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1B calcium dysregulation Flashcards

(43 cards)

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1
Q

Describe the hormonal control in the increase of serum calcium

A
  • Vitamin D
    • Synthesised in skin or intake via diet
  • Parathyroid Hormone (PTH) (secreted by parathyroid glands)
  • Main regulators of calcium (and phosphate) homeostasis via actions on kidney, bone and gut
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2
Q

Describe the hormonal control in the decrease of serum calcium

A
  • Calcitonin (secreted by thyroid colloid)

Can reduce calcium acutely, but no negative effect if parafollicular cells are removed eg thyroidectomy

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3
Q

What are the 2 types and sources of Vitamin D?

A
  • Vitamin D2 (ergocalciferol) from diet e.g. oily fish
  • Vitamin D3 (cholecalciferol) synthesised in skin when exposed to sunlight
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4
Q

How is vitamin D3 made and both D2 and D3 metabolised?

A

Vitamin D becomes activated after undergoing both hydroxylation steps

1,25(OH)2 cholecalciferol is aka calcitriol - the active form of vitamin D

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5
Q

What is serum 25-OH cholecalciferol a good indicator of?

A

Body vitamin D status, as calcitriol is difficult to measure in blood

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6
Q

How does calcitriol regulate its own synthesis?

A

It decreases transcription of 1 alpha hydroxylase - negative feedback

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7
Q

What are the effects of calcitriol on the bone?

A

Increases Ca2+ reabsorption by binding to calcitriol receptors on osteoblasts which release OAFs → Osteoclasts > osteoblasts (ONLY AT LOW SERUM CALCIUM)

  • in normal serum calcium, calcitriol works to increase bone formation → osteoblasts > osteoclasts
  • n.b. Increase of reabsorption of Ca2+ from the bones itself INTO the blood stream
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8
Q

What are the effects of calcitriol on the kidney?

A

Increases Ca2+ and phosphate reabsorption into blood by kidney from urine

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9
Q

What are the effects of calcitriol on the gut?

A

Increases Ca2+ and phosphate absorption from food into blood

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10
Q

What are the effects of PTH on the bone?

A

Increases reabsorption of calcium from bone

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11
Q

What are the effects of PTH on the kidney?

A
  • Increases calcium reabsorption from kidney from urine
  • Increases phosphate excretion
  • Increases 1-alpha-hydroxylase activity → Increases calcitriol synthesis
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12
Q

What are the effects of PTH on the gut?

A

Through increase in 1-alpha-hydroxylase activity and through increased calcitriol synthesis, there is increase in Ca2+ and phosphate absorption from gut.

So PTH doesn’t directly affect gut

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13
Q

What is the overall affect of PTH on plasma calcium levels?

A

Overall increase

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14
Q

What is the overall affect of PTH on plasma phosphate levels?

A

Net loss → the phosphate loss from the kidney tends to outweigh the phosphate reabsorption from the gut.

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15
Q

What specifically happens when PTH interacts with bone?

A
  • PTH binds to PTH receptor on osteoblasts (cells that build bone)
  • Stimulates osteoblasts to make osteoclast activating factors (OAFs) e.g. RANKL (receptor activator of nuclear factor kappa-B ligand)
  • Osteoclasts (cells that consume bone) are switched on and dissolve bone, releasing calcium into the blood stream
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16
Q

How does phosphate reabsorption in kidneys happen?

A
  • Phosphate is reabsorbed via sodium-phosphate co-transporter - this also results in less sodium excretion in urine
  • Increased phosphate loss in urine would lower serum phosphate levels
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17
Q

How does PTH work in phosphate reabsorption?

A
  • PTH inhibits renal phosphate reabsorption by inhibiting these transporters
  • In primary hyperparathyroidism, serum phosphate is low due to increased urine phosphate excretion
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18
Q

What is FGF23 and what does it do?

Study These Flashcards
A
  • Fibroblast Growth Factor 23 (hormone) is derived from bone
  • Also inhibits phosphate reabsorption in kidneys by inhibiting Na+/PO43- co-transporters
  • Also inhibits calcitriol synthesis causing less phosphate absorption from gut from food
19
Q

What is hypocalcaemia?

Study These Flashcards
A

Low serum calcium

20
Q

How does hypocalcaemia affect action potential generation?

Study These Flashcards
A
  • There’s low extracellular calcium so this enables greater Na+ influx as there’s less competition for Na+ to move across membrane
  • Means MORE membrane excitability
21
Q

What are clinical symptoms of hypocalcaemia?

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A
  • It sensitises excitable tissues
  • Paraesthesia (tingling) of hands, mouth, feet, lips
  • Convulsions- fits
  • Arrhythmias- unusual heart rhythms
  • Tetany- contract muscles but can’t relax again
  • Mnemonic- CATs go numb
22
Q

What is Chvostek’s sign?

Study These Flashcards
A
  • You tap facial nerve just below zygomatic arch (cheekbone)
  • Since there’s more membrane excitability, you get a positive response of twitching of facial muscles
  • Indicates neuromuscular irritability due to hypocalcaemia
23
Q

What is Trousseau’s sign?

Study These Flashcards
A
  • Inflate a BP cuff for several minutes around patient’s arm
  • This induces carpopedal (fingers) spasm and muscles contract and can’t relax again (tetany)
  • This is due to neuromuscular irritability due to hypocalcaemia
24
Q

What are 2 causes of hypocalcaemia?

Study These Flashcards
A
  • Vitamin D deficiency
  • Low PTH levels- hypoparathyroidism
25
What are causes of vitamin D deficiency?
1. Malabsorption or dietary insufficiency 2. Inadequate sun exposure 3. Liver disease 4. Renal disease 5. Vit D receptor defects (rare)
26
What are the consequences of vitamin D deficiency?
- There is a lack of bone mineralisation causing 'soft bones' - In children they get rickets (bowing of bones) - In adults, bones are more formed so they get osteomalacia (predisposed to fractures and proximal myopathy (especially thigh muscles))
27
What are four causes of low PTH levels?
- Surgical- neck surgery could have damaged parathyroid glands - Auto-immune- one of the most common reasons - Magnesium deficiency- it's needed to make PTH - Congenital (agenesis of parathyroid gland i.e. it doesn't develop in embryo- rare)
28
What are causes of hypercalcaemia?
- Primary hyperparathyroidism (commonest) - Malignancy - Vitamin D excess (rare)
29
How does primary hyperparathyroidism cause hypercalcaemia?
- Too much PTH - Usually due to a parathyroid gland adenoma - No negative feedback- high PTH, but high calcium
30
What malignancies can be seen in hypercalcaemia?
- Bony metastases produce local factors to activate osteoclasts - Certain cancers (e.g. squamous cell carcinomas) secrete PTH-related peptide that acts at PTH receptors
31
What is the relationship between PTH and calcium?
- If calcium falls, parathyroid glands sense this and release more PTH - If we have too much calcium, there's negative feedback and parathyroid glands don't release PTH
32
What happens in primary hyperparathyroidism?
- If we get a parathyroid adenoma it produces too much PTH - Calcium increases but there's no negative feedback to PTH due to autonomous PTH secretion from adenoma
33
What is the biochemistry of primary hyperparathyroidism?
- High calcium - High PTH (not suppressed by hypercalcaemia negative feedback) - Low phosphate- increased renal phosphate excretion (inhibition of sodium-phosphate transporter in kidney)
34
What is the treatment of primary hyperparathyroidism?
Parathyroidectomy is the main treatment
35
What are the risks of untreated primary hyperparathyroidism?
- Osteoporosis due to osteoclasts constantly breaking down bone - Renal calculi (stones) - Psychological impact of hypercalcaemia- mental function, mood
36
What happens in secondary hyperparathyroidism?
- It's a normal physiological response to hypocalcaemia - Calcium will be low or normal - PTH will be high (hyperparathyroidism) **secondary** to the low calcium - This is different from primary hyperparathyroidism where calcium is high
37
What are the causes of secondary hyperparathyroidism?
- Most common cause is vitamin D deficiency due to diet, reduced sunlight - Less common, due to renal failure- can't make calcitriol in renal failure
38
What is the treatment for secondary hyperparathyroidism in people with and without kidney failure?
Vitamin D replacement
39
What vit D replacement can patients with normal renal function receive?
- 25 hydroxy vitamin D- inactive vit D - They convert it to 1,25 dihydroxy vitamin D via 1alpha hydroxylase - Can give ergocalciferol (25 hydroxy vitamin D2) or cholecalciferol (25 hydroxy vitamin D3) - Can get at chemists/supermarket
40
What vit D replacement can patients with renal failure get?
- There's inadequate 1alpha hydroxylation, so can't activate 25 hydroxy vitamin D - We give them **alfacalcidol** - 1alpha hydroxycholecalciferol- this is active vitamin D - Reserved for renal failure patients so needs to be prescribed
41
What happens in tertiary hyperparathyroidism?
- It's rare - When you have chronic renal failure you can't make calcitriol so you have chronic vit D deficiency - Parathyroid glands start secreting more PTH to make up for drop in calcitriol so calcium doesn't become low - One or more of these glands enlarge (hyperplasia) to the point where they can't be switched off - Autonomous PTH secretion happens causing hypercalcaemia
42
What is the treatment for tertiary hyperparathyroidism?
Parathyroidectomy
43
What happens in hypercalcaemia due to malignancy?
- There is high calcium - There is low or suppressed PTH

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