Rheumatology Flashcards
arthropathy
disease of joint
arthritis
inflammation of the joint
Arthralgia
Pain in the joint
seropositive arthritis
RA, lupus, scleroderma, vasculitis, sjogrens
seronegative
AS, psoriatic, reactive and IBD
OA
• Wear and tear with age. Alongside this, associated inflammation can cause periodic flaring of the OA
generally accepted that an imbalance exists between wear and repair of cartilage within joints
Environmental factors, hobbies and type of work may have an influence and joints with abnormal alignment
o Previous injuries = secondary OA
o No definitive cause for primary OA
Risk factors for OA
- Age
- Female versus male sex
- Obesity
- Muscle weakness
- Proprioceptive deficits
- Genetic elements
- Acromegaly
Secondary causes of OA
- Congenital dislocation of the hip
- Perthes
- SUFE
- Previous intra‐articular fracture
- Extra‐articular fracture with malunion
- Osteochondral / hyaline cartilage injury
- Crystal arthropathy
- Inflammatory arthritis (can give rise to mixed pattern arthritis)
- Meniscal tears
- Genu Varum or Valgum
OA signs/symptoms
- Pain – typically worse on activity and relieved by rest. (mechanical pain)
- May progress to be present with less activity and at rest or at night.
- Stiffness – usually morning stiffness lasts less than 30 mins. Inactivity gelling.
- Pain on very minimal movement
OA X ray findings
L - loss joint space
O - Osteophytes
S- Sclerosis
S - subchondral cyst
Clinical features of OA: hands, knee, hip and spine
Hand:
• DIP, PIP and 1st CMC joints
• Bony enlargements: DIPs (Heberdens nodes) and PIPs (Bouchards nodes)
• Squaring of the hand
Knee:
• Osteophytes, effusions, crepitus and restriction of movement
• Genu varus (towards the midline) or valgus (away from the midline) deformities
• Bakers cyst
Hip:
• Pain may be felt in groin or radiating to knee
• Pain felt in hip may be radiating from the lower back.
• Hip movements restricted
Spine:
• Cervical – pain and restriction of neck movement
• Lumbar – Pain on standing or walking for some time, osteophytes can cause spinal stenosis if encroach on spinal canal or pinch the nerve root
OA Mx
Non-pharmacologic:
o Physiotherapy - muscle strengthening, proprioceptive
o ‘Common sense measures’ - weight loss exercise, trainers, walking stick, insoles
Pharmacologic:
o Analgesia – paracetamol, compound analgesics, topical analgesia
o NSAIDs - topical/systemic,
o Pain modulators – tricyclics e.g. amitriptyline, anti-convulsants eg. Gabapentin
o Intra-articular – Steroids, Hyaluronic acid (injections)
Surgical:
o Arthroscopic washout, Loose body, soft tissue trimming.
o Joint replacement
Inflammatory arthritis features
- Joint pain with associated swelling
- Morning stiffness lasting more than 30 minutes
- Improvement in symptoms with exercise
- Synovitis on examination
- Raised inflammatory markers (CRP and plasma viscosity)
- Extra-articular symptoms
RA
- Rheumatoid arthritis is an auto‐immune inflammatory symmetric polyarthropathy which most commonly affects the small joints of the hands and feet.
- Larger joints such as the knees, shoulders and elbows can also be affected as the disease progresses.
- Female x3 > Male
- 35-50 years old
- Potential triggers include infections and cigarette smoking.
RA pathogenesis
Environmental (smoking) causes epigenetic changes and in combination with genetic predisposition and causes altering in DNA transcribing
• Therefore, susceptibility genes lead to conversion of the amino acid arginine into the amino acid citrulline – occurs in synovium
• This results in protein unfolding due to loss of positive charge (change in protein shape)
• Unfolded protein acts as antigen and foreign
• Citrullinated proteins
are recognized by anti-citrullinated peptide antibodies
• The anti-citrullinated peptide antibodies are distributed through the circulation and form immune complexes with citrullinated proteins produced in an inflamed synovium and release of cytokines
• This is associated with the infiltration and activation of neutrophils
• Inflammatory pannus forms which then attacks and denudes articular cartilage leading to joint destruction
• Tendon ruptures and soft tissue damage can occur leading to joint instability and subluxation.
RA signs/symptoms
- Morning stiffness >30 minutes
- Involvement of small joints of hands and feet (PIPs/MCPs and MTPs):
- Symmetric distribution
- Positive compression tests of metacarpophalangeal(MCP) and metatarsophalangeal (MTP) joints
- Tenosynovitis
- Prolonged: Atlantial-axial sublaxation – cervical cord compression
Extra-articular manifestations of RA
- Rheumatoid nodules (RA) – anywhere but can be found on pressure points
- Lungs - Pleural effusions, interstitial fibrosis and pulmonary nodules.
- Cardiovascular morbidity and mortality are increased in patients with RA.
- Ocular involvement is common in individuals with RA and includes keratoconjunctivitis sicca, episcleritis, uveitis, and nodular scleritis that may lead to scleromalacia.
RA Ix
RF and Anti-CCP antibodies
increase in CRP, ESR and PV
X-Ray:
o Early features can include peri-articular osteopenia (bone thinning) and soft tissue swelling.
o Periarticular erosions can occur later in the disease and subluxation .
US: Synovial gout inflammation and synovitis
RA Mx
DMARD within 3 months
short term: simple analgesia, NSAIDs and Intramuscular/intra-articular and oral steroids.
DMARD: methotrexate (1st line), sulphasalazine, hydroxychloroquine and leflunomide
No responce to DMARD: Biologics
- tender joint count, swollen joint count, CRP/ESR and visual analogue score
need over 5.1 on DAS28 score
At least 2 DMARDs (combination)
Biologic examples
Anti TNF agents- Infliximab, Etanercept, Adalimumab, Certolizumab, Golimumab
T cell receptor blocker-Abatacept.
B cell depletor-Rituximab
IL-6 blocker-Tocilizumab.
JAK inhibitors-Tofacitinib, Baricitinib
Patients can take them in pregnancy – safe to use
DMARD side effects
o Bone marrow suppression – WBC count – blood tests done regularly and liver is not becoming inflamed o Infection o Liver function derangement o Pneumonitis o Nausea o Teratogenic
Biologic side effects
o Risk of infection (esp. TB)
o Question over risk of malignancy (esp. skin cancer)
o Contraindicated in certain situations e.g. pulmonary fibrosis, heart failure
RA Conservative and surgery Mx
• physio, OH, podiatrists and orthotists
Surgery • Synovectomy • Joint replacement • Joint excision • Tendon transfers • Arthrodesis (fusion) • Cervical spine stabilisation
Seronegative inflammatory
arthropathies
common extraarticular
• Sacroiliitis, uveitis & conjunctivitis, dactylitis (inflammation of a digit) and enthesopathies are common (especially achilles insertional tendonitis and plantar fasciitis)
AS
- Chronic inflammatory disease of the spine and sacro‐iliac joints which can lead to eventual fusion of the intervertebral joints and SI joints.
- It is part of the seronegative spondyloarthropathy group of conditions relating to the HLA B27 gene.
- Hallmark- Sacroiliac joint involvement (sacroiliitis)
- Over time there is loss of spinal movement and development of a “question mark” spine, with loss of lumbar lordosis and increased thoracic kyphosis
AS signs/symptoms
• Back pain (neck, thoracic, lumbar) and stiffness and sacroiliac pain in the buttock region.
o The pain and stiffness is worse with rest and improves with movement.
o It takes at least 30 minutes for the stiffness to improve in the morning and it gets progressively better with activity throughout the day.
• Symptoms can fluctuate with “flares” of worsening symptoms and other periods where symptoms improve.
• Enthesitis
• Peripheral arthritis (shoulders, hips) – rare
• Extra articular features:
o weight loss and fatigue
o Chest pain related to costovertebral and costosternal joints
o Enthesitis is inflammation of the entheses. This is where tendons or ligaments insert in to bone. This can cause problems such as plantar fasciitis and achilles tendonitis.
o Dactylitis is inflammation in a finger or toe.
o Anaemia
o Anterior uveitis
o Aortitis is inflammation of the aorta
o Heart block can be caused by fibrosis of the heart’s conductive system
o Restrictive lung disease can be caused by restricted chest wall movement
o Pulmonary fibrosis at the upper lobes of the lungs occurs in around 1% of AS patients
o Inflammatory bowel disease is a condition associated with AS
AS A disease
- Axial Arthritis
- Anterior Uveitis
- Aortic Regurgitation
- Apical fibrosis
- Amyloidosis/ Ig A Nephropathy
- Achilles tendinitis
- Plantar Fasciitis
AS Ix
schobers test
• Tragus/occiput to wall
• Chest expansion
• X-rays may show sclerosis and fusion of the sacroiliac joints and bony spurs from the vertebral bodies, known as syndesmophytes, which can bridge the intervertebral disc resulting in fusion, producing a “bamboo spine”.
• MRI shows early disease (bone marrow oedema)
• Inflammatory parameters (ESR, CRP, PV) and HLA B27 -not diagnostic
AS Mx
• Physiotherapy (stop spinal fusion), exercise, Bisphosphonates (osteoporosis)
• NSAIDs: can be used to help with for pain. If the improvement is not adequate after 2-4 weeks of a maximum dose then consider switching to another NSAID.
• Steroids can be use during flares to control symptoms. This could oral, intramuscular slow release injections or joint injections.
• DMARDS = no impact on spinal disease, only if peripheral inflammation e.g. MTX, SZP
• anti-TNF inhibitors: Infliximab, Certolizumab, Adalimumab and Etanercept in severe AS
• Only consider biologics if they are not getting vaccination
• Surgery
o reserved for hip and knee arthritis
o Kyphoplasty to straighten out the spine is controversial and carries considerable risk.
Psoriatic arthritis
• Inflammatory arthritis associated with psoriasis, but 10 -15% of patients can have PsA without psoriasis
Psoriatic arthritis signs/symptoms
asymmetrical oligoarthritis, but may also affect the hands in a pattern similar to RA.
• Sacroiliitis: often asymmetric and may be associated with spondylitis
• Nail involvement (Pitting, onycholysis)
• Dactylitis
• Enthesitis: Achilles tendinitis & Plantar fasciitis
• Extra articular features (eye disease)
• Arthritis of DIP of fingers and toes
• No Rheumatoid nodules
Clinical subgroups of psoriatic arthritis
- Confined to distal interphalangeal joints (DIP) hands/feet
- Symmetric polyarthritis (similar to RA)
- Spondylitis (spine involvement) with or without peripheral joint involvement
- Asymmetric oligoarthritis (2 or 4 joints) with dactylitis
- Arthritis mutilans – very aggressive and destructive form
PA Ix
• CRP, PV and ESR, HLA-B27 and negative RF • X-rays: o Marginal erosions and “whiskering” o “Pencil in cup” deformity o Osteolysis
PA Mx
• Medical
o NSAIDs
o Corticosteroids/joint injections
o Disease Modifying Drugs (Methotrexate, Sulfasalazine, Leflunomide)
o Anti TNF in severe disease unresponsive to NSAIDs and Methotrexate
o Secukinumab (anti-IL17)
• Non-medical
o Physiotherapy
o Occupational Therapy
o Orthotics, Chiropodist
• Joint replacement can be considered in larger joints which are severely affected and DIP joint fusion can occasionally help.
Enteropathic arthritis
inflammatory arthritis involving the peripheral joints and sometimes spine, occurring in patients with inflammatory bowel disease (Crohn’s disease and Ulcerative Colitis).
Enteropathic arthritis signs/symptoms
- It tends to be a large joint asymmetrical oligoarthritis
- Worsening of symptoms during flare-ups of inflammatory bowel disease
- GI- loose, watery stool with mucous and blood – up to 20 times per day
- Weight loss, low grade fever
- Eye involvement ( uveitis)
- Skin involvement ( pyoderma gangrenosum)
- Enthesitis ( Archilles tendonitis, plantar fasciitis, lateral epicondylitis)
- Oral- apthous ulcers
Enteropathic arthritis Ix
- Upper and lower GI endoscopy with biopsy showing ulceration/ colitis
- Joint aspirate- no organisms or crystals
- Raised inflammatory markers- CRP, PV
- X ray/ MRI showing sacroiliitis and inflammation
- USS showing synovitis/ tenosynovitis – if soft tissue
Enteropathic arthritis Mx
- Treat Inflammatory Bowel Disease in order to control arthritis
- NSAID: may exacerbate inflammatory bowel disease. Paracteamol, Cocodamol instead
- Steroids ( oral, intraarticular, intramuscular)
- Disease Modifying Drugs (Methotrexate, Sulfasalazine Azathioprine): agreement with GI
- Anti-TNF- Infliximab, Adalimumab licensed for both Crohn’s disease and inflammatory arthritis – so end up treating both which is good
Reactive Arthritis
- Occurs in response to an infection in another part of the body, most commonly genitourinary infections (Chlamydia, Neisseria) or GI infections (Salmonella, Campylobacter).
- Large joints eg the knee become inflamed around 1‐4 weeks following the infection.
- The infection triggers an autoimmune arthropathy.
Reactive Arthritis signs/symptoms
- Some patients have a triad of symptoms of urethritis, uveitis or conjunctivits and arthritis known as Reiter’s syndrome (can’t pee, see or climb a tree)
- General Symptoms (fever, fatigue, malaise)
- Asymmetrical monoarthritis or oligoarthritis
- Enthesitis
- Mucocutaneous lesions: Keratodema Blenorrhagica, Circinate balanitis, painless oral ulcer and hyperkeratotic nails
- Ocular lesions (unilateral or bilateral): Conjunctivitis &Iritis
- Visceral manifestations: Mild Renal disease & Carditis
Reactive arthritis Ix
- ESR,CRP,PV, FBC, U&Es and HLA B27 (rarely necessary)
- Cultures (blood, urine, stool)
- Joint fluid analysis (rule out infection)
- X-ray of affected joints
- Ophthalmology opinion
Reactive arthritis Mx
- Most cases are self‐limiting whilst others (15‐ 30%) are chronic or have frequent relapses.
- NSAIDs
- Corticosteroids: Intra articular (once sepsis ruled out), Oral & Eye drops
- Antibiotics for underlying infection eg respiratory/ GI
- DMARDs (SZP) - If resistant/chronic
- Non medical: Physiotherapy and Occupational therapy
Systemic Lupus Erythematosus
- Systemic autoimmune condition that can affect almost any part of the body
- Immune system attacks cells and tissue resulting in inflammation and tissue damage
- Immune complexes form and precipitate causing further immune response
SLE Pathogenesis
defect in apoptosis that causes increased cell death and a disturbance in immune tolerance.
• Necrotic cells release nuclear materials which act as auto-antigens
• The defective clearance of the apoptotic cell debris allows for the persistence of nuclear antigens and immune complex production.
• Auto-immunity results from exposure to nuclear and cellular auto-antigens
• B and T cells are stimulated. Autoantibodies are produced
• Complexes of antigens and auto-antibodies form and circulate
• Deposition of immune complexes (clinical manifestations) in basement membrane (skin and kidney) and in small blood vessels
• Activation of complement which attracts leucocytes which release cytokines
• Cytokine release perpetuates inflammation which causes necrosis and scarring
SLE signs/symptoms
- Constitutional: fever, fatigue and weight loss
- Musculoskeletal: arthralgia, myalgia (pain) and inflammatory arthritis
- Muco-cutaneous: malar rash, photosensitivity, discoid lupus, subacute cutaneous lupus, oral/nasal ulceration and Raynauds phenomenon.
- Renal: lupus nephritis
- Respiratory: pleurisy, pleural effusion, pneumonitis, pulmonary embolism, pulmonary hypertension, and interstitial lung disease.
- Haematological: leukopenia, lymphopenia, anaemia (may be haemolytic), and thrombocytopenia
- Neuropsychiatric: seizures, psychosis, headache, aseptic meningitis, delirium
- Cardiac: pericarditis, pericardial effusion, pulmonary hypertension, sterile endocarditis and accelerated ischemic heart disease.
- Gastrointestinal: less common but include autoimmune hepatitis, pancreatitis and mesenteric vasculitis
SLE Ix
• FBC may show anaemia, leucopenia and thrombocytopenia
Anti-nuclear antibody (ANA)
Anti-dsDNA antibody
Anti-Sm
• Anti Ro (neonatal lupus and congenital heart block), anti-La and anti-RNP - may be seen in SLE but may also be seen in other conditions
• C3/4 levels - low when disease active, especially renal disease – good to monitor
• Urinalysis to look for evidence of glomerulonephritis
o Proteinuria >0.5g in 24 hours
o Biopsy proven nephritis
o Red cell casts
o Creatine and urea will be normal
• Imaging studies may be used to look for evidence of organ involvement
o CT chest for interstitial lung disease
o MRI brain for cerebral vasculitis
o Echo for pericardial effusion.
