Calcium Flashcards

1
Q

What are the functions of calcium?

A

bone and tooth structure, mineral store, action potentials, membrane excitability, second messenger, co-factor in metabolic pathways, blood clotting factor

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2
Q

How can we be certain that cause of tooth weakness after development is not due to Ca deficiency?

A

detine/enamel cannot be broken down to recover Ca because odontoclasts/ameloclasts do not exist

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3
Q

Examples of Ca acting as a second messenger

A

muscle (excitation-contraction coupling), gland secretion, non-steroid hormone action (non-steroid therefore cannot penetrate membrane)

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4
Q

What is meant by diffusible calcium?

A

calcium that is available - it is either ionised or bound to citrate

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5
Q

What is the concentration of ionised calcium?

A

1.2 mmol/l

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6
Q

What is the concentration of diffusible calcium bound to citrate?

A

0.2mmol/l

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7
Q

What is non-diffusible calcium?

A

calcium that’s bound to proteins

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8
Q

What is the concentration of calcium bound to protein (non-diffusible)?

A

1.2 mmol/l

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9
Q

What is the total concentration of calcium in the body?

A

2.6 mmol/l (diffusible 1.4 + non-diffusible 1.2)

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10
Q

Where do we get calcium from?

A

our diet

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11
Q

Where is calcium absorbed from our diet?

A

GI tract

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12
Q

What happens to the calcium that is not absorbed in the GIT?

A

the calcium is excreted in faeces

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13
Q

What is the name of the type of bone that is remodelled to achieve Ca balance?

A

exchangeable bone

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14
Q

What is the name of the type of bone that is not demineralised/remodelled?

A

stable bone

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15
Q

Where does the Ca that is absorbed from the GIT go?

A

Ca enters the plasma and interstitial fluid

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16
Q

How is excess Ca excreted from the plasma?

A

blood is filtered by the kidneys and excess Ca is excreted in urine

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17
Q

How does Ca become incorporated into bone?

A

Ca from the plasma/interstitial fluid is used to mineralise osteoid of exchangeable bone which then becomes stable bone

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18
Q

Which substances are required for calcium homeostasis?

A

parathyroid hormone, calcitonin, vitamin D

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19
Q

Where is PTH secreted from?

A

parathyroid glands

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20
Q

When in PTH secreted?

A

when plasma [Ca2+] is low

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21
Q

Function of PTH

A

increases plasma calcium

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22
Q

How does PTH increase plasma calcium?

A

increased bone resorption, increased Ca2+ resorption in kidney (in exchange with decreased PO4 resorption), increased Ca2+ uptake from intestines (assisted by vit D)

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23
Q

Which cells carry out bone resorption?

A

osteoclasts

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24
Q

What is the effect of PTH on the kidney?

A

increases Ca2+ resorption, increases PO4 excretion, increases 1,25 (OH)2 vit D (calcitriol) formation

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25
Q

What is the effect of PTH on bone?

A

bone resorption - releases Ca2+ and PO4

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26
Q

What is the overall effect of PTH on PO4 concentration?

A

no effect - although there is increased PO4 excretion from kidney, bone resorption releases PO4

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27
Q

How is absorption of Ca from the intestines increased?

A

PTH increases the formation of 1,25 (OH)2 vit D (calcitriol) in the kidneys which aids the absorption of Ca from the GIT

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28
Q

Where is calcitonin secreted from?

A

C cells (parafollicular) in the thyroid gland

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29
Q

When is calcitonin released?

A

When plasma [Ca2+] is high

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30
Q

What is the function of calcitonin?

A

reduces plasma [Ca2+]

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31
Q

How does calcitonin lower plasma calcium?

A

increases bone formation and decreases Ca2+ resorption in the kidneys

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32
Q

Which cells are involved in bone formation?

A

osteoblasts

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33
Q

Why does it seem that calcitonin does not play a major role in calcium homeostasis?

A

a lack of calcitonin has no pathological effects

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34
Q

What is the effect of calcitonin on kidneys?

A

increases Ca2+ excretion

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35
Q

What is the effect of calcitonin on bone?

A

increases bone deposition

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36
Q

Where is vitamin D derived from?

A

dietary vitamin D and 7-dehydrocholesterol synthesised in the skin

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37
Q

What is the name of the precursor to vitamin D synthesised in the skin in sunlight?

A

7-dehydrocholesterol

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38
Q

What is the first product from dietary vitamin D and 7-dehydrocholesterol?

A

vitamin D3 (cholecalciferol)

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39
Q

What is vitamin D3 (cholecalciferol) converted into?

A

25 (OH) cholecalciferol

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40
Q

How is vitamin D3 (cholecalciferol) converted into 25 (OH) cholecalciferol?

A

vitamin D3 (cholecalciferol) is hydroxylated by 25-hydroxylase in the liver

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41
Q

Where is vitamin D3 (cholecalciferol) hydroxylated into 25 (OH) cholecalciferol?

A

in the liver by 25-hydroxylase

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42
Q

What is 25 (OH) cholecalciferol converted into?

A

1,25 (OH)2 cholecalciferol (calcitriol)

43
Q

How is 25 (OH) cholecalciferol converted into 1,25 (OH)2 cholecalciferol?

A

hydroxylated by 1a (alpha) hydroxylase in the kidney

44
Q

Which enzyme converts 25 (OH) cholecalciferol into 1,25 (OH)2 cholecalciferol (calcitriol)?

A

1 alpha hydroxylase (in the kidney)

45
Q

Which hormone regulates the hydroxylation of 25 (OH) cholecalciferol into 1,25 (OH)2 cholecalciferol in the kidney?

46
Q

What is the active form of vitamin D?

A

1,25 (OH)2 cholecalciferol (calcitriol)

47
Q

What is the overall function of 1,25 (OH)2 cholecalciferol (calcitriol)?

A

increase plasma Ca and PO4

48
Q

How does 1,25 (OH)2 cholecalciferol (calcitriol) increase plasma Ca and PO4?

A

increases Ca absorption from intestines, increase Ca and PO4 retention in kidneys, and increases Ca and PO4 release from bone

49
Q

What is the effect of 1,25 (OH)2 cholecalciferol (calcitriol) on the intestine?

A

increases Ca absorption in intestine

50
Q

What is the effect of 1,25 (OH)2 cholecalciferol (calcitriol) on the kidneys?

A

increases Ca and PO4 retention

51
Q

What is the effect of 1,25 (OH)2 cholecalciferol (calcitriol) on bone?

A

increases Ca and PO4 release

52
Q

What is a similarity in the effects of vitamin D (calcitriol) and PTH?

A

both increase plasma [Ca]

53
Q

What is a difference between the effects of PTH and vitamin D (calcitriol)?

A

PTH doesn’t affect [PO4] as PO4 excretion from kidney is increased whereas calcitriol increases PO4 retention in the kidneys resulting in an overall [PO4] increase (bone resorption increases PO4 too)

54
Q

Which hormones increase bone formation/mass?

A

calcitonin, growth hormone, IGF-1, insulin, oestrogen, testosterone

55
Q

Which hormones increase bone resorption and therefore decrease bone mass?

A

cortisol, parathyroid hormone, thyroid hormones

56
Q

Function of osteoblasts

A

synthesis and secrete collagen fibres forming a matrix (osteoid) which is later mineralised by calcium salts

57
Q

How do osteocytes arise?

A

when osteoblasts become trapped in the matrix they mature into osteocytes

58
Q

Where are osteocytes found?

A

in bony lacunae

59
Q

How do osteocytes communicate?

A

via long cytoplasmic processes

60
Q

Describe the structure of an osteoclast

A

a large, multinucleate cell

61
Q

What cells are osteoclasts derived from?

A

monocyte/macrophage lineage

62
Q

Function of osteoclasts

A

resorb bone

63
Q

Where are osteoclasts found?

A

in depressions called Howship’s lacunae

64
Q

What concept underpins orthodontic treatment?

A

bone remodelling

65
Q

Function of bone remodelling

A

allows a constant source of Ca

66
Q

What is the term for raised [Ca2+]?

A

hypercalcaemia

67
Q

What is the term for reduced [Ca2+]?

A

hypocalcaemia

68
Q

What condition may result from low calcium levels in the blood?

A

Hypocalcaemic tetany

69
Q

What does hypocalcaemic tetany cause?

A

involuntary muscle contractions

70
Q

What are the causes of hypocalcaemic tetany?

A

decreased Ca2+ intake, excessive Ca2+ loss, alkalosis

71
Q

What is alkalosis?

A

condition where blood plasma pH is too high

72
Q

How can alkalosis contribute to hypocalcaemia?

A

a high blood plasma pH increases protein binding of calcium which decreases ionised calcium (diffusible)

73
Q

How does low [Ca2+] impact nerve excitability?

A

low [Ca2+] increases nerve excitability

74
Q

What are the symptoms of low [Ca2+]?

A

pins and needles, muscle spasms

75
Q

What are the 2 clinical indicators of hypocalcaemia?

A

Trousseau’s sign and Chvostek’s sign

76
Q

What is Trousseau’s sign?

A

involuntary contractions of muscles in hand and wrist due to hypocalcaemia

77
Q

What is Chvostek’s sign?

A

tapping of the facial nerve resulting in muscle contraction due to hypocalcaemia

78
Q

What can cause alkalosis?

A

hyperventilation (increase in O2 which expels more CO2 causing increase alkalinity of blood)

79
Q

What is the treatment for alkalosis due to hyperventilation?

A

trapping CO2 in the lungs by rebreathing expired air from a bag

80
Q

Which hormones can cause calcium regulation disorders if they are over or under secreted?

A

parathyroid hormone, vitamin D, calcitonin

81
Q

What is the consequence of hyperparathyroidism?

A

increased bone resorption

82
Q

Which condition can result from hyperparathyroidism?

A

osteitis fibrosa cystica

83
Q

What is osteitis fibrosa cystica?

A

areas of demineralisation in skull and leg bones

84
Q

What is unusual about the name of the disease, osteitis fibrosa cystica?

A

it names features that do not occur in the condition - there is no inflammation of the bone, no fibrous tissue or cysts

85
Q

How would osteitis fibrosa cystica be diagnosed?

A

no infection, no cysts, teeth vital. Panoramic radiograph of the skull shows other areas of radiolucency / lesions. Refer to GP to test [Ca2+]

86
Q

What consequence does hypoparathyroidism have on teeth?

A

defective teeth mineralisation due to low blood [Ca2+] from under secretion of PTH (congenital as enamel is not broken down following development)

87
Q

What is the cause of vitamin D deficiency?

A

dietary deficiency results in failure to synthesise 1,25 (OH)2 cholecalciferol (calcitriol)

88
Q

What are the consequences of vitamin D deficiency?

A

decreased Ca uptake from GIT, undermineralised bone causing a lack of rigidity

89
Q

What is the condition of a lack of bone rigidity in children?

90
Q

What is the name of the condition in which adults lack bone rigidity?

A

osteomalacia

91
Q

Cause of rickets / osteomalacia

A

vitamin D deficiency

92
Q

What are the symptoms of rickets?

A

bowlegged, cowboy walk, flexible bones

93
Q

What are the consequences of increased or decreased calcitonin levels?

A

no obvious clinical consequences - so calcitonin is likely not essential for plasma [Ca2+] regulation

94
Q

Which bone disease results in a decreased bone mass and density?

A

osteoporosis

95
Q

Which bone disease results in an increased bone mass and density?

A

osteopetrosis

96
Q

Which part of the population is more affected by osteoporosis?

97
Q

Although osteoporosis affects both men and women, why is it evident earlier in women?

A

due to menopause (decreased oestrogen)

98
Q

Causes of osteoporosis

A

menopause, corticosteroids (cortisol increases bone resorption), nutritional deficiency

99
Q

How does osteopetrosis affect blood supply?

A

osteopetrosis reduces blood supply

100
Q

What are the consequences of osteopetrosis?

A

bone is prone to fracture and chronic infection, difficult extractions and healing

101
Q

Why is bone healing reduced in osteopetrosis?

A

due to reduced blood vessels

102
Q

Why are tooth roots indistinct from bone on radiographs in patients with osteopetrosis?

A

osteopetrosis results in more radiopaque bone which is difficult to distinguish from teeth

103
Q

How do the maxilla and mandible compare in osteopetrosis?

A

mandible is enlarged and has a greater density than mandible