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calcium Flashcards

1
Q

what % of body calcium is in the bones?

A

99%

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2
Q

what % of bone calcium is exchangeable with the ECF?

A

1%

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3
Q

what % of blood calcium is protein bound?

A

50%

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4
Q

what does blood calcium bind to?

A

(40% albumin, 10% globulin)

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5
Q

what binds the same biding sites on albumin molecules?

A

hydrogen

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6
Q

what happens to ionised calcium in acidosis?

A

increases

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7
Q

what happens to ionised calcium levels in alkalosis?

A

decreases

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8
Q

why does alkalosis cause tingling of the lips and fingers?

A

hyperventilation causes respiratory alkalosis bc you’re blowing off excess CO2. Tinging of the lips and fingers occurs in hyperventilation  fall in ionised calcium
• More calcium outside the cell than inside the cell

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9
Q

what are the 5 phases of cardiac APs and what happens during them?

A
  • 4 – resting membrane, -ve potential maintained by Na/K exchanger – 3 Na for 2 K
  • 0- Opening of fast Na+ channels – stabilised by extracellular calcium
  • 1 – Early repolarisation as fast sodium channels close
  • 2 - plateau phase: Na-Ca exchanger: Na in and calcium out, maintains positive potential
    1. Repolarisation – sodium and calcium channels close
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10
Q

how does calcium cause tetany and tachyarrhythmias?

A

• Ca2+ can sit in the Na+ membrane and block it
• Drop in extracellular Ca2+ means less Na+ channels are blocked. Na+ can enter the cell freely and uncontrolled depolarisations happen  tetany and tachyarrhythmias
o Hypocalcaemia reduces the threshold for APs to fire

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11
Q

what effect does hypercalcaemia have on nerve firing? what effect does this have on the body?

A

• Hypercalcaemia slows nerve firing
o Slows muscle contraction
o Slows nerve firing in the brain  depression and inability to concentrate
o Slows nerve firing in the smooth muscle of the gut  slows peristalsis  constipation

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12
Q

how much of body phosphate is mineralised in bone?

A

85%

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13
Q

how much of serum phosphate is ionised?

A

almost all

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14
Q

what is extracellular calcium needed for?

A

o Bone mineral
o Blood coagulation
o Membrane excitability

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15
Q

what is intracellular calcium needed for?

A

signalling

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16
Q

what is extracellular phosphate needed for?

A

bone mineral

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17
Q

what is intracellular phosphate needed for?

A

o Structural
o High energy bonds
o Phosphorylation

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18
Q

what effect does calcium have on PTH?

A

high levels of calcium inhibits PTH

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19
Q

what does PTH act on?

A

o Get calcium from bone
o Stop losing calcium from the kidneys
o Absorb more calcium from the gut

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20
Q

what are the 2 cell types in the parathyroid gland? what do they do?

A

oxyphilic cells - nothing important lol

chief cells - secrete PTH

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21
Q

what cells secrete PTH?

A

chief cells of the parathyroid gland

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22
Q

when are oxyphilic cells useful?

A

useful when imaging for if someone has an overactive gland. It takes up technetium-sestambi which helps identify which gland is overactive

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23
Q

how is PTH processed?

A
  • PreproPTH is cleaved by the RER to proPTH
  • ProPTH is cleaved by the Golgi to PTH
  • PTH is secreted in vesicles
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24
Q

what type of receptor is the calcium sensing receptor?

A

GPCR

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25
Q

what does the calcium sensing receptor do?

A
  • Reduces PTH secretion
  • Increases breakdown of stored PTH
  • Suppresses transcription of PTH gene
  • Inactivating mutations lead to FHH
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26
Q

what is FHH?

A

(familial hypocalciuric hypercalcaemia) – calcium levels are higher than normal without any clinical consequences

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27
Q

what is activated vitamin D?

A

Calcitriol - 1,25-dihydroxycholecalciferol

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28
Q

what stimulates and suppressed PTH gene transcription?

A
  • activated vitamin D suppresses PTH gene transcription

- phosphate stimulated PTH gene transcription

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29
Q

what activates CASR and reduces calcium levels?

A

cinacalcet

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30
Q

what does CASR activation restrain?

A

parathyroid proliferation

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31
Q

what organs does PTH act on and what effect does this have?

A
  • Kidney: decreases calcium excretion and increases phosphate excretion
  • Bone: increases calcium and phosphate resorption
  • Intestine: increases absorption of calcium and phosphate; some evidence for direct effects but mainly indirectly through calcitriol
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32
Q

how is calcium handled in the PCT?

how much is reabsorbed? how? what drives it? and is PTH involved?

A
  • 65% reabsorption
  • Paracellular
  • PTH-independent
  • Driven by voltage gradient
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33
Q

how much calcium is reabsorbed in the LoH?

A

20%

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34
Q

how does calcium pass into the LoH?

A

para/transcellular

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35
Q

what is the effect of CASR on the LoH and how?

A

• CASR downregulates NaK2Cl

o Calcium sensing receptor on the PTH cells is the same one of the LoH cells

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36
Q

what inhibits calcium reabsorption in the LoH and how?

A

• Inhibited by loop diuretics
o Loop diuretics inhibit NaK2Cl cells
o Furosemide inhibits Na+, K+, Cl- reabsorption, which reduces the gradient for calcium reabsorption
o Serum calcium will fall and urine calcium will increase

37
Q

how much calcium is reabsorbed in the distal tubule?

A

10%

38
Q

what does PTH upregulate in the distal tubule?

A

o TRPV calcium channels
o Calcium ATPase
o Na/Ca exchanger

39
Q

what diuretic acts on the distal tubule and what effect does it have?

A

• Thiazide diuretics target Na+/Cl-channels
o Have opposite effects to loop diuretics
o Na+ levels fall in the cell  increases gradient across opposite cell membrane
o Na+ can therefore enter down the conc gradient while calcium passes out the other way
o Thiazide diuretics increase serum calcium

40
Q

what other effects does PTH have on the kidney?

A
  • Down-regulation of NaPi transporters - Reduced phosphate reabsorption
  • Vitamin D Activation - Stimulation of 25(OH) D3  1,25(OH)2 D3
  • Proximal tubule gluconeogenesis
  • Inhibits sodium/water/bicarbonate reabsorption via effects on Na/H exchanger and Na/K ATPase
41
Q

what is bone made of mainly?

A

Bone = Collagen plus Hydroxyapatite

42
Q

what is mineralisation made of?

A

calcium + phosphate + alkaline phosphatase

43
Q

what are osteoblasts made from>

A

mesenchymal cells

44
Q

what do osteoblasts do?

A

o Produce mineral and signal to osteoclasts to resorb bone
o When mineralisation is complete they differentiate into osteocytes
• Osteoblasts release RANKL – promotes osteoclastogenesis and osteoclast function

45
Q

what are osteoclasts derived from?

A

myeloid origin

46
Q

what stimulates RANKL production?

A

PTH and calcitriol

47
Q

what downregulates OPG?

A

PTH and calcitriol

48
Q

what is OPG? what does it do?

A

osteoprotegerin

inhibits osteoclastogenesis

49
Q

what increases gut calcium absorption and how?

A

Calcitriol increases RANKL which increases gut calcium absorption

50
Q

what effet does glucocorticoid have on bone remodelling?

A

reduce osteoblast numbers and mineral production; increase RANKL

51
Q

what effect does oestrogen have on bone remodelling?

A

epiphyseal closure; reduce cytokine sensitivity and inhibits bone remodelling

52
Q

what causes osteoperosis?

A

high levels of PTH causes breakdown of bone

53
Q

what does vitamin D deficiency lead to?

A

osteomalacia

54
Q

what does primary hyperparathyroidism present with?

A
  • Terminal tuft erosion – breakdown of bone in the fingers
  • Rugger jersey spine – breakdown of bone in the spine so it looks stripy.
  • Subperiosteal erosion
  • Brown tumour – focal area where there were really high levels of PTH and excess remodelling. Isn’t a tumour but can be mistaken for a malignancy
55
Q

what is vitamin D produced from?

A

cholesterol

56
Q

what is vitamin D hydroxylated into?

A

25-hydroxyvitamin D

57
Q

in the liver, what is vitamin D converted to?

A

25(OH)D

58
Q

what is the vitamin D receptor?

A
  • Nuclear receptor found on DNA in a heterodimer with the retinoid acid receptor
  • Also a membrane bound receptor
59
Q

explain the negative feedback inhibition involving the vitamin D receptor?

A

In most cells there is a negative feedback inhibition: activation of the VDR inhibits the action of 1α hydroxylase, therefore reducing the amount of activated vitamin D able to bind to the VDR.

60
Q

where are activated macrophages found?

A

TB and sarcoid granulomata

61
Q

how can granulomas lead to hypercalcaemia?

A

• Can lead to high levels of vitamin D leaking into the circulation from the granuloma –> hypercalcaemia

62
Q

what is the role of calcitrol?

A

increasing gut calcium and phosphate absorption

63
Q

what factors determine calcium absorption?

A

bile salts, free fatty acids and fibre in the diet; gastric acidity

64
Q

what effect do PPIs have on calcium?

A

PPIs reduce calcium uptake

65
Q

what effect does vitamin D have on the parathyroid?

A

reduction in PTH transcription

66
Q

what effect does vitamin D have on the bone?

A

reduces expression of type 1 collagen; increases levels of osteocalcin & RANKL; facilitates osteoclast differentiation

67
Q

why can vitamin D deficiency lead to myopathy?

A

bc vitamin D is needed to increase amino acid uptake

68
Q

what are the bones like in osteomalacia?

A

soft bones

69
Q

what are the bones like in osteoperosis?

A

porous, brittle bones

70
Q

what effect do osteoperosis and osteomalacia have on BMD?

A

cause a reduction in BMD

71
Q

what is FGF23?

A

phosphatonin, hormone that reduces serum phosphate levels secreted by osteocytes

72
Q

what does a mutation in FGF23 lead to?

A

Autosomal dominant hypophosphataemic rickets

73
Q

what does paraneoplastic FGF23 lead to?

A

tumour induced osteomalacia

74
Q

what do low levels of FGF23 lead to?

A

familial tumoural calcinosis

75
Q

what is calcitonin a marker for?

A

medullary thyroid cancer

76
Q

where is calcitonin released from?

A

thyroid c-cells

77
Q

what is the role of calcitonin in humans?

A

role unclear

78
Q

what is PTHrP important for?

A

important in lactation and embryological development

79
Q

how may an asymptomatic patient with primary hyperparathyroidism present?

A 
o	Low BMD
o	Renal calculi
o	Renal impairment
o	Calcium > 3.0mmol/l
o	Age < 50
80
Q

how do you diagnose primary hyperparathyroidism?

A 
o	Serum calcium and PTH
o	24 hr urine calcium
o	Urine calcium creatinine excretion index
o	Renal ultrasound
o	DXA scan
81
Q

how do you localise an adenoma in primary hyperparathyroidism?

A

o Neck USS
o MIBI scan
o CT scan
o Parathyroid Venous Sampling

82
Q

what are signs and symptoms of hypocalcaemia?

A

convulsions, confusion, tetany, tachyarrhythmias

83
Q

what causes hypocalcaemia?

A

Vitamin D deficiency, Chronic kidney disease, PTH resistance

84
Q

how is hypoparathyroidism treated acutely?

A

IV or oral calcium replacement

85
Q

how is hypoparathyroidism treated chronically?

A

alfacalcidol (1,25 vitamin D3) orally

86
Q

why is there a risk of kidney stones with chronic treatment of hypoparathyroidism?

A

However, the lack of PTH means that calcium will continue to be lost from the kidneys at a high rate. This hypercalciuria will increase the risk of kidney stones, even if the serum calcium is low!

87
Q

why cant PTH be given orally?

A

peptide hormone

88
Q

how can PTH be given?

A

continuous subcutaneous infusions of PTH, given via an insulin pump

89
Q

what does FHH cause and how?

A
  • Inactivating mutations of the CaSR
  • Parathyroid can’t sense high calcium
  • PTH not suppressed by high calcium
  • CaSR in kidney not activated
  • PTH-calcium curve shifts to the right
  • High serum Ca, low urine Ca, high serum Mg

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