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Kat's Pathology > Calcium Metabolism > Flashcards

Calcium Metabolism Flashcards

1
Q

What are the roles of calcium in the body? (2)

A

Skeleton strength.

Metabolic actions.

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2
Q

What are the metabolic actions of calcium? (2)

A

Action potentials.

Intracellular signalling.

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3
Q

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

A

99%

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4
Q

What three organ systems are involved in calcium uptake/excretion in the body?

A

Digestive system.
Bone.
Kidneys.

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5
Q

What percentage of the body’s calcium is present in serum?

A

1%

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6
Q

What three forms is serum calcium present in? (3)

A

Free (ionised) - approximately 50%
Protein-bound - approximately 40%
Complexed - approximately 10%

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7
Q

What form of plasma calcium is the biologically active form?

A

Free (ionised calcium)

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8
Q

What protein is calcium bound to in the serum?

A

Albumin.

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9
Q

What is serum calcium complexed with?

A

Citrate/phosphate.

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10
Q

What is the normal range of serum calcium?

A

2.2-2.6mmol/L

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11
Q

What is normally reported when looking at calcium levels in the body?

A

‘Corrected’ Calcium

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12
Q

How is the correct calcium calculated?

A

serum calcium + 0.02 x (40-serum albumin in g/L)

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13
Q

What other form of calcium is measured in the blood (Apart from corrected)

A

Ionised calcium.

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14
Q

Why is it important to measure the corrected calcium in the blood?

A

If you have low albumin, the bound calcium will be low, but the free calcium will be normal.
The corrected calcium allows you to see where the problem lies.

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15
Q

Why is it important to maintain a normal level of circulating calcium? (2)

A

Important for normal nerve and muscle function.

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16
Q

What happens to circulating calcium levels in calcium and vitamin D deficiency?

A

Plasma concentration must be maintained despite calcium and vitamin D deficiency.
Chronic calcium deficiency thus results in loss of calcium from bones in order to maintain circulating calcium.

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17
Q

What is the homeostatic response to low calcium? (2)

A

Hypocalcaemia is detected by the parathyroid gland.

The parathyroid gland releases PTH.

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18
Q

Where does PTH obtain calcium from? (3)

A

Bone.
Gut (absorption - increased 1,25(OH) vitamin D).
Kidney (resorption and renal 1 alpha hydroxylase activation)

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19
Q

How does PTH obtain calcium from the gut?

A

Through vitamin D.

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20
Q

How does PTH obtain calcium from the kidneys? (2)

A

Actions of PTH direction.

Vitamin D actions.

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21
Q

How does PTH obtain calcium from bone?

A

Direct action of PTH.

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22
Q

What type of hormone is vitamin D?

A

Steroid hormone.

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23
Q

Where is PTH released from?

A

Parathyroids.

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24
Q

How many amino acids make up PTH?

A

84 amino acid protein.

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25
Q

What are the roles of PTH? (3)

A

Bone and renal calcium resorption.
Stimulates 1,25(OH)2 vitamin D synthesis (through 1-alpha-hydroxylation)
Also stimulates renal phosphate wasting.

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26
Q

What is the pathway for vitamin D synthesis? (4)

A

7-dehydrocholesterol –> cholecalciferol (D3) ((sun))

cholecalciferol (D3) –> 25-hydroxycholecalciferol (25-OH D3) ((liver))

25-hydroxycholecalciferon (25-OH D3) –> 1,25-dihydroxycholecalciferol (1,25(OH)2 D3) ((kidneys))

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27
Q

What is the physiological active form of vitamin D?

A

1,25(OH)2 D3 (1,25-dihydroxycholecalciferol)

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28
Q

What is ergocalciferol?

A

Vitamin D2 - a plant vitamin.

Active form.

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29
Q

What is cholecalciferol?

A

Vitamin D3 - synthesised in the skin.

Active form.

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30
Q

What enzyme in the liver hydroxylates cholecalciferol –> 25- hydroxycholecalciferol

A

25-hydroxylase.

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31
Q

Is 25-hydroxycholecalciferol active or inactive?

A

Inactive - this is the stored and measured form of vitamin D.

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32
Q

Where does activation of vitamin D occur?

A

Kidney.

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33
Q

What enzyme in the kidney activates vitamin D?

A

1-alpha-hydroxylase.

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34
Q

From where can 1-alpha-hydroxylase be secreted from? (2)

A

Kidney.

Rarely from lung cells of sarcoid tissue.

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35
Q

What is the mechanism of action of 1,25-dihydroxycholecalciferol? (4)

A

Intestinal calcium absorption.
Intestinal phosphate absorption.
Critical for bone formation.

Vitamin D receptor controls many genes (e.g. for cell proliferation, immune system, etc…)

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36
Q

What is vitamin D deficiency associated with? (3)

A

Cancer.
Autoimmune disease.
Metabolic syndrome.

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37
Q

What is the rate limiting step in vitamin D synthesis?

A

Activation of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol.

Rate limiting in the kidney under PTH control.

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38
Q

What is the role of the skeleton? (8)

A

Metabolic role in calcium homeostasis.
Main reservoir of calcium, phosphate and magnesium.

Structural framework. 
Strong. 
Relatively lightweight. 
Mobile. 
Protects vital organs. 
Capabel of orderly growth and remodelling.
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39
Q

What are the main types of metabolic bone disease? (5)

A

Osteoporosis.
Osteomalacia.
Paget’s disease.

Parathyroid bone disease.
Renal osteodystrophy.

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40
Q

How does vitamin D deficiency affect the bone?

A

Defective bone mineralisation.

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41
Q

What does vitamin D deficiency lead to? (2)

A

Childhood –> Rickets.

Adulthood –> Osteomalacia.

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42
Q

What percentage of UK adults have vitamin D deficiency? (2)

A

50% of adults have insufficient vitamin D.

16% have severe deficiency during winter and spring.

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43
Q

What are some risk factors for vitamin D deficiency? (7)

A

Lack of sunlight exposure.
Dark skin.
Dietary.
Malabsorption.

Renal failure.
Anticonvulsants induce breakdown of vitamin D.
Chappatis (phytic acid)

44
Q

What are the clinical features of osteomalacia? (4)

A

Bone and muscle pain.
Increased risk of fracture.
Looser’s zones on x-ray (pseudofractures).
Biochemical abnormalities - low calcium, low phosphate, raised ALP.

45
Q

What are the biochemical abnormalities in osteomalacia? (3)

A

Low calcium.
Low phosphate.
Raised ALP.

46
Q

What are the clinical features of rickets? (4)

A

Bowed legs.
Costochondral swelling.
Widened epiphyses at the wrists.
Myopathy.

47
Q

What is the underlying pathology of osteomalacia?

A

Demineralisation of bone.

48
Q

What is osteomalacia caused by?

A

Vitamin D deficiency.

49
Q

What is the underlying pathology of osteoporosis?

A

Loss of bone mass, leading to pathological fractures.

50
Q

Is the bone abnormal in osteoporosis?

A

No, residual bone is normal in structure.

51
Q

What age does bone density decrease from?

A

20.

52
Q

What is the strongest risk factor for osteoporosis?

A

Increasing age.

53
Q

How is calcium level affected in osteoporosis?

A

It isn’t - normal calcium.

54
Q

What is the biochemistry in osteoporosis? (3)

A

Normal calcium.
Normal phosphate.
Normal ALP.

55
Q

How does osteoporosis normally first present?

A

Asymptomatic until a fracture occurs.

56
Q

What are the most common areas for osteoporotic fractures to occur? (3)

A

NOF.
Vertebral.
Wrist (Colle’s)

57
Q

How is osteoporosis diagnosed?

A

DEXA scan (Dual energy X-ray absorptiometry)

58
Q

What areas of the body are scanned using a DEXA scan? (2)

A

Hip (femoral neck)

Lumbar spine.

59
Q

What is the T-score in a DEXA scan?

A

SD from mean of young healthy population

60
Q

What is the T-score used for in DEXA scanning?

A

Useful to determine fracture risk.

61
Q

What is the Z-score in DEXA scanning?

A

SD from mean of age-matched controls.

62
Q

What is the Z-score used for in DEXA scanning?

A

Useful to identify accelerated bone loss in younger patients.

63
Q

What T score indicates osteoporosis?

A
64
Q

What T score indicates osteomalacia?

A

Between -1 and -2.5.

65
Q

What are the causes of osteoporosis? (4)

A

Age-related decline in bone mass (e.g. menopause).
Failure to attain peak bone mass (e.g. childhood illness).
Early menopause.
More rapid bone loss during adulthood (e.g. lifestyle: sedentary, alcohol, smoking, low BMI/nutritional; endocrine: hyperprolactinaemia, thyrotoxicosis, Cushing’s; Drugs: steroids; other: genetic, prolonged intercurrent illness).

66
Q

What are the lifestyle treatments for osteoporosis? (3)

A

Weight-bearing exercise.
Stop smoking.
Reduce alcohol.

67
Q

What are the drug treatments for osteoporosis? (6)

A

Vitamin D/calcium.
Bisphosphonates (e.g. alendronate) - reduced bone resportion.
Teriparatide (PTH derivative) - anabolic actions.
Strontium - anabolic and anti-resorptive actions.
Oestrogens (HRT)
SERMs (e.g. reloxifene)

68
Q

What are the symptoms of hypercalcaemia? (3)

A

Polyuria/polydipsia.
Constipation.
Neurological - confusion/seizures/coma.

69
Q

What calcium level is required for symptoms of hypercalcaemia to develop?

A

> 3mmol/L

70
Q

What is the normal physiological response to hypercalcaemia?

A

Suppression of PTH.

71
Q

What are the two most important questions to ask when faced with a patient with hypercalcaemia?

A

Is it a genuine result (repeat).

What is the PTH?

72
Q

What are the causes of hypercalcaemia without PTH suppression (2)

A

Inappropriate PTH response to hypercalcaemia = primary problem with PTH regulation.

  1. primary hyperparathryoidism (most common).
  2. Familial hypocalciuric hypercalcaemia (rare)
73
Q

What are the causes of hypercalcaemia with PTH suppression? (2)

A

Appropriate PTH response to hypercalcaemia = seek other causes.

  1. Malignancy (most common)
  2. Others (rare) - sarcoid, vitamin D excess, thyrotoxicosis, milk alakali syndrome.
74
Q

What is the most common cause of hypercalcaemia?

A

Primary hyperparathyroidism.

75
Q

What are the causes of primary hyperparathyroidism? (3)

A

Parathyroid adenoma, hyperplasia, carcinoma.

76
Q

What syndrome is parathyroid hyperplasia associated with?

A

MEN1.

77
Q

Who is more often affected by primary hyperparathyroidism?

A

Women more often affected than man.

78
Q

What is the biochemistry of primary hyperparathroidism? (4)

A

Raised serum calcium.
Raised or inappropriately normal PTH.
Low serum phosphate.
Raised urine calcium (due to hypercalcaemia)

79
Q

What is the best way to remember to symptoms of primary hyperparathyroidism?

A

Bones (PTH bone disease).
Stones (renal calculi).
Abdominal Moans (constipation, pancreatitis).
Psychic Groans (confusion).

80
Q

Where is the calcium sensing receptor present? (CaSR)

A

Parathyroids - regulates PTH release.

Renal - influences calcium resorption (PTH independent)

81
Q

What is the defect in familial hypocalciuric hypercalcaemia (FHH/FBH).

A

CaSR mutation.

Higher set point for PTH release –> mild hypercalcaemia
Reduces urine calcium.

82
Q

What are the most common malignancies that cause hypercalcaemia? (3)

A 
Hymoural hypercalcaemia of malignancy (e.g. small cell lung carcinoma) 
Bone metastases (e.g. breast carcinoma causing local one osteolysis). 
Haematological malignancy (e.g. myeloma - cytokines).
83
Q

What are some other causes of non-PTH driven hypercalcaemia (apart form malignancy) (5)

A

Sarcoidosis (non-remal 1-alpha hydroxylation).
Thyrotoxicosis (thyroxine –> boen resportion)
Hypoadrenalism (renal calcium transport).
Thiazide diuretics (renal calcium transport)
Excess vitamin D (e.g. sunbeds).

84
Q

What is the acute treatment for hypercalcaemia? (3)

A

FLUIDS
FLUIDS
Bisphosphonates (if cause is known to be cancer) - OTHERWISE AVOID.

85
Q

What is the long-term management of hypercalcaemia?

A

Treat the underlying cause.

86
Q

What are the clinical signs of hypocalcaemia? (4)

A

Neuro-muscular excitability (e.g. trousseau’s sign, hyperreflexia, chvostek’s sign, convulsions).
Laryngeal spasm (stridor)
ECG - prolonged QT interval.
Choked optic disc.

87
Q

What is the treatment for hypocalcaemia? (2)

A

Calcium and vitamin D

usually activated - i.e. 1-alpha forms, except simple vitamin D deficiency

88
Q

What are the two questions you have to ask when faced with a result showing hypocalcaemia (2)

A

Is it a genuine result - repeat and adjust for albumin.

What is the PTH?

89
Q

What are the two broad causes of hypocalcaemia?

A

Non-PTH driven

Due to low PTH

90
Q

What are some non-PTH driven causes of hypocalcaemia? (3)

A 
Vitamin D deficiency (dietary, malabsorption, lack of sunlight). 
Chronic kindney disease (1-alpha hydroxylation) 
PTH resistance (pseudohypoparathyroidism - PTH will be raised)
91
Q

What are some causes of hypocalcaemia due to low PTH? (4)

A

Surgical (including post thyroidectomy)
Auto-immune hypoparathyroidism.
Congenital absence of parathyroids (e.g. DiGeorge syndrome).
Magnesium deficiency (PTH regulation)

92
Q

What is Paget’s disease of the bones.

A

Focal disorder of bone remodelling.

93
Q

What are the clinical signs of Paget’s disease of the bones.

A

Focal pain, warmth, deformity, fractures, SC compression

94
Q

What are some causes of Paget’s disease of the bones (2)

A

Malignancy.

Cardiac failure.

95
Q

What bones are most often affected in Paget’s disease of the bones? (4)

A

Pelvis.
Femur.
Skull.
Tibia.

96
Q

What is the biochemical sign of Paget’s disease of the bones?

A

Elevated ALP.

97
Q

How is Paget’s diagnosed on imaging? (2)

A

Nuclear medical scan.

X-ray.

98
Q

What is the treatment for Paget’s disease of the bone?

A

Bisphosphonates for the pain.

99
Q

Which has the lowest calcium?

Primary hyperparathyroidism
Secondary hyperparathyroidism 
Osteoporosis 
Paget's disease of the bone 
Breast Cancer
A

Secondary hyperparathyroidism

100
Q

What is a cause of primary hyperparathyroidism?

A

Osteitis fibrosa.

101
Q

What is the cause of renal osteodystrophy?

A

Due to secondary hyperparathyroidism and retention of aluminium from dialysis fluid.

102
Q

What is the biochemistry in osteoporosis?

A 
Normal calcium. 
Normal phosphate. 
Normal PTH.
Normal vitamin D. 
Normal ALP.
103
Q

What is the biochemistry in osteomalacia/rickets?

A 
Low calcium. 
Low phosphate. 
Raised PTH. 
Low vitamin D. 
Raised ALP.
104
Q

What is biochemistry of Paget’s?

A 
Normal calcium. 
Normal phosphate. 
Normal PTH. 
Normal vitamin D. 
Raised ALP.
105
Q

What is the biochemistry in parathyroid bone disease?

A 
Raised calcium. 
Low phosphate. 
Raised PTH. 
Normal vitamin D. 
Raised/normal ALP.
106
Q

What is the biochemistry in renal bone disease?

A 
Normal/low calcium. 
Raised phosphate. 
Raised PTH. 
Normal vitamin D. 
Normal/raised ALP.

Kat's Pathology (105 decks)

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