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Year 2 - ENDO > 12 - calcium and phosphate regulation > Flashcards

12 - calcium and phosphate regulation Flashcards

1
Q

Where are the parathyroid glands and what do they produce?

A

4 of them , located behind the thyroid gland

produce parathyroid hormone (PTH)

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2
Q

What ion does PTH regulate?

A

calcium

PTH increases serum calcium

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3
Q

State the 3 functions of PTH

A
  • interacts the kidney to absorb calcium (excrete less calcium)
  • promotes calcium release from the bones
  • regulates the conversion of inactive vitamin D (25-hydroxy-vitamin-D) -> active vitamin D (calcitriol)
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4
Q

What is the action of active vitamin D (calcitriol)?

A

it promotes calcium reabsorption from the gut and bones -> increases serum Ca

(and increases absorption of phosphate from the gut)

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5
Q

How is phosphate reabsorbed in the kidney?

A

in the proximal convoluted tubule, phosphate is reabsorbed using sodium-transport co-transporters - phosphate leaves the nephron tubules indenters the cells

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6
Q

Describe the mechanism by which PTH affects the mechanism of phosphate reabsorption in the kidney nephron

A

inhibits the sodium-transport co-transporters

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7
Q

Describe the excretion and serum levels of phosphate in a person with primary hyperparathyroidism

A

increased phosphate excretion.

low serum phosphate due to inhibition of phosphate reuptake at the proximal convoluted tubule.

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8
Q

What is FGF 23? Where does it come from?

A

Fibroblast growth factor 23 from osteocytes

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9
Q

In which 2 ways does FGF 23 inhibit the reabsorption of phosphate?

A

1- via the sodium-phosphate cotransporter

2- inhibits calcitriol (calcitriol assists phosphate reabsorption from gut).

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10
Q

Describe the mechanism of regulation of PTH secretion

A

Parathyroid cells have calcium-sensing receptors on their surface.

When you have high calcium in the ECF, calcium binds to these receptors.
THIS INHIBITS PTH SECRETION - when your Ca is high, PTH is inhibited.

When you have a low serum calcium in the ECF, less calcium binds to these receptiors -> less PTH inhibition -> more PTH release -> mechanisms to increase serum Ca.

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11
Q

What are 2 ways in which the body can get vitamin D?

A
  • from the diet (ergocalciferol)

- via UVB light

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12
Q

Describe the mechanism by which we can get vitamin D via UVB light and the role of PTH in this process

A
  • UVB light converts 7-dehydrocholesterol -> cholecalciferol
  • In the liver, cholecalciferol is converted to 25-OH-D3 (BIOLOGICALLY INACTIVE)
  • 1α-hydroxylase in the KIDNEY converts 25-OH-D3 -> 1,25-(OH)2-D3 (BIOLOGICALLY ACTIVE)
    NOTE: ^this conversion is stimulated by PTH.
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13
Q

What is the role of vitamin D in calcium (and phosphate) homeostasis (4)

A

Active vitamin D:

  • promotes Ca and phosphate reabsorption in the gut
  • promotes Ca maintenance in the bones
  • increases renal Ca reabsorption
  • produces negative feedback on PTH (calcitriol receptors on PT cells).

(calcitriol and vitamin D work together to increase Ca2+)

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14
Q

State the causes of vitamin D deficiency (5)

A
  • A poor diet and malabsorption
  • not enough sunlight exposure/too much sun cream
  • Liver and renal diseases of ANY CAUSE - because both organs are critical for vitamin D production
  • vitamin D resistant rickets – vitamin D production is normal, but there are receptor defects (rare)
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15
Q

HOW DO CHANGES IN EXTRACELLULAR CALCIUM AFFECT NERVE AND SKELETAL MUSCLE EXCITABILITY?
(remember generation of an AP in nerves/skeletal muscle requires Na+ influx across cell membrane)

A
  • HIGH EC calcium (HYPERcalcaemia) = Ca2+ blocks Na+ influx, so LESS membrane excitability
  • LOW EC calcium (HYPOcalcaemia) = enables GREATER Na+ influx, so MORE membrane excitability

(i.e. Na+ and Ca2+ compete)

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16
Q

State the normal range for serum calcium

A

2.2–2.6 mmol/L

17
Q

How can we assess for hypocalcaemia in a patient?

A

using Chvostek’s sign and Trousseau’s sign

assess for neuromuscular irritability

18
Q

What are the general signs and symptoms for hypocalcaemia?

A
  • involve sensitisation of excitable tissues (muscle cramps/tetany, tingling) - nerve hyperexcitability
  • Paraesthesia (hands, mouth, feet lips), convulsions (EXTREME), arrhythmias and tetany may occur
    (PCAT)
19
Q

How do you test a patient for Chvostek’s sign?
What is a positive indicator response?
What does it indicate?

A
  • Tap the facial nerve just below the zygomatic arch (cheek bone)
  • A positive response will involve twitching of the facial muscles
  • This indicates neuromuscular irritability due to hypocalcaemia
20
Q

How do you test a patient for Trosseau’s sign?
What is a positive indicator response?
What does it indicate?

A
  • You inflate a BP cuff and leave it like that for several minutes
  • This induces carpopedal spasm = neuromuscular irritability (hand contracts and can’t be relaxed)
21
Q

State the causes of hypocalcaemia

A

• Vitamin D deficiency
• hypoparathyroidism
—–> surgical causes (neck surgery)
—–> auto-immune
—–> magnesium deficiency (needed for PTH)
• PTH resistance e.g. pseudohypoparathyroidism (receptor defects)
• Renal failure: Impaired 1a hydroxylation -> decreased production of 1,25(OH)2D3

22
Q

Describe the effect of hypercalcaemia on neuronal excitability.

A

It reduces neuronal excitability and you get atonal muscles

23
Q

What are the main signs and symptoms of hypercalcaemia?

A

Stones, abdominal moans and psychic groans

Stones – renal effects
• Polyuria + polydipsia
• Nephrocalcinosis = deposition of calcium in the kidneys (can cause renal colic)
Abdominal moans – GI effects
• Anorexia, nausea, constipation, pancreatitis, dyspepsia
Psychic groans – CNS effects
• Fatigue, depression, impaired concentration, altered mentation, coma

24
Q

State the causes of hypercalcaemia (4)

A
  • 1° hyperparathyroidism
  • Malignancy – tumours/metastases often secrete a PTH-like peptide
  • Conditions with high bone turnover (hyperthyroidism, Paget’s disease of bone – immobilised patient)
  • Vitamin D excess (rare)
25
Q

Give the normal physiological response that would occur when serum Ca2+ falls

A

PTH increases
-> Increased calcium reabsorption from the kidney
-> Increased production of calcitriol
-> Increased calcium reabsorption from bones
PTH exerts negative feedback, to stop production of PTH and maintain normal serum calcium

26
Q

Describe how you would differentiate between primary hyperparathyroidism and malignancy causing hypercalcaemia.

A

(look at PTH levels)
In 1° hyperparathyroidism there is no negative feedback because the parathyroid adenoma will be producing PTH autonomously
• PTH = HIGH
• Plasma Calcium = HIGH
In malignancy, the negative feedback will be intact as it is due to increased bone turnover due to bony metastases
• PTH = LOW
• Plasma Calcium = HIGH

27
Q

What is the treatment if primary hyperparathyroidism?

A

parathyroidectomy

28
Q

Define Vitamin D Deficiency

A

lack of mineralisation in bone

29
Q

What does vitamin D deficiency cause? State some symptoms.

A 
Lack of bone mineralisation 
Softening of bone (can lead to bowing of the legs)
Bone deformities 
Bone pain
Severe proximal myopathy
30
Q

What are the different names for vitamin D deficiency in children and adults?

A

Children – Rickets

Adults – Osteomalacia

31
Q

What are the serum levels in secondary hyperparathyroidism? What is the usual cause?

A

PTH is high, secondary to low Ca2+

usually due to vitamin D deficiency

32
Q

Describe what happens in tertiary hyperparathyroidism

A
  • Initial chronic low plasma calcium ion concentration
  • The parathyroid gland is being massively stimulated for a long time
  • Eventually, the PTH becomes autonomous and stops responding to negative feedback

(causes an increased plasma calcium ion level - similar to 1° hyperparathyroidism)

33
Q

PRIMARY and TERTIARY hyperparathyroidism are associated with _________

A

HYPERCALCAEMIA

34
Q

Describe the biochemical finding in vitamin D deficiency

A 
(very difficult to measure calcitriol)
Plasma 25-hydroxycholecalciferol = LOW
Plasma Calcium = LOW 
Plasma Phosphate = LOW 
Plasma PTH = HIGH (2° hyperparathyroidism stimulated by the hypocalcaemia)
35
Q

Describe the treatment of vitamin D deficiency in the case of normal renal function.

A

Give 25-hydroxy vitamin D
This can be in the form of:
• Ergocalciferol = 25-hydroxy vitamin D2)
• Cholecalciferol = 25-hydroxy vitamin D3

36
Q

Describe the treatment of vitamin D deficiency in the case of renal failure.

A

Alfacalcidol = 1-hydroxycholecalciferol (active vitamin D)

37
Q

What can vitamin D excess lead to?

A

Hypercalcaemia and hypercalciuria (due to increased intestinal absorption of calcium)

38
Q

What can vitamin D excess result from?

A
  • Excessive treatment with active metabolites of vitamin D, as in patients with chronic renal failure (wrong dose)
  • Granulomatous disease – granulomatous tissue has 1-hydroxylase so it can be a source of ectopic calcitriol

Year 2 - ENDO (20 decks)

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