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CNSLF Path - Ca Metabolism & Disorders of Ca Balance (ii)…
CNSLF Path - Ca Metabolism & Disorders of Ca Balance (ii) Hypercalcaemia
Intro
increased tissue potential - slowing
no reliable physical findings
Ca has loop diuretic effect: polyuria - dehydration - AKI
type 1 (distal) renal tubular acidosis
shortened QT interval
"Stones, bones, groans + psychiatric overtones"
nephrolithiasis
can lead to CKD due to nephrocalcinosis (chronic ca salt deposition in the renal parenchyma - damages distal tubules - DI)
bone pain + weakness
groans: abdo pain due to stones or constipation
depression, confusion, lethargy
Causes
PTH excess
hyperparathyroidism
primary
usually detected as incidental lab abnormality
patient is usually well - mild hypercalc, normal exam
by far the commonest cause in ambulant (not confined to bed) asymp outpatients
onset over wks-months
usually <3mmol/L
tertiary
CKD
due to low calcitriol leading to low ionised Ca
known as CKD mineral bone disease
renal osteodystrophy (bone disease that occurs when kidneys fail to maintain proper blood levels of Ca + phosphorus)
extraosseus calcifications
also causes hyperphosphataemia (decreased PO4 excretion)
PTHrP secreting cancer (mimics primary hyperthyroidism)
Lithium
familial hypocalciuric hypercalcaemia (genetic mutation of CaSR - set point changed)
Vit D excess
increased intake
granulomatous disorders - ectopic calcitriol production - e.g. sarcoid
Hormone-independent increased bone turnover
osteolytic bone mets
Paget's disease
hyperthyroidism
immobilisation
Increased Ca intake - Milk-Alkali syndrome (e.g. osteoporosis supplement overdose)
thiazide diuretics
don't cause hypercalcaemia by themselves, but can exacerbate the hypercalcaemia of hyperparathyroidism or any other cause of increased input of Ca into the bloodstream that is not suppressed by hypcalcaemia
increases Ca reabsorption in DT
malignancy + immobility = most common causes in inpatients
poor prognostic factor
50% survival @ 1 month
malignancy...
can be severe (<3mmol/L)
onset over days-wks
abnormal exam
Dx
1) find Cacorr (correcting for hyperalbuminaemia)
2) physical exam + CXR (look for cancer + granulomatous disease, but usually obvious @ this stage)
3) check PTH level
high/normal: primary hyperparathyroidism
suppressed: measure PTHrP, calcidiol (Ca in diet), calcitriol
elevated PTHrP: malignancy
elevated calcidiol: vit D excess
evaluated calcitriol but not calcidiol: ectopic production
none elevated: bone mets, rare causes
Tx
0.9% saline
aggressive rehydration until euvolaemia restored (patients often dehydrated)
then can start diuretics
frusemide
inhibits ca reabsorption in DCT
admin only after euvolaemia restored
bisphosphonates
if Ca levels v high
inhibit clast bone resorption
pamidronate IV infusion most common used
SE = osteonecrosis of jaw, esp if dental disease
steroids only for granulomatous diseases (prednisolone 10-40mg daily)