calcium and phosphate regulation Flashcards
summarise calcium homeostasis *
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
describe phosphate regulation
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
describe teh regulation of PTH secretion *
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
describe the synthesis of Vit D *
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)
what are the effects of calcitriol *
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
what are the causes of vitamin D deficiency *
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
hypercalcaemia effect on afferent nerve and skeletal musclee excitability *
high extracellular ca blocks na influx = less membrane excitability because less able to generate AP
hypocalcaemia effect on affernet nerve and skeletal muscle excitability *
low ca enables greater na influx = more membrane excitability because not much competition with Ca = generate more AP easily
clinical features of hypocalcaemia *
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)
what is hypocalcaemia *
ca below 2.2mmol/L
what is chvostek’s sign *
tap facial nerve below zygomatic arch
positive response is twitching of the facial muscles - indicates neuromuscualr irritability due to hypocalcaemia
wat is trousseau’s sign *
inflate bp cuff for several minutes = induce carpopedal spasm = neuromuscular irritability due to hypocalcaemia
what are the causes of hypocalcaemia *
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
what is hypercalcaemia *
Ca >2.6mmol/L
what are the signs and symptoms of hypercalcaemia *
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
what are the causes of hypercalcaemia *
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
what is the physiological pt response to low ca *
increase
what are the ca and pth levels in primary hyperparathyroidism and why *
adenoma makes too much pth = increase in ca
no negative feedbacj because autonomous PTH prroduction = pth stays high
therefore both ca and pth high
what is teh physiological pth response to high ca 8
pth reduces under -ve feedback
what is the phosphate level in primary hyperthyroidism *
low
pth (which is igh) inhibits phosphate resorption from the kidney = more lost in urine
what is the ca and pth levels in hypercalcaemia of malignancy and why *
malignancy in bone = high ca
pth is switched off by -ve feedback so pth low
what is vit D deficiency *
lack of mineralisation in bone
what are the consequences of vit D deficiency *
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
what is the treatment of hyperparathyroidism *
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)
