Osteomalacia, Pagets, Osteoporosis Flashcards
what is osteomalacia
severe prolonged vitamin D deficiency (rickets in children)
what happens in osteomalacia to the amount of bone and mineralisation
normal amount of bone, decr mineral content- have excess uncalcified osteoid and cartilage
what are the causes of vitamin D deficiency
diet, poor sunlight, Asian, anti convulsant therapy, malabsorption, renal failure, vitamin D resistance
what is the difference between rickets and osteomalacia
rickets- if process occurs during period of bone growth. osteomalacia- after fusion of epiphyses
signs of rickets
growth retardation, hypotonia, apathy, knock kneed, bow legged
signs of osteomalacia
bone pain, tender, fractures (typically femoral neck), proximal myopathy, osteoporosis
causes of osteomalacia
vit D deficiency, renal osteodystrophy, drug induced, vit D resistance, liver disease, tumour induced
investigations in osteomalacia
plasma- decr Ca, decr PO4, incr ALP, incr PTH, decr vit D. biopsy- incomplete mineralisation of bone, muscle normal. x ray- loss of cortical bone, partial fractures without displacement especially- lateral border scapula, inferior femoral neck, medial femoral shaft
treatment osteomalacia
vit D. dietary- calcium D3 Forte. malabsorption- ergocalciferol or parenteral calcitriol. renal or vit D resistance- alfacalcidol or calcitriol
what is another term for Pagets
osteitis deformans
what is Pagets
increased bone turnover, incr number of osteoclasts and osteoblasts- with remodelling, bone enlargement, deformity, weakness. woven bone
clinical features Pagets
asymptomatic in >70%. deep boring pain, bony deformity and enlargement- pelvis, lumbar spine, skull, femur, tibia- bowed sabre tibia.
complications Pagets
fractures, OA, incr Ca, nerve compression due to bony enlargement,osteosarcoma
diagnosis Pagets
x ray- localised enlargement bone, patchy cortical thickening- sclerosis, osteolysis, deformity. bloods- incr ALP, Ca and PO4 normal. isotope bone scan- incr uptake.
treatment Pagets
analgesia, bisphosphonates- zoledronate, pamidronate, risedronate, alendronate
what is osteoporosis
low bone mass. deterioration of bone mass.
where are the common sites of fracture osteoporosis
spine, neck of femur, wrist
what happens in bone remodelling osteoporosis
bone resorption is greater than bone formation- osteoclasts resorb greater amount of bone, osteoblasts lay down smaller amount of bone than was resorbed
what are the primary and secondary causes osteoporosis
primary- age related. secondary- another condition or drugs
what happens if trabecular bone is affected osteoporosis
crush fractures of vertebrae common
why is osteoporosis more common in women
oestrogen low after menopause
risk factors osteoporosis
SHATTERED- Steroids; Hyperthyroidism, hyperparathyroidism, hypercalciuria; Alcohol and tobacco; Thin; Testosterone decr; Early menopause; Renal/liver failure; Erosive; Dietary
what are the complications of osteoporosis over time
kyphosis, loss of height, indigestion/reflux, pain, neck weak and head falls forward, breathing difficulties, stress incontinence
investigations osteoporosis
x ray, DEXA (dual energy x ray absorptiometry). bloods- ca, po4, alp normal
what is measures from DEXA
T score- number of standard deviations the BMD is from youthful average -2.5 or worse is osteoporosis. -1 to -2.5 is osteopenia
indications for DEXA
prev low trauma fracture, FH, early menopause, prior to long term prednisolone, osteopenia, bone and remodelling disordera
how do steroids predispose to osteoporosis
promote osteoclast bone resorption, decr muscle mass, decr Ca absorption from gut
management osteoporosis lifestyle
stop smoking, weight bearing exercise, good calcium intake, HRT women early menopause.
management osteoporosis pharmacological
bisphosphonates (alendronate 10mg/day SE photosensitivity, GI upset); calcium and vit D; strontium ranelate (decr fracture rates); HRT (prevent not treat); raloxifene (oestrogen receptor modulator); teriparatide; calcitonin; testosterone; denosumab