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Phase 1b - Endocrinology > Calcium Dysregulation > Flashcards

Calcium Dysregulation Flashcards

-> Function of endocrine glands: Summarise the function of the key endocrine glands, including the synthesis, regulation and physiological effects of their hormones. -> Endocrine disorders: Describe the clinical features and treatment options of endocrine disorders.

1
Q

What is the surrogate marker to measure inactive Vitamin-D?

A
  • 25-Hydroxy vitamin D
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2
Q

Which cells detect serum calcium in parathyroid gland?

A
  • G-coupled calcium sensing receptors on the parathyroid cells
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3
Q

What increases serum calcium & phosphate (2)?

A
  • Increase in Vitamin D (synthesised in skin or intake via diet)
  • Increase in parathyroid hormone (PTH) (secreted by parathyroid glands)
  • Main regulators of calcium & phosphate homeostasis via actions on kidney, bone & gut
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4
Q

What is the precursor molecule of pre-vitamin D3?

A

7-dehydrocholesterol

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5
Q

What is the precursor molecule of Vitamin D3?

A

Pre-Vitamin D3

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6
Q

Which enzyme catalyses the conversion of vitamin D3 to 25-hydroxycholecalciferol?

A
  • Hepatic 25-hydroxylase
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7
Q

Which enzyme catalyses the conversion of 25-hydroxycholecaliciferol to 1,25 dihydroxycholecaliciferol?

A
  • Renal 1-alpha hydroxylase
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8
Q

What are the effects of calcitriol (1,25 dihydroxycholecaliciferol / active form of vitamin D) (4)?

A
  • Increased osteoblast activity
  • Increased enterocyte calcium absorption (Calbindin-D expression)
  • Increased serum phosphate absorption
  • Increased renal calcium and phosphate reabsorption
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9
Q

What are the effects of PTH (6)?

A
  • Increased calcium resorption from bone
  • Increased dietary calcium absorption
  • Increased dietary phosphate absorption
  • Increased renal renal calcium reabsorption
  • Increased renal phosphate excretion
  • Increased 1-alpha-hydroxylase activity -> Increased renal vitamin D synthesis

Therefore increase in plasma [calcium].

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10
Q

What is the relationship between PTH and calcium ions?

A
  • There is an inverse relationship between calcium concentration and PTH production

Increased calcium concentration inhibits PTH release.

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11
Q

What is the normal physiological response to hypercalcaemia for PTH?

A
  • PTH decreases (suppressed)
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12
Q

Which transporter is responsible for phosphate renal reabsorption?

A
  • NPT2
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13
Q

What effects does PTH have on renal phosphate reabsorption?

A
  • Inhibits NPT2 transporter → Increase urine phosphate excretion
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14
Q

What effect does FGF-23 have on calcitriol?

A
  • Inhibits the synthesis of calcitriol
    • Less phosphate reabsorption from gut
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15
Q

What decreases serum calcium & phosphate (1)?

A
  • Increase in calcitonin (secreted by thyroid parafollicullar cells)
    • Can reduce calcium acutely, but no negative effect if parafollicular cells are removed
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16
Q

What are the clinical features of hypocalcaemia (4)?

Mnemonic - [CATs go numb]

A
  • Paraesthesia (hands, mouth, feet, lips, Chvostek’s sign - facial paraesthisia)
  • Convulsions
  • Arrhythmias
  • Tetany
17
Q

What are the causes of hypocalcaemia (4 PTH / 1 Vit D)?

A
  • Low PTH levels (Hypoparathyroidism):
    • Surgical - neck surgery
    • Autoimmune
    • Magnesium deficiency
    • Congenital
  • Low vitamin D levels (Deficiency):
    • Diet
    • UV light
    • Malabsorption
    • Impaired production (renal failure)
18
Q

What are the signs of hypercalcaemia (Stones (1), Moans (5) and Groans (5))?

A
  • Stones - renal effects:
    • Nephrocalcinosis (kidney stones and renal colic)
  • Abdominal moans - GI effects:
    • Anorexia
    • Nausea
    • Dyspepsia
    • Constipation
    • Pancreatitis
  • Psychic groans:
    • Fatigue
    • Depression
    • Impaired concentration
    • Altered mentation
    • Coma
19
Q

What are the causes of hypercalcaemia (3)?

A
  • Primary hyperparathyroidism
    • Excess production of PTH (parathyroid gland adenoma)
    • There is no negative feeadback (elevated production of PTH)
  • Malignancy
    • ​Bony metastases, produce local factors to activate osteoclast)
    • Certain cancer (squamous cell carcinoma), secrete PTH related peptide that acts at PTH receptors
  • Excess vitamin D
20
Q

What is the treatment for hypocalcaemia (2)?

A
  • Oral calcium
  • Vitamin D supplements
21
Q

What is the main cause of primary hyperparathyroidism?

A
  • Parathyroid adenoma
    • ​Elevated production of PTH
    • Calcium increases, however there is no negative feedback to PTH
22
Q

What is the biochemistry of primary hyperparathyroidism (3)?

A
  • High PTH
  • High calcium
  • Low phosphate - increased renal phosphate excretion (inhibition of NPT2)
  • Normal Vitamin D

Because the blood serum doesn’t require any additional calcium the production and conversion of vitamin D is down-regulated as a protective mechanism for the body. This is why over 60% of patients with primary hyperparathyroidism have a lower than normal vitamin D level.

23
Q

What is the main treatment of primary hyperparathyroidism?

A
  • Parathyroidectomy
24
Q

What are the associated risks of untreated primary hyperparathyroidism (3)?

A
  • Osteoporosis
  • Renal caliculi
  • Mental function & mood is impaired
25
Q

What is the biochemistry of secondary hyperparathyroidism (2)?

A
  • High PTH
  • Low serum calcium, physiological response to hypocalcaemia
26
Q

What are the common causes of secondary hyperparatyroidism?

A
  • Vitamin D deficiency
    • Common: Diet / Reduced sunlight
    • Less common: Renal failure
27
Q

What is the treatment of secondary hyperparathyroidism in patients without renal failure?

A
  • Vitamin D replacement
    • 25-hydroxy vitamin D

Patient converts this to 1,25 dihydroxy vitamin D via 1a hydroxylase

Ergocalciferol 25 hydroxy vitamin D2
Cholecalciferol 25 hydroxy vitamin D3

28
Q

What is the treatment for secondary hyperparathyroidism in patients with renal failure?

A
  • Alfacalcidol (1a hydroxycholecalciferol)

Due to nadequate 1-alpha hydroxylation

29
Q

What is the common cause of tertiary hyperparathyroidism?

A
  • Chronic renal failure
    • Parathyroid gland hyperplasia- autonomous PTH secretion causes hypercalcaemia
30
Q

What is the biochemistry of tertiary hyperparathyroidism (2)?

A
  • High PTH
  • High serum calcium
31
Q

Explain the biochemistry of tertiary hyperparathyroidism.

A
  • Occurs in chronic renal failure
  • Can’t make calcitriol
  • PTH increases (hyperparathyroidism)
  • Parathyroid glands enlarge (hyperplasia)
  • Autonomous PTH secretion causes hypercalcaemia
32
Q

What is the treatment for tertiaty hyperparathyroidism?

A
  • Parathyroidectomy
33
Q

What is Chvostek’s sign? What is it a sign of?

A
  • Twitching of the zygomatic arch
  • Sign of hypocalcaemia
34
Q

What is Trousseau’s sign? What is it a sign of?

A
  • Carpopedal spasm
  • Sign of hypocalcaemia

Phase 1b - Endocrinology (19 decks)

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