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Path - Chempath > Calcium metabolism > Flashcards

Calcium metabolism Flashcards

1
Q

What is calcium fundamental for?

A

Muscle and nerve function

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2
Q

Where must calcium be tightly regulated?

A

in the BLOOD PLASMA

It must be maintained regardless of any calcium /vit D deficiency, so bone may be sacrificed for this

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3
Q

What portions of calcium is intracellular (bone) / extracellular (plasma)

A 
Intracell = 99% 
Extracell = 1%
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4
Q

Explain the three forms serum calcium is found in

A

Free - 50%
Protein bound - 40% (to albumin)
Complexed - 10% (citrate/phosphate)

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5
Q

What occurs to total serum calcium in liver disease?

A

Liver disease means lower albumin
This means lower protein bound calcium
So the total serum calcium seems lower

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6
Q

What must we do to correct for these low albumin levels?

A

CORRECTED CALCIUM

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7
Q

How do you work out corrected calcium values?

A

Corrected calcium = serum calcium + 0.02 x (40- serum albumin)

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8
Q

Explain the physiological response to low calcium

A
  1. Fall in ionised calcium
  2. Release of PTH from parathyroid gland
  3. PTH causes:
    - increased bone calcium resorption
    - increased renal calcium resorption
    - increased 1,25OH vitamin D
    - Increased intestinal absorption of Calcium
  4. This causes a rise in plasma calcium
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9
Q

What organ secretes PTH?

A

Parathyroid gland

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10
Q

Which three organs are involved in increasing plasma calcium?

A

KIDNEY (absorption + 1a hydroxylase production)
GI (absorption)
BONE (resporption)

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11
Q

What is the role of PTH?

A

Liberate calcium from bone
Reabsorb calcium from kidneys and increase kidney secretion of 1alpha hydroxylase
Stimulate renal phosphate excretion in urine

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12
Q

Which organ produces 1alpha hydroxylase?

A

KIDNEY

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13
Q

What does the urine sample of someone with high PTH look like?

A

HIGH PO

LOW Ca

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14
Q

What are the two forms of Vitamin D?

A

D2 ergocalciferol

D3 cholecalciferol

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15
Q

Where is Vit D2 derived from?

A

From plants

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16
Q

Where is Vit D3 derived from?

A

mammals

When UV light hits the skin and converts 7-dehydrocholesterol to cholecalciferol

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17
Q

What organ produces 25 hydroxylase?

A

LIVER

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18
Q

What triggers the liver to produce 25 hydroxylase?

A

NOTHING

The liver produces it itself, constantly

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19
Q

What is the function of 25 hydroxylase?

A

Conver cholecalciferol to 25-hydroxycholecalciferol

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20
Q

What is the rate limiting step in 1,25OH 2 D3 synthesis?

A

1alpha hydroxylase converting 25 OH D3 to 1,25OH2 D3

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21
Q

What organ secretes 1 alpha hydroxylase

A

kidney

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22
Q

What triggers 1alpha hydroxylase production in the kidney?

A

PTH release from the parathyroid gland

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23
Q

What is Calcitriol?

A

The drug equivalent of 1,25 OH2 D3

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24
Q

Who is Calcitriol prescribed to

A

To patients with renal dysfunction

So they cannot produce 1alpha hydroxylase

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25
Q

What other tissue type can abnormally produce 1a hydroxylase?

A

Lung cells of sarcoid tissue

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26
Q

When is it likely that lung cells of sarcoid tissues produce 1a hydroxylase?

A

Summer months

Because there is more sunlight > more vitamin D activation

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27
Q

What are the functions of activated via D?

A

Increase intestinal Calcium absorption
Increase intestinal phosphate absorption
Critical for bone formation

28
Q

What enzyme will be high with high bone turnover?

A

Alkaline phosphatase

29
Q

What is the skeleton a reservoir for?

A

Calcium
Phosphate
Magnesium

30
Q

What is osteomalacia

A

Normal bone density, but abnormal bone structure

Caused by Vitamin D deficiency

31
Q

What is the mineralisation state of bone in osteomalacia?

A

DEMINERALISED

32
Q

What are risk factors for Vit D deficiency?

A

lack of sunlight
dark skin
Dietary
Malabsorption

33
Q

What are clinical features of osteomalacia ia?

A

bone, muscle pain

increased fracture risk

34
Q

What are biochemical findings of osteomalacia ?

A

Low Ca
Low PO
High ALP

35
Q

What are radiological findings of osteomalacia?

A

Looser zones

36
Q

What are clinical features of rickets?

A

Bowed legs

Myopathy

37
Q

What are radiological findings of rickets?

A

Costochondral swelling
widened epithets at risk
Loozer zone on X ray

38
Q

What drugs can trigger osteomalacia?

A

Anticonvulsants

because anticonvulsants promote vitamin D breakdown

39
Q

What type of food can trigger osteomalacia?

A

Phytic acid e.g. chapatis

Phytic acid chelates vitamin D in the gut and reduces absorption

40
Q

What is osteoporosis’

A

Normal bone mineralisation and structure, but loss of bone density

41
Q

What symptoms does osteoporosis present with

A

NONE

other than pathological fractures

42
Q

What are risk factors / precipitants for osteoporosis?

A

Old age (bone disuse)
Hyperthyroidism, Cushings
Acromegaly
Early menopause (loss of protective effect of oestrogen)

43
Q

What fracture is typical in postmenopausal women?

A

Colles fracture (of wrist)

44
Q

What is the biochemistry of someone with osteoporosis?

A

normal Ca, Po

45
Q

How do you diagnose osteoporosis?

A

DEXA scan

46
Q

What is a T score

A

Number of st dev from mean of young healthy population (20yo)

47
Q

What is a Z score

A

Number of st dev from mean of age matched control population (20yo)

48
Q

Define osteoporosis:

A

T score below -2.5

49
Q

Define osteopoenia

A

T score between -1 and -2.5

50
Q

What are lifestyle treatments for osteoporosis?

A

Weight bearing exerciser
Stop smoking
Reduce alcohol consumtion

51
Q

What are drug treatments for osteoporosis?

A 
vitamin D/ calcium
Biphosphonates 
Teriparatide 
Strontium 
HRT 
SERMS e,.g. raloxifere
52
Q

How do biphosphonates work?

A

Osteoblasts incorporate calcium BIPHOSPHONATE into bone
Osteoclasts can’t break this down
Very strong bone is produced
However long term, this bone is brittle

53
Q

What are symptoms of Hypercalcemia?

A

Poluyuria/polydipsia
Constipation
Neuro - seizures, confusion, coma

54
Q

Above what Ca level do hypercalcaemia symptoms occur?

A

> 3

55
Q

What are causes of hypercalcaemia?

A

Suppressed PTH:

  • malignancy
  • sarcoidosis
  • vit D overdose
  • thyrotoxicosis

Non suppressed PTH

  • Primary hyperparathyroidism
  • Familial hypercalciuric hypercalcaemia
56
Q

What causes - Primary hyperparathyroidism

A

Parathyroid adenoma
Parathyroid hyperplasia
Parathyroid carcinoma

57
Q

What is the biochemistry in - Primary hyperparathyroidism

A

high Ca
Low PO
Raised PTH (inappropriate)

58
Q

What are clinical features of - Primary hyperparathyroidism

A

BONES STONES MOANS GROANS

BONES: loss of calcium in bone > fracture
STONES: calcium phosphate stones as phosphate is “thrashed”
MOANS: abdominal pain due to constipation, pancreatitis
GOANS: psychiatric features e.g. confusion

59
Q

What receptor does the parathyroid gland use to detect calcium?

A

Calcium Sensing Receptor (CaSR)

60
Q

Explain familial benign hypercalcaemia

A

Mutation in CaSR

There is a slightly increased set point for PTH release, leading to mild hypercalcaemia

61
Q

What are the three types of hypercalcaemia of malignancy

A

Humoral Hypercalcemia of malignancy (PTHrP)
Bone metastases (e.g. breast cancer)
Haematological malignancy

62
Q

How do you treat hypercalcaemia?

A

Acutely - FLUIDS
If cancer - BIPHOSPHONATES
Treat underlying cause

63
Q

What are symptoms of hypocalcaemia?

A 
Due to heightened neuromuscular excitability 
- Carpo pedal spasm 
Trusseau 
Chvostek 
Convulsions 
Hyperreflexia
64
Q

What are causes of hypocalcaemia?

A

Due to low PTH:

  • surgical
  • AI thyroiditis
  • DiGeorge

Non-PTH driven

  • Vit D deficiency
  • CKD
  • Pseudohypoparathyroidism (PTH resistance)
65
Q

How do you treat hypocalcaemia?

A

Calcium + vit D

66
Q

what is renal osteodystrophty

A

Renal failure > no 1alpha hydroxylase > no Ca absorption. > altered bone formation

Path - Chempath (23 decks)

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