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Year 2 - endocrinology > Calcium and phosphate regulation > Flashcards

Calcium and phosphate regulation Flashcards

1
Q

What do osteoclasts and osteoblasts do?

A

Osteoblasts produce bone

Osteoclasts break bone down

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2
Q

What are the 3 functions of PTH?

A
  • PTH instructs the kidney to absorb calcium
  • PTH also promotes calcium release from the bones
  • PTH regulates the conversion of inactive vitamin D (25-hydroxy-vitamin-D) to active vitamin D (calcitriol)
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3
Q

How is phosphate concentration regulated?

A

In the nephron (PCT), phosphate is reabsorbed using sodium-transport co-transporters – phosphate leaves the nephron lumen and enters the cells
- PTH inhibits this

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4
Q

What happens to phosphate excretion in primary hyperparathyroidism?

A

Increase in phosphate excretion. These patients have a low serum phosphate due to inhibition of phosphate reuptake at the proximal convoluted tubule.

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5
Q

How does FG23 affect reabsorption of phosphate?

A
  • Via the sodium-phosphate cotransporter

- Inhibits calcitriol (calcitriol assists phosphate reabsorption from gut).

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6
Q

How do parathyroid cells detect calcium?

What happens if calcium level is high?

A

They 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.

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7
Q

Where is vitamin D obtained from?

A
  • Diet (ergocalciferol)

- Via UVB light (converts 7-dehydrocholesterol -> cholecalciferol (vit D3))

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8
Q

What happens to cholecalciferol in the liver and is the product made active?

A

Cholecalciferol is converted to 25-OH-D3 – biologically inactive

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9
Q

What happens to 25-OH-D3 in the kidneys?

A

It is converted into 1,25-(OH)2-D3 which is buologically active. This is timulated by PTH

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10
Q

What are the roles of vit D?

A
  • Promotes calcium reabsorption from the gut and bones
  • It increases renal Ca reabsorption, and produces negative feedback on PTH
  • Helps phosphate reabsorption from the gut
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11
Q

What are the causes of vitamin D deficiency?

A
  • A poor diet and malabsorption (e.g. coeliac disease)
  • Lack of sun /too much sun cream,
  • Liver and renal diseases
  • A rare cause is vitamin D resistant rickets – vitamin D production is normal, but there are receptor defects (recessive, rare)
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12
Q

What is the normal serum range for calcium?

A

2.2–2.6 mmol/

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13
Q

What is chvostek’s sign and its use?

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
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14
Q

What is trousseau’s sign and its use?

A
  • Also assesses for neuromuscular irritability in a patient with hypocalcaemia
  • 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)
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15
Q

What are the causes of hypocalcaemia?

A
  • Vitamin D deficiency
  • Low PTH levels = hypoparathyroidism
  • Can be surgical causes (neck surgery), auto-immune or magnesium deficiency (needed for PTH)
  • PTH resistance e.g. pseudohypoparathyroidism (patient can make PTH but have receptor defects)
  • Renal failure: Impaired 1a hydroxylation -> decreased production of 1,25(OH)2D3
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16
Q

What are the effects of hypercalcaemia?

A

Stones (renal effects of hypercalcaemia)

  • Polyuria & thirst
  • Nephrocalcinosis, renal colic, chronic renal failure
Abdominal moans (GI effects of hypercalcaemia)
- Anorexia, nausea, dyspepsia, constipation, pancreatitis
Psychic groans (CNS effects of hypercalcaemia)
- Fatigue, depression, impaired concentration, altered mentation, coma (usually >3mmol/L)
17
Q

How can hypocalcaemia be assessed for?

A

using chvostek’s sign and trousseau’s sign

18
Q

What are the causes of hypercalcaemia?

A
  • Primary 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)
19
Q

What is primary hyperparathyrodism?

Pattern of hormone and calcium/phosphate levels?

Treatment?

A
  • Tumour in the parathyroid causes a large increase in PTH secretion
  • Because it is a tumour it is unlikely to be regulated by the normal negative feedback
  • It will continue to produce large amounts of PTH leading to an increased plasma calcium ion concentration
  • Raised calcium, low phosphate, raised PTH
  • Treatment is parathryroidectomy
20
Q

What would hypercalcaemia of malignancy look like?

How can you differentiate between hypercalcaemia of malignancy and primary hyperparathyroidism?

A

Patients present with high calcium, but this is not due to a parathyroid adenoma making too much PTH. There is -ve feedback as serum calcium rises, PTH falls (nothing wrong with the parathyroid gland). High calcium and supressed PTH. This is how you differentiate between the two causes.

21
Q

What does vit D deficiency lead to?

A
  • Lack of mineralisation in bone
  • Softening of bone, bone deformities, bone pain; severe proximal myopathy
  • In children –> rickets
  • In adults –> osteomalacia
22
Q

What is secondary hyperparathyroidism?

A
  • Usually due to vitamin D deficiency -> low calcium
  • Some people have low plasma calcium concentration for a variety of other reasons such as renal failure
  • Renal failure leads to loss of calcium in the urine which will stimulate the parathyroid to release PTH
  • PTH will do its best to maintain the plasma calcium ion level by increasing
23
Q

What is 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
24
Q

What are the biochemical findings in vit D deficiency?

*calcium, phosphate, PTH levels

A
  • Plasma [25(OH)D3] usually low (we don’t measure 1,25 (OH)2 D to assess body vitamin D stores
  • Plasma [Ca2+] will be low (may be normal if secondary hyperparathyroidism has developed)
  • Plasma [PO43-] will be low (due to reduced gut absorption)
  • [PTH] high (secondary hyperparathyroidism)
25
Q

How is vit D deficiency treated in patients with and without renal failure?

A

NORMAL

  • Give 25 hydroxy-vitamin D as can covert themselves
  • Can be given as ergocalciferol or cholecalciferol

RENAL FAILURE

  • Inadequate 1a hydroxylation (can’t activate 25-hydroxyl vitamin D preparations)
  • Give Alfacalcidol (1a-hydroxycholecalciferol) which is active
26
Q

What can cause vit D excess?

A
  • Excessive treatment with active metabolites of vitamin D e.g. Alfacalcidol (e.g. wrong dose)
  • 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 – VERY RARE
27
Q

What can vit D excess lead to?

A

Hypercalcaemia and hypercalciuria due to increased intestinal absorption of calcium

28
Q

Which types of hyperparathyroidisms lead to hypercalcaemia?

A

Primary and tertiary

Year 2 - endocrinology (18 decks)

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