MSK Flashcards
define osteoporosis
reduced bone density (T score < -2.5) increases fracture risk
- cancellous bone affected => crush fractures
- cortical bone affected => long bone fractures
causes of osteoporosis (ME DR G/ SHATTERED)
Primary
- idiopathic
- post-menopausal
Secondary
- Malignancy (myelomas)
- Endocrine (cushings, thyrotoxicosis, hyperparathyroidism, hypogonadism)
- Drugs (steroids, heparin)
- Rheumatological (RA, ankylosing spondylitis)
- Gastrointestinal (liver/ renal problems, malabsorption- low Ca2+)
or
Steroid
Hyperparathyroidism
Alcohol
Thin
Testosterone (low)
Early menopause
Renal/ liver disease
Erosive bone disease (RA)
Dietary calcium (low)
presenting symptoms of osteoporosis
- usually asymptomatic till fracture
=> NOF- after minimal trauma
=> vertebral- stooped posture, pain on lifting
=> colles -radius fracture after falling on outstretched hand
examination findings of osteoporosis
none usually till fracture
- pain on external hip rotation + flexion (NOF fracture)
- tenderness over vetebrae
- thoracic kyphosis (over multiple vertebrae)
investigations + findings for osteoporosis
- Bloods (calcium, phosphate, ALP => usually normal in primary osteoporosis)
- X-ray (diagnose fracture- biconcave vertebrae/ crush fractures)
- DEXA scan (T
Management for osteoporosis
- bisphosphonates (alendronic acid)- reduce osteoclast function
- Selective oestrogen receptor modulators (raloxifene)
- PTH - stimulates osteoblasts
- Ca2+/ Vit D supplements
- HRT (for menopausal women)
The heart in ankylosing spondylitis
Conduction defects
AV block
Aortic regurgitation
Ankylosing spondylitis
Chronic inflammatory disease of spine + sacroiliac joint
Aetiology of ankylosing spondylitis
Unknown
Strong genetic/environmental interplay
Typical presentation of ankylosing spondylitis
Gradual onset of lower back pain
Worse during the night
Spinal morning stiffness
Relieved by exercise
Radiates from sacroiliac joints to hips/buttocks
Improves towards end of day
Progression of ankylosing spondylitis
Variable disease course
Progressive loss of spinal movement in all directions (therefore, decreased thoracic expansion)
Kyphosis
Neck hyperextension
Spinocranial ankylosis
Features of ankylosing spondylitis
Enthesitis (Achilles tendinitis, plantar fasciitis, tibial/ischial tuberosities, iliac crests)
Costochondritis
Acute iritis
Osteoporosis
Aortic valve incompetence
Pulmonary apical fibrosis
Testing for and diagnosing ankylosing spondylitis
Clinical supporting by imaging
MRI - detection of active inflammation and destructive changes
XR
- SI joint space narrowing/widening, sclerosis, erosions, ankylosis/fusion
- bony proliferation from enthesitis between ligaments and vertebrae
FBC normocytic anaemia
Increased ESR, CRP
Management of ankylosing spondylitis
Exercise not rest ideally with specialist physio
NSAIDs relieve symptoms and may slow radiographic progress
Local steroid injections
TNF-α blockers in severe cases
Surgery - hip replacement, spinal Ostrogoth (rare)
Ankylosing spondylitis prognosis
Worse if:
ESR > 30
onset < 16
Early hip e0cement
Poor response to NSAIDs
define Osteomalacia
Low mineral content of bone
Rickets - mineralisation problem during bone growth
Osteomalacia - after fusion of epiphyses
Signs and symptoms of rickets
Infants:
Growth retardation
Hypotonia
Apathy
Once walking:
Knock kneed
Bow legged
Deformities of metaphysical epiphyseal junction
Features of decreased Ca2+ (mild)
Signs and symptoms of osteomalacia
Bone pain and tenderness
Fractures (especially femoral neck)
Proximal myopathy (waddling gait)
Decreased phosphate
Vit D deficiency
Causes of osteomalacia
Vitamin D deficiency
Vitamin D resistance
Liver disease
Renal osteodystrophy
Tumour induced
Drug induced
How does vitamin D deficiency contribute to osteomalacia
Malabsorption, poor diet, or lack of sunlight
How does vitamin D resistance contribute to osteomalacia
Mainly inherited conditions
Responsive to high doses of vitamin D
How does liver disease contribute to osteomalacia
Reduced hydroxylation of vit D to 25-hydroxy-cholecalciferol
Malabsorption of vitamin D
How does renal osteodystrophy cause osteomalacia
Renal failure causes 1,25-dihydroxy-cholecalciferol deficiency
Tumour induced osteomalacia
raised tumour production of phosphate in FGF-23 which causes hyperphosphaturia
Low serum phosphate often causes myalgia and weakness
Investigations for osteomalacia
Plasma serum levels
Biopsy
X ray
Plasma investigation findings in osteomalacia
Reduced:
- calcium (mild but may be severe)
- phosphate
- 25OH-vit D (except in vit D resistance)
- 1,25(OH)2-vit D in renal failure
Increased:
- ALP
- PTH
biopsy findings in osteomalacia
incomplete mineralisation
muscle biopsy normal
x ray findings in osteomalacia
loss of cortical bone
partial fractures without displacement, esp. on:
- lateral border of scapula
- inferior femoral neck
- medial femoral shaft
cupped, ragged, metaphysical surfaces seen in rickets
treatment of osteomalacia due to dietary insufficiency
vitamin D
calcium D3 tablet
treatment of osteomalacia due to malabsorption or hepatic disease
vitamin D2 (ergocalciferol) parenteral calcitriol
treatment of osteomalacia due to renal disease/vit D resistance
alfacalcidol
calcitriol
can cause dangerous hypercalcaemia
what needs to be done alongside medication for osteomalacia
monitor plasma calcium
initially weekly
and if nausea/vomiting
risk factors for septic arthritis
pre-existing joint disease
DM
immunosuppression
chronic renal failure
recent joint surgery
prosthetic joints
IV drug abuse
age > 80 yrs
investigations for septic arthritis
joint aspiration for synovial fluid microscopy & culture
blood cultures
plain radiograph and CRP may be normal
ddx for septic arthritis
crystal arthropathies
treatment of septic arthritis
empirical IV antibiotics after aspiration until sensitivities are known
IV antibiotics for approx. 2 weeks
consider orthopaedic review for arthrocentesis, washout, and debridement
urgent referral if there is prosthetic joint involvement
common causative organisms of septic arthritis
staph aureus
streptococci
neisseria gonococcus
gram -ive bacteria
Define Osteoarthritis
Degeneration of cartilage and underlying bone
Usually primary (generalised)
Can be secondary to joint disease or other conditions
Signs and symptoms of localised disease in osteoarthritis
- pain and crepitus on movement
- background ache at rest
- worse with prolonged activity
- brief stiffness after rest
- joints may feel unstable
Signs and symptoms of generalised disease in osteoarthritis
- nodal OA (DIP, PIP, CMC joints, and knees in post menopausal females)
- joint tenderness, derangement, and bony swelling
- reduced range of movement and mild synovitis
Testing for osteoarthritis
Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts
Elevated CRP
Management of osteoarthritis
Core treatments:
- exercise
- weight loss if overweight
Analgesia:
- paracetamol +/+ NSAIDs
- codeine/short term oral NSAID
- topical capsaicin
- intra-articular steroid
Non-pharmacological:
- physios, OTs
- heat/ice packs
- walking aids
- stretching/manipulation
Surgery:
- joint replacement
define rheumatoid arthritis
chronic inflammatory condition affecting small joints of hands/feet
- x3 more common in females
- Autoimmune disease (HLA-DR1/DR4)
- associated with other autoimmune diseases (Sjorens)
presenting symptoms of rheumatoid arthritis
- gradual onset
- symmertrical joint pain + swelling (polyarthritis -multiple small joints affected)
- morning stiffness
- common systemic symptoms (fever, fatigue, weight loss, pericarditis, pleurisity) FFWPP
- RARE extrarticular features (LEAF) - lung fibrosis, episcleritis, amyloidosis, fetty syndrome (splenomegaly, RA, leucopenia)
examination findings of rheumatoid arthritis
early
- swelling of MCP/PIP joints (usually symmetrically)
- warm/tender joints
- reduced joint movement
late
- ulnar deviation due to subluxation (partial dislocation) of MCP
- radial deviation of wrist
- swan neck deformity
- boutteniere deformity
- z line deformity of thumb
- muscle wasting
- palmar erythema
- rheumatoid nodules (elbows/hands)
investigations for rheumatoid arthritis
bloods:
- FBC- low Hb, high platelets (inflammation)
- high CRP/ESR- inflammation
- +ve Rhematoid factor
- Anti-cyclic citrulinated peptide antibodies (specific)
Joint aspiration- exclude septic arthritis
Joint X-ray (BONDS)
- Bone erosions
- Osteopenia (low bone density)
- Narrow joint space
- Deformity
- Swelling
US/MRI of joint => check for synovitis
management of rheumatoid arthritis
mild disease
- DMARDs - Methotrexate
- NSAIDs -
- Corticosteroid/ immunosuppresant - Prednisilone (avoid long term use)
Use biologics for severe disease (anti-TNF = infliximab, anti-CD20 antibody = Rituximab)
if pregnant
- corticosteroids (SAFER)
- hydroxychloroquinolone/ sulfasalzine - DMARDs
*DMARDs= disease modifying anti-rheumatic drugs
define reactive arthritis
inflammation of larger joints after an extra-articular infection (GI/urogenital)
- affects men more comonly (20-40)
- Reiter’s syndrome (reactive arthritis, uveitis, conjuctivitis)
- affects more large joints + lower extremeties
- HLA-B27 involvement
causes of reactive arthritis (pathogens)
GI infection
- salmonella
- shigella
- campylobacter
- yersinia
Urogenital infection
- chlamydia
presenting symptoms of reactive arthritis
symptoms can occur up to 30 days after infection
- burning during urination (urethritis)
- asymetrical joint swelling - lower extremities (arthritis)
- lower back pain (sacroillitis)
- (enthesitis- tendon/ligament attaches to bone PAINFUL)
- conjuctivitis -red painful eye
examination signs of reactive arthritis
- Arthritis- asymmetrical oligoarthritis, sausage digits
- circinate Balnatis- red painless patches on glans of penis
- Conjuctivitis- painful red eye
- Keratoderma Belenhorragia- browinsh red maccules on SOLES/PALMS
investigations for reactive arthritis
Bedside
- Stool culture/ Urine culture- check for STIs -chlamydia
Bloods
- FBC
- high ESR/CRP
- HLA B27 testing
- anti-nuclear antibody/ rheuamtoid factor - rule out other arthritis
Joint aspiration - rule out septic/crystal arthritis
Joint X-ray - see sarcoillitis
Management for reactive arthritis
symptomatic relief
- NSAIDs- naproxen/ibuprofen
- corticosteroid- prednisilone
chronic arthritis
- DMARDs - sulfasalazine
define crystal arthropathy
joint inflammation due to crystal deposition
- gout
- pseudogout
Epidemeiology for crystal arthropathy
gout
- more common in older males
pseudogout
- more common in elderly
pathophysiology of gout
- deposition of monosodium urate (uric acid) crystals in joints/tissue
- engulfed by phagocytes
- pro-inflammatory cytokines (TNF-a) are released causing joint inflammation
causes of gout (hyperuricemia)
- increased uric acid synthesis/production
- increased purine intake -red meat, seafood
- increased nucelic cell turnover -lymphoma/leukaemia
- reduced uric acid excretion
- alcohol
- dehydration => AKI
- drugs (loop diuretics, cyclosporine)
- renal dysfunction
risk factors for gout
- XS alcohol
- family Hx of gout, hyperuricemia, renal disease
- diabetes
- hypertension
- obesity
- CVD
- chemotherapy/radiation
- high purine rich diet (seafood, red meat)
presenting symptoms of gout
Acute:
- SUDDEN joint pain (SEVERE)
- usually affects metatarsalphalangeal (MTP) joints usually BIG TOE
- joint swelling
- joint stiffness
- resolves 7-10 days
- RECURRENT ATTACKs
Chronic
- low-grade fever
- painful tophi (urate crystal deposits on ear, elbows)
- symptoms of renal calculi (dysuria)
examination findings of gout
- examine other joints
- check for arthritis signs (red, warm, swollen joints, painful on movement)
- check for tophi (urate deposits on elbows, pinna of ear)
investigations for gout
- Generally clinical diagnosis unless doubt
Bloods: FBC, U&Es, LFTs, HbA1c, lipid profile
Joint aspiration
- crystals - needle shaped monosodium urate crystals (uric acid)
- light microscopy- negative befringence
- MC&S- exclude septic arthritis
X-ray
- later stage: rat-bite erosions
- non-specific soft tissue swelling
Check for complications
- CVD
- renal disease (AXR/CT KUB- renal stones)
management for gout
Acute
- NSAIDs (+ gastro protection e.g. omeprazole)
- oral colchicine
Prevent recurrent attacks:
- allopurinol - not for acute attacks as it can worsen acute gout
pathophyisology of pseudogout
- deposition of calcium pyrophosphate dihydrate (CPPD) crystals in joint cartilage causing inflammation
causes/ triggers for pseudogout
Precipitating factors:
- surgery
- illness
- trauma
RARE CAUSES:
- Haemochromatosis
- Hyperparathyroidism
- Hypomagnesaemia
- Hypophosphatasia
- acromegaly (XS GH), Wilson’s disease (XS copper)
presenting symptoms of pseudogout
- ACUTE joint PAIN and swelling
- affects larger joints (knees, elbows)
- symptoms of arthtitis (stiffness, swelling, reduced movement)
- systemic: fever, chills
- RESOLVES weeks-months
- can have tendon inflammation (tendinitis)
examination findings of pseudogout
acute
- RED, swollen, hot, tender joints
- restricted movement
- mild fever
chronic
- crepitus
- deformity
- bony swelling
- restricted movement
investigations for pseudogout
Bloods
- high WCC
- high ESR
- blood culture - exclude septic arthritis
Joint aspiration
- crystals- CPPD crystals, brick shaped
- light microscopy- positive befringence
- MC&S- exclude septic arthritis
X-ray (signs of osteoarthritis)
- Loss of joint space
- Osteophytes
- Subcondral cysts
- Sclerosis
management of pseudogout
- treat symptoms
- ice pack, rest
- NSAIDs/ colchicine
define osteomyelitis
infection of bone leading to inflammation, necrosis and new bone formation
- acute- SUSPECT IN UNWELL LIMPING CHILD/ immunocompromised patient
- chronic- adults with open fractures, previous orthopaedic surgery
common organisms that cause osteomyelitis
- Staph. Aureus
- Group B streptococcus?
risk factors for osteomyelitis
Acute:
- YOUNG CHILDREN
Chronic:
- DIABETES
- traumatic injury
- IV drug user
- immunocompromised
- previous surgery
- previous osteomyelitis
- sickle cell
- rheumatoid arthritis
presenting symptoms of osteomyelitis
- fever
- malaise/rigors
- pain in area affected
- restricted movement/ limping
- PMHx: open fracture, orthopaedic surgery
- Risk factors
examination findings of osteomyelitis
- red, warm, tender, swollen joints
- signs of previous surgery- scars, flaps, fixed fractures
- acute/healed sinus tracts (signs of wound drainage)
- reduced range of movement
- reduced sensation (diabetic foot)
- pus/discharge from ulcers
investigations for osteomyelitis
Bloods:
- FBC- high WCC (infection)
- ESR/CRP
- Blood culture - identify organism
X-ray (diagnostic)
- osteopenia (reduced bone density- due to bone destruction) 6-7days after infection
- bone sequestrum (dead bone separated from normal bone during necrosis)
- soft tissue swelling
Bone scan - show areas of bone density
Management of osteomyelitis
- antibiotics (adults- flucloxacillin, children - ceftriaxone)
- more severe/ pressing on spinal chord/ pus leakage => surgery (debridment, revascularise, amputate)
complications of osteomyelitis
- septic arthritis
- squamous cell carcinoma
- destruction of surrounding soft tissue
- pathological fracture
- secondary amyloidoses
define polymylagia rheumatica
chronic, systemic inflammatory disease charachterised by aching and morning stiffness in neck/shoulder/pelvic girdle
risk factors for polymylagia rheumatica
- older age (>50)
- giant cell arteritis
- female (more common in)
- north european
- infection (high rates in winter season)
presenting symptoms of polymylagia rheumatica
- shoulder/pelvic girdle pain and stiffness >2 weeks
- morning stiffness (lasting >45 mins)
- rapid repsonse to corticosteroids
- Risk factors:
- systemic: low-grade fever, weight loss, fatigue, anorexia, depression
investigations for polymylagia rheumatica
Bloods: (exclude other causes)
- ESR/CRP - inflammation
- FBC
- TSH (exclude hypothyroidism)
- RF (exclude rheumatoid arthritis)
- anti-CCP (exclude RA)
- U&Es, LFTs
- Ca2+, ALP
- creatine kinase
Other:
- protein electrophoresis (exclude myeloproliferative disorders)
Imaging:
- US (check for bursitis, tne
- MRI
Management for polymylagia rheumatica
- corticosteroids (gradually reduce dose when symptoms fully controlled)
- treat complications: osteoporosis
- refer to rheumatologist if corticosteroids needed for >2yrs/ can’t reduce steroid dose without relapse.
