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Year 2 - LCRS - Endocrinology > Calcium and Phosphate Regulation > Flashcards

Calcium and Phosphate Regulation Flashcards

1
Q

1,25 (OH)2 Vitamin D3 - other names

A

Calcitriol

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2
Q

What is the effect of PTH?

A

Increases serum Ca2+

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3
Q

How does PTH increase serum Ca2+?

A
  • Bone: binds to PTHRs on osteoblasts which release OAFs (incl RANKL) that activate osteoclasts to break down bone and release Ca2+ and PO43- into the bloodstream.
  • Kidneys: Binding of PTH causes increased reabsorption of Ca2+ and increased excretion of PO43-
    Also: increases the production of 1-alpha-hydroxylase which increases calcitriol concentration and causes increased absorption of phosphate and calcium in the small intestine.
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4
Q

In what form is calcium found in bones?

A

hydroxyapatite crystals (containing calcium and phosphate)

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5
Q

How is phosphate regulated?

A
  • in the gut and in the kidneys
  • FGF23 -> inhibits the Na+/PO43- cotransporter in cells of proximal convoluted tubule -> reduces reabsorption, increases excretion in urine
  • FGF-23 also has a negative effect on calcitriol and there is less phosphate absorption in the kidney

FGF-23 reduces the levels of phosphate in the blood.

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6
Q

How is phosphate reabsorbed?

A
  • in the proximal convoluted tubule cells in the kidney

- via a sodium phosphate cotransporter which is inhibited by FGF23 and PTH

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7
Q

Where is FGF 23 derived from?

A

Bone (from osteocytes)

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8
Q

What are the serum phosphate levels in primary hyperparathyroidism?

A
  • low because there is a lot of phosphate excretion via urine
  • PTH inhibits sodium phosphate cotransporter
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9
Q

How are parathyroid cells regulated?

A
  • high serum calcium -> binding of Ca2+ to calcium receptors inhibits PTH release
  • low serum calcium, less binding -> less inhibition -> more PTH release
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10
Q

What are the effects of calcitriol?

A
  • increased Ca absorption in the gut
  • Ca2+ maintenance in bone
  • negative feedback on PTH
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11
Q

What are the 2 sources of vitamin D?

A
  • ergocalciferol (Vitamin D2) from the diet

- 7-dehydrocholesterol is turned into VitaminD3 (cholecalciferol) via UVB light

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12
Q

What are the 5 main causes of Vitamin D deficiency?

A
  1. Malabsorption or dietary insufficiency (e.g. coealiac disease, IBD)
  2. Lack of access to UVB light / lack of sunlight
  3. Liver disease / liver failure
  4. Renal disease / renal failure
  5. Receptor defects (very rare, autosomal recessive, resistant to vitamin D treatment)
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13
Q

What is the role of the liver with regards to vitamin D?

A
  • stores inactive precursor
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14
Q

HOW DO CHANGES IN EC CALCIUM AFFECT NERVE AND SKELETAL MUSCLE EXCITABILITY?

A
  • To generate an AP in nerves/skeletal muscle requires Na+ influx across cell membrane
  • HIGH ec calcium (HYPERcalcaemia) = Ca2+ blocks Na+ influx, so LESS membrane excitability
  • LOW ec calcium (HYPOcalcaemia) = enables GREATER Na+ influx, so MORE membrane excitability
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15
Q

What are the signs and symptoms of HYPOcalcameia?

A
  • Ca2+ below normal range (2.2 - 2.6 mmol/L)
  • sensitises excitable tissues (muscle cramps/ tetany, tingling)
  • parasthesia (= pins and needles, hands, mouth, feet, lips)
  • convulsions & seizures if it drops very fast
  • arrythmias
  • tetany

-> CATs go numb

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16
Q

What is chvosteks sign? What does it indicate?

A
  • Tap facial nerve just below zygomatic arch
  • Positive response = twitching of facial muscles
  • Indicates neuromuscular irritability due to hypocalcaemia
17
Q

What is trousseaus sign?

A

Inflation of BP cuff for several minutes induces carpopedal spasm = neuromuscular irritability due to hypocalcaemia

18
Q

What are some causes of hypocalcaemia?

A
  • Vitamin D deficiency
  • Low PTH levels = hypoparathyroidism
    Surgical – neck surgery
    Auto-immune (AI destruction of PT glands is possible)
    Magnesium deficiency
  • PTH resistance eg pseudohypoparathyroidism
  • Renal failure
    Impaired 1a hydroxylation
    decreased production of 1,25(OH)2D3
19
Q

What are the signs and symptoms of hypercalcaemia?

A
  • moans, bones, stones and groans
  • reduced neuronal excitability; atonal muscles.
  • stones = renal effects (polyuria and thirst (not known why) nephrocalcinosis, renal cholic, chronic renal failure
  • abdominal moans = GI effects (anorexia, nausea, dyspepsia, constipation, pancreatitis) -> gut has slowed down
  • psychic groans = CNS effects (fatigue, depression, impaired concentration, altered mentation, Coma (usually >3mmol/L)
20
Q

What are the signs and symptoms of hypercalcaemia?

A
  • moans, bones, stones and groans
  • reduced neuronal excitability; atonal muscles.
  • stones = renal effects (polyuria and thirst (not known why) nephrocalcinosis, renal cholic, chronic renal failure
  • abdominal moans = GI effects (anorexia, nausea, dyspepsia, constipation, pancreatitis) -> gut has slowed down
  • psychic groans = CNS effects (fatigue, depression, impaired concentration, altered mentation, Coma (usually >3mmol/L)
21
Q

What are some causes of hypercalcaemia?

A
  • Parathyroid adenoma
  • some tumors secrete a PTH-like peptide
    (these first 2 are the cause of hypercalcaemia 90% of the time)
  • conditions with high bone turnover (hyperthyroidism, Paget’s disease of bone - immobilised patient)
  • vitamin D excess (rare) -> would be e.g. if someone is taking tablets containing calcium
22
Q

What happens in primary hyperparathyroidism?

A
  • there is an adenoma of the PTG that produces PTH inappropriately and increases serum calcium.
  • there is NO negative feedback: Autonomous PTH secretion DESPITE hypercalcaemia
23
Q

Blood biochemistry in primary hyperparathyroidism

A
  • Raised calcium
  • Low phosphate
  • Raised (unsuppressed) PTH
24
Q

Hypercalcaemia of malignancy

A
  • raised calcium
  • suppressed PTH

(in HC of malignancy there are two reasons why Ca2+ might be increased”
- tumor secretes a PTH like peptide.
- in bony metastases: cancer spreads to bone and causes calcium release
(treat with bisphosphonates)

25
Q

What does vitamin D deficiency cause?

A
  • Definition: lack of mineralisation in bone
  • Results in “softening” of bone, bone deformities, bone pain; severe proximal myopathy.
  • Rickets in children
  • osteomalacia in adults
26
Q

Treatment of primary hyperparathyroidism?

A

Surgery - parathyroidectomy

27
Q

Secondary Hyperparathyroidism

A
  • PTH increases appropriately to try and increase serum calcium levels
  • e.g. vitamin D deficiency causing hypocalcaemia
28
Q

What are the biochemical findings in vitamin D deficiency?

A
  • low 25-hydroxy-vitamin D3
  • plasma Ca2+ low (may be normal if secondary hypreparathyroidism has developed)
  • low PO43- in plasma
  • high PTH in secondary hyperparathyroidism
29
Q

How is vitamin D measured in the blood?

A
  • generally measure 25-hydroxy Vitamin D

- calcitriol is very difficult to measure because you would have to have special tubes and with special foil etc.

30
Q

How do you treat vitamin D deficiency?

A 
In patients with normal renal function:
- 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
Gives as tablets.

In patients with renal failure
- inadequate 1a hydroxylation, so can’t activate 25 hydroxyl vitamin D preparations
Give Alfacalcidol - 1a hydroxycholecalciferol

31
Q

Excess vitamin D

A
  • intoxication
  • Can lead to hypercalcaemia and hypercalciuria due to increased intestinal absorption of calcium
  • Can occur as a result of:
    • 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 - LCRS - Endocrinology (18 decks)

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