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Orthopaedics > Metabolic bone disease > Flashcards

Metabolic bone disease Flashcards

1
Q

define osteoporosis

A

syndrome associated with low bone mineral density and microarchitectural deterioration of bone tissue leading to an increased risk of fractures

asymptomatic until fractures occur

risk of fractures rise as bone density falls

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2
Q

basic pathophys of osteoporosis 2

A

imbalance between bone formation and bone resorption

increased activity of both osteoclasts and osteoblasts leads to bone loss and osteoclast resoprtion takes weeks and osteoblast bone formation takes months

microscopically
-loss of trabecular bone (both mineralised and collagen components)

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3
Q

risk factors for osteoporosis reducing bone density 9

A

deficiency of oestrogen in females
deficiencey of androgens in males

sharp drop in bone density in early menopause (multifactorial)

endocrine
-DM
-hyperthyroidism
-hyperparathyroidism

GI conditions
-crohns
-UC
-coeliac diseae
-chronic pancreatitis

CKD

Chronic liver disease

COPD

immobility

BMI <18.5

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4
Q

risk factors for osteoprosis independent of bone denisty 7

A

age-

oral corticosteroids

smoking

alcohol

previous fragility fracture

rheumatolgy conditions: RA, other arthropathies

parental history of hip fracture

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5
Q

risk factors for osteoporosis mechanism unclear 6

A

SSRIS

PPIs

anticonvulsants- carbamazepine

aromatase inhibor

GnRH antagonists

TZDs

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6
Q

define bone mineral denisty

A

measure of amount of bone mineralisation

measured with DEXA scan

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7
Q

define DEXA scan

A

compares observed BMD with that of normal young adult (T-score)

and that of aged-matched controls (Z score)

measured at lumbar spine (L1+4) + Femoral neck

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8
Q

how is osteoporosis defined by DEXA scnan

A

T score <-2.5

> -1=normal

<-1 but >-2.5 represents osteopaenia

> -2.5 & fracture= osteoporosis

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9
Q

describe common fragility fractures

A

occurs with low energy mechanisms that would not normally be expected to result in a fracture

most commonly simple fall:
-hip fractures
-vertebral (crush) fractures
-distal radius fractures
-humeral neck fractures

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10
Q

tools to determine fracture risk 3

A

FRAX
-fracture risk assessment tool

Qfracture

DEXA

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11
Q

who should undergo assessment of fragility fracture risk

A

all women age 65y and older
men age 75 and older
regardless of clinical risk factors

all women 50-64 and men 50-74 with:
-previous osteoporosis fragility fractures
-use of oral steroids
-Hx of falls
-low BMI
-smoker
-high alcohol intake

people under 50 with:
-current or frequent oral steroid use
-untreated premature menopause
-previous fragility fracture

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12
Q

considerations for treatment of osteoporosis

A

exclude non-osteoporotic causes for fragility fractures:
-metastatic disease
-Myeloma
-osteomalcia
-Pagets

exclude vit D deficiency and inadequate calcium intake

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13
Q

treatment for osteoporosis 8

A

excersise- weight bearing activity

reduce fizzy drinks - esp colas

HRT for menopause <40yo

vit D ± calcium (if calcium intake inadequate)

bisphosphonates

raloxifene

calcitonin

denosumab

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14
Q

MOA of bisphosphonates

A

reduce bone resporption and bone tunrover

*-issues with compliance

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15
Q

MOA of raloxifine

A

selective oestrogen receptor modulation (SERM)

agonist on bone and cholesterol

antagonist on mammary/uterine tissue

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16
Q

MOA of calcitonin

A

thyroid hormone

binds to osteoclasts and inhbits bone resoprtion

salmon calcitonin has much higher affinity for human calcitonin receptors than human calcitonin

has some antigenic side effects

17
Q

MOA of denosumab

A

monoclonal antibody to RANKL

inhibits osteoclast formation

18
Q

MOA of teriparatide

A

recombinat PTH

anabolic effect
-actiavtes osteoblasts more than osteoclasts

19
Q

define osteomalaica and rickets and the difference between them

A

a qualitative bone disorder due to defective mineralisation of osteoids

may happen before skeletal maturity-> rickets

or after skeletal maturity-> osteomalacia

BOTH USUALLY DUE TO VIT D DEFICIENCY
-VIT D INDEPENDENT FORMS ALSO

20
Q

basic pathophys of rickets (osteomalacia)

A

poor calcification of cartilage matrix of growing long bones

occurs at zone of provisional calcification
-fraying and widening of metaphysis called cupping

leads to increased physeal width and cortical thinning and bowing

21
Q

Vit D dependent forms of rickets (osteomalacia) 4

-and causes (0,2,4)

A

low exposure to UV radiation

low oral intake
-low dietary intake
-breast milkd has low amounts of vit D

low intestinal absorption
-CF
-chronic pancreatiis
-coeliac disease
-gastrectomy

underlying problems
-defective Vit D metabolism
drugs
-cytochrome P450 inducers
-anticonvulsatns (pheytoin, carbamazepine, phenobarbitone)

hepatbobilary disea
renal disease
alcoholism
tumours

22
Q

Vit-D independent forms of rickets (osteomalacia)

A

partial defects in renal tubular functioning (renal tubular acidosis, fanconi syndrome)

drugs
-bisphosphonates
-fluoride
-excessive use of phosphate binding antacits

23
Q

clinical features of rickets 6

A

aching bones and joints

lower limb abnormalities:
-in toddlers genu varum (bow legs)
-in older children - genu valgum (knock knees)

‘rickety rosary’ - swelling at the costochondral junction

kyphoscoliosis

craniotabes - soft skull bones in early life

Harrison’s sulcus

24
Q

treatment for rickets (osteomalacia) 5

A

replace missing components
-vit D
-calcium ± vit D
-calcitriol (syntehtic D3)
-phosphate

surgical correction in selected cases

25
Q

osteomalacia clinical features 4

A

bone pain

bone/muscle tenderness

fractures: especially femoral neck

proximal myopathy: may lead to a waddling gait

26
Q

define pagets disease
-what cuases it

A

disorder of bone remodelling
starts with increased osteoclast activity
can be monostotic or polyostotic

-likely viral aetiology
-paramyxovirus + genetic susceptibility

27
Q

3 phases of pagets disease

A

lytic- active

mixed- active

sclerotic (inactive)

*-all three phases may coexist in the same bone

28
Q

comon sites of pagets disease

A

femur

tibia

pelvis

skull

spine

29
Q

biochem findings in pagets disease 3

A

calcium and phosphate normal

alkaline phosphate raised

urinary hydroxyproline raised

30
Q

clinical features of pagets disease 6

A

localised pain and tenderness

increased focal temperature due to hyperaemia (due to hypervascularity)

increased bone size

bowing deformites

kyphosis of spine

decreased ROM

(75% asymptomatic at time of diagnosis)

31
Q

complications of pagets disease 8

A

increassed deformity and pathological fractures risk

increased risk of OA

hearing loss
-sensorineural hearing loss
-conductive hearing loss

neural compression

malignant transformation - eg osteosarcoma (1% of cases)

high output congestive cardiac failure

hyperparathyroidism

intramedullary haematopoesis

32
Q

radiological features of pagets disease in the skull 4

A

osteoprososi circumscripta

cotton wool appearance

diploic widening

tam o’shanter sign

33
Q

radiological features of pagets disease in the pelvis 3

A

coritcal thickening and sclerosis of iliopectineal and ischiopubic lines

acetabular protrusion

enlargement of pubic rami and ischium

34
Q

radiological features of pagets disease in the long bones

A

blade of grass or candle flame sign

lateral curvature of femur

anterior curvature of tibia

35
Q

radiological features of pagets disease in the spine

A

picture frame sign

squaring

vertical trabecular thickening

36
Q

treatment of pagets diseas 3

A

expectant if syx minimal

bispphosphonates first line

cacitonin

37
Q

what needs to be watched when treating pagets disease 2

A

excessive bleeding during arthroplasty/fracture fixation

issues with limb alignment with significant deformiteis in knee arthroplasty

38
Q

other conditions affecting bone mineralisation

A

Hypoparathyroidism
Hyper/hypocalcaemia
Hyper/hypophosphataemia
Hypercalciuria
Renal osteodystrophy
Osteogenesis imperfecta
Osteopetrosis
Hypophosphatasia
Fibrous dysplasia

Orthopaedics (15 decks)

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