MSK and Rheum Flashcards
What is reactive arthritis?
synovitis as a reaction to a recent infective trigger
aka Reiter Syndrome
Difference between septic arthritis vs reactive arthritis
reactive arthritis doesn’t have an infection in the joint
Most common infections that trigger reactive arthritis
gastroenteritis or STIs
Chlamydia causes _____arthritis
Gonorrhoea causes ______ arthritis
reactive, septic
What gene is linked to reactive arthritis?
HLA B27
What are the associations of reactive arthritis?
- bilateral conjunctivitis
- anterior uveitis
- circinate balanitis
‘can’t see, pee or climb a tree’
How should reactive arthritis be managed?
- Bloods - FBC, CRP, HLA-B27
- Stool or urethral swab
- Urinalysis
- Joint aspiration to check for septic or crystal
How does septic arthritis present?
- hot, red, swollen and painful joint
- stiffness and reduced range of motion
- systemic symptoms such as fever, lethargy and sepsis
What bacteria commonly cause septic arthritis?
- Staphylococcus aureus most common
- Neisseria gonorrhoea in sexually active
- Haemophilus influenza
- E.coli
How should septic arthritis be managed?
- have a low threshold
- aspirate and send for staining, crystal microscopy, culture
- empirical IV antibiotics before sensitivities are known
- flucloxacillin plus rifampicin
- vancomycin plus rifampicin for penicillin allergy
- clindamycin is alternative
Which joints are affected in ankylosing spondylitis?
- sacroiliac joints and vertebral column joints
How does ankylosing spondylitis present?
- young male
- symptoms develop gradually over 3 months
- lower back pain and stiffness
- sacroiliac pain in buttock region
- worse at night
- improves with time
_____ fractures are a key complication of ankylosing spondylitis
vertebral
Associations with ankylosing spondylitis
- weight loss and fatigue
- chest pain due to costovertebral and costosternal joints
- enthesitis causing plantar fasciitis and achilles tendonitis
- dactylitis
- anaemia
- anterior uveitis
- aortitis
- heart block caused by fibrosis of heart’s conductive system
- restrictive lung disease
- pulmonary fibrosis
- IBD
What is Schober’s test?
- part of spine exam
- line at L5, line 10cm above and 5cm below
- bend over
- less than 20cm gap = restriction and may support ankylosing spondylitis
Investigations for ankylosing spondylitis
- inflammatory markers
- HLA B27 test
- X-ray of spine
- MRI of spine can show bone marrow oedema early in the disease
- look for bamboo spine, squaring of vertebral bodies, subchondral sclerosis, fusion of the joints
Management of ankylosing spondylitis
- NSAIDs
- Steroids
- Anti-TNF medications
- Monoclonal antibodies
- physiotherapy
- exercise and mobilisation
- avoid smoking
- bisphosphonates to treat osteoporosis
- treatment of complications
- surgery for deformities
Risk factors for gout
- male
- obese
- high purine diet (meat and seafood)
- alcohol
- diuretics
- cardiovascular or kidney disease
- family history
Presentation of gout
- gouty tophi at DIP, elbow and ear
- base of metatarsophalangeal joint
- wrists
- base of thumb
How is gout diagnosed?
Clinically or by an aspiration - exclude septic arthritis!
- X-ray
- Aspiration will show no bacteria, needle shaped crystals, negative birefringence
- monosodium urate crystals
- joint space maintained but lytic lesions, punched out erosions, sclerotic borders with overhanging edges
Management of gout
Acute = NSAIDs, colchicine (if renal impairment or significant heart disease), steroids
Prophylaxis: allopurinol to reduce uric acid levels, lifestyle changes (weight loss, hydration, stop alcohol)
How should pseudogout be diagnosed?
- aspiration shows no bacteria, calcium pyrophosphate crystals, rhomboid shaped crystals, positive birefringence
X-ray = chondrocalcinosis (white line in the middle of the joint caused by calcium deposition)
- loss of joint space, osteophytes, subarticular sclerosis, subchondral cysts
How should pseudogout be managed?
NSAIDs, colchicine, joint aspiration, steroid injections, oral steroids
There is a strong association between polymyalgia rheumatica and _________
giant cell arteritis
Who is usually affected by polymyalgia rheumatica?
- over 50
- women
- Caucasian
What are the features of polymyalgia rheumatica?
- symptoms present for at least 2 weeks
- bilateral shoulder pain that may spread to the elbow
- bilateral pelvic girdle pain
- worse with movement
- interferes with sleep
- stiffness for at least 45 mins in the morning
- weight loss, upper arm tenderness, carpel tunnel syndrome, pitting oedema
How should polymyalgia rheumatica be diagnosed?
- clinical presentation and response to steroids
- rasied CRP
- FBC
- calcium
- creatine kinase
- rheumatoid factor
- ANA
- anti-CCP
How should polymyalgia rheumatica be treated?
15mg prednisolone per day
Assess after a week and after 3-4 weeks
Start reducing regime
Inform about sick day rules and give steroid treatment card
Bisphosphonates and calcium and vitamins D supplements to prevent osteoporosis
PPIs to protect gastric lining
What are the risk factors for osteoporosis?
- old
- female (especially post-menopausal)
- reduced mobility and activity
- low BMI
- RA
- alcohol and smoking
- long term corticosteroids
- certain medications (SSRIs, PPIs, anti-epileptics, anti-oestrogens)
What is the FRAX tool?
- prediction of a fragility fracture in the next 10 years
- first step in assessing risk of osteoporosis
- age, BMI, co-morbidities, smoking, alcohol, family history
How is bone mineral density and what can we infer from the score?
DEXA scan which gives a T score
T more than -1 = normal
T -1 to -2.5 = osteopenia
T less than -2.5 = osteoporosis
T less than -2.5 with a fracture = severe osteoporosis
How should osteoporosis be assessed?
- Do a FRAX assessment
- If intermediate risk then go for a DEXA scan
- If high risk then offer treatment
How should osteoporosis be managed?
- activity and exercise
- healthy weight
- adequate calcium intake
- adequate vitamin D
- avoiding falls
- stop smoking
- reduce alcohol consumption
Bisphosphonates are first-line (alendronate, risedronate, zoledronic acid)
What is osteomalacia?
defective bone mineralisation causing soft bones, results from insufficient vitamin D
How does osteomalacia present?
- fatigue
- bone pain
- muscle weakness
- muscle aches
- pathological or abnormal fractures
Investigations for osteomalacia
- serum 25-hydroxyvitamin D
- less than 25 nmol/L = deficient
- 25-50 nmol/L = insufficient
75 nmol/L or above = optimal - serum calcium is low
- serum phosphate is low
- serum alkaline phosphatase may be high
- PTH may be high
- Xrays may show osteopenia
- DEXA scan shows low bone mineral density
How should osteomalcia be treated?
- supplementary vitamin D
Risk factors for vitamin D deficiency
- inadequate sunlight exposure
- malabsorption issue
- chronic kidney disease
- not enough in diet
- darker skin
What is osteomyelitis?
inflammation in a bone and bone marrow, usually caused by bacterial infection
What is the most common causative organism of osteomyelitis?
Staphylococcus aureus
What is haematogenous osteomyelitis?
when a pathogen is carried through the blood and seeded in the bone
What are the 2 ways in which osteomyelitis can occur?
haematogenous or direct contamination
What are the risk factors for osteomyelitis?
- open fracture
- orthopaedic operations (particularly prosthetic joints)
- diabetes, especially foot ulcers
- peripheral arterial disease
- IV drug use
- immunosuppression
How does osteomyelitis present?
- fever
- pain and tenderness
- erythema
- swelling
Quite non-specific, with generalised symptoms of infection such as lethargy, nausea and muscle aches
How should osteomyelitis be investigated?
- X-rays often don’t show any changes early on so cannot exclude osteomyelitis with them but they can show periosteal reactions, localised osteopenia or destruction
- MRI scan is best imagine
- Raised inflammatory markers
- Blood cultures
- Bone cultures
How should osteomyelitis be managed?
- surgical debridement of infected bone and tissues
- antibiotics
flucloxacillin
alternatives = clindamycin or vancomycin
Osteomyelitis with prosthetic joints may require complete revision surgery
What are the risk factors for OA?
obesity, age, occupation, trauma, female, family history
Which joints are commonly affected by OA?
- hips
- knees
- sacro-iliac joints
- DIPs
- carpometacarpal join
- wrist
- cervical spine (cervical spondylosis)
X-ray changes for OA
LOSS
- loss of joint space
- osteophytes
- subchondral sclerosis
- subchondral cysts
How does OA present?
- joint pain and stiffness
- worse on activity and at end of day
- bulky, bony enlargement of joint
- restricted range of motion
- crepitus on movement
- effusions around the joint
Signs of OA in the hands
- Heberden’s nodes (DIP)
- Bouchard’s nodes (PIP)
- squaring at the base of the thumb at the carpometacarpal joint
- weak grip
- reduced range of motion
How is OA diagnosed?
- no investigations needed if over 45, typical pain and no morning stiffness
-
How should OA be managed?
- patient education to lose weight, physiotherapy, occupational therapy, orthotics
- Oral paracetamol and topical NSAIDs
- Oral NSAIDs and PPIs
- Opiates e.g. codeine and morphine
- Intra-articular steroid injections
- Joint replacement
What are the causes and genetic associations of rheumatoid arthritis?
- autoimmune disease
- unknown cause
- HLA-DR1 and HLA-DR4
Presenting symptoms of rheumatoid arthritis
- gradual onset
- joint pain
- swelling
- morning stiffness
- impaired function
- symmetrical joins affected
- fever, fatigue, weight loss
Signs of rheumatoid arthritis on examination
- spindling of fingers, swelling of MCP and PIP joints, warm and tender joints, reduction in range of movement
- rheumatoid nodules on elbows, ulnar margin, palms and over extensor surfaces
Investigations for rheumatoid arthritis
- clinical
- check rheumatoid factor
- check anti-CCP antibodies
- CRP
- x-ray
Extra-articular manifestations of RA
- pulmonary fibrosis
- bronchiolitis obliterans
- felty’s syndrome (RA, neutropenia, splenomegaly)
- anaemia of chronic disease
- cardiovascular
- episcleritis and scleritis
- rheumatoid nodules
- lymphadenopathy
How should RA be managed?
- NSAIDs or COX-2 inhibitors with PPIs to treat flare-ups
- DMARDs: methotrexate, leflunomide, sulfasalazine, hydroxychloroquine.
- Add a biologic, usually a TNF inhibitor (adalimumab, infliximab and entanercept)
- Rituximab (monoclonal antibody targeting the CD20 protein)
Methotrexate side effects
works by interfering with metabolism of folate and suppressing components of the immune system
- mouth ulcers
- liver toxicity
- pulmonary fibrosis
- bone marrow suppression and leukopenia
- teratogenic
Leflunomide side effects
works by interfering with pyrimidines
- mouth ulcers
- increased blood pressure
- rashes
- peripheral neuropathy
- liver toxicity
- bone marrow suppression
- teratogenic
Sulfasalazine side effects
- temporary male infertility
- bone marrow suppression
Hydroxychloroquine side effects
- nightmares
- reduced visual acuity
- liver toxicity
- skin pigmentation
Side effects of anti-TNF drugs
- vulnerability to severe infections and sepsis
- reactivation of TB and hepatitis B
Side effects of rituximab
- vulnerability to severe infections and sepsis
- night sweats
- thrombocytopenia
- peripheral neuropathy
- liver and lung toxicity
What is systemic lupus erythematosus?
inflammatory autoimmune connective tissue disease
- often takes a relapsing-remitting course
Which antibodies are found in SLE?
anti-nuclear antibodies
SLE presentation
- fatigue
- weight loss
- arthralgia
- myalgia
- fever
- photosensitive malar rash
- lymphadenopathy
- SOB
- pleuritic chest pain
- mouth ulcers
- hair loss
- Raynaud’s phenomenon
How should SLE be investigated?
- autoantibodies (ANA and dsDNA)
- FBC (normocytic anaemia)
- C3 and C4 (decreased)
- ## Immunoglobulins (raised)
How is SLE treated?
- anti-inflammatory drugs and immunosuppression
- no cure, aim is to reduce symptoms and complications
- NSAIDs, steroids, hydroxychloroquine
- methotrexate, azathioprine, tacrolimus, leflunomide, ciclosporin
- rituximab, belimumab
