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calcium Flashcards

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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
what does the calcium sensing receptor do?
* Reduces PTH secretion * Increases breakdown of stored PTH * Suppresses transcription of PTH gene * Inactivating mutations lead to FHH
26
what is FHH?
(familial hypocalciuric hypercalcaemia) – calcium levels are higher than normal without any clinical consequences
27
what is activated vitamin D?
Calcitriol - 1,25-dihydroxycholecalciferol
28
what stimulates and suppressed PTH gene transcription?
- activated vitamin D suppresses PTH gene transcription | - phosphate stimulated PTH gene transcription
29
what activates CASR and reduces calcium levels?
cinacalcet
30
what does CASR activation restrain?
parathyroid proliferation
31
what organs does PTH act on and what effect does this have?
* 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
32
how is calcium handled in the PCT? | how much is reabsorbed? how? what drives it? and is PTH involved?
* 65% reabsorption * Paracellular * PTH-independent * Driven by voltage gradient
33
how much calcium is reabsorbed in the LoH?
20%
34
how does calcium pass into the LoH?
para/transcellular
35
what is the effect of CASR on the LoH and how?
• CASR downregulates NaK2Cl | o Calcium sensing receptor on the PTH cells is the same one of the LoH cells
36
what inhibits calcium reabsorption in the LoH and how?
• 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
how much calcium is reabsorbed in the distal tubule?
10%
38
what does PTH upregulate in the distal tubule?
o TRPV calcium channels o Calcium ATPase o Na/Ca exchanger
39
what diuretic acts on the distal tubule and what effect does it have?
• 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
what other effects does PTH have on the kidney?
* 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
what is bone made of mainly?
Bone = Collagen plus Hydroxyapatite
42
what is mineralisation made of?
calcium + phosphate + alkaline phosphatase
43
what are osteoblasts made from>
mesenchymal cells
44
what do osteoblasts do?
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
what are osteoclasts derived from?
myeloid origin
46
what stimulates RANKL production?
PTH and calcitriol
47
what downregulates OPG?
PTH and calcitriol
48
what is OPG? what does it do?
osteoprotegerin | inhibits osteoclastogenesis
49
what increases gut calcium absorption and how?
Calcitriol increases RANKL which increases gut calcium absorption
50
what effet does glucocorticoid have on bone remodelling?
reduce osteoblast numbers and mineral production; increase RANKL
51
what effect does oestrogen have on bone remodelling?
epiphyseal closure; reduce cytokine sensitivity and inhibits bone remodelling
52
what causes osteoperosis?
high levels of PTH causes breakdown of bone
53
what does vitamin D deficiency lead to?
osteomalacia
54
what does primary hyperparathyroidism present with?
* 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
what is vitamin D produced from?
cholesterol
56
what is vitamin D hydroxylated into?
25-hydroxyvitamin D
57
in the liver, what is vitamin D converted to?
25(OH)D
58
what is the vitamin D receptor?
* Nuclear receptor found on DNA in a heterodimer with the retinoid acid receptor * Also a membrane bound receptor
59
explain the negative feedback inhibition involving the vitamin D receptor?
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
where are activated macrophages found?
TB and sarcoid granulomata
61
how can granulomas lead to hypercalcaemia?
• Can lead to high levels of vitamin D leaking into the circulation from the granuloma --> hypercalcaemia
62
what is the role of calcitrol?
increasing gut calcium and phosphate absorption
63
what factors determine calcium absorption?
bile salts, free fatty acids and fibre in the diet; gastric acidity
64
what effect do PPIs have on calcium?
PPIs reduce calcium uptake
65
what effect does vitamin D have on the parathyroid?
reduction in PTH transcription
66
what effect does vitamin D have on the bone?
reduces expression of type 1 collagen; increases levels of osteocalcin & RANKL; facilitates osteoclast differentiation
67
why can vitamin D deficiency lead to myopathy?
bc vitamin D is needed to increase amino acid uptake
68
what are the bones like in osteomalacia?
soft bones
69
what are the bones like in osteoperosis?
porous, brittle bones
70
what effect do osteoperosis and osteomalacia have on BMD?
cause a reduction in BMD
71
what is FGF23?
phosphatonin, hormone that reduces serum phosphate levels secreted by osteocytes
72
what does a mutation in FGF23 lead to?
Autosomal dominant hypophosphataemic rickets
73
what does paraneoplastic FGF23 lead to?
tumour induced osteomalacia
74
what do low levels of FGF23 lead to?
familial tumoural calcinosis
75
what is calcitonin a marker for?
medullary thyroid cancer
76
where is calcitonin released from?
thyroid c-cells
77
what is the role of calcitonin in humans?
role unclear
78
what is PTHrP important for?
important in lactation and embryological development
79
how may an asymptomatic patient with primary hyperparathyroidism present?
``` o Low BMD o Renal calculi o Renal impairment o Calcium > 3.0mmol/l o Age < 50 ```
80
how do you diagnose primary hyperparathyroidism?
``` o Serum calcium and PTH o 24 hr urine calcium o Urine calcium creatinine excretion index o Renal ultrasound o DXA scan ```
81
how do you localise an adenoma in primary hyperparathyroidism?
o Neck USS o MIBI scan o CT scan o Parathyroid Venous Sampling
82
what are signs and symptoms of hypocalcaemia?
convulsions, confusion, tetany, tachyarrhythmias
83
what causes hypocalcaemia?
Vitamin D deficiency, Chronic kidney disease, PTH resistance
84
how is hypoparathyroidism treated acutely?
IV or oral calcium replacement
85
how is hypoparathyroidism treated chronically?
alfacalcidol (1,25 vitamin D3) orally
86
why is there a risk of kidney stones with chronic treatment of hypoparathyroidism?
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
why cant PTH be given orally?
peptide hormone
88
how can PTH be given?
continuous subcutaneous infusions of PTH, given via an insulin pump
89
what does FHH cause and how?
* 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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