Rheumatology Flashcards
What is rheumatoid arthritis?
Symmetrical inflammatory arthritis affecting mainly the peripheral synovial joints including both articular and extra-articular structures.
Can lead to systemic involvement of lung, kidney and cardiovascular.
What is the gender ratio for rheumatoid arthritis?
Females:males = 3:1.
What is the term given for rheumatoid arthritis in children?
Juvenile idiopathic arthritis.
What is the genetic basis of rheumatoid arthritis?
Genetics: HLA-DR4 mediated.
Environmental trigger triggers genetic predisposition leading to autoimmune cascade.
What main structure is targeted in rheumatoid arthritis?
Synovium and tenosynovium.
What is the main difference between osteoarthritis and rheumatoid arthritis?
Osteoarthritis: non-inflammatory, cartilage affected.
Rheumatoid arthritis: inflammatory, synovium affected.
What is pannus?
RA causes an inflammatory response to synovium that leads to the formation of a hypervascular abnormal tissue called rheumatoid pannus if left untreated.
What is the pathogenesis of rheumatoid arthritis
APCs present self-antigen to T cells which stimulate B cells and macrophages.
Macrophages release pro-inflammatory cytokines.
B cells produce rheumatoid factor and other inflammatory cytokines.
Net result is increased osteoclast stimulation leading to inflammation and joint destruction.
What time length is the therapeutic window for rheumatoid arthritis?
3 months.
Early rheumatoid is defined as less than 2 years since symptom onset.
How can rheumatoid arthritis be diagnosed?
History/clinical exam.
Routine blood testing for anaemia of chronic disease (normochromic/normocytic anaemia), raised platelets, FBC (MCV normal, Hb low).
Inflammatory markers (CRP, ESR/plasma viscosity) - raised.
Autoantibodies.
X-rays of hands, feet and chest.
What are the clinical features of rheumatoid arthritis?
Prolonged morning stiffness lasting longer than an hour.
Involvement of small joints of the hands and feet.
Symmetric distribution.
Positive compression tests of MCP and MTP joints.
What are the clinical presentations of rheumatoid arthritis?
PIP, MCP, wrist, MTP synovitis.
Monoarthritis.
Tenosynovitis.
Trigger finger.
Carpal tunnel syndrome.
Polymyalgia rheumatica.
Palindromic rheumatism.
Systemic symptoms.
Poor grip strength.
Which autoantibodies are associated with rheumatoid arthritis? How specific/sensitive are they?
Rheumatoid factor (produced by B cells) - sensitivity 50-80%; specificity 70-80%.
Anti-cyclic citrullinated peptide (CCP) - sensitivity 60-70%; specificity 90-99%.
What clinical findings of rheumatoid arthritis can be seen on plain xrays?
Soft tissue swelling.
Periarticular osteopenia.
Erosions.
There may be absence of findings in early disease.
What clinical findings of rheumatoid arthritis can be seen by ultrasound?
Increased sensitivity for synovitis in early disease.
Can detect up to 7 times more MCP joint erosions than plain xray in early RA.
What clinical findings of rheumatoid arthritis can be seen by MRI?
Bone marrow oedema on MRI associated with inflammatory joint disease.
Integrity of tendons can be assessed.
Can distinguish synovitis from effusions.
Can detect erosions earlier.
Can be used to monitor disease activity..
What is the management of rheumatoid arthritis?
Early recognition and diagnosis.
Early treatment by DMARDs for all patients with RA.
Importance of tight control with target of remission or low disease activity.
Use of NSAIDs and steroids only as adjuncts.
Steroids serve as a bridge between diagnosing the patient and starting the immunosuppressants as they can take up to 8 weeks to work.
Patient education.
Why is regular blood monitoring needed for patients on DMARDs?
They cause bone marrow suppression.
Can lead to infection, liver function derangement, pneumonitis (if on methotrexate).
When would a patient with rheumatoid arthritis be put on a biologic agent?
Failure to respond to 2 DMARDs including Methotrexate and DAS 28 greater than 5.1 on two occasions 4 weeks apart.
When would you use steroids as a treatment for rheumatoid arthritis?
As a bridging therapy and for flares only.
What is osteoarthritis?
Articular cartilage thinning or loss (loss of joint space seen on xray).
What are the risk factors for cartilage loss in osteoarthritis?
Age.
Female versus male sex.
Obesity.
Previous injury (occupation, sports activities).
Muscle weakness.
Proprioceptive deficits.
Genetic elements.
Acromegaly.
Joint inflammation.
Crystal deposition in cartilage.
What is the pathogenesis of osteoarthritis?
Cartilage breaks down by initially becoming thinner and then crack occur on the surface.
Gaps in the cartilage expand until they reach the bone.
Synovial fluid leaks into the cracks causing further damage and can lead to cysts in the bone and other deformities.
What types of osteoarthritis are there?
Idiopathic.
Secondary (previous injury, calcium crystal deposition disease, rheumatoid arthritis, etc.).
What joints are normally affected by osteoarthritis?
What is the clinical presentation of osteoarthritis?
Pain (worse on activity, relieved by rest; mechanical pain).
Stiffness (usually morning stiffness lasting less than 30 mins and can occur after periods of inactivity).
What signs are found on examination of osteoarthritis?
Crepitus.
Joint swelling - bony enlargements due to osteophytes.
Joint tenderness.
Joint effusion - in late cases.
What are Heberden’s nodes?
Hard bony swellings that can develop in the DIP joints.
What are Bouchard’s nodes?
Hard bony swellings of the PIP joints.
How is osteoarthritis diagnosed?
Clinical (history/exam) and radiographs.
What radiographic findings suggest osteoarthritis?
Loss of joint space.
Subchondral sclerosis.
Subchondral cysts.
Osteophytes.
What is the non-pharmacologic management of osteoarthritis?
Physiotherapy - muscle strengthening, proprioceptive.
Weight loss.
Exercise.
Trainers.
Walking stick.
Insoles.
What is the pharmacologic management of osteoarthritis?
Analgesia – paracetamol, compound analgesics, topical anagesia.
NSAIDs - topical/systemic, may give additional symptomatic relief, consider risk/benefit ratio.
Pain modulators – tricyclics (amitriptyline), anti-convulsants (Gabapentin).
Intra-articular – Steroids, (Hyaluronic acid).
What is the surgical management of osteoarthritis?
Arthroscopic washout, loose body, soft tissue trimming.
Joint replacement.
What is gout?
Inflammation in the joint triggered by uric acid crystals.
What can cause hyperuricaemia from increased urate production?
Inherited enzyme defects.
Myeloproliferative/Lymphoproliferative disorders.
Psoriasis.
Haemolytic disorders.
Alcohol (beer, spirits).
High dietary purine intake (red meat, seafood, corn syrup).
What can cause hyperuricaemia from reduced urate excretion?
Chronic renal impairment.
Volume depletion e.g. heart failure.
Hypothyroidism.
Diuretics.
Cytotoxics, e.g. cyclosporin.
What is the gender ration of gout?
UK = male:female = 4:1.
USA = male:female = 9:1.
What is the classical clinical presentation of acute gout?
Monoarthropathy of the 1st MTP>ankle>knee.
How long will it take for gout to settle without treatment?
About 10 days.
How long will it take for gout to settle with treatment?
About 3 days.
What is chronic tophaceous gout?
Chronic joint inflammation often diuretic associated.
High serum uric acid.
Tophi present.
May get acute attacks.
What investigations will suggest a diagnosis of gout?
Raised inflammatory markers.
Serum uric acid raised (may be normal during acute attack).
Synovial fluid polarising microscopy.
Renal impairment (may be cause or effect).
Xrays (acute attack will be normal).
What will uric acid crystals appear as under polarising microscopy?
Needle-shaped, negatively birefringent crystals.
What is the acute treatment for gout?
NSAIDs.
Colchicine.
Steroids.
What is the prophylaxis treatment for gout?
Allopurinol.
Febuxostat.
Start 2-4 weeks after an acute attack.
When would you give someone prophylaxis treatment for gout?
If a patient has had more than 2 attacks in a year.
What are the types of calcium pyrophosphate deposition disease?
Calcium pyrophosphate crystals (pseudogout).
Calcium hydroxyapatite crystals (Milwaukee shoulder).
What joints are affected by calcium pyrophosphate deposition disease?
It affects the fibrocartilage in the knees, wrists and ankles.
What would calcium pyrophosphate crystals look like under polarising microscopy?
Envelope-shaped, mildly positively birefringent.
What is the treatment of pseudogout?
NSAIDs.
Colchicine.
Steroids.
Rehydration.
Why does hydroxyapatite crystal deposition cause acute and rapid deterioration?
It causes release of collagenases, serine proteinases and IL-1.
What is the treatment for calcium hydroxyapatite deposition?
NSAIDs.
Intra-articular steroid injection.
Physiotherapy.
Partial/total arthroplasty.
What is soft tissue rheumatism?
General term used to describe pain that is caused by inflammation/damage to ligaments, tendons, muscles or nerves near a joint rather than either the bone or cartilage.
Pain should be confined to a specific site e.g. shoulder, wrist, etc.
What structure is affected by soft tissue rheumatism of the neck?
Muscular - usually self-limiting.
What structure is affected by soft tissue rheumatism of the shoulder?
Commonest area for soft tissue pain which could be from:
- Adhesive Capsulitis.
- Rotator cuff tendinosis.
- Calcific tendonitis.
- Impingement.
- Partial rotator cuff tears.
- Full rotator cuff tears.
What soft tissue rheumatisms can occur in the elbow?
Medial and lateral epicondylitis - cubital tunnel syndrome.
What soft tissue rheumatisms can occur in the wrist?
De-Quervains tenosynovitis - carpal tunnel syndrome.
What soft tissue rheumatisms can occur in the pelvis?
Trochanteric.
Iliopsoas.
Ischiogluteal.
Bursitis and stress enthesopathies.
What soft tissue rheumatisms can occur in the foot?
Plantar fasciitis.
What investigations can aid diagnosis of soft tissue rheumatism?
Tests usually unnecessary.
X-ray (shows calcific tendonitis).
MRI if it fails to settle.
Identify precipitating factors.
What treatment is used for soft tissue rheumatism?
Pain control.
Rest and ice compressions.
Physiotherapy.
Steroid injections.
Surgery.
What are the features of joint hypermobility?
Presents with arthralgia.
Premature osteoarthritis.
Investigations normal.
60 year old patient who is experiencing knee pain for 5 years seen by GP who organised xray. Can it differentiate osteoarthritis from rheumatoid arthritis?
Yes.
Is hyperuricaemia a prerequisite for gout?
Yes.
50 year old lady who is otherwise fit and well, presents with pain in hip when walking for 1 year. Examinations show relatively normal range of movement in the hip. What is the best treatment option?
NSAIDs and physiotherapy.
75 year old lady presented with acute swelling of the knee and therefore, unable to walk. O/E, patient is pyrexial and looking slightly unwell. Knee is markedly swollen, skin over the joint is red and joint is hot to touch. Range of movement is markedly reduced. What is the most likely diagnosis?
Septic arthritis.
What are connective tissue diseases?
Spontaneous overactivity of the immune system that produces specific auto-antibodies.
What is SLE?
A systemic autoimmune disease that can affect any part of the body, where the immune system attacks the body’s cells and tissue damage.
Antibody-immune complexes precipitate and cause a further immune response.
What is the gender ratio of lupus?
Females:males = 9:1.
What are the risk factors for SLE?
Increased oestrogen exposure (early menarche, on oestrogen containing contraceptives and HRT).
Smoking.
Genetic predisposition.
SLE is more common in which ethnic populations?
African-American, African-Caribbean, Asian.
What is the pathogenesis of SLE?
Loss of immune regulation.
Increased and defective apoptosis.
Necrotic cells release nuclear material which act as auto-antigens.
Speed of clearance of dead cells is reduced allowing internal cellular components to be exposed to immune system for longer.
Autoimmunity results from exposure to nuclear and intracellular auto-antigens.
B and T cells stimulated.
Auto-antibodies produced.
How does renal disease occur in SLE?
Deposition of immune complexes (nuclear antigens and anti-nuclear antib odies) in mesangium.
Activate complement which attracts leukocytes -> release cytokines.
Cytokine release perpetuates inflammation -> necrosis and scarring.
What pathogenesis drives SLE disease?
Immune complex formation.
What drug treatment should be given for SLE?
NSAIDs and simple analgesia.
Hydroxychloroquine - all SLE patients should have this.
Steroids - for flares only.
Immunosuppressives - moderate/severe disease.
Biologics.
