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endo - yr2 > calcium and phosphate regulation > Flashcards

calcium and phosphate regulation Flashcards

1
Q

summarise calcium homeostasis *

A

Parathyroid hornone is made by the parathyroid glands

PTH increase calcium resorption from bone and kidney

PTH inccrease calcitriol production in kidney - increases Ca absorption in SI

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2
Q

describe phosphate regulation

A

phosphate reabsorbed from urine throug Na/K cotransporter - this transporter inibited by PTH and fibroblast growth factor 23 (FGF23) = phosphate loss via urine

FGF23 also inibits calcitriol (calcitriol increase phosphate absorption from SI) = reduced phosphate absorption from SI

therefore high PTH and FGF23 = low serum phosphate

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3
Q

describe teh regulation of PTH secretion *

A

high ca = more binding to calcium-sensing receptor

receptor activation = inhibition of PTH secretion

low ca = less receptor activation = more PTH stimulation to increase Ca conc

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4
Q

describe the synthesis of Vit D *

A

in skin 7-dehydrocholestrol is precurser - UVB light convert this to vit D3 (cholecalciferol).

or vit D2 from diet (ergocalciferol)

they go into liver and are hydroxylated once = 25 OH D3 - inactive d3

renal a1 hydroxylase is stimulated by PTH - does 2nd hydroxylation = calcitriol (1,25 OH D3)

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5
Q

what are the effects of calcitriol *

A

Ca phosphorus and mg absorption in the gut

Ca maintenance in bone - increase osteoblast activity

increased renal ca reabsorption and decreased phos reabsorbtion in the kidney

-ve feedback on PTH - dont want more active vitamin D made

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6
Q

what are the causes of vitamin D deficiency *

A

no UVB light - from sun, eg elderly dont go outside

malabsorption or dietry insufficiency - poverty, coeliac, inflammatory bowel disease

liver disease - cant store the inactive precursor

renal disease - cant do 2nd hydroxylation

receptor defects - rare, autosomal recessive, resistant to vit d treatment - vit D receptor rickets

anticonvulsants can increase vit d breakdown

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7
Q

hypercalcaemia effect on afferent nerve and skeletal musclee excitability *

A

high extracellular ca blocks na influx = less membrane excitability because less able to generate AP

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8
Q

hypocalcaemia effect on affernet nerve and skeletal muscle excitability *

A

low ca enables greater na influx = more membrane excitability because not much competition with Ca = generate more AP easily

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9
Q

clinical features of hypocalcaemia *

A

parasthesia - pins and needles in hands, mouth, feet, lips

Convulsions - seizures - if drop very low or quickly

Arrhythmias - heart needs ca to contract and conduct

Tetany - muscles contract and cant relax

(pneumonic - CATs go numb)

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10
Q

what is hypocalcaemia *

A

ca below 2.2mmol/L

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11
Q

what is chvostek’s sign *

A

tap facial nerve below zygomatic arch

positive response is twitching of the facial muscles - indicates neuromuscualr irritability due to hypocalcaemia

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12
Q

wat is trousseau’s sign *

A

inflate bp cuff for several minutes = induce carpopedal spasm = neuromuscular irritability due to hypocalcaemia

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13
Q

what are the causes of hypocalcaemia *

A

vut D deficiency

low PTH - hypoparathyroidism: neck surgery/injury (perminant or transient), autoimmune destruction of parathyroid glands, mg deficiency (needed for PTH release and production)

PTH resistance eg pseudohypoparathyroidism - make PTH but resistant

renal failure - impaired 1a hydroxylation = decreased active vit D

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14
Q

what is hypercalcaemia *

A

Ca >2.6mmol/L

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15
Q

what are the signs and symptoms of hypercalcaemia *

A

stones, abdominal moans and psychhic groans

stones- renal effects - dehydration therefore early have polyuria and thirst, then nephrocalcinosis (try to filter more ca = deposits in kidney, calcium stones ), renal colic (try to pass stones), chronic renal failure (because of undiagnosed stones damaging kidney), neprogenic diabetes insipidis

abdo moans - GI effects - gut slowed down = anorexia, nausea, dyspepsia (heart burn), constipation, pancreatitis, pruritis (itchy skin)

psychic groans - CNS - fatigue, depression, impaired concentration, confused, altered mentation when >3mmol/L

cardiac - dysrhythmia,short QT, hypertension

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16
Q

what are the causes of hypercalcaemia *

A

primary hhyperparathyroidism

malignancy - tumours/metastasis secreting Pth like peptide (ectopic cancer)

primary hyperparathyroidism and cancer make up 90% of the causes

conditions with igh bone turnover - hyperthyroidism, paget’s disease of bone - immobilised pt)

vit D excess - rare

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17
Q

what is the physiological pt response to low ca *

A

increase

18
Q

what are the ca and pth levels in primary hyperparathyroidism and why *

A

adenoma makes too much pth = increase in ca

no negative feedbacj because autonomous PTH prroduction = pth stays high

therefore both ca and pth high

19
Q

what is teh physiological pth response to high ca 8

A

pth reduces under -ve feedback

20
Q

what is the phosphate level in primary hyperthyroidism *

A

low

pth (which is igh) inhibits phosphate resorption from the kidney = more lost in urine

21
Q

what is the ca and pth levels in hypercalcaemia of malignancy and why *

A

malignancy in bone = high ca

pth is switched off by -ve feedback so pth low

22
Q

what is vit D deficiency *

A

lack of mineralisation in bone

23
Q

what are the consequences of vit D deficiency *

A

softening of bine

bone deformities - bones are bowed because cant take the weight of body

bone pain

severe proximal myopathy

in children = rickets

in adults = osteomalacia = fractures and pain - low bone mineral density

24
Q

what is the treatment of hyperparathyroidism *

A

1st give 2L of non-caffeine containing fluid a day - brings down ca

parathyroidectomy do ultrasound (anatomical) or sestamibi scan (functional scan - nuclear medicine taken up by over active thyroid gland)

25
Q

what are the ca and pth signs in secondary hyperparathyroidism and why *

A

ca low eg from vit d deficiency

pth increases to try to normalise serum ca - this is the normal -ve feedback repsonse

26
Q

what are the biochemical findings in vit d deficiency *

A

inactive 25 OH D3 low (dont measure active - difficult)

plasma ca adn phos low/possibly normal if secondary hyperparathyroidism has developed

plasma phosphate low - reduced gut absorption

pth conc high - trying to increase ca to reference range - increase by -ve feedback

27
Q

what is the treatment of vit d deficiency in pts with normal renal function *

A

give 25 OH D - inactive - patient can activate this in the kidney via 1a hydroxylase

the medication is ergocalciferol (25 OH D2) - IM injections

or cholecalciferol (25 OH D3)

28
Q

what is te treatment of vit d deficiency in pts with renal failure *

A

they have inadequate 1a hydroxylation so cant activate 25 hydroxyl vit D preparations

so give alfacalcidol - 1a hydroxycholecalciferol (active vit D)

29
Q

what are the causes of vit d excess *

A

excessive treatment with active metabolites eg alcalciferol

granulomatus disease eg sarcoidosis, leprasy and TB, macrophages in granuloma produce 1a hydroxylase to make active vit D

30
Q

what is the consequence of vit d excess *

A

hypercalcaemia and hypercalciuria - due to increased intestinal absorption of ca

31
Q

what are teh actions of pth *

A

increase ca reabsorption from the kidney and phosphate excretion

stimulat 1a hydroxylase to make active vit d

cause bone resorption to increase ca

32
Q

what are the risk factors for vitamin D deficiency *

A

if south asian - darker skin so need more prolongued skin exposure

live in uk - not much sun

if vegetarian - oily fish, red meat, liver and egg yolk are sources

33
Q

why would alkaline phosphtase be high with vit d *

A

alp is a marker of bone turnover - if it is high show bone working hard - trying to make more bone but cat because has no vit d and so no ca

34
Q

what does microscopic haematuria mean

A

cant see the blood by eye - need a microscope

35
Q

what is teh diagnosis if have high pth and ca but low phos *

A

primary hyperparathyroidism

high pth mean more ca is absorbed from bone, more vit d activation, more absorption of ca from kidney and more phosphate loss from kidney

36
Q

why is primary hyperparathyroidism found most commonly in post menopausal women

A

oestrogen has a protective effect on bone resorption - ie less bone resorption

37
Q

what is the cause of loin pain in primary hyperparathyroidism *

A

the hypercalcaemia - causes kidney stones

38
Q

what is the diagnosis if you have a high ca and suppressed pth *

A

cancer - skeletal metastises

acronym: bridget bardows kinky pink tights - breast, bhroncus, kidnye, prostate and thyroid cancers spread to bone

some cancers secrete pth related peptide - increase ca but not detected as normal pth

39
Q

when does pth related peptide increase physiologically

A

pregnancy - for baby and breast feeding

40
Q

how can primary hyperthyroidism cause osteoporosis *

A

it means hhigh pt which absorbes bone

also calcium accumulates aroundjoints causing pseudo gout

endo - yr2 (24 decks)

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