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chem path > Calcium > Flashcards

Calcium Flashcards

1
Q

what is the normal range of calcium

A

2.2-2.6 mmol/L

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2
Q

where is most of the calcium found

A

bone - 99%

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3
Q

in serum how how is calcium found

A

50% ionised (free)
40% bound to albumin (so affected by albumin)
10% bound to phosphate/citrate complexes

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4
Q

what is the corrected calcium formula

A

serum calcium + 0.2 x (40-serum albumin)

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5
Q

why use the corrected calcium

A

to check if free calcium concentration is normal in the presence of abnormal albumin level

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6
Q

what is vitamin D2

A

plant vitamin (diet)
-ergocalciferol

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7
Q

what is vitamin D3

A

synthesised by animals through the conversion of 7-dehydrocholesterol under UV light (cholecalciferol)

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8
Q

what vitamin D do we measure in blood

A

25-OH vitamin D

*25(OH)cholecalciferol

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9
Q

what happens to cholecalciferol in liver

A

converted by enzyme 25 hydroxylase into 25(OH)cholecalciferol

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10
Q

what happens to 25(OH)cholecalciferol in the kidney

A

converted by enzyme 1 alpha hydroxylase into 1,25(OH)2cholecalciferol
(calcitriol = active)

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11
Q

where is vitamin D activated and by what enzymes

A

1) liver = 25 hydroxylase
2) kidney = 1 alpha hydroxylase

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12
Q

which is the rate limiting step in vitamin D activation

A

1-alpha hydroxylase step in kidney

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13
Q

where is vitamin D absorbed

A

jejunum

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14
Q

what are the 2 main hormones involved in calcium metabolism

A

PTH
calcitonin

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15
Q

what does PTH do

A

overall: increases plasma calcium concentration & reduces phosphate

-increases vitamin D activation in the kidney
-increases bone resorption through osteoclasts to mobilise calcium
-increases renal calcium reabsoprtion
-increases calcium resorption In gut
-increases renal phosphate excretion (phosphate trashing hormone = PTH)

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16
Q

what does calcitonin do

A

overall: lowers calcium serum concentration

-inhibits calcium reabsorption in kidney & gut
-promoted deposition of calcium in bone (inhibits osteoclasts & stimulates osteoblasts)

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17
Q

where is calcitonin produced

A

parafollicular C cells of thyroid

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18
Q

what does calcitriol do

A

-increases calcium & phosphate reabsorption from gut & kidney
-increases ostebolast activity to build and remodel bone

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19
Q

what are symptoms of hypocalcaemia

A

perioral paraesthesia
carpopedal spasm (Trousseaus sign)
laryngospasm
anxious/irritable
hypertonia
chosteks sign - tapping on jaw makes it twitch - spasm
prolonged QT (less Ca+ influx into cardiac muscle so repolarisation delayed)

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20
Q

what are the causes of hypocalcaemia

A

1) hypoparathryoidism:
-primary: DiGeorge
-post-thyroidectomy (most common)
-magnesium deficiency
-pseudohypoparathyroidism
2) low vitamin D
3) CKD

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21
Q

what electrolytes would you see in hyperparathyroidism (eg. diGeorge)

A

PTH low
calcium low
phosphate high
ALP low/normal
vitamin D normal

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22
Q

what electrolytes would you see in vitamin D deficiency

A

low calcium
low phosphate
high PTH
ALP high
vitamin D normal

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23
Q

what does vitamin D deficiency cause in adults

A

osteomalacia

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24
Q

what does vitamin D deficiency cause in kids

A

rickets

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25
Q

why can magnesium deficiency cause low PTH?

A

magnesium needed for synthesis and release of PTH

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26
Q

most common cause of hypothyoridism

A

post-surgical (eg. thyrodiectomy)

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27
Q

what happens in digeorge syndrome

A

3rd/4th brachial clefts not formed so doesnt make PTH glands - genetic

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28
Q

what is pseudohypoparathyroidism

A

resistance to PTH
-high PTH, low calcium, high phosphate

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29
Q

what is albright hereditary osteodystrophy and what are features

A

-hereditary pseudohypoparathyroidism
-resistance to PTH so low calcium despite high PTH
-short 4th/5th fingers + obesity & round face

(not alBright - they are obese and have stubby ass fingers)

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30
Q

what is pseudopseudohypoparathyroidism

A

same phenotype as albrights hereditary osteodystrophy but normal biochemical findings + no resistance to PTH

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31
Q

treatment of hypocalcaemia

A

-symptomatic or severe (<1.9) = 10% IV calcium gluconate

-not symptomatic or >1.9 = oral calcium supplement (not taken at meal times) + vitamin D supplement

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32
Q

how do you supplement vitamin D in different people

A

CKD: alfacalidol
others: vitamin D2 or D3

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33
Q

symptoms of hypercalcaemia

A

stones (renal), bones (pain), groans (psych), moans (abdominal pain) + polyruria

34
Q

most common cause of hypercalcaemia in community

A

primary hyperparathyroidism

35
Q

why does sarcoidosis cause hypercalcaemia

A

macrophages in granulomas increase 1 alpha hydroxylase which converts vitamin D to active form.

35
Q

why does myeloma cause hypercalcaemia

A

osteoclast activating cytokines

35
Q

causes of hypercalcaemia?

A

low PTH: malignancy (PTHrp, bone mets, myeloma), sarcoidosis
high PTH: hyperparathyroidism, FHH
normal: maybe tertiary hyperparathyrodisim

36
Q

most common cause of hypercalcaemia in hospitalised inpatients

A

malignancy

37
Q

most common cause of primary hyperparathyroidism

A

single parathyroid adenoma

37
Q

what is primary hyperparathyroidism

A

problem with parathyroid gland causing increased PTH production. most commonly single parathyroid adenoma

38
Q

electrolytes in primary hyperparathyrodism

A

-PTH: high or normal (should be suppressed!!!)
-high calcium, low phosphate
-high/normal ALP
-normal vitamin D

39
Q

what are some features of primary hyperparathyroidism

A

affects wrists - colles fracture
pepperpot skull
osteitis fibrosa cystica (bone cysts) + brown tumours

40
Q

what is secondary hyperparathyroidism

A

pathology outside parathyroid gland (eg. CKD, vit D deficiency) causes PTH gland to produce more PTH

41
Q

what are causes of secondary hyperparathyoridism

A

CKD
vitamin D deficiency
malabsoprtion syndrome

42
Q

what is renal osteodystrophy

A

when secondary hyperPTH from CKD causes bone damage

43
Q

electrolytes in secondary hyperparathyrodism

A

low calcium (trigger)
high PTH
high phosphate (cant really excrete)
high ALP
low/normal vitamin D

44
Q

what is tertiary hyperparathyrodiism

A

autonomous PTH secretion. prolonged secondary hyperparathyroidism causes upregulated secretion of PTH

45
Q

electrolytes in tertiary hyperparathyroidism

A

high/normal calcium
-low or high phosphate
-high PTH
-high/normal ALP
-N vitamin D

46
Q

when does sarcoid hypercalcaemia increase

A

in summer

47
Q

treatment of hypercalcaemia

A

IV fluids - fluids, fluids, fluids
-cancer? bisphosphonates (otherwise avoid
-treat cause

48
Q

what is band keratopathy due to

A

calcium deposits in centre of cornea

49
Q

what is familial hypocalciuric hypercalcaemia

A

CASR mutation
-less calcium sensitivity in PTH gland
-more calcium is needed to suppress PTH so hypercalcemia
-less calcium is really excreted so hypocalciuria

50
Q

where is mutation in familial hypocalciuric hypercalcaemia

A

CASR gene (calcium sensing gene)
*cinacalcet sensitising this gee

51
Q

how to differentiate FHH from primary hyperparathyroidism

A

calcium/creatinine clearance ratio lower in FHH
-can be confirmed with genetic testing

52
Q

features of rickets

A

constochondral swelling (rachitic rosary), bowed legs, myopathy, wide epiphysis on wrist

53
Q

osteomalacia features

A

myalgia, bone pain, loosers zones (sclerotic bone)

54
Q

why chapatis cause osteomalacia

A

chapatis high in phytic acid which chelates vitamin D

55
Q

why ALP high in osteomalacia

A

PTH raised so more bone resorption (osteoclasts) so osteoblasts activity to mend it (blasts release ALP)

56
Q

osteoporosis common fractures

A

colles (distal radius), NOF, vertebral (thus kyphosis and short stature with age)

57
Q

first symptom of osteoporosis

A

fracture

58
Q

bone profile in osteoporosis

A

everything normal

59
Q

what medications can help osteoporosis

A

-vit D
-bisphosphoates (eg. alendronate)
-PTH analogue (teriparatide)
-oestrogen
-raloxifene (SERM)

60
Q

what do bisphosphonates do

A

bind to hydroxiapatite on bone, osteoclasts bind to them, they suppress osteoclast activity & bone turnover
-problem: cant remodel well

61
Q

side effects of bisphosphonates

A

gastric ulcers, oesophagitis (must take it sitting up), jaw osteonecrosis

62
Q

pagets disease bone profile

A

isolated raised ALP

63
Q

treatment for primary hyperPTH?

A

total parathyroidectomy

64
Q

what are risk factors for renal stones

A

dehydration
abnormal urine pH (eg. meat intake, renal tubular acidosis)
-some stones eg. calcium more in acidic urine
-struvite stones more in alkali urine
-urine infection
-anatomical abnormalities

65
Q

what. is calcium level like usually in calcium stones

A

normal

65
Q

what do calcium stones occur from

A

-hyperoxaluria
-hypcalciuria

66
Q

how to prevent calcium stones

A

avoid dehydration
lessen oxalate intake
normal calcium intake
thiazide (cause hypocalciuria)
citrate (alkanalises urine)

67
Q

what is the x ray appearance of calcium stones

A

radio-opaque (more bright)

68
Q

what does a struvite (triple phosphate stone) look like on x ray

A

radioopaque
staghorn (huge and looks like a branching fern)

69
Q

what does uric acid stone look like on x ray

A

radiolucent (cant see it well)

70
Q

what does a cysteine stone look like

A

semi-opaque (ground glass)

71
Q

risk factor for struvite stones

A

UTI (proteus mirabilis, klebsiella)

72
Q

what is a risk factor for uric acid stones

A

chemotherapy for leukaemia (eg. tumour lysis syndrome)

73
Q

analgesia for renal stones

A

IM diclofenac

74
Q

management for renal stones =< 5mm (small)

A

conservative mangement (let them pass)

75
Q

management for renal stones 6-20 mm

A

shockwave lithotripsy/uteroscopy

76
Q

management for renals tones >20mm

A

percutaneous neprholithotomy

77
Q

management for renal stones 5-10mm

A

lithotripsy

78
Q

rank the following conditions in terms of calcium level from lowest to highest

-osteoporosis
-osteomalacia
-primary hyperPTH
-secondary hyperPTH
-PTH carcinoma

A

lowest to highest

-osteomalacia
-secondary hyperPTH
-osteoporosis
-primary hyperPTH
-PTH carcinoma

chem path (20 decks)

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