Calcium and phosphate regulation Flashcards
Calcium homeostasis diagram.
PTH, vit D interaction.
Phosphate regulation at proximal convoluted tubule🍆🍆🍆🍆🍆 diagram.
How is PTH regulated?
ECF [Ca2+] negative feedback
High - Ca2+ binds to receptor, less PTH release. Vice versa.
What is the net effect of FGF23 secretion?
look up
Diagram showing vit D synthesis + its physiological effects.
Diagram showing causes of vit D deficiency.
How does high/low ECF Ca2+ effect nerve + skeletal muscle excitability?
High - less membrane excitability. Na+ influx blocked.
Low - more membrane excitability. Greater Na+ influx.
Define hypocalcaemia?
serum Ca2+ < 2.2mmol/L
What are the signs and symptoms of hypocalcaemia?
oParasthesia(hands, mouth, feet , lips)
oConvulsions
oArrhythmias
oTetany
What is Chvostek’s sign for hypocalcaemia?
Tap facial nerve below zygomatic arch. +ve response = twitching of facial muscles - indicates neuromuscular irritability.
What is Trousseau’s sign?
Inflate BP cuff for several minutes. Carpopedal spasm - neuromuscular irritability.
outline potential causes of hypocalcaemia.
- Vitamin D deficiency
- Low PTH levels = hypoparathyroidism
Surgical – neck surgery
Auto-immune
Magnesium deficiency
- PTH resistance egpseudohypoparathyroidism
- Renal failure
Impaired 1ahydroxylation
decreased production of 1,25(OH)2D3
What are the clinical features of hypercalcaemia?
•Stones – renal effects
Polyuria & thirst
Nephrocalcinosis, renal colic, chronic renal failure
•Abdominal moans - GI effects
Anorexia, nausea, dyspepsia, constipation, pancreatitis
•Psychic groans - CNS effects
Fatigue, depression, impaired concentration, altered mentation, coma (usually >3mmol/L)
What are the primary causes of hypocalcaemia?
- Primary hyperparathyroidism
- Malignancy – tumours/metastases often secrete a PTH-like peptide
- Conditions with high bone turnover (hyperthyroidism, Paget’s disease of bone – immobilisedpatient)
- Vitamin D excess (rare)
What causes primary hyperparathyroidism?
-ve feedback loop not functional. Autonomous PTH secretion despite hypercalcaemia.
What are the characteristics of primary hyperparathyroidism?
- Raised calcium
- Low phosphate
- Raised (unsuppressed) PTH
What is hypercalcaemia of malignancy? What are the characteristics of these?
High bone turnover due to tumour releasing ca2+.
Raised Ca2+, low PTH due to appropriate physiological response to raised Ca2+
What is the consequence of vitamin D deficiency?
What is it called in children/adults?
·“softening” of bone, bone deformities, bone pain; severe proximal myopathy.
Children - rickets
Adults - osteomalacia.
How is primary hyperparathyroidism treated?
parathyroidectomy
What is secondary hyperparathyroidism?
Raised PTH due to need to normalise Ca2+
Outline the biochemical findinds in Vitamin D deficiency
(Plama 25OHD3, plasma Ca2+, plasma PO43-, PTH)
How is vitamin D deficiency treated?
Normal renal function -
- Give 25 hydroxyvitamin D (25 (OH) D)
- Patient converts this to 1,25 dihydroxyvitamin D (1,25 (OH)2D) via 1ahydroxylase
Ergocalciferol25hydroxyvitamin D2
Cholecalciferol25hydroxyvitamin D3
Renal failure -
- inadequate1ahydroxylation, so can’t activate 25 hydroxyl vitamin D preparations
- GiveAlfacalcidol - 1ahydroxycholecalciferol
What can Vitamin D excess cause?
hypercalcaemiaandhypercalciuriadue to increased intestinal absorption of calcium
What can cnause Vitamin D excess?
·excessive treatment with active metabolites of vitamin D egAlfacalcidol
·granulomatous diseases such as sarcoidosis, leprosy and tuberculosis (macrophages in the granuloma produce 1ahydroxylase to convert 25(OH) D to the active metabolite 1,25 (OH)2D
