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Endo yr 2 > calcium regulation > Flashcards

calcium regulation Flashcards

1
Q

what substances in the blood can increase serum calcium?

A

-vitamin D (skin or diet)
-PTH SECRETED by parathyroid gland

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2
Q

what subst in blood can decrease serum calcium?

A

calcitonin, significant effect however its removal (after parathyroid cells removed) doesnt make a difference interestingly

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3
Q

what organs are the main regulators of calcium and phospate

A

gut, kidney, bone

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4
Q

(look at ipad) what reactions happen in skin cells in vit d synthetic process?

A

7- dehydrocholesterol -> pre vitamin D3 -> vitamin D3

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5
Q

what is vitamin d3 converted to? where? by what enzyme?

A

25 (OH) CHOLECALCIFEROL BY 25 HYDROXYLASE IN TH ELIVER

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6
Q

what is 25 (OH) cholecalciferol converted to? where? by what enzyme?

A

1,25 (OH)2 cholecalciferol by 1 alpha hydroxylase in the kidney

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7
Q

what is calcitriol?

A

1,25 (OH)2 cholecalciferol / active vit D

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8
Q

what is the measured indicator for vit d?

A

25-OH cholicalciferol (or 25-OH vit d)

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9
Q

how does calcitriol regulate its synthesis?

A

by decreasing the transcription of 1 alpha hydroxylase

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10
Q

what are the effects of lacitriol on calcium and phosphate absorption/ reabsorbtion/ secretion in gut bone and kidn?

A

kidney and gut both incr serum calcium bc incr reabsorption/ absorption
bone: decreases serum calcium because incr OSTEOBLAST activity

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11
Q

what are the direct actions of pth on calcium adn phosphate levels

A

increases OSTEOCLAST activity in bone so increasing calcium in serum

in kidney:
-incr calcium reabsorption
-incr phosphate EXCRETION

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12
Q

what are the indirect effects of pth on calcium and phosphate levels? what substance is involved?

A

PTH increases 1 a hydroxylase activity :
-> increases 1,25 (OH)2D3 synthesis
-> increases ca and po reabsorption in GUT

(SO OVERALL: PTH: KIDNEY AND BONE: DIRECT, GUT: INDIRECT)

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13
Q

what is the effect of hyperparathyroidism on serum phosphate levels? what is the mechanism?

A

remember: P.T.H: please transporter halt

-phosphate is reabsorbed in the kidney by na/ phosphate co-transporters
-PTH inhibits this transporter
- leads in less phosphate reabsorption so low phosphate in serum and more excreted

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14
Q

what is FGF23 derived form? what are its mechanisms for influencing serum phosphate levels?

A

derived from bone,
1) inhibits same transporters as PTH
2) Inhibits calcitriol ( leads to less phosphate reabsorption form gut) (indirect)

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15
Q

signs and sympotms of hypocalcemia

A

CAT goes numb

convulsions
arrhythmias
tetany

paraesthesia (nmbness in mouth, hands, feet, lips)

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16
Q

what is tetany

A

involuntary contraction of muscles due to LOW calcium levels

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17
Q

what are convulsions

A

rapid uncontrolable muscle movements like spasm

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18
Q

what is chvosteks’ sign

A

a specific facial paresthesia: when you tap check below eye and they close their eye on that side

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19
Q

what is trousseaus sign?

A

a specific type of tetany: carpopedal spasm (basically tetany below wrist/ palm)

20
Q

causes of hypocalcaemia

A
  • Low PTH levels
    -low vitamin D
21
Q

DEFICIENCY in what chemical element/ mineral can cause low pth levels

A

magnesium

22
Q

causes of low PTH:

A

SURGery in neck
autoimmune
congenital (agenesis: rare)
MAGNESIUM DEFICIENCY

23
Q

causes of vit d def

A

poor diet/ malabsorption
low uv exposure
impaired productIon (RENAL FAILURE) !!!

24
Q

what happens to calcium levels in hypoparathyroidism?

A

decrease (hypocalcaemia)

25
Q

AS a rule of thumb are systems underacting or overacting in hypercalcaemia?

A

under- so they overeact in hypo

26
Q

what are the specific symptoms in hypercalcaemia?

A

broken bones, stones, psychic groans and abdominal moans, low muscles tones

27
Q

specific renal effects- what si the medical name of having stones

A

nephrocalcinosis: kidney stones, renal colic (pain cuased by kidney trying to pass urine when theres kidney stone)

28
Q

specific abdominal symptoms - GI effects

A

Anorexia (loss of apetite), nausea, dyspepsia, constipation, pancreatitis (mechanism is unclear )

29
Q

Psychic groans - CNS effects specific, in which cases do these usually arise?

A

Fatigue, depression, impaired concentration, altered mentation, coma (usually >3mmol/L : probably very intense symptoms)

30
Q

causes of hypercalcaemia and most common cause

A

primary hyperparathyroidism (most common) , malignancy, vit d excess (rare)

31
Q

what happens in primary hyperparathyroidism, what is the cause?

A

too much pth,
usually due to parathyroid gland adenoma (benign tumour)
no negative feedback, due to AUTONOMOUS PTH SECRETION from adenoma: (body has enough calcium and pth is still abnormally released: more calcium absorbed)

32
Q

what cancers usually cause hypercalcaemia and how?

A

bony metastases produce local factors to activate osteoclasts

Certain cancers (eg squamous cell carcinomas) secrete PTH-related hormones (like a peptide that acts at PTH receptors

33
Q

HOW TO REMEMBER SPECIFIC LITTLE differences in pth and calcitriol effcets on excretions and absorptions

A

they both generally increase both calcium and phosphate from everywhere except from:
1) calcitriol: in bone: osteoblasts: steal ca from blood
2) pth: in kidney: increases phosphate EXCRETION - remove from blood

34
Q

effect of primary hyperparathyroidism on phosphate?

A

low phosphate: increased renal phosphate excretion (inhibition of Na+/PO43- transporter in kidney)

35
Q

what is the treatment of primary hyperparathyroidsim?

A

Parathyroidectomy is treatment of choice for primary hyperparathyroidism

36
Q

what are the risks of untreated hyperparathyroidism?

A

Osteoporosis
Renal calculi (stones) (Hypercalcemia: bad on bones too much calcium deposition makes them brittle )
Psychological impact of hypercalcaemia – mental function, mood

37
Q

what is secondary hyperparathyroidism? (what pth and ca levels and why)

A
  • clacium low or normal
  • PTH high as a responce/ secondary to the low calcium
38
Q

difference bwteen prim and secondary hyperparathyroidsim?

A

both pth high, calcium high in primary, low in secondary (means problem is not in the actual gland-like in primary, its in the calcium level)

39
Q

what is the most common cause of secondary hyperparathyroidism?

A

vit d deficiency
commonly: diet and sunlight

less common: renal failure: cant make calcitriol (Active vit d)

39
Q

common type of vit d in food

A

vit d2- ergocalciferol Ithing of ergo- energy in food)

39
Q

treatment of secondary hyperparathyroidism if renal function normal?

A
  • vit d replacement: Give 25 hydroxy vitamin D: either
    1) ergocalciferol: 25 hydroxy vitamin D2 or
    2)cholecalciferol: 25 hydroxy vitamin D3
40
Q

treatment of secondary hyperparathyroidism if renal function abnormal?

A

inadequate 1a hydroxylation, so can’t activate 25 hydroxy vitamin D preparations (no point in giving vit d they cant do anything with it so they need special vit d cant use over counter )

-need alfacalcidol -1a hydroxycholecalciferol

41
Q

what is the difference between secondary and tertiary hyperparathyroidism? describe mechanism of disease in tertiary- treatment?

A

-the have same biochemistry : high pth low calcium but tertiary is when there is CHRONICALLY low calcium,

-so the parathyroids have been overworking for a long time to produce PTH so they start growing (all 4 glands hyperplasia) and releasing “basally” more pth than normal (diseased glands)

  • this means that in contrast to secondary, parathyroids are damaged and treatment is removal (parathyroidectomy)
42
Q

why does renal failure cause vit d def?

A

bc a 25 hydrohylase is in kidney and calcitriol produced by it in kidney

43
Q

most common cause of tertiary hyperparathyroidism and on eless common in uk maybe more in developing counr

A

1) chronic renal failure
2) chronic malnutrition

44
Q

when is there low PTH and hypercalcaemia?

A

malignancyy (bc parathyroid is doing its job fine, issue is alciujm secretion atopically)

45
Q

Management of hypercalcaemia of malignancy? (bone cancer)

A

1) hydration
2) if nauseus??:
BISPHOSPHONATES – INHIBIT OSTEOCLASTS AND STOP THEM FROM ABSORBING BONE
LOWERS CALCIUM, LESS BONY PAIN

Endo yr 2 (11 decks)

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