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Year 2 Endocrinology > Calcium and Phosphate regulation > Flashcards

Calcium and Phosphate regulation Flashcards

1
Q

Interaction between PTH and vitamin D

A

PTH increases serum Ca2+ , increases Ca2+ reabsorption in bone and causes kidney to absorb Ca2+. It regulates the production of active vitamin D. Inactive vitamin D is from liver and undergoes 1a hydroxylation under control of PTA increasing the serum Ca2+ by increasing Ca2+ reabsorption by the gut

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2
Q

What is PTH’s effect on phosphate

A

PTH inhibits Na, Phosphate cotransporter so phosphate can’t be reabsorbed into the proximal convoluted tubule cell from the urine

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3
Q

What is the effect of FGF23 on phosphate regulation

A

It inhibits reabsorption of phosphate in the kidney by inhibiting the NNa+/PO43- cotransporter so more phosphate lost in urine and it also inhibits calcitriol production so less vit D so less phosphate reabsorption from the gut

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4
Q

What does FGF23 stand for

A

Fibroblast growth factor 23 from osteocytes

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5
Q

What receptor on the parathyroid cells that respond to calcium called

A

Calcium sensin receptor

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6
Q

High calcium causes what effect on parathyroid cells

A

Inhibits PTH secretion - makes sense as pth increases serum calcium

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7
Q

What is the effect of low calcium in ECF on parathyroid cells

A

Ca not bound to receptor, no inhibition, PTH secreted and PTH action in body leads to increased Ca in ECF

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8
Q

How to obtain Vitamin D

A

Vitamin D from diet (ergocalciferol)
Sunshine (cholecalciferol)
these form inactive vitamin D

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9
Q

What is the problem with 25 OH-D3?

A

Not useful in calcium metabolism, inactive calcium

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10
Q

What regulates the second hydroxylation of vitamin D (from the inactive form)

A

negative feedback by PTH in the kidney

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11
Q

What enzyme makes 25 OH-D3 into 1,25 (OH)2 D3?

A

renal 1 alpha hydroxylase enzyme

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12
Q

What are stages in the production of vitamin D that can go wrong and cause vitamin D deficiency?

A
  1. malabsorption or dietary insufficiency
  2. lack of sunshine
  3. liver disease - coeliac disease, inflam bowel disease
  4. renal disease - renal failure, liver failure
  5. receptor defects - rare
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13
Q

What is the effect of high EC calcium on the nerve and skeletal muscle excitability

A

Ca2+ blocks Na+ influx so less membrane excitability

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14
Q

What is the effect of high EC calcium on the nerve and skeletal muscle excitability

A

enables greater Na+ influx so more membrane excitability

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15
Q

What are signs and symptoms of hypocalcaemia?

A 
Parasthesia (pins and needles, hands mouth feet and lips)
Convulsions
Arrhythmias
Tetany
(Sensitises excitable tissues;
muscle cramps/tetany, 
tingling)
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16
Q

What is chvostek’s sign? How do you test for it

A

When you tap the facial nerve just below the zygomatic arch and a positive response leads to a twitching of facial muscles. This indicates a neuromuscular irritability due to hypocalcaemia

17
Q

What is trousseau’s sign? How do you test for it?

A

Inflation of BP cuff for several minutes to induce a carpopedal spasm - neuromuscular irritability due to hypocalcaemia

18
Q

What are causes of hypocalcaemia?

A
  • Vitamin D deficiency
  • Low PTH levels = hypoparathyroidism
  • Surgical – neck surgery, auto-immune, magnesium deficiency
  • PTH resistance eg pseudohypoparathyroidism
  • Renal failure
  • Impaired 1a hydroxylation -> decreased production of 1,25(OH)2D3
19
Q

What are signs or symptoms of hypercalcaemia?

A
  • 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)
    (reduced neuronal excitability; atonal muscles)
20
Q

What are causes of hypercalcaemia?

A
  • Primary hyperparathyroidism
  • Malignancy: tumours or metastases often secrete a PTH-like peptide
  • Conditions with high bone turnover (hyperthyroidism, Paget’s disease of bone – immobilised patient)
  • Vitamin D excess (rare)
21
Q

If Ca2+ drops a bit, what is the normal physiological response

A

PTH is made, leading to calcium going up. Then negative feedback and PTH goes down again

22
Q

What is a diagnostic sign of primary hyperparathyroidism

A

High calcium, high PTH showing no negative feedback. Raised calcium. Low phosphate. Raised (unsuppressed PTH)

23
Q

What is a diagnostic sign of hypercalcaemia of malignancy

A

Raised calcium but a suppressed PTH (no issue with parathyroid, but a cancer in bone releasing calcium)

24
Q

What is the definition of vitamin D deficiency

A

Lack of mineralisation in bone

25
Q

What does vitamin D deficiency result in?

A

‘softening’ of bone, bone deformities, bone pain; severe proximal myopathy

26
Q

What is vitamin D deficiency in children called? What is it called in adults

A

Children: rickets
Adults: osteomalacia

27
Q

What is the diagnostic sign of secondary hyperparathyroidism?

A

Low Ca2+ but high PTH. PTH increases to try normalise serum calcium but there is vitamin D deficiency

28
Q

What are biochemical findings in vitamin D deficiency?

A
  • Plasma [25(OH)D3] usually low
  • Plasma [Ca2+] low (may be normal if 2o hyperparathyroidism has developed)
  • Plasma [PO43-] low
  • [PTH] high (2o hyperparathyroidism)
29
Q

Do you measure active vitamin D to assess body vit D stores

A

No. It’s too much faff

30
Q

Treatment for vitamin D deficiency in patients with normal renal function

A

Give 25 hydroxy vitamin D (25 (OH) D)
Patient converts this to 1,25 dihydroxy vitamin D (1,25 (OH)2 D) via 1a hydroxylase
Ergocalciferol 25 hydroxy vitamin D2
Cholecalciferol 25 hydroxy vitamin D3

31
Q

Treatment of vitamin D in patients with renal failure

A

inadequate 1a hydroxylation, so can’t activate 25 hydroxyl vitamin D preparations
Give Alfacalcidol - 1a hydroxycholecalciferol

32
Q

What does vitamin D excess lead to?

A

Can lead to hypercalcaemia and hypercalciuria due to increased intestinal absorption of calcium

33
Q

What can be a reason for vitamin D excess?

A
  • excessive treatment with active metabolites of vitamin D eg Alfacalcidol
  • granulomatous diseases such as sarcoidosis, leprosy and tuberculosis (macrophages in the granuloma produce 1a hydroxylase to convert 25(OH) D to the active metabolite 1,25 (OH)2 D

Year 2 Endocrinology (21 decks)

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