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

Calcium and Phosphate Regulation Flashcards

1
Q

What are the organs and hormones involved in regulating serum calcium?

A

Vitamin D which enters the liver and is converted to Calcidiol which enters the kidney where it is converted to calcitriol before acting on the bones and small intestine.

PTH (parathyroid hormone) is released from the parathyroid glands and acts on the kidneys and bones.

PTH
Vitamin D
Calcidiol (25-OH-D)
Calcitriol (1,25-(OH)2-D)

Parathyroid glands
Liver
Kidneys
Bones
Small intestine
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2
Q

Where is PTH released from, where does it act, and what effects does it have on those tissues?

A
  • Released from the parathyroid glands
  • Acts on bone, increasing release of calcium and phosphorus
  • Acts on kidneys, increasing calcitriol formation and decreasing excretion of calcium
  • Regulates the enzyme that converts calcidiol to calcitriol so activates it when it acts on the kidney
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3
Q

Where does vitamin D travel to once absorbed, where is it converted and into what?

A

Enters the body and enters the liver
- converted to 25-OH-D aka calcidiol in the liver
Then enters the kidneys
- converted to 1,25-(OH)2-D aka calcitriol
Calcitriol is the active form of vitamin D

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4
Q

What is the name of the active form of vitamin D, where is it released from, where does it act, and what is its effects on those tissues?

A
  • Calcitriol (1,25-dihydroxy-vitaminD - 1,25-OH-D)
  • Released from kidneys after conversion from calcidiol
  • Acts on small intestine, increasing absorption of dietary calcium
  • Acts on bone, releasing calcium and phosphorus
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5
Q

What do the effects of both vitamin D (calcitriol) and PTH lead to?

A

Increased serum calcium

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6
Q

How does PTH influence phosphate regulation?

A

Phosphates are reabsorbed from the urine in the proximal convoluted tubule by the Na+/PO4(3-) co-transporter
- PTH inhibits the co-transporter thus reducing phosphate reabsorption/increasing phosphate excretion

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7
Q

What is FGF23 and what effects does it have?

A

FGF23 is Fibroblast growth factor 23 and it comes from osteocytes

  • causes phosphate excretion in the urine as it also inhibits reabsorption, like PTH
  • it also inhibits calcitriol thus reducing phosphate reabsorption in the gut

Overall reduces phosphate reabsorption in kidneys and gut

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8
Q

How is PTH secretion regulated?

A

Regulated by levels of Ca2+ in the extracellular fluid (ECF)
Parathyroid gland cells have Ca2+ receptors at one end (apical membrane) and PTH-containing vesicles at the opposite end (basolateral membrane)
- When Ca2+ is high in the ECF, Ca2+ ions bind to the receptors which inhibits PTH release from the parathyroid gland
- When Ca2+ is low in the ECF, Ca2+ does not bind to the receptors thus there is no inhibition of PTH release so PTH is released in an attempt to raise the serum calcium levels

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9
Q

How is vitamin D produced in its different forms?

A
  • In the skin, UVB light stimulates conversion of 7-dehydrocholesterol to vitamin D3 (cholecalciferol)
  • Vitamin D2 comes from the diet
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10
Q

Where is vitamin D converted to its inactive and active forms and what enzyme is involved in the kidney which PTH stimulates?

A
  • Vitamin D3 and D2 are both converted to 25-OH-D3 in the liver, the inactive form
  • 25-OH-D3 is converted to 1,25-(OH)2-D3 in the kidneys by renal 1alpha-hydroxylase, the active form
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11
Q

What are the 4 main effects of calcitriol (1,25-OH-D3) after its been produced in the kidneys?

A
  • Increase Ca2+ absorption in the gut
  • Ca2+ maintenance in the bone
  • Negative feedback on PTH
  • Increased renal Ca2+ reabsorption (PCT)
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12
Q

What are the 4 causes of vitamin D deficiency?

A

1) Malabsorption or dietary insufficiency
- aren’t taking it in or not absorbing it

2) Lack of UVB light
- Can be unfortunate country, not much sunlight
- Can be old and not get out much
- Can be due to ethnicity, some require more sunlight to make sufficient vitamin D

3) Liver disease
- may be unable to convert vitamin D to calcidiol so vitamin D chain is broken

4) Renal disease
- may be unable to make the final conversion of calcidiol to calcitriol due to general kidney disease or specific 1alpha-hydroxylase deficiency/insufficiency

5) Receptor defects
- defective receptors on target tissues (small intestine, gut etc)

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13
Q

Summarise the causes of vitamin D deficiency?

A
  • Diet
  • Lack of sunlight
  • GI malabsorption (coeliac disease, inflam. bowel disease)
  • Renal/Liver failure
  • Vitamin D receptor defects (autosomal recessive, rare, resistant to vitamin D treatment)
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14
Q

Why is vitamin D deficiency re-emerging as a problem in the UK?

A

Mainly due to inadequate diet and lack of sunlight

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15
Q

What is needed in nerves/skeletal muscle to generate an action potential?

A

Requires Na+ influx across the cell membrane

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16
Q

How is Na+ influx affected by high extracellular (EC) Ca2+, how does this affect membrane excitability, and what is the name for high EC Ca2+?

A

Less Na+ influx
Less excitability

If there is high extracellular Ca2+, it blocks Na+ influx so the membrane becomes LESS excitable
- This is hypercalcaemia

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17
Q

How is Na+ influx affected by low extracellular (EC) Ca2+, how does this affect membrane excitability, and what is the name for low EC Ca2+?

A

Greater Na+ influx
Greater excitability

If there is low extracellular Ca2+, there is no blockade of Na+ influx and actually enables GREATER Na+ influx so the membrane becomes MORE excitable
- this is hypocalcaemia

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18
Q

What are the signs and symptoms of hypocalcaemia?

A

Paresthesia (tingling, itching sensation) (hands, mouth, feet, lips)
Convulsions
Arrhythmias
Tetany

Sensitises excitable tissues

  • muscle cramps/tetany
  • tingling
19
Q

What is the normal range of serum calcium?

A

2.2-2.6 mmol/L

20
Q

What are the two signs we look for that appear in hypocalcaemic patients?

A

Chvostek’s sign

Trousseau’s sign

21
Q

How do you test for Chvostek’s sign and what does this indicate?

A

Tap facial nerve just below zygomatic arch (high and lateral on the cheek)
- Positive response = twitching of the facial muscles

This indicates neuromuscular irritability due to hypocalcaemia

22
Q

How do you test for Trousseau’s sign, what does this indicate, and what is the caution about testing it?

A

Inflation of BP cuff for several minutes induces CARPOPEDAL spasm

  • this is a sort of clawing of the hand as a form of induced tetany so they can’t relax their hand
  • indicates neuromuscular irritability due to hypocalcaemia

This test is quite painful and uncomfortable for the patient so as soon as the sign appears you release the blood pressure cuff

23
Q

What are the causes of hypocalcaemia?

A

Vitamin D deficiency
Low PTH levels (hypoparathyroidism)
- surgical - neck surgery (damage/removal of parathyroid glands)
- Auto-immune
- Magnesium deficiency
PTH resistance (called pseudohypoparathyroidism)
Renal failure
- impaired 1alpha-hydroxylation leads to decreased production of 1,25-(OH)2-D3

24
Q

Why is PTH resistance named pseudohypoparathyroidism and what is the distinguishing feature from ‘real’ hypoparathyroidism?

A

Patient has low calcium because PTH can’t act on PTH receptors as they’re defective so can’t reabsorb calcium from small intestine/bones.

  • When you check PTH it is high as the parathyroid glands are fine but the problem lies with the receptors
  • PTH would be low in ‘real’ hypoparathyroidism
25
Q

What are the signs and symptoms of hypercalcaemia?

A

Overall reduced neuronal excitability - atonal muscles

Can be remembered as ‘stones, abdominal moans, and psychic groans’

Stones - renal effects
- polyuria and thirst
- nephrocalcinosis (calcium deposition resulting in kidney stones), renal colic (trying to get rid of the stone), chronic renal failure (if stones left untreated)
Abdominal moans
- anorexia, nausea, dyspepsia, constipation, pancreatitis
Psychic groans
- Fatigue, depression, impaired concentration, altered mentation, coma (usually >3mmol/L)

26
Q

What are the causes of hypercalcaemia?

A
  • Primary hyperparathyroidism - too much PTH
  • Malignancy - tumours/metastases, often secrete PTH-like peptide which works like PTH
  • Conditions with high bone turnover (hyperthyroidism, Paget’s disease of bone, immobilised patient)
  • Vitamin D excess (rare)
27
Q

What happens in primary hyperparathyroidism?

A

Ca2+ goes up and usually would have a negative feedback effect on PTH release, reducing it.
If you have an adenoma in the parathyroid glands, there is no negative feedback effect so PTH continues to be produced result in continuously rising Ca2+ levels

28
Q

What test results should you see in a patient with primary hyperparathyroidism?

A
  • Raised calcium
  • Raised (unsuppressed) PTH
  • Low phosphate (as a result of the unsuppressed PTH
29
Q

What happens in hypercalcaemia of malignancy?

A

Usually due to metastases in bone

  • Causes high Ca2+ due to the metastases but the negative feedback loop is still intact so PTH is low
  • this distinguishes it from primary hyperparathyroidism
30
Q

What test results would you expect to see in patients with hypercalcaemia of malignancy?

A
  • Raised calcium
  • Suppressed PTH
  • Normal phosphate (potentially high with continually suppressed PTH)
31
Q

What is the definition of vitamin D deficiency state?

A

Lack of mineralisation in bone

32
Q

What does vitamin D deficiency result in?

A

‘Softening’ of bone
Bone deformities
Bone pain
Severe proximal myopathy

33
Q

What is vitamin D deficiency called in children and adults?

A

Children - Rickets

Adults - Osteomalacia

34
Q

What happens in primary hyperparathyroidism and what is the treatment?

A

High Ca2+ and high PTH
- no negative feedback due to autonomous PTH secretion despite hypercalcaemia

Treatment is parathyroidectomy (surgical removal of the gland)

35
Q

What happens in secondary hyperparathyroidism?

A

Low Ca2+ (usually due to vitamin D deficiency)

- PTH increases above normal levels to try to normalise serum calcium

36
Q

What would be the biochemical findings in vitamin D deficiency?

A
  • Plasma calcidriol (25-OH-D) usually low
  • Plasma Ca2+ low (may be normal if secondary hyperparathyroidism has developed)
  • Plasma phosphate (PO4(3-)) low
  • PTH high (secondary hyperparathyroidism)
37
Q

What are the states of serum calcium in primary and secondary hyperparathyroidism?

A

Primary - hypercalcaemia (Ca2+ rises to try and inhibit PTH but fails)

Secondary - low to normal calcaemia

38
Q

How is vitamin D deficiency treated in patients with normal renal function?

A

Give 25-OH-D (calcidriol replacement)

- Patient then converts this, as by the natural process, to 1,25 dihydroxy vitamin D (calcitriol) via 1alpha-hydroxylase

39
Q

What are the names of the 25-hydroxy-vitaminD2 and 25-hydroxy-vitaminD3?

A

Ergocalciferol - 25-OH-D2

Cholecalciferol - 25-OH-D3

40
Q

How is vitamin D deficiency treated in patients with renal failure?

A

These patients have inadequate 1alpha-hydroxylase so can’t activate 25-OH-D2/3 preparations

  • Give Alfacalcidol - 1alpha-hydroxycholecalciferol
  • Very potent, not available over the counter
41
Q

What can vitamin D excess (intoxication) cause?

A

Can lead to:
- Hypercalcaemia
- Hypercalciuria
due to increased intestinal absorption of calcium

42
Q

What can cause vitamin D excess (intoxication)?

A
  • Excessive treatment with active metabolites of vitamin D e.g. alfacalcidol (wrong prescription basically)
  • Granulomatous diseases such as sarcoidosis, leprosy and tuberculosis
43
Q

How do granulomatous diseases cause vitamin D excess?

A

Macrophages in the granuloma produce 1alpha-hydroxylase to convert calcidriol to calcitriol which is active and more potent thus providing a new source of active vitamin D causing excess vitamin D effects
- case reports of patients with sarcoidosis who have become hypercalcaemic due this phenomenon

LCRS Year 2 - Endocrinology (21 decks)

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