distal tubule
A
  • Proximal tubule: paracellularly
  • Loop of henle: para/transcellularly
  • Distal tubule: via TRPV Ca2+ channels
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10
Q

What is the effect of PTH and calcitriol on RANKL and OPG?

A
  • stimulate RANKL

- downregulate OPG

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11
Q

What is the role of RANKL?

A

RANKL is released by osteoblasts

  • RANKL is a receptor activator for nuclear factor kB ligand and colony stimulating factor 1
  • promotes osteoclastogenesis and osteoclast function
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12
Q

What is the role of OPG?

A

OPG = osteoprotegerin

- inhibits osteoclastogenesis

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13
Q

What is the effect of PTH on IGF1 and IL1?

A

Increases both

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14
Q

What can primary hyperparathyroidism result in?

A
  • terminal tuft erosion
  • rugger jersey spine
  • subperiosteal erosion
  • brown tumour
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15
Q

What type of receptor is vitamin D receptor?

A

nuclear and membrane bound

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16
Q

What occurs when vitamin D receptor is activated?

A
  • inhibits action 1-alpha hydroxylase
  • this reduces the amount of 1,25-vitamin D able to bind to VDR

*function of the VDR is to increase calcium and phosphate absorption from the gut and kidneys

17
Q

Apart from inside the kidney, where else is calcitriol produced and why? In what situations doe this occur?

A

Macrophages

  • inside a macrophage calcitriol acts as a cytokines
  • modulates body defences against microbial invaders stimulating the innate immune response

Occurs when macrophages are activated (such as in TB and sarcoid granulomata) –> can lead to hypercalcaemia

18
Q

Explain how calcium is absorbed from the gut.

A
  • calcium in the lumen can travel to interstitial space in the gut para/transcellularly
  • calbindin is produced in the gut cells (enterocytes) –> it grabs Ca2+ inside the cell and releases it into the interstitium
  • Ca2+ in the interstitium can enter the blood
19
Q

What are the effects of vitamin D on parathyroid glands?

A
  • modest reduction in PTH transcription
20
Q

What are the effects of vitamin D on bones?

A
  • reduces expression of type 1 collagen
  • increases level of osteocalcin + RANKL
  • facilitates osteoclast differentiation
21
Q

What are the effects of vitamin D on phosphate?

A
  • increases phosphate absorption from the gut

- increases levels of FGF23 to remove it via renal excretion

22
Q

What are the effects of vitamin D on amino acids?

A

increases amino acid uptake

*deficiency in vitamin D results in myopathy

23
Q

What can vitamin D deficiency lead to?

A
  • rickets
  • osteomalacia
  • osteoporosis
24
Q

What is FGF23?

A

phosphatonin - hormones that reduces serum phosphate

  • it is secreted by osteocytes
  • actives inhibition of vitamin D
25
Q

What is the result of an activating mutation in FGF23?

A

Autosomal dominant hypophosphataemic rickets

26
Q

What is the result of a benign neoplasm that inappropriately produces fibroblast growth factor 23?

A

tumour-induced osteomalacia

27
Q

What effect does familial tumoral calcinosis have on FGF23 levels?

A

FGF23 levels are low

28
Q

Where is calcitonin produced? What is its role?

A

Produced by thyroid C cells

Lowers calcium levels

29
Q

What are potential causes of primary HPT?

A
  • parathyroid adenoma
  • carcinoma
  • hyperplasia
30
Q

What are potential causes of secondary HPT?

A
  • physiological compensation for hypocalcaemia

- vitamin D deficiency

31
Q

What are potential causes of tertiary HPT?

A
  • autonomous PTH production following chronic secondary PHPT
32
Q

What are the S+S/is the result of HPT?

A
  • hypercalcaemia
  • polyuria and polydipsia
  • kidney stones
  • osteoporosis
  • mood disorder
33
Q

How is primary HPT diagnosed?

A
  1. serum calcium and PTH
  2. 24h urine calcium
  3. urine calcium creatinine excretion index
  4. renal ultrasound
  5. DEXA scan
34
Q

What are the S+S of hypocalcaemia?

A
  • convulsions
  • confusion
  • tetany
  • tachyarrhythmia
35
Q

What are the causes of hypocalcaemia?

A
  • hypoparathyroidism: iatrogenic, autoimmune, genetic
  • vitamin D deficiency
  • chronic kidney disease
  • PTH resistance
36
Q

How would you treat acute and chronic hypoparathyroidism?

A
  1. acute: IV/oral calcium replacement
  2. chronic: alfacalcidol orally - increases gut absorption of calcium
    - however there will still be hypercalciuria = increased risk of kidney stones

Met2 (26 decks)

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