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CNSLF Bone Path 1&2 (iii) - Metabolic Bone Disease (Paget's…
CNSLF Bone Path 1&2 (iii) - Metabolic Bone Disease
Dx
careful hx
physical exam
radiology
lab tests
bone bx rare but may be indicated
Osteoporosis
common
progressive reduction in bone mass
mineralisation normal
localised or generalised
causes
primary
senile
post-menopausal oestrogen deficiency
genetic factors (vit D R polymorphism)
idiopathic
secondary
immobility
insufficient Ca intake
hormones
drugs (steroids)
neoplasia
after 30 y/o women lose 0.5-1% of their bone mass each yr until age 50 or menopause
after menopause rate of bone loss increases (as high as 6.5%)
pathogenesis: increased bone resorption by clasts (normally inhibited by calcitonin) + decreased new bone formation by blasts
bone pain
fractures
loss of height (compression fracture of vertebral column)
deformity
dx
imaging techniques that measure bone density - dexa scan
x-ray (when 30-40% of bone mass is lost)
serum Ca, phosphate, PTH, ALP normal
prevention + tx
exercise
oral Ca + vit to limit bone loss
HRT
calcitonin
bisphosphonates (suppress clasts)
glucocorticoids CIed
Osteomalacia/Rickets
inadequate bone mineralisation
osteoid production normal
rickets
= disease of children (skeletal deformities)
inadequate mineralisation of epiphyseal cart - lack of osteoid mineralisation
skull deformity (craniotabes - softening/thinning), front bossing, squared appearance of head
thickening of knees, wrists
enlargement of costchrondral junctions of ribs (ricketic rosary)
protrusion of sternum - pigeon-breast
retraction of softened rib - Harrison's groove
lumbar lordosis
bowing of long bones of legs
osteomalacia = disease of adults (bone pain, micro fractures - losers zone)
due to vit D deficiency + the exacerbating effects of compensatory increase in PTH
dietary
malabsorption
chronic renal failure
liver disease
inadequate sunlight exposure
end organ vit D resistance (R defect)
drugs
wide osteoid seams with prominent osteoblasts
osteoclasts are rare (unmineralised osteoid doesn't stim osteoclastic reaction)
biochem: high Ca + PO4, high PTH, high ALP
tx = vit D
Paget's disease (osteitis deformans)
common - affects 5% of elderly
more common in Europe, US, whites
1 bone in 15%, multiple in 85% (but not entire skeleton)
collagen matrix madness
initial osteoclastic phase - resorption
mixed osteolytic-osteoblastic phase - haphazard bone production
fibrosis of BM spaces
quiescent (dormant) osteosclerotic phase (gain in bone mass)
late stage: coarse thickened trabeculae
hallmark = 'mosaic pattern' (haphazard arrangment)
cause unknown - possible slow virus (paramyxovirus)
viral particles have been identified in cytoplasm + nuclei of osteoclasts of affected patients
hereditary component (locus of chromo 18q)
bone pain
increased hat size
deafness/hearing loss (impinges on Ns)
lion-like faces (thickened facial bone)
isolated elevated ALP due to blast activation
fractures
deformity
N or cord compression
comps
osteoarthritis
high output HR
malignant transformation (osteosarcoma)
Hyperparathyroidism
primary - adenoma/hyperplasia - high Ca
secondary - hypocalcaemia response - low/normal Ca
PTH induces clast activity - resorption - cavities in trabeculae of cancellous bone, fibrosis, micro fractures, haemorrhage
osteitis fibrosis cystica (von Recklinghausen disease of bone) = brown 'tumours'
changes can regress after control
rare to be dxed + txed @ early stage
Renal osteodystropy
bone disease secondary to renal failure
can be osteitis fibrosa cystica, osteomalacia, osteosclerosis or osteoporosis
hypocalc + PO4 retention - compensatory PTH increase
loss of renal mass - less vit D activation - osteomalacia
aluminium present in dialysis solutions cam bind to osteoid + inhibit its mineralisation - osteomalacia
metabolic acidosis - increase resorption + release of ca hydroxyapatite from matrix - osteomalacia
steroids (e.g. for GN) can cause osteoporosis)
deposition of amyloid in bone (beta-2 micro globulin