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brs (phase 1b) > (endo) calcium dysregulation > Flashcards

(endo) calcium dysregulation Flashcards

review phase 1a calcium + phosphate regulation cards before these ones

1
Q

review phase 1a ‘regulation of calcium and phosphate’ cards before this deck

A

good going champ

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2
Q

how does the parathyroid gland respond to low serum calcium levels?

A

low serum calcium levels
= detect by the calcium-sensing receptors on chief cells
= increase PTH secretion
= stimulates more Ca2+ reabsorption in the gut and kidney and more bone resorption
= increases serum Ca2+

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3
Q

how does the parathyroid gland respond to high serum calcium levels?

A

high serum calcium levels
= detect by the calcium-sensing receptors on chief cells
= reduce PTH secretion
= results in less Ca2+ reabsorption in the gut and kidney and less bone resorption
= reduces serum Ca2+

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4
Q

what are the three types of hyperparathryoidism?

A

primary, secondary and tertiary hyperparathyroidism

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5
Q

what is primary hyperparathyroidism?

A

parathyroid adenoma autonomously producing too much PTH

calcium increases continuously due to lack of negative feedback system

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6
Q

what blood test results are expected in a patient w primary hyperparathyroidism?

A 
PTH = extremely elevated
calcium = extremely elevated
phosphate = low
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7
Q

why are PTH and calcium elevated in primary hyperparathyroidism?

A

calcium increases in response to increased PTH by cannot stop increasing as the pituitary adenoma does not respond to negative feedback

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8
Q

why is phosphate low in primary hyperparathyroidism?

A

increased PTH so increased inhibition of the renal apical sodium-phosphate co-transporter
= so increased urinary loss of phosphate

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9
Q

what is the impact of PTH on phosphate levels in a normal healthy state?

A

on kidney = increased phosphate EXCRETION

on gut = increased phosphate ABSORPTION

(usually, these two action are balanced)

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10
Q

what is the impact of PTH on phosphate levels in a hyperparathyroid state?

A

pathology overtakes and more PTH acts on the kidney to stimulate more excretion

(overall excretion&raquo_space; absorption)

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11
Q

how is primary hyperparathyroidism treated?

A

parathyroidectomy

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12
Q

what are the risks of untreated hyperparathyroidism?

A

1) osteoporosis
2) renal caliculi (stones)
3) psychological impacts of hypercalcaemia = altered mentation, depression

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13
Q

why does hyperparathyroidism lead to kidney stones?

A

excess PTH
= excess calcium
= excess calcium in urine
= increased risk of calcium kidney stone formation

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14
Q

why does hyperparathyroidism lead to osteoporosis?

A

excess PTH
= increased stimulation of OAFs (osteoclast activating factors) via osteoblasts
= increased osteoclastic bone resorption

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15
Q

what is secondary hyperparathyroidism?

A

the normal physiological response to hypocalcaemia

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16
Q

how does primary hyperparathyroidism compare to secondary?

A

primary = elevated PTH, elevated Ca

secondary = low Ca, elevated PTH

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17
Q

what blood test results are expected in a patient w secondary hyperparathyroidism and why?

A 
PTH = elevated
Ca = low

hypocalcaemia is sensed by the calcium-sensing receptors of the chief cells that stimulates in turn, PTH secretion

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18
Q

what are the causes of secondary hyperparathryoidism?

A

causes of hypocalcaemia: less PTH (not possible), less vitamin D (MAIN cause)

so, causes of vitamin D deficiency

  • malabsorption or poor dietary intake
  • inadequate sun exposure
  • renal failure
  • liver failure
  • vit D receptor defects
19
Q

what is the most common cause of secondary hyperparathyroidism?

A

vitamin D deficiency

20
Q

explain how vitamin D deficiency leads to secondary hyperparathyroidism

A

calcitriol deficiency
= less Ca2+ absorption in the gut and kidney
= reduced serum Ca2+ levels
= parathyroid glands respond by increasing PTH secretion significantly

21
Q

how is secondary hyperparathyroidism treated in patients with NORMAL renal function?

A

give 25-OH vitamin D (either ergocalciferol or cholecalciferol)

with normal renal function, they can 1-alpha hydroxylase it to form calcitriol

22
Q

how is secondary hyperparathyroidism treated in patients with IMPAIRED renal function?

A

give alfacalcidol (1-alpha hydroxycholecalciferol = an analogue of vitamin D)

with impaired renal function, they cannot 1-alpha hydroxylase it themselves so better to directly give vitamin D (analogue)

23
Q

differentiate between cholecalciferol and ergocalciferol

A

ergocalciferol (from diet) = 25-hydroxy vitamin D2

cholecalciferol (from skin) = 25-hydroxy vitamin D3

24
Q

what is tertiary hyperparathyroidism?

A

an overactive parathyroid gland as a result of chronic renal failure or chronic vitamin D deficiency

25
Q

what are the two main reasons for tertiary hyperparathyroidism?

A

1) chronic renal failure

2) chronic vitamin D deficiency

26
Q

explain the pathophysiology of tertiary hyperparathyroidism

A

in chronic renal failure/vitamin D deficiency
= impaired function of 1-alpha hydroxylase
= chronic lack of calcitriol synthesis
= low serum Ca2+ levels

= PTH increases (hyperparathyroidism)
= parathyroid glands enlarge (hyperplasia)
= continuous autonomous PTH secretion

27
Q

how is tertiary hyperparathyroidism treated?

A

parathyroidectomy

28
Q

what is the main consequence of tertiary hyperparathyroidism?

A

continuous, autonomous secretion of PTH from the hyperplastic parathyroid glands
= HYPERCALCAEMIA

29
Q

how common is tertiary hyperparathyroidism?

A

extremely rare

= only happens in the context of CKD/chronic renal failure/chronic vit D deficiency

30
Q

what is the normal response to hypercalcaemia?

A

hypercalcaemia

= causes PTH to fall

31
Q

what do the following blood results indicate:

  • elevated Ca2+
  • low/suppressed/undetectable PTH
A

could be
1) normal physiological response to hypercalcaemia

OR//

2) hypercalcaemia of malignancy

32
Q

what is hypercalcemia of malignancy?

A

hypercalcaemia caused either by

1) bony metastases that activate OAFs to stimulate osteoclastic bone resorption
2) certain cancers that produce PTH-related peptides that act on the PTH receptors of osteoblasts

= both ultimately result in increased serum calcium

33
Q

how can hypercalcaemia of malignancy and primary hyperparathyroidism be differentiated?

A

hypercalcaemia of malignancy
= high Ca2+, low/undetectable PTH

primary hyperparathyroidism
= high Ca2+, high PTH

34
Q

what is the most likely diagnosis if a patient with hypercalcaemia has a high PTH?

A

if renal function is normal = primary hyperparathyroidism (e.g. parathyroid adenoma)

if chronic renal failure = tertiary hyperparathyroidism (all four glands are hyperplastic)

35
Q

what blood report is expected for a patient with vitamin D deficiency?

A

Ca2+ = low
PTH = elevated
25-OH cholecalciferol = low

= secondary hyperparathyroidism (secondary to the hypocalcaemia)

36
Q

in what form is vitamin D measured and why?

A

measure 25-OH cholecalciferol

as calcitriol (1,25-dihydroxycholecalciferol) is very difficult to measure

37
Q

summarise primary hyperparathyroidism

A

autonomous secretion of PTH by a parathyroid adenoma, hypercalcaemia and high PTH

38
Q

summarise secondary hyperparathyroidism

A

due to low vitamin D, calcium falls, PTH increases (secondary to low calcium)

39
Q

summarise tertiary hyperparathyroidism

A
  • a complication of chronic renal failure
  • unable to make calcitriol (active vitamin D) over a prolonged period
  • parathyroid glands become hyperplastic and autonomous
  • high PTH drive causes hypercalcaemia
40
Q

when you spot hypercalcaemia, what should you look at first?

A

PTH levels

41
Q

what is the most likely cause of hypercalcaemia and suppressed PTH?

A

hypercalcaemia of malignancy

42
Q

what is the most likely cause of hypercalcaemia and elevated PTH?

A

in renal function normal = primary hyperparathyroidism

if chronic renal failure = tertiary hyperparathyroidism

43
Q

what is the most likely cause of hypocalcaemia and elevated PTH?

A

vitamin D deficiency

brs (phase 1b) (71 decks)

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