calcium Flashcards

1
Q

what is the function of osteoclasts?

A

for bone reabsorption
release calcium and phosphate out of the bone

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2
Q

what do osteoclasts express to increase activity?

A

RANK ligaments receptors

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3
Q

what do osteoblasts do?

A

bone formation/ ossifications

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4
Q

what controls bone remodelling?

A

oestrogen, PTH, glucocorticoids, IGH-1, growth hormone and insulin

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5
Q

how does oestrogen effect bone remodelling?

A

inhibits osetoblastic cytokine stimulators
lack of oestrogen - leads to osteoporosis

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6
Q

what does PTH do in relation to bone remodelling?

A

enhances bone turnover

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7
Q

what does VItD do in relation to bone remodelling?

A

enhances osetoblast activity

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8
Q

hwo do glucocorticoids effect bone remodelling?

A

: initially inhibit osteoclast activity
- Prolonged use can cause osteoblast inhibition  osteoporosis

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9
Q

what does IGH-1 do in relagtion to bone remodelling?

A

: initially inhibit osteoclast activity
- Prolonged use can cause osteoblast inhibition  osteoporosis

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10
Q

can untreated diabetes effects bones?

A

insulin enhances bone formation
untreated diabetes can lead to osetoporosis

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11
Q

what are the functions of calcium?

A
  • Coagulation
  • 2nd messenger – cell signalling
  • Nerve function
  • Muscular contraction
  • Cardiac action potential
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12
Q

where is calcium found?

A
  • 99% found in bone – 1% is either unbound or bound to albumin
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13
Q

what are normal calcium values?

A
  • 2.2-2.6nmol/L
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14
Q

how does PTH affect calcium?

A

increase serum calcium

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15
Q

how does calcitonin affect calcium?

A

reduces serum calcium

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16
Q

what is unbound calcium affected by?

A

plasma protein - albumin
and pH

17
Q

what happens to calcium in alkalotic conditions?

A

more Ca bound to albumin eg anxiety attack causing resp alkalosis

18
Q

what happens to calcium in acidotic conditions?

A

more free Ca in blood eg hypercapnic

19
Q

what stimulates PTH secretion?

A

low serum calcium
increased serum phosphate

20
Q

what inhibits secretion of PTH?

A

raised serum calcium or calcitriol (activated VitD)

21
Q

what are the effects on bones, intestines and kidneys of PTH?

A
  • Bone: enhances osteoblast and clast  more bone reabsorption and Ca/ phosphate release
  • Intestine: increases Ca absorption via 1,25 dihydroxy vitD
  • Kidneys: increases Ca reabsorption, inhibits phosphate reabsorption, activates 1,25 hydroxy VitD
22
Q

where does vitD come from?

A

UV and skin

23
Q

where is vitD metabolised to be activated?

A
  • Metabolised by liver and proximal tubular cells in kidneys to be activated
24
Q

what are the effects of VItD in bone, gut and kidneys?

A
  • Bone: increases osteoblast activity  strengthens bone
  • Gut: enhances calcium and phosphate absorption
  • Gut and kidney: increase serum ca and phosphate for bone mineralisation
25
where is calcitonin secreted from?
secreted from C cells of thyroid by increased Ca levels
26
what is the aetiology of hypercalcaemia?
- Excessive PTH: primary hyperparathyroidism, tertiary hyperparathyroidism, ectopic PTH secretion - Malignancy: myeloma, bony mets, paraneoplastic syndromes eg parathyroid adenomas - Excess vitD: exogenous excess/ granulomatous disease eg sarcoidosis - Renal: severe AKI - Drugs: thiazide like diuretics/ lithium - Hereditary: familial hypocalciuric hypercalcaemia
27
what are the symptoms of hypercalcaemia?
BONES, STONES, GROANS, MOANS and THRONES - Bones: bone pain and pathological fracture (not caused by trauma) - Renal stones: calculi  renal colic - Abdo groan: abdo pain, vomiting, pancreatitis - Psychic moans: confusion, hallucinations, lethargy, depression - Thrones: constipation
28
what would you do with >3nmol/L calcium levels?
- >3nmol/L want to urgently admit  normal saline IV – 4L/24hrs - Hypercalcemia refractory to rehydration may require bisphosphonates (promote osteoblasts)
29
what is defined as hypocalcaemia?
<2.2mmol/L
30
what is the aetiology of hypocalcaemia?
- PTH deficiency: primary hypoparathyroidism (autoimmune), parathyroid damage (post thyroid/ parathyroid surgery or post neck irradiation), hypomagnesium - vitD deficiency/ osteomalacia - acute pancreatitis - CKD - drugs: bisphosphonates, calcitonin
31
what symptoms are seen with hypocalcaemia?
- muscle weakness/ cramps - muscle tetany/ spasm - perioral paraesthesia - psychological disturbances - seizures
32
what is trousseaus sign indicating hypocalcaemia?
occlusion of brachial artery eg with blood pressure cuff cuff and leads to involuntary contraction of hand/ wrist
33
what is chvosteks sign indicating hypocalcaemia?
tapping over facial nerve causes contraction of facial nerve  mouth moves towards site of tapping
34
what ECG changes can be seen in hypocalcaemia?
ECG may show OT prolongation - torsades de pointes and cardiac arrest
35
what is the management of hypocalcaemia?
- replacing calcium while investigating and finding initial cause - eg oral calcium - severe or ECG changes present  calcium gluconate
36