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Rheumatology > Calcium > Flashcards

Calcium Flashcards

1
Q

In what form is calcium stored in the bone?

A

Hydroxyapatite

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2
Q

What % of the body’s total calcium is stored in the bone?

A

99%

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3
Q

What is meant by being in positive calcium balance?

A

Absorption of dietary calcium exceeds the intestinal+renal losses of calcium by around 400mg per day (e.g. in growing children)

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4
Q

What is the normal serum calcium concentration?

A

2.2-2.6g

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5
Q

How does serum calcium exist?

A
  • 47% as uncomplexed calcium ions
  • 44% associated with serum albumen
  • 9% complexed with citrate

(N.B. latter two forms are unavailable to cells since they are unable to enter via the calcium ion transporter)

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6
Q

What are the roles of calcium in the body?

A
  • Structural role is in the skeleton
  • Calcium is also required for a number of calcium-dependent cellular processes including:
  • Muscle contraction
  • Cardiac action potential
  • Calcium dependent protein kinases
  • Secretion of hormones and neurotransmitters (calcium allows fusion of secretory vesicles with plasma membrane)
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7
Q

How much calcium is injested each day?

A

25mmol

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8
Q

How much calcium is absorbed from the gut each day?

A

10-14mmol (50% of daily ingested calcium)

BUT half of this absorbed amount (7mmol) is re-secreted into the gut every 24 hours

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9
Q

How is the majority of calcium excreted?

A

Faecal

Remainder is excreted via the kidneys in the urine

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10
Q

What is the normal phosphate concentration?

A

0.6-1.3mmol/L in an adult (higher in children)

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11
Q

What happens if serum phosphate falls?

A

It is replaced by mobilisation of bone mineral

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12
Q

What happens if serum phosphate rises?

A

Serum phosphate complexes free serum calcium. The free calcium is replaced by mobilisation of bone mineral

I.E. both reduced and increased levels of serum phosphate can cause demineralisation of bone

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13
Q

What hormones/chemicals coordinate calcium homeostasis?

A

Parathyroid hormone
Calcitriol (vit D)
Calcitonin

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14
Q

Which of the hormones/chemicals that coordinate calcium homeostasis increase serum calcium?

A

PTH

Calcitriol

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15
Q

Which of the hormones/chemicals that coordinate calcium homeostasis decrease serum calcium?

A

Calcitonin

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16
Q

How do PTH and calcitriol increase serum calcium?

A
  • Increase the activity of osteoclasts–> increased calcium mobilisation from bone
  • Increase calcium reabsorption from the distal kidney tubules
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17
Q

How does calcitonin decrease serum calcium?

A
  • Inhibits osteoclast function

- Inhibits calcium reabsoption from the distal kidney tubules

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18
Q

What can cause hypocalcaemia in premature babies?

A
  • Secretion of parathyroid hormone requires magnesium

- Magnesium deficiency in premature babies can impair PTH secretion–>hypocalcaemia

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19
Q

Describe the relationship between serum calcium concentration and PTH concentration?

A

At serum calcium levels bewteen 1.5-2.7, plasma conc. of PTH is inversely proportional to calcium concentration

  • Increased serum calcium concentration–> decreased secretion of PTH
  • Decreased serum calcium concentration –> increased secretion of PTH
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20
Q

How does PTH increase serum calcium?

A
  • PTH binds to G-protein receptors found on osteoblasts and in the renal tubules
  • It’s binding causes an increased in cAMP
  • In osteoblasts, increased cAMP leads to increased generation of osteoclast activating factors which increase resorbtion of calcium
  • PTH also increases intestinal absorption of calcium by increasing synthesis of calcitriol through stimulation of renal 1a-hydroxylase
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21
Q

Describe how vitamin D3 in the skin is converted to enable biological activity

A
  1. Hydroxylation in the liver at position C25 by 25-hydroxylase to 25-hydroxy-vitamin D3
  2. Further hydroxylation in the kidney at position C1 by 1a-hydroxylase to the active form, 1, 25,-dihydroxy-vitamin D3
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22
Q

What is 25-hydroxy-Vitamin D3 converted to in the kidney?

A

Hydroxylation of 25-hydroxy-Vitamin D3 can either occur ar:

  • Position C1, catalysed by 1a-hydroxylase, creating the active form 1, 25-dihydroxy-Vitamin D3
  • Position C24, catalysed by 24-hydoxylase, which renders the 25-hydroxy-Vitamin D3 biologically inactive
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23
Q

How is vitamin D metabolism controlled?

A
  • Serum calcium concentration: low serum calcium maximises activity of 1a-hydroxylase, as serum calcium increases, 24-hydroxylase activity increases
  • PTH increases 1a-hydroxylase activity
  • Calcitonin inhibits 1a-hydroxylase
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24
Q

How does vitamin D3 serum calcium?

A
  • The active metabolite of vitamin D3 (1, 25-dihydroxy-Vitamin D3) increases the expression of an intestinal calcium transporter increasing intestinal uptake of calcium
  • In addition in acts in osteoblasts to increase the transcription of osteoblast activating factors that stimulate resorption of calcium and phosphate from bone by osteoclasts
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25
Q

Where is calcitonin synthesised?

A

The para-follicular C-cells of the thyroid gland

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26
Q

What is the action of calcitonin?

A

Over the calcium concentration range of 2.1-3.0mmol/L serum calcitonin increases in direct proportion to calcium concentration. This relationship is believed to prevent hypercalcaemia on intake of a high calcium load. Calcitonin inactivates osteoclasts leading to reduced bone demineralisation (i.e. prevents release of calcium from bone)

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27
Q

What is the definition of osteoporosis?

A

Bone mineral density (BMD) more than 2.5 SDs below the young adult mean

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28
Q

What is the definition of osteopenia?

A

Bone mineral density (BMD) 1-2.5 SDs below the young adult mean

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29
Q

What are the risk factors for osteoporosis?

A
  • Female sex
  • Caucasian/Asian
  • Increasing age
  • Previous fracture
  • FHx of hip fracture
  • Low BMI
  • Smoking
  • Alcohol abuse
  • Immobilisation
  • Chronic liver disease
  • Chronic renal disease
  • COPD
  • Low dietary calcium intake
  • Vitamin D insufficiency
  • Drugs
  • Endocrine diseases: Cushing’s, hyperthyroidism, hyperparathyroidism
  • RA
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30
Q

Describe the aetiology of osteoporosis

A

Osteoporosis is related either to inadequate peak bone mass and/or ongoing bone loss. Peak bone mass is achieved in early adult life. Then age related bone loss occurs with an accelerated rate in women, starting around the menopause

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31
Q

What factors affect peak bone mass?

A

Genetic factors
Nutritional factors
Sex hormone status
Physical activity

32
Q

What drugs can cause osteoporosis?

A

Steroids
Heparin
Ciclosporin
Anticonvulsants

33
Q

What are the four sites where osteoporotic fractures typically occur?

A

Thoracic vertebrae
Lumbar vertebrae
Femoral neck
Distal radius (Colles’ fracture)

34
Q

What are the clinical features of thoracic vertebral fractures?

A

Kyphosis

Loss of height (widow’s stoop)

35
Q

What is the gold standard measurement of bone density?

A

Dual energy X-ray absorptiometry (DXA)

36
Q

What are the secondary causes of osteoporosis?

A 
Thyrotoxicosis
Myeloma
Primary hyperparathyroidism
Hypogonadism
Coeliac disease
37
Q

In which individuals with osteoporosis should blood tests be arranged to look for secondary causes?

A

Men

Premenopausal women

38
Q

What are the indications for DXA scanning?

A

Radiographic osteopenia
Previous fragility fracture (in those <19
Maternal history of hip fracture

39
Q

If a patient presents with height loss and/or kyphosis, what is the initial investigation? What will this investigation show?

A

Inital investigation is thoracic spine x-ray

shows loss of anterior vertebral body height and wedging due to fracture

40
Q

What is the Risk Factor Assessment Tool for osteoporosis?

A

FRAX: A WHO tool for estimating the 10 year probability of hip fracture or major osteoporotic fractures combined for an untreated patient aged 40-90. It integrates clinical risk factors with femoral neck bone-mineral density. It is a guide only and is not helpful in all patients

41
Q

In the UK, at what level on FRAX is treatment for osteoporosis started?

A

4% 10-year risk of hip fracture (3% in the US)

42
Q

How are new vertebral fractures treated?

A 
Bed-res for 1-2 weeks and strong analgesia
Muscle relaxants (e.g. diazepam 2mg, 3x daily), subcutaneous calcitonin or IV pamidronate are also given for pain relief
43
Q

What lifestyle advice is given to people with osteoporosis?

A 
Stop smoking
Reduce alcohol intake
Adequate intake of calcium (700-1000mg/day; 1500mg post menopausally)
Adequate intake of Vitamin D
Regular weight bearing exercises
44
Q

What is the first line treatment for osteoporosis?

A

Bisphosphonates + calcium and vit D supplementation

45
Q

What is the second line treatment of osteoporosis?

A

Raloxifene or denosumab

46
Q

What treatment is given if bisphosphonates and raloxifene are not tolerated?

A

1st line: teripartide

2nd line: HRT or denosumab

47
Q

How do bisphosphonates work?

A

They inhibit bone resorption through inhibition of osteoclast activity

48
Q

Name 3 common bisphosphonates

A

Alendronate
Risendronate
Zoledronate

49
Q

What are the side effects of bisphosphonates?

A
  • GI (dyspepsia, nausea, vomiting, abdo pain, diarrhoea, constipation)
  • Flu-like symptoms
  • Oesophageal reactions e.g. ulcers and strictures: can be severe. Patients are therefore advised to take the tablets with a full glass of water on rising, to take them on an empty stomach at least 30 minutes before the first food of the day and to stand/sit for 30 minutes after taking them
  • Osteonecrosis of the jaw (greatest risk in patients taking IV bisphosphonates for cancer indications)

-

50
Q

What is the action of raloxifene?

A

It is a selective oestrogen receptor modulator (SERM). It activates oestrogen receptors on bone while having no stimulatory effect on endometrium.

51
Q

What treatment may be indicated in severe cases of osteoporosis in women who are intolerant of or fail to respond to other therapies?

A

Recombinent human parathyroid peptide (teriparatide) given by subcutaneous injection and stimulates bone formation. Hypercalcaemia is a side effect

52
Q

What treatment may be given to men with osteoporosis and biochemical evidence of hypogonadism?

A

Testosterone

53
Q

What treatment is given to all patients >65 taking corticosteroid treatment?

A

Bisphosphonates or teriparatide

54
Q

What is osteonecrosis?

A

Also known as AVN. Death of bone and marrow cells due to reduced blood supply.

55
Q

What are the causes of osteonecrosis?

A 
Medication (glucocorticoids, bisphosphonates)
Alcohol abuse
Sickle cell disease
Trauma
Radiation
HIV infection
56
Q

What is the commonest site affected by osteonecrosis?

A

Femoral neck

57
Q

How does osteonecrosis present?

A

Pain
Arthropathy
Bony collapse if untreated

58
Q

How is osteonecrosis diagnosed?

A

MRI (x-ray doesn’t show early changes)

59
Q

What is Paget’s disease?

A

A focal disorder of bone remodelling in which there is increased osteoclastic bone resorption followed by formation of weaker new bone, increased local bone blood flow and fibrous tissue. Incidence increases with age. Rare in <40s but affects 10% of adults at 90

60
Q

What are the most common sites of Paget’s disease?

A 
Pelvis
Lumbar spine
Femur
Thoracic spine
Skull
Tibia
61
Q

What are the clinical features of Paget’s disease?

A
  • Most cases are asymptomatic
    Possible symptoms include:
  • Pain in the bone or nearby joint
  • Deformities: enlargement of the skull, bowing of the tibia
  • Complications: nerve compression (causing deafness or paraparesis); pathological fractures; rarely high-output cardiac failure (due to increased bone blood flow) and osteogenic sarcoma
62
Q

What are the biochemical findings in Paget’s disease?

A

Normal calcium and phosphate. Greatly raised alkaline phosphate

63
Q

What characteristic changes are seen on X-ray in Paget’s disease?

A 
Localised bony enlargement and distortion
Sclerotic changes (increased density)
Osteolytic areas (loss of bone and reduced density)
64
Q

How is Paget’s disease treated?

A

Bisphosphonates

65
Q

For which patients with Paget’s disease is pharmacological treatment indicated?

A

Symptomatic patients

Asymptomatic patients at risk of complications e.g. fracture or nerve entrapment

66
Q

How is disease activity monitored in Paget’s disease?

A

Symptoms

Measurement of serum alkaline phosphatase or urinary hydroxyproline

67
Q

What are the clinical manifestations of vitamin D deficiency?

A

Rickets (in children)

Osteomalacia in adults

68
Q

Which individuals are at risk of vitamin D deficiency?

A
  • Those with pigmented skin
  • Use of sunscreen
  • Concealing clothing
  • The elderly and institutionalised (esp. nursing home residents)
  • Malabsoption disorders
  • Renal disease (due to inadequate conversion of 25, hydroxy-vitamin D3 to 1,25, dihydroxy-vitamin D3
  • Liver diease
69
Q

Which drugs can increase risk of vitamin D deficiency?

A
  • Anticonvulsants
  • Rifampicin
  • HAART
70
Q

What are the common symptoms of osteomalacia?

A

Proximal muscle weakness and pain

71
Q

What features may present with severe vitamin D deficiency?

A

Hypocalcaemia
Tetany
Siezures

72
Q

How does rickets present in children?

A

Bone deformity (knock knees, bowed legs) and impaired growth

73
Q

What are the biochemical findings in osteomalacia?

A

Low calcium and phosphate. High alkaline phosphatase

74
Q

What is the X-ray appearance in osteomalacia?

A

Defective mineralization

Looser’s zones (low density bands extending from the cortex inwards in the shafts of the long bones)

75
Q

How is vitamin D deficiency treated?

A

Oral calciferol (10,000 IU daily for 8-12 weeks then maintenance dose of 1000 IU daily)

76
Q

How is vitamin D deficiency treated in patients with severe malabsorbtion?

A

IM calciferol 300,000 IU monthly for 3 months, then yearly maintenance dosease

77
Q

What adverse health effects are associated with vitamin D deficiency

A

Increased risk of type II DM
Cancer
CVD

Rheumatology (13 decks)

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