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BRS YR2 > Calcium Dysregulation > Flashcards

Calcium Dysregulation Flashcards

1
Q

What is the key characteristic used to identify tertiary hyperparathyroidism?

A

Renal failure

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2
Q

What causes secondary hyperparathyroidism?

A

Vitamin D deficiency

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3
Q

What increase serum calcium?

A
  • vitamin D (skin or diet)
  • PTH (parathyroid glands)
    via actions on: kidney, bone and gut
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4
Q

What decreases serum calcium?

A
  • calcitonin (thyroid parafollicular cells)

can reduce calcium acutely, no negative effect if parsafollicular cells are removed

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5
Q

What is the active form iof vitamin D?

A

calcitriol

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6
Q

What is the relationship between 1,25(OH)2 vitamin D (calcitriol) and 1 alpha hydroxylase?

A

calcitriol regulates it’s own synthesis by decreasing transcription of 1 alpha hydroxylase

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7
Q

What are the effects of calcitriol?

A

bones: increased osteoblast activity
kidney: increased calcium and phosphate reabsorption
gut: phosphate and calcium reabsorption

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8
Q

What are the effects of PTH?

A

bone: increased calcium resorption from bone
(increased osteoclast activity)
kidney: increased calcium reabsorption, increased phosphate excretion and increased calcitriol synthesis.
gut: the increased calcitriol from the kidney’s effects mean increased calcium and phosphate reabsorption

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9
Q

What is the net effect of phosphate?

A

fairly neutral

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10
Q

Does PTH increase calcium?

A

yes

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11
Q

What is FGF23?

A

regulate phosphate

more FGF23, greater phosphate excretion

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12
Q

Where is FGF23 made?

A

osteocytes

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13
Q

How does FGF23 lower phosphate levels in the body?

A
  • inhibits sodium/phosphate co-transporter, must be lost to the urine
  • inhibits calcitriol formation, therefore less phosphate is reabsorbed.
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14
Q

What is the sodium/phosphate channel inhibited by?

A
  • PTH

- FGF23

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15
Q

What is the effect of hypocalcaemia?

A

sensitisation of excitable tissues; muscle cramps, tetany and tingling

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16
Q

What are the signs/symptoms of hypocalcaemia?

A
  • paraethesia
  • convulsions
  • arrhythmias
  • tetany
  • Chvosteks’ sign
  • Trousseau’s sign
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17
Q

What is paraesthesia?

A

pins and needles in hands, mouth, feet…

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18
Q

What is Chvosteks’ sign?

A

facial parasthesia

19
Q

What is trousseau’s sign?

A

carpopedal spasm

20
Q

What is tetany?

A

the ability to contract muscles, but can’t relax them

21
Q

What are the 2 causes of hypocalcaemia?

A
  • low PTH levels (hypoparathyroidism)

- low vitamin D levels

22
Q

What can cause low PTH levels?

A
  • surgery (neck)
  • autoimmune issues
  • magnesium deficiency
  • congenital causes
23
Q

What can cause low vitamin D levels?

A

Deficiency

  • diet
  • UV light
  • malabsorption
  • impaired production (renal failure)
24
Q

What are the signs/symptoms of hypercalcaemia?

A 
'stones, abdominal bones and psychic groans'
\+ atonal muscles
stones:
- nephrocalcinosis: kidney stones, renal colic
abdominal moans:
- anorexia, nausea, dyspepsia, constipation, pancreatitis
psychic groans:
- fatigue
- depression
- impaired concentration
- coma (>3mmol/L)
- altered mentation
25
Q

What are the possible causes of hypercalcaemia?

A
  • primary hyperparathyroidism
  • malignancy
  • vitamin D excess (rare)
26
Q

How can primary hyperparathyroidism cause hypercalcaemia?

A
  • usually: parathyroid gland adenoma

- no negative feeback (high PTH, high calcium)

27
Q

How can malignancy cause hypercalcaemia?

A
  • bony metastases produce local factors to activate osteoclasts
  • certain cancers (eg: squamous cell carcinomas) secrete PTH-related peptide that acts on PTH receptors
28
Q

What is the relationship between PTH and calcium?

A

inverse relationship

29
Q

What are the different types of hyperparathyroidism?

A

primary, secondary and tertiary hyperparathyroidism

30
Q

What happens when there is a hyperparathyroid adenoma?

A
  • excess PTH is produced
  • calcium increases, no negative feedback due to autonomous PTH secretion from the adenoma
  • primary hyperparathyroidism
31
Q

What is the biochemistry of primary hyperparathyroidism?

A
  • high calcium
  • low phosphate
    (increased renal phosphate excretion - sodium/phosphate transporter inhibited)
  • high PTH (not suppressed)
32
Q

How do you treat hyperparathyroidism?

A

parathyroidectomy (removal of the gland)

33
Q

What are the effects of untreated hyperparathyroidism?

A
  • osteoporosis
  • renal calculi (stones)
  • psychological impact
34
Q

What happens in secondary hyperparathyroidism?

A

normal physiological response to hypocalcaemia

  • low calcium
  • normal feedback response
  • increased PTH (high secondary to calcium)
35
Q

What causes secondary hyperparathyroidism?

A 
Vitamin D deficiency
commonly:
- diet
- reduced sunlight
rarely:
- renal failure
(no calcitriol in renal failure)
36
Q

How do you treat secondary hyperparathyroidism?

A 
Normal kidney function 
- 25 hydroxy vitamin D 
- produceds D2 + D3.
Renal failure
- inadequate-1-alpha hydroxylation, can't activiate it.
- alfacalcidol (active vitamin D)
37
Q

What happens in tertiary hyperparathyroidism?

A
  • chronic renal failure
  • chronic vitamin D deficiency
  • low vitamin D
    (can’t make calcitriol)
  • over production of PTH (PTH glands hyperplasia)
  • causes hypercalcaemia
38
Q

How do you treat tertiary hyperparathyroidism?

A

parathyroidectomy

39
Q

What should be done first when a patient presents with high calcium?

A

look at PTH

40
Q

How do you differentiate between primary hyperparathyroidism and hypercalcaemia due to malignancy?

A

look at PTH levels, high in primary, low in malignancy

41
Q

What is a key characteristic of tertiary hyperparathyroidism?

A
  • chronic renal failure

- all 4 glands are enlarged (hyperplastic)

42
Q

How is vitamin D measured?

A

25 (OH) vitamin D

43
Q

What is the normal progression of hyperparathyroidism?

A

secondary to tertiary hyperparathyroidism

switch due to constant PTH production due to vitamin D deficiency

BRS YR2 (70 decks)

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