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Y2 ENDOCRINOLOGY > Calcium dysregulation > Flashcards

Calcium dysregulation Flashcards

1
Q

what are the two main regulators of calcium and phosphate via the kidney, bone and gut?

A

vitamin D and parathyroid hormone (PTH)

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2
Q

Outline the process of vitamin D metabolism

A

D3 made in the skin in response to sunlight. D2 taken in the diet and transported to liver. First hydroxylation via 25 hydroxylase forming 25(OH) cholecalciferol, second hydroxylation via 1-alpha- hydroxylase in the kidneys to produce 1,25(OH)2 cholecalciferol - calcitriol

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3
Q

what is the name of the bio-active form of vitamin D?

A

calcitriol - 1,25(OH)2 cholecalciferol

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4
Q

what hormone acts to decrease serum calcium and phosphate?

A

calcitonin, secreted by thyroid parafollicular cells, reduces calcium acutely.

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5
Q

How do we know that the effect of calcitonin and calcium levels is acute?

A

there is no negative effect if the thyroid parafollicular cells are removed.

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6
Q

How does vitamin D act to increase serum calcium and phosphate?

A

stimulates reabsorption from the kidney, in the gut, and promotes bone calcium mineralisation via osteoblasts

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7
Q

How does PTH act to increase serum calcium and phosphate?

A

stimulates osteoclasts, releasing Ca2+ . Stimulates 1-alpha-hydroxylase increasing vit.D metabolism. inhibits sodium phosphate transporter cells

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8
Q

How does vitamin D regulate its own synthesis?

A

through negative feedback, increased vitamin D results in a decreased transcription of 1-a-hydroxylase

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9
Q

Where does the FGF23 hormone come from?

A

is derived from osteocytes

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10
Q

describe the relationship between calcium and PTH

A

when serum calcium falls is detected via calcium-sensing receptor which stimulates the production of PTH

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11
Q

how is phosphate reabsorbed in the gut and kidneys?

A

via sodium phosphate transporter cells

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12
Q

What is the action of FGF23?

A

inhibition of sodium phosphate transporter cells and the synthesis of calcitriol resulting indirectly in less phosphate absorption from the gut

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13
Q

How does hypocalcaemia present?

A

CATs go numb: convulsions, arrhythmias, tetany and paraesthesia

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14
Q

What tests (not blood related) can be used to test for hypocalcaemia?

A

Chvosteks sign and trousseaus sign

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15
Q

What are the causes of hypocalcaemia?

A

hypoparathyroidism, surgical, auto-immune, congenital, deficiency, renal failure

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16
Q

How does hypercalcaemia present?

A

Stones, moans and abdominal groans. Stones: renal effects, results in nephrocalcinosis. Abdominal moans: GI effects such as constipation, anorexia, dyspepsia, pancreatitis. Psychic groans: CNS effects such as fatigue, depression, impaired concentration, altered ment action and even coma

17
Q

What are the three causes of Hypercalcaemia?

A

Primary hyperparathyroidism, malignancy, vitamin D excess (rare)

18
Q

How does primary hyperparathyroidism cause hypercalcaemia?

A

Too much PTH from parathyroid glands but no negative feedback resulting in high PTH bit high calcium

19
Q

How does Malignancy result in hypercalcaemia?

A

Bony metastases produce local factors to activate osteoclasts, and certain cancers secrete PTH-related peptide that acts at PTH receptors

20
Q

How does renal failure cause Hypocalcaemia?

A

No 1-a-hydroxylase step therefore no calcitriol

21
Q

Outline the biochemistry behind primary hyperparathyroidism

A

Parathyroid adenoma producing too much PTH which increases calcium. Low phosphate due to increased renal phosphate excretion because of inhibition of sodium phosphate transporters in the kidney. the high PTH is not suppressed by hypercalcaemia

22
Q

how is primary hyperparathyroidism treated?

A

parathyroidectomy is treatment of choice for primary hyperparathyroidism

23
Q

what are the risks associated with untreated primary parathyroidism?

A

osteoporosis, renal calcinosis, psychological impact of hypercalcemia - mental function and mood

24
Q

what is secondary hyperparathyroidism?

A

normal physiological response to hypocalcaemia

25
Q

what will be seen in serum blood markers for secondary hyperparathyroidism?

A

low/normal calcium. high PTH

26
Q

what is the main cause of secondary hyperparathyroidism?

A

vitamin D deficiency

27
Q

how is seconday hyperparathyroidism treated?

A

Vit. D replacement. if normal renal function then 25 hydroxy vitamin D. If renal failure then Alfacalcidol

28
Q

why are patients with renal failure given Alfacalcidol rather than 25 hydroxy vitamin D?

A

patients with renal failure have inadequate 1-a hydroxylation so cannot activate calcitriol preparations

29
Q

What do we measure vitamin D as?

A

25 (OH) vitamin D as calcitriol is very difficult to measure

30
Q

what is seen in the blood serum markers of a patient with vitamin D deficiency?

A

low/normal calcium but high PTH

31
Q

When looking at hypercalcaemia, what is the most important blood marker to investigate?

A

PTH, normal PTH response to hypercalcaemia is for PTH to fall, if PTH is low, can be hypercalcaemia due to malignancy, if PTH is high, can be hyperparathyroidism

32
Q

what is tertiary hyperparathyroidism?

A

chronic vit.D deficiency that occurs in renal failure resulting in high PTH and hyperplasia of parathyroid cells

33
Q

what can form as a result of autonomous PTH secretion?

A

hypercalcaemia

34
Q

How do we distinguish between primary and tertiary hyperparathyroidism?

A

primary if normal renal function. in tertiary all 4 parathyroid glands will be hyperplastic and patient will have renal failure

35
Q

what affects does PTH have on the kidneys?

A

increased calcium reabsorption and phosphate excretion. increased 1-a-hydorxylase activity

36
Q

what affect does PTH have on the gut?

A

increased calcium and phosphate absorption

Y2 ENDOCRINOLOGY (13 decks)

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