Calcium and phosphate regulation

Question 1

Calcium homeostasis diagram.

PTH, vit D interaction.

Answer 1

Question 2

Phosphate regulation at proximal convoluted tubule🍆🍆🍆🍆🍆 diagram.

Answer 2

Question 3

How is PTH regulated?

Answer 3

ECF [Ca2+] negative feedback

High - Ca2+ binds to receptor, less PTH release. Vice versa.

Question 4

What is the net effect of FGF23 secretion?

Answer 4

look up

Question 5

Diagram showing vit D synthesis + its physiological effects.

Answer 5

Question 6

Diagram showing causes of vit D deficiency.

Answer 6

Question 7

How does high/low ECF Ca2+ effect nerve + skeletal muscle excitability?

Answer 7

High - less membrane excitability. Na+ influx blocked.

Low - more membrane excitability. Greater Na+ influx.

Question 8

Define hypocalcaemia?

Answer 8

serum Ca2+ < 2.2mmol/L

Question 9

What are the signs and symptoms of hypocalcaemia?

Answer 9

oParasthesia(hands, mouth, feet , lips)

oConvulsions

oArrhythmias

oTetany

Question 10

What is Chvostek’s sign for hypocalcaemia?

Answer 10

Tap facial nerve below zygomatic arch. +ve response = twitching of facial muscles - indicates neuromuscular irritability.

Question 11

What is Trousseau’s sign?

Answer 11

Inflate BP cuff for several minutes. Carpopedal spasm - neuromuscular irritability.

Question 12

outline potential causes of hypocalcaemia.

Answer 12

• 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

Question 13

What are the clinical features of hypercalcaemia?

Answer 13

•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)

Question 14

What are the primary causes of hypocalcaemia?

Answer 14

• 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)

Question 15

What causes primary hyperparathyroidism?

Answer 15

-ve feedback loop not functional. Autonomous PTH secretion despite hypercalcaemia.

Question 16

What are the characteristics of primary hyperparathyroidism?

Answer 16

• Raised calcium
• Low phosphate
• Raised (unsuppressed) PTH

Question 17

What is hypercalcaemia of malignancy? What are the characteristics of these?

Answer 17

High bone turnover due to tumour releasing ca2+.

Raised Ca2+, low PTH due to appropriate physiological response to raised Ca2+

Question 18

What is the consequence of vitamin D deficiency?

What is it called in children/adults?

Answer 18

·“softening” of bone, bone deformities, bone pain; severe proximal myopathy.

Children - rickets

Adults - osteomalacia.

Question 19

How is primary hyperparathyroidism treated?

Answer 19

parathyroidectomy

Question 20

What is secondary hyperparathyroidism?

Answer 20

Raised PTH due to need to normalise Ca2+

Question 21

Outline the biochemical findinds in Vitamin D deficiency

(Plama 25OHD3, plasma Ca2+, plasma PO43-, PTH)

Question 22

How is vitamin D deficiency treated?

Answer 22

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

Question 23

What can Vitamin D excess cause?

Answer 23

hypercalcaemiaandhypercalciuriadue to increased intestinal absorption of calcium

Question 24

What can cnause Vitamin D excess?

Answer 24

·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