Calcium and phosphate regulation Flashcards
Describe how phosphate levels are regulated at the levels of the kidneys?
PTH and FGF23 both inhibit the phosphate sodium transporter found on the apical membrane so increase excretion in urine. FGF23 also inhibits calcitriol in the gut so reduces phosphate reabsorption in the gut.
How is PTH secretion regulated?
High Ca binds to receptor and inhibits secretion of PTH from parathyroid cells. Low Ca means its not detected at the receptor and thus PTH secretion isn’t inhibited.
Describe production of calcitriol?
7 dehydrocholectrol is converted into vitamin d3 or cholecalciferol by UV light. Ergocalciferol is taken in via diet. Both ergocalciferol and cholecalciferol are converted to 25 OH D3 in the liver. Then this is converted into calcitriol (1,25 OHD3) by 1 alpha hydroxylase in the kidneys.
Describe the actions of calcitriol?
Increases renal reabsorption of calcium, increases reabsorption in the gut and negatively feedbacks with PTH.
Describe causes of vitamin D deficiency?
Lack of UV light, malabsorption and dietary deficiency, liver disease, renal disease and receptor defects? ,
How do changes in calcium concentration affects nerve activity?
High calcium blocks Na influx so reduces nerve excitability, low calcium has opposite effect. Normal range Is 2.2 to 2.6mmol/L. Hypocalaemia causes parathesis, convulsions, arrhythmia and tetany.
What are 2 signs for hypocalcaemia?
Chvosteks sign…tap facial nerve below zygomatic arch and you get twitching. Trousseau’s sign…inflation of blood pressure cuff for several minutes causes carpopedal spasm.
What are the causes of hypocalcaemia?
Vitamin D deficiency, hypoparathyroidism, PTH resistance and renal failure due to impaired 1 alpha hydroxylase.
What are the causes of hypercalcaemia?
Hyperparathyroidism, vitamin D excess, conditions with high bone turnover e.g. Paget’s, malignancy (tumours can secrete a PTH like peptide).
What at the symptoms of hypercalcaemia?
Gallstones, renal colic, renal failure, anorexia, nausea, constipation, pancreatitis, fatigue, depression, coma.
How do you differentiate between hypercalcaemia due to primary hypoparathyroidism and hypocalcaemia of malignancy.
Both have high calcium but in PHP you get it driven by high PTH whereas with malignancy the high calcium inhibits PTH secretion.
What is vitamin D deficiency state?
Lack of mineralisation of bone, causing softening of the bone, increased risk of fracture, bone pain, and proximal myopathy. In children its called rickets and in adults called osteomalasia.
How do you differentiate between primary and secondary hyperparathyroidism?
With primary you get high PTH driving high calcium and no negative feedback is present. With secondary a low calcium concentration is corrected by elevating the levels of PTH?
What are the biochemical findings in vitamin D deficiency?
Low 25OH Vit D3, low calcium, low phosphate and high PTH (secondary hyperparathyroidism).
How do you treat a vitamin D deficiency?
In patients with normal renal function give cholecalciferol or ergocalciferol and their 1 alpha hydroxylase will convert these into calcitriol. In patients with compromised renal function give Alfacalcidol - 1a hydroxycholecalciferol as they lack 1 alpha hydroxylase so can’t activate 25 hydroxyl vitamin D preparations.
