locomotor Flashcards
who gets osteoarthritis
older (>50)
W>M
causes of osteoarthritis
unknown but thought variety of minor incidental traumas and abnormal biomechanics can trigger repair processes
repairs result in structurally altered but symptom free joints. sometimes repair cannot completely sort dmaage and get symptomatic osteoarthritis
joints most affected by osteoarthritis
knee
hip
hands
risk factors for osteoarthritis
genetics
constitutional factors - ageing, female, obesiy, high bone desnity, low bone density (progression)
local, risk factors - joint injury, occupatinal and recreational stresses, reduced muscle strength, joint laxity, joint malalignment, metabolic stresses (diabetes or too much iron)
presentation of osteoarthritis
> 45
with no obvious signs of inflammation (no morning stiffness, large effsion or hot joint)
pain - during and after movement
stiffness awakening or after inactivity
tenderness
loss of flexibility
grating sensation - crepitus
bone spurs
swelling
signs on examination of osteoarthritis
gelling - pain and stiffnes caused by inactivity. once activity resumes, pain and stiffness resolves ore quickly than inflammatory arthritis
bony swellings and joint deformities, crepitus, restricted range of movement, joint tenderness, muscle wasting and weatness, warmth and instability
only a few joints problematic at one time
investigations for osteoarthritis
working diagnosis
radiology - loss of joint space, osteophytes, subchondral bone thickening and/or cysts
treatment of osteoarthritis
depend on eprsons ICE, pain level, mood and comorbidieis
physio to strengthen surrounding muscle
painkillers
topical capsaicin
intra-articular corticosteroids
surgery for knee and hip
who gets gout?
very common
more i men
older people
black and maoris ethnicity
causes of gout
common and complex form of arthritis
accumulation of urate crystals in joint, causing inflammation and intense pain of a gout attack
risk factors gout
diet - red meat, shellish, alcohol, fruit sugar
overweight
medical conditons - HTN, diabetes, obesity, metabolic syndrome, heart and kidney
medications - aspirin, diuretics, ACEi, beta blockers, antirejection drugs
family hsitory
men, then women post menopause, older
recent surgeyr or truama
= all increase levels of uric acid
presentation of gout
intense joint pain - normally big toe, most severe 4-12hrs
lingering discomfort
inflammation and redness
limited range of motion
tophi - firm white translucent nodules (10yr after first attack)
signs on examination of gout
arthritis - swelling, redness, warmth and pain on passive movement. big toe most common, bootlace area, heel, nkle, knee, finger, wrist, elbow. lower limb more than upper limb
tophi - firm white transluecnt nodules, assymmetric to joint involvement. heberdens nodes in post menopausal women taking diuretics
investigations for gout
joint fluid test - needle draw up fluid from joint for microscopy
blood test - limited in sure intially as serum uric acid can be normal during acute attack and if taking certain drugs - aspirin, corticosteroids
xray maging - rule out other causes of inflammation
USS - detect urate crystals in join and trophi
DECT- visualise urate crystals in joints
treatment of gout
reduce inflammation and pain - NSAIDs, colchicine, corticosteroids
prevent gout complications by lowering uric acid in blood - block production= allopurinol, febuxostat
- improve removal = probenecid (kidney excretion increased)
diet changes - less alcohol, less purine high foods
exercise and lose weight
causes of septic arthritis
infection with pyogenic organism, most commonly staph A
more common in immunosuppressed and elderly
infected by direct injury or by blood borne infection from infected skin lesion or other site
risk factors for septic arthritis
prosthetic joints
pre-existing joint disease
recent intra-articular steroid injection
diabetes mellitus
presentation of septic arthritis
hot, painful, swollen, red joints acutely
fever and evidenc eof infection elsewhere
high index in suspeciion in ledelry, immunosuppresed and RA
more than one joint in 20%
prosthetic joints within 3 months
investigations of septic arthritis
joint aspiration (USS guidance if needed) and synovial fluid analysis
- appearance and white cell count: septic = opaque, 75,000 WCC/mm, nostly neurtrophils
- gram stain and culture
- polarized light microscopy for crystals (gout and pseudogout)
blood - FBC, erthryocyte, sedimentation rate, CRP, blood cultures
Xrays to affected joint
swab of urethra, cervix and anorectum if gonococcal infection possible
treatment of septic arthritis
pending sensitivies - flucloxacillin IV, oral fusidic acid, and gentamicin (if immunosuppressed, for gram neg)
modify treatment depending on culture and sensitivity and continue with 2 antibiotics for 6 weeks
adequate joint drainage
refer to orthopaedic surgeon
immobilise in acute phase, mobilise early to avoid contractures
NSAIDs for pain refleif
who gets prolapsed discs
20-40yo (in older, disc degenerations prevent collapse)
cuases of prolapsed disc
usually strenuous activity
presentation of prolapsed disc
+/- sciatica
sudden onset severe back pain following strenuous activity
pain related to position and aggravated by movement
muscle spasms lead to sideways tilt when standing
radiation and pain and clinical findings depend on disc effected
most common prolapsed discs?
lowest 3
L4/L5 and L5/S1 account for 90%
investigations of prolapsed disc
limited value in acute disc disease and xrays are often normal
MRI reserved to patients whom surgery is considered
treatment of prolapsed disc
releif of symptoms
little effect on duration of disease
acute stage - bed rest on firm mattress, analgesia, occasional epidural corticosteroid injection if severe
surgeyr if severe or increasing neurological impairment (bladder, foot drop)
physio
who gets rheumatoid arthritis
increases with age - 40s-50s most common
F:M 3:1
pathophysiology of rheumatoid arthritis
synovitis with thickening of the synovial lining and infiltration by inflammatory cells
synovium proliferates and grows out over surface of cartilage = pannus, destroys articular cartilage and subchondral bone causing bony erosions
risk factors for RA
FHx
genetics
presentation of RA
insidious onset of pain
early morning stiffness
swelling of small joints of hands and feet
spindling of fingers caused by swelling of PIPJs but not DIPJs
weakening of joint capsule casuing joint instability
characteristic deformities: ulnar deviation, boutonniere deformity and swan neck deformity
investigations of RA
good history and multiple tests:
- blood count, shows anaemia (normocytic normochromic), ESR and CRP raised
- serum antibodies anti-CCP distinguish RA from acute transient synovitis
- Xray of affected joints
- synovial fluid sterile with high neutrophil count in uncomplicated diseasee
xray signs on RA
soft tissue swelling
joint narrowing
erosions at joint margins
porosis of periarticular bone and cysts
treatment of RA
goals are remission of symptoms, no cure
NSAIDs for pain
corticosteroids to suppress disease activity
DMARDS such as methotrexate
biological DMARDs work by TNF alpha
who gets oesteoporosis
increased with age
women, especially post menopause
causes of osetoporosis
imbalance in normal process of bone remodelling by osteoclasts and osteoblasts
decreased bone mineral density and changes in bone composition, archiectural size, geometry
risk factors of osteoporosis
things that affect bone strength - endocrine disease, malabsorption, CKD, chronic liver disease, COPD, menopause, immobility, BMI <18.5
age, oral corticosteroids, smoking, alcohol, prev fagility fractures, rehumatological conditions, parental Hx of hip fracture
presentation of osteoporosis
asymptomatic and remains undiagnosed until fragility fracture occurs
investigations of osteoporosis
DEXA bone scan
>2.5SDs below the mean density of bone classifies as osteoporotic
treatment of osteoporosis
bisphosphonate (alendronate)
calcium if they need it along with vitamin D
