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Clinical Pathology (RIP) > T3 - L5 calcium metabolism > Flashcards

T3 - L5 calcium metabolism Flashcards

1
Q

What type of ion is calcium?

A

Divalent cation (Ca2+)

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2
Q

In which processes is calcium physiologically important?

A
  • muscle contraction
  • neuronal excitation
  • enzyme activity (Na/K ATPase, hexokinase etc)
  • blood clotting
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3
Q

How is calcium structurally important?

A

Key component of hydroxyapatite Ca10(PO4)6(OH)2 - the predominant mineral in bone

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4
Q

What type of ion is phosphate?

A

Monovalent anion (PO4-)

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5
Q

Why is phosphate physiologically important?

A
  • the P in ATP
  • intracellular signalling
  • cellular metabolic processes eg. glycolysis
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6
Q

Why is phosphate structurally important?

A
  • backbone of DNA
  • component of hydroxyapatite
  • membrane phospholipids
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7
Q

Is phosphate predominantly intracellular or extracellular?

A

Predominantly intracellular

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8
Q

When these electrolytes are out of balance, it can be attributed to what…

A
  • increased or reduced intake
  • increased or reduced excretion/loss
  • increased or reduced storage
  • tissue redistribution
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9
Q

Calcium is normally tightly regulated at what levels?

A

2.20-2.60mmol/L

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10
Q

The two key controlling factors for calcium are..

A
  • PTH

- vitamin D and metabolites

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11
Q

There are complex but well-characterised relations between calcium and what?

A
  • GI uptake
  • renal clearance
  • bone
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12
Q

how would you work out the total Ca2+t?

A

Total Ca = Ionised Ca + Bound Ca + Complexed Ca

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13
Q

Which form of calcium is the physiologically active fraction?

A

Ionised calcium

  • calcium sensing receptor
  • cellular effects
  • regulation of PTH
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14
Q

Is bound calcium active?

A

Physiologically INACTIVE

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15
Q

when calcium circulates bound to plasma proteins, what is the most common protein for it to be bound?

A

Albumin

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16
Q

What are complexed calcium compounds?

A

Salts - calcium phosphate and calcium citrate

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17
Q

Calcium values can be corrected for what? (adjusted calcium)

A

Corrected for changes in albumin

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18
Q

What is adjusted calcium?

A

Total calcium + (40-Alb) x 0.025

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19
Q

What is the reference range for adjusted calcium?

A

Same as normal

2.20-2.60mmol/L

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20
Q

Describe the calcium distribution in the plasma

A

ionised calcium = 1.3mmol/L

bound calcium = 0.95mmol/L

complexed calcium = 0.05mmol/L

roughly

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21
Q

Total calcium doesn’t necessarily reflect ionised calcium; why?

A
  • total calcium affected by albumin

- pH influences ionised Ca

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22
Q

Describe the ways that pH influences ionised/bound calcium

A

acidosis = reduced Ca-albumin

alkalosis = increases Ca-albumin

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23
Q

Why does acidosis reduce Ca-albumin so reduce the amount of bound calcium?

A

Calcium and H+ ions compete for the albumin binding sites

  • this means less bound calcium and more ionised calcium
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24
Q

How does the distribution of calcium change in alkalosis?

A

Increased bound calcium and decreased ionised calcium

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25
Q

How does a reduction in binding protein change calcium distribution?

A
  • decrease in bound calcium
  • ionised calcium and complexed calcium stay the same
  • overall decrease in total calcium
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26
Q

Calcium levels tend to increase as levels of which protein increase?

A

Albumin

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27
Q

What are the albumin levels reference range?

A

35-55g/L

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28
Q

Give examples of artifactual causes of hypocalcaemia

A
  • EDTA contamination (chelates calcium ions)

- venestasis will cause low adjusted calcium (total calcium is unaffected)

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29
Q

Which calcium disorder involves low serum ionised calcium and low plasma PTH?

A

Primary hypoparathyroidism

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30
Q

Which calcium disorder involves low-normal serum ionised calcium but high plasma PTH?

A

Secondary hyperparathyroidism (usually renal or nutritional)

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31
Q

Which calcium disorder involves high serum ionised calcium and but low plasma PTH?

A

PTH independent hypercalcaemia (eg. malignancy, vitamin D toxicity)

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32
Q

Which calcium disorder involves high serum ionised calcium and high plasma PTH?

A

Primary hyperparathyroidism

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33
Q

Calcium at what levels is a medical emergency requiring immediate treatment?

A

Over 3.5mmol/L or under 1.6mmol/L

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34
Q

how would a standard biochemistry test become contaminated with EDTA?

A
  • Purple tube used for full blood count contain EDTA

- if used first it can contaminate other samples.

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35
Q

what happens if your blood sample is contaminated by EDTA?

A
  • chelate the calcium

- cause of spuriously raised potassium (pseudohyperkalemia).

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36
Q

what colour tube is used for a full blood count?

A

purple

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37
Q

what 3 main forms does calcium circulate the body in?

A
  • ionised “free” Ca2+ (50%) - biologically active
  • bound to plasma proteins (41%) - predominantly albumin
  • complexed to anions (9%) - e.g. phosphate, citrate, bicarbonate
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38
Q

which of the 3 forms of calcium that circulate the body is the biologically active form?

A

Ionised “free” Ca2+ (50%)

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39
Q

how much is Total body phosphorous? and how is this distributed between bone, intracellular and extracellular?

A

Total body phosphorous (23 mol, ~700g)

  • bone 85%
  • intracellular 14%
  • extracellular 1%
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40
Q

what two main forms does phosphorus circulate in the blood?

A
  • Organic form (covalently bound) ~70%
    e. g. phospholipids
  • Inorganic form as phosphate ~30%
    Predominantly HPO42- & H2PO4-
41
Q

what is the adult reference range for phosphate?

A

0.8 - 1.5mmol/L

42
Q

PTH is secreted by the parathyroid glands, stimulated in response to what?

A
  • low calcium
  • high phosphate
  • high magnesium in low calcium environments
43
Q

how does magnesium effect the secretion of PTH?

A
  • Mg acts on Ca Receptor
  • intimates negative feed back loop (in place of calcium)
  • high Mg = decreased secretion of PTH
  • However high Mg is only able to reduce PTH when parathyroid glands were exposed to low Ca concentrations.
  • With normal to high Ca concentrations, only an extremely high Mg concentration of 5.0 mM was able to decrease PTH secretion
44
Q

what direct action does PTH have on bone?

A

drive resorption of Ca and PO4

45
Q

what direct action does PTH have on the kidneys?

A
  • increase reabsorption of Ca from the filtrate

- increase excretion of PO4

46
Q

what indirect action does PTH have on the kidneys?

A

increase conversion of vitamin D to its active
form (1,25(OH)2 vitamin D)

NB: this increases Ca and PO4 absorption from the gut

47
Q

what is the active form of Vitamin D?

A

(1,25(OH)2 vitamin D)

calcitriol (also known as 1,25-dihydroxycholecalciferol)

48
Q

high calcium has what affect on PTH release?

A

decrease the release of PTH

High calcium results in negative feedback on PTH release (via calcium sensing receptors of
the parathyroid gland)

49
Q

where can we get Vitamin D from?

A
  • Diet (especially oily fish)
  • Synthesis in the skin from a cholesterol precursor by the action of UV-B from the
    sunlight
50
Q

where does Vitamin D have to go to become “Activated”?

A
  • The liver to undergo the first hydroxylation
  • The kidneys to undergo the second hydroxylation step by 1α-hydroxylase

NB: This last step produces the active form of Vitamin D (1,25(OH)2 vitamin D)

51
Q

which enzyme in the liver hydroxylates vitamin D to its active form?

A

1α-hydroxylase

52
Q

how does PTH increase the activation of Vitamin D?

A

PTH acts on the kidneys to increase the activity of 1α-hydroxylase enzyme to increase the activation of Vitamin D

53
Q

why is the precursor of Vitamin D measured in the lab instead of the active form of Vitamin D?

A

As it is present at a greater concentration in the blood and more stable

54
Q

what does the active form of vitamin D act on?

A

Acts on the intestine to increase the absorption of Calcium and Phosphate

NB: Has some other effects including beneficial effects for the immune system and
anti-cancer effects]

55
Q

For bone health, is 25-OH Vitamin D < 75 nmol/L sufficient?

A

NO

25-OH Vitamin D < 75 nmol/L is deficient or depleted

56
Q

For bone health, is 25-OH Vitamin D >75 nmol/L sufficient?

A

YES

25-OH Vitamin D >75 nmol/L is sufficient

57
Q

For bone health, is 25-OH Vitamin D > 500 nmol/L sufficient?

A

NO

25-OH Vitamin D > 500 nmol/L suggests toxicity

58
Q

For bone health, is 25-OH Vitamin D 54 nmol/L sufficient?

A

NO

25-OH Vitamin D < 75 nmol/L is deficient or depleted

59
Q

For bone health, is 25-OH Vitamin D 95 nmol/L sufficient?

A

YES

25-OH Vitamin D >75 nmol/L is sufficient

60
Q

For bone health, is 25-OH Vitamin D 632 nmol/L sufficient?

A

NO

25-OH Vitamin D > 500 nmol/L suggests toxicity

61
Q

what percentage of under 18s in the UK have insufficient vitamin D (<50 nmol/L)?

A

29%

62
Q

Due to children having insufficient vitamin D in the UK, there has been a resurgence of what disease?

A

rickets

63
Q

what factors affect your vitamin D level?

A
  • season
  • latitude/climate
  • clothing
  • use of sunscreen
  • time spent indoors/outdoors
  • skin tone
  • age
  • diet
  • body fat and BMI
64
Q

how does the season affect vitamin D levels

A

more sun in summer

65
Q

how does your clothing affect vitamin D levels?

A

More susceptible to Vitamin D deficiency when

choosing to cover up

66
Q

how does your skin tone affect vitamin D levels?

A

Darker skin tones contain more melanin will require more exposure to sunlight to
synthesise the same amount of Vitamin D as someone with lighter skin

67
Q

what is FG23?

A

Fibroblast growth factor 23

68
Q

FG23 is secreted by osteocytes in response to what?

A

increase in the active form of vitamin D (calcitriol)

69
Q

what does FG23 do?

A
  • Suppresses 1α hydroxylation of vitamin D by the kidneys (negative feedback)
  • Increases renal phosphate excretion
70
Q

what affect does FG23 have on the active form of vitamin D?

A

less active vitamin D secreted

  • Suppresses 1α hydroxylation of vitamin D by the kidneys (negative feedback)
71
Q

Calcitonin is secreted by the C-cells of the thyroid gland in response to what?

A

increased calcium

concentration

72
Q

what does calcitonin do?

A

Opposes the effect of PTH by acting on osteoclasts to inhibit bone resorption

NB: Function is usually insignificant in the regulation of normal calcium homeostasis

73
Q

list some signs and symptoms of hypocalcaemia.

A
  • tetany
  • Paraesthesia (pins and needles)
  • cramps
  • convulsions
  • psychosis
74
Q

what is hypocalcaemia?

A

low level of calcium in the blood

75
Q

list some causes of hypocalcaemia.

A
  • vitamin D deficiency
  • Inadequate dietary calcium intake
  • Hypoproteinaemia
  • Hypoparathyroidism
  • Pseudo-hypoparathyroidism
  • High phosphate
  • High citrate
  • EDTA contamination
76
Q

what is the most common cause of hypocalcaemia?

A

vitamin D deficiency

77
Q

what is Hypoproteinaemia?

A

abnormally low level of protein in the blood

78
Q

how can you distinguish between a vitamin D deficiency and hypoparathyroidism?

A
  • Patient with high PTH has vitamin D deficiency

- Patient with almost undetectable PTH has hypoparathyroidism

79
Q

list some signs and symptoms of hypercalcaemia.

A
  • renal stones
  • bone pain/osteoporosis
  • lethargy, fatigue, depression
  • Abdominal pain, constipation, nausea, vomiting
  • dehydration
80
Q

how does hypercalcaemia cause dehydration?

A

via renal resistance to ADH

81
Q

list some causes of hypercalcaemia?

A
  • hyperparathyroidism
  • malignancy
  • medications
  • vitamin D excess
  • hyperthyroidism
  • bone disease/immobilisation
82
Q

how can hyperparathyroidism cause hypercalcaemia?

A

[Too much PTH causing too much resorption of Ca from bones and urine]

83
Q

which medications can cause hypercalcaemia?

A

Thiazides [diuretics], lithium

84
Q

how can hyperthyroidism cause hypercalcaemia?

A

[Thyroid hormones act on the bones to drive ongoing resorption]

85
Q

how can you differentiate between hyperparathyroidism and bone metastases?

A
  • Patient with appropriately suppressed PTH as expected with high
    Ca has bony metastases
  • Patient with inappropriately high PTH and high calcium has
    hyperparathyroidism
86
Q

what are the first line biochemical investigations for hypo- hypercalcaemia?

A
  • consider adjusted calcium equation
  • bone profile
  • vitamin D
  • Magnesium
  • Simultaneous measurement of Ca & PTH
87
Q

what are symptoms of phosphate deficiency?

A
  • Haemolysis, thrombocytopenia and poor granulocyte function
  • Severe muscle weakness, respiratory muscle failure [most severe result] and
    rhabdomyolysis
  • Convulsions, coma, death
  • Chronic phosphate deficiency will cause rickets (children) / osteomalacia (adults)
88
Q

what is refeeding syndrome?

A

When feeding a patient after a prolonged period of malnutrition or
starvation, the arrival of calories prompts the secretion of insulin,
stimulating glycolysis & other processes e.g. protein synthesis & lipogenesis

this can lead to a phosphate deficiency

89
Q

what is Hyperphosphataemia?

A

elevated level of phosphate in the blood

90
Q

what type of ion is Mg?

A

Divalent cation, Mg2+

91
Q

what is the physiological importance of Mg?

A

● Cofactor for ATP – our fuel!
● Neuromuscular excitability
● Enzymatic function
● Regulates ion channels

92
Q

what is the structural importance of Mg?

A

Comprises 0.5 – 1% of bone matrix

93
Q

how much is the total body magnesium? and how is this distributed between, bone, intracellular and extracellular?

A

Total body magnesium (~1.1 mol)

● Bone (54%)
● Intracellular (45%)
● Extracellular (1%)

94
Q

what are the 3 forms of Mg that circulate the body?

A

similar to calcium -

  • ionised “free” Mg 60\5
  • bound to plasma proteins (25%) predominantly albumin
  • complexed to anions (15%) e.g. phosphate, citrate, bicarbonate
95
Q

what is the reference range for magnesium?

A

0.7 - 1.0mmol/L

96
Q

where does homeostasis of Mg occur?

A

predominantly in the kidneys

97
Q

a decrease in Mg stimulates the release of PTH, so why does severe hypomagnasaemia result in hypercalcaemia?

A

PTH release is stimulated by a decrease in magnesium and inhibited by an increase in
magnesium (but calcium is a much more potent stimulus)

● HOWEVER, PTH release is magnesium-dependent, so severe hypomagnasaemia will
inhibit PTH release and cause hypocalcaemia.

98
Q

Hypermagnesaemia is rare since kidneys have a large capacity to excrete excess, therefore it is usually iatrogenic. What does this mean?

A

caused by medical examination or treatment.

Clinical Pathology (RIP) (49 decks)

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