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Endocrinology - Rachel Doohan Y5 > calcium and phosphate regulation > Flashcards

calcium and phosphate regulation Flashcards

1
Q

calcium homeostasis

A

is a complex process involving the following 4 components

  • serum calcium
  • serum phosphate
  • parathyroid hormone
  • 1,25-dihydroxyvitamin D3 (calcitriol)
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2
Q

more than

A

99% of total body calcium is stored in bone predominantly as hydroxyapatite, only a very small portion of calcium is available for exchange in the serum

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3
Q

parathyroid hormone is

A

released by the parathyroid glands in response to low levels of calcium

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4
Q

PTH end organ targets are

A
  • kidneys
  • bone
  • skeletal system
  • GI tract
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5
Q

in the Kidneys PTH

A

increases renal calcium resorption and phosphate excretion, it does so by blocking the reabsorption of phosphate in the proximal tubular and promotes reabsorption of calcium in the ascending loop of henle, distal tubule and collecting tubule

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6
Q

In the bone

A

PTH promotes absorption of calcium from the bone in 2 ways; rapid and slow phase

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7
Q

rapid phase

A
  • the rapid phase brings about a rise in serum calcium within minutes and occurs at the levels of osteoblasts and osteocytes, although it seems counter-intuitive that cells that promote deposition of bone are involved in resorption, these cells form an interconnected network known as the osteolytic membrane overlying the bone matrix, but with a small layer of interposed fluid called bone fluid when PTH binds to receptors on these cells, the osteolytic membrane pumps calcium ions from the bone fluid into the extra-cellular fluid
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8
Q

slow phase

A

bone resorption which takes several days, osteoclasts are activated to resorb bone and then the osteoclasts proliferate

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9
Q

PTH also

A

converts 25-hydroxyvitamin D to its more active metabolite 1,25-dihydroxyvitamin D3 (calcitriol) by activation of enzyme 1-hydroxylase in the proximal tubules of the kidney

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10
Q

vitamin D3 otherwise known as

A

cholecalciferol

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11
Q

cholecalciferol is formed

A

in the skin when a cholesterol precursor (7-dehydroxycholesterol) is exposed to UV light, activation of cholecalciferol then occurs when the substance undergoes 25-hydroxylation in the liver and 1-hydroxylation in the kidney to form calcitriol

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12
Q

primary action of calcitriol

A

promotes gut absorption of calcium by stimulating formation of calcium binding protein within the interstitial epithelial cells and it also promotes the intestinal absorption of phosphate

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13
Q

calcium in the serum

A

is normally bound to albumin and only free calcium is biologically active, therefore if a patient has low albumin levels (i.e. liver of renal failure), calcium levels may be measured as low but the patient does not have hypocalcaemia (i.e. there calcium levels are normally or even high) so you have to work out there corrected calcium level

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14
Q

corrected calcium

A

Ca+ 0.8x(4-albumin)

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15
Q

calciums affect on neuronal membranes

A

calcium stabilises and discharges neuronal membranes therefore, significant disturbances in serum calcium levels will always cause neurological disturbances

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16
Q

overall net affect of PTH is to

A

increase calcium and decrease phosphate

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17
Q

calcitonin

A

is released by the parafollicualr C cells of the thyroid gland in response to hypercalcemia and has the opposite affect to PTH

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18
Q

affect of calcitonin

A
  • inhibits the activation of osteoclasts
  • reduces reabsorption of calcium and phosphorous in the GI tract
  • reduces reabsorption of calcium in the kidneys
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19
Q

causes of hypercalcaemia

A
  • primary hyperparathyroidism is the most common cause
  • malignancy= bone demineralisation caused by metastases to bone or PTHrP
  • Drugs
  • familial hypocalciuric hypercalcaemia
  • sarcoidosis
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20
Q

PTHrP

A

squamous cell lung cancer can release parathyroid hormone resembling peptide which mimics PTH

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21
Q

drugs causing hypercalcaemia

A

Vitamin D toxicity, Thiazide diuretics, lithium

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22
Q

why do thiazide diuretics cause hypercalcaemia

A

they promote potassium and magnesium excretion but inhibit calcium excretion

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23
Q

familial hypocalciuric hypercalcaemia

A
  • autosomally dominant inherited condition caused by mutations in the CASR gene
  • Biologically characterised by moderate hypercalcaemia but inappropriate levels of PTH and urinary calcium
  • PTH levels are normal and calcium in the urine is low
  • rarey ever causes any symptoms and is usually an incidental finding and requires no treatment
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24
Q

sarcoidosis

A

causes hypercalcemia due to the uncontrollable synthesis of 1,25- dihydroxyvitamin D3 (CALCITRIOL) by macrophages

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25
Q

saying for remembering the symptoms of hypercalcaemia

A

stones, groans, bones and psychiatric overtones

26
Q

symptoms of hypercalcaemia

A 
ACUTE= thirst, dehydration, confusion, polyuria 
CHRONIC=  Myopathy, nephrolithiasis, osteoporosis, abdominal pain, pancreatitis, nephrogenic diabetes insidious
27
Q

why does hypercalcaemia cause nephrogenic diabetes insipidus

A

because Calcium is a competitive inhibitor of ADH

28
Q

primary hyperparathyroidism

A

overactivity of the parathyroid gland causing the excessive production of PTH, high PTH and High Calcium (BUT PTH CAN BE INNAPROPRIATLEY NORMAL)

29
Q

causes of primary hyperparathyroidism

A
  • most commonly caused by a benign adenoma
  • more rarely caused by parathyroid hyperplasia associated with MEN 1 and MEN2A Syndromes
  • even more rarely caused by a parathyroid carcinoma
30
Q

diagnosis of primary hyperparathyroidism

A
  • Raised PTH, Raised Calcium, increased urinary calcium excretion
  • Sestimibi scan to plan for surgery
31
Q

treatment of acute hypercalcaemia

A
  • 0.9% NaCl 4-6 litres over 24 hours to treat the dehydration
  • Loop diuretics (which diurese calcium) but only after rehydration
  • Bisphosphonates= but work over 2-3 days so not useful acutely
  • In life-threatening scenarios IV calcitonin but this has to be used with extreme caution as it can cause deadly hypocalcaemia
32
Q

definitive management for primary hyperparathyroidism

A

Parathyoidectomy (but only if indicated)

33
Q

indications for surgery

A

end organ damage caused by hypercalcaemia, very high serum calcium (greater than 2.85mmol/l), under age 50, EGFR less than 60ml/min

34
Q

end organ damage caused by hypercalcaemia

A
  • osteitis fibosa et cystica= skeletal disorder resulting in loss of bone mass and the weakening of bones caused by peri-trabecular fibrosis
  • gastric ulcers
  • renal stones
  • osteoporosis
  • salt and pepper sign of skull= tiny well-defined lucencies in the skull vault caused by the resorption of trabecular bone
35
Q

hypercalcaemia caused by malignancy

A

RAISED CALCIUM AND ALP BUT LOW PTH BECAUSE OF NEGATIVE FEEDBACK

36
Q

investigations for hyperclacaemia caused by malignancy

A

X-rays, CT, MRI, isotope bone scan

37
Q

secondary hyperparathyroidism

A

is not a disease it is the normal physiological increase in the secretion of PTH in response to low levels of calcium (most commonly caused by renal failure which causes renal diuresis) but chronic secondary hyperparathyroidism can cause tertiary hyperparathyroidism

38
Q

tertiary hyperparathyroidism

A

persistent hyperparathyroidism despite treating the underlying cause of the secondary hyperparathyroidism

39
Q

biochemistry of primary hyperparathyroidism

A
  • HIGH PTH
  • HIGH CA
  • LOW PHOSPHATE
  • HIGH CALCITRIOL
40
Q

biochemistry of secondary hyperparathyroidism

A
  • HIGH PTH
  • LOW CA
  • HIGH PHOSPHATE
  • LOW CALCITRIOL
41
Q

biochemistry of tertiary hyperparathyroidsim

A
  • HIGH PTH
  • HIGH CA
  • HIGH PHOSPHATE
  • LOW CALCITRIOL
42
Q

kidneys are responsible for

A

excreting phosphate and converting cholecalciferol to calcitriol which is why phosphate is high and calcitriol is low in secondary hyperparathyroidism because the kidneys cannot function properly, despite the increase in PTH, calcium cannot rise in response because calcitriol isn’t made so it can’t be absorbed through the gut

43
Q

treatments of secondary hyperparathyroidism

A
  • treat the underlying chronic kidney disease, calcitriol, restrict dietary intake of phosphate
44
Q

treatment of tertiary hyperparathyroidism

A

calcitriol, and restrict dietary intake of phosphate, if refractory to medical management parathyroidecotmy could be considered

45
Q

hypocalcaemia is most commonly caused by

A

hypoparathyroidism (particularly post-thyroidecomty)

46
Q

hyocalcaemia can also be caused by

A
  • vitamin D deficiency (malnutrition, malabsorption)
  • chronic renal failure
  • pancreatitis
  • hyperventilation
  • rhabdomyolysis
  • loop diuretics and bisphosphonates
  • congenital absence (digeourge syndrome)
  • hypoamgnaesaemia
47
Q

symptoms of hypocalcaemia

A
  • neuronal hyperactivity- parasethesia, hyperactive reflexes, muscles spasms, seizures, prolongation of the QT interval, tetany, muscle weakness
48
Q

signs seen in hypocalcaemia

A
  • chovsteks sign= percussion of the facial nerve causes twitching of the facial muscles
  • trousseau sign= carpopedal spasm when the upper arms is compressed by a blog pressure cuff
49
Q

management of hypoparathyroidism

A

calcium and vitamin D supplementation

50
Q

why does hypomagnasaemia cause hypoparathyroidism

A

calcium release from cells is dependant on magnesium, in mageniusm deficiency, intra-cellular calcium is high so PTH release is inhibited and skeletal and muscle receptors become less sensitive to PTH

51
Q

management of hypomaganseamia causing hypocalcaemia

A

calcium and magnesium replacement

52
Q

causes of hypomagnasaemia

A
  • alcohol, drugs (thiazide diuretics and PPIS), pancreatitis, malabsorption
53
Q

psuedophyoparathyroisim

A

generic defect caused by mutation of GNAS 1 gene

- low calcium but PTH concentrations are elevated because of PTH resistance

54
Q

presentation of psudeohypoparathyroidism

A
  • bone abnormalities (mcewan albright)
  • obesity
  • subcutaneous clarification
  • learning disability
  • brachydactyly (4th metacarpal)
55
Q

pseudo-psuedohypoparathyoidism

A

is the exact same as pseudo-hypoparathyroidism but patients have NORMAL CALCIUM

56
Q

rickets and osteomalacia

A

same disease except rickets is the name given when it occurs in children

57
Q

what is rickets/ osteomalacia

A

deficiency in calcium and phosphorous causing weakened bones

58
Q

people with chronic renal disease may have high

A

25-hydroxyvitaminD3 levels so have to check there 1,25-hydroxyviatmin D3 levels

59
Q

long term consequences of vitamin D deficiency

A
  • demineralisation/ fractures
  • osteomalacia/ rickets
  • malignant especially of the colon
60
Q

X-linked hypophosphataemia

A

vitamin D resistant rickets

  • PHEX or FGF23 gene mutation
  • FGF 23 regulates phosphate levels in plasma and is secreted by osteocytes in response to calcitriol
  • low phosphate but high vitamin D
  • treat with phosphate and Vitamin D supplementation

Endocrinology - Rachel Doohan Y5 (28 decks)

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