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Medicine year 4 CDM > Block 9: Reactive arthritis, RA > Flashcards

Block 9: Reactive arthritis, RA Flashcards

1
Q

Reactive arthritis

A
  • Aseptic arthritis arising 1-6 weeks following gastrointestinal (Salmonella, Shigella Campylobacter) or urogenital pathogens (Chlamydia trachomatis). Chlamydia is the most common cause
  • A seronegative spondyloarthropathy
  • Triad of asymmetric oligoarthritis, urethritis and conjunctivitis
  • Typical patient is a young male with lower back pain, heel pain, myalgia and multiple joint pain, stiffness or swelling with redness of eye
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2
Q

Seronegative spondyloarthropathy

A
  • Includes reactive arthritis, psoriatic arthritis, ankolysing spondylitis and arthritis due to inflammatory bowel disease
  • Association with HLA-B27
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3
Q

Clinical features of reactive arthritis- arthritic symptoms

A
  • Peripheral arthritis: normally asymmetric oligoarthritis (knee, ankle and/or heel pain). Present especially in the morning. Some patient can develop chronic or recurrent arthritis, sacroiliitis and or spondylitis lasting more than 6 months
  • Dactylitis: sausage digit- painful inflammation of an entire finger or toe
  • Enthesitis: inflammation of ligaments and tendons
  • Axial arthritis: spinal inflammation (sacroiliac joint and lumbosacral spine) manifests as nonspecific lower back pain and/or buttock pain and stiffness- especially during inactivity
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4
Q

Reactive arthritis: extra-articular manifestations

A
  • Occular: conjunctivitis (normally appears during flares of arthritis), anterior uveitis, keratitis, corneal ulceration
  • Genitourinary symptoms: prostatitis, urethritis and haemorrhagic cystitis
  • Gastrointestinal symptoms: mild diarrhoea
  • Mucosal and skin manifestations: Keratoderma blennorhagicum, Circinate balantitis, oral ulcers, nail changes like onycholysis, subungal keratosis or nail pitting
  • Cardiac manifestations: pericarditis, aortic disease and conduction abnormalities
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5
Q

Reactive arthritis investigations

A
  • Blood tests: ESR and CRP elevated
  • Genetic and immunological markers: Rheumatoid factors and ANA, HLA-B27
  • Urine test: leukocytes, haematuria and mild proteinuria. NAAT to detect Chlamydia
  • Stool tests: Test for Salmonella, shigella, Campylobacter and Yersinia
  • Radiography: changes only found in long standing disease (chronic ReA)
  • MRI: to assess enthesitis and involvement in sacroiliac joints
  • Synovial fluid analysis
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6
Q

ASAS classification criteria for axial SpA

A
  • Back pain for 3 months or longer
  • Age at onset < 45 years
  • Sacroiliitis on imaging (radiographs or MRI) plus one or more SpA features or HLA-B27 plus two or more other SpA features
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7
Q

ASAS classification criteria for peripheral SpA

A
  • Absence of back pain and the presence, usually in a person under 45 years old, of peripheral arthritis (usually lower limb predominant and asymmetric), enthesitis, or dactylitis, alone or in combination, along with one of two sets of additional features.
  • One or more of the following from thefirst setconsists: Psoriasis, Inflammatory bowel disease, Preceding infection, Sacroiliitis on imaging (radiographs or MRI)
  • Two or more features: Arthritis, Enthesitis, Dactylitis, past history or inflammatory back pain, positive family history of SpA
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8
Q

Reactive arthritis: treatment for arthritic symptoms

A
  • NSAID’s
  • Corticosteroids: in flare or unresponsive to NSAID’s. Intra-articular injections
  • DMARD’s: second line, in chronic or erosive disease or when NSAID’s and steroids fail. Sulfasalazine is effective in peripheral. Methotrexate effective in acute and chronic disease
  • Anti-TNF alpha therapy: third line
  • Physiotherapy
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9
Q

Treatment in reactive arthritis

A
  • Antibiotics in acute infection but not established reactive arthritis. Don’t use in gastrointestinal infections
  • Remission: doxycycline or azithromycin combined with rifampicin for 6 months
  • Circinate balanitis and mild to moderate keratoderma blennorrhagica should be treated with topical steroids.
  • Anterior uveitis: systemic corticosteroids
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10
Q

Complications of reactive arthritis

A
  • Secondary arthritis
  • Ankylosing spondylitis
  • Ocular complications: recurrent iritis/uveitis can cause cataracts, cystic macular oedema
  • Keratoderma blennorrhagicum: pustular or plaque like lesions typically on the soles or palms
  • Cardiac complication: proximal aortitis
  • Rarely severe glomerulonephritis and immunoglobulin A nephropathy
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11
Q

Reactive arthritis: factors associated with poor outcome

A
  • Nature of infection: ReA caused due to genitourinary pathogen have a worse outcome than those caused by gastrointestinal pathogens.
  • Presence of HLA-B27 gene
  • Heel and foot pain at the beginning of the disease
  • Elevated ESR
  • Unresponsiveness to nonsteroidal anti-inflammatory drugs (NSAIDs)
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12
Q

Key symptoms on reactive arthritis

A
  • Bilateral conjunctivitis(non-infective)
  • Anterior uveitis
  • Urethritis(non-gonococcal)
  • Circinate balanitis(dermatitis of the head of the penis)
  • ‘Can’t see, can’t pee, can’t climb a tree’
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13
Q

Initial investigations for reactive arthritis

A

Patient presenting with an acute warm, swollen painful joint should have septic arthritis excluded. Antibiotics can be given until exclusion. Joint aspiration is required. Synovial fluid is sent formicroscopy,culture and sensitivity testingfor infection, andcrystal examinationfor gout and pseudogout.

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14
Q

Reactive arthritis prognosis

A

Most cases resolve within 6 months and do not recur. Recurrent cases may require DMARD’s or anti-TNF medication. Can have chronic reactive arthritis which has a relapsing/remitting pattern. Can cause secondary arthritis and deformity

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15
Q

Rheumatoid arthritis

A

Chronic inflammation of the synovial lining of the joints, tendon sheaths and bursa.

Tends to be symmetrical and affect multiple joints. It is a symmetrical polyarthritis

Risk factors: women, middle age (40-60), family history, smoking, western diet, certain gut bacteria

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16
Q

RA: genetic association

A
  • HLA DR4- present in RF positive patients
  • HLA DR1- present in RA patients
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17
Q

RA: antibodies

A
  • Rheumatoid factor- autoantibody present in 70% of RA patients, targets the FC portion of the IgG antibody. Can be positive in autoimmune inflammatory conditions, hepatitis C, TB, AIDS
  • Cyclic citrullinated peptide antibodies (anti-CCP antibodies)- more specific then rheumatoid factor, can be positive whilst RF is negative
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18
Q

RA bloods

A
  • U&E’s- NSAID’s can cause renal impairment
  • LFT- treatment can be hepatotoxic
  • FBC- normocytic anaemia due to chronic disease. Treatments can cause bone marrow suppression. Platelets are increased with inflammation.
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19
Q

X-ray RA

A
  • L- loss of joint space
  • E- erosions
  • S- soft tissue swelling
  • S- soft bones (peri-articular osteopenia, decreased density)
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20
Q

X-ray: OA

A
  • L- loss of joint space
  • O- osteophytes
  • S- subchondral sclerosis
  • S- subchondral cysts
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21
Q

When would you refer urgently with RA (within 3 days)

A
  • Small joints of the hands or feet are affected
  • More than one joint is affected
  • There has been a delay of three months or longer between the onset of symptoms and the person seeking medical advice
22
Q

RA symptoms

A

Presents with symmetrical distal polyarthropathy. Worse after rest, improves with activity

Key symptoms: pain, swelling, stiffness. Tends to affect the small joints of the hand and feet, typically the wrist, ankle, MCM and PIP joints in the hands.

Systemic symptoms: fatigue, weight loss, flu like illness, muscle aches and weakness

23
Q

Palindromic rheumatism

A

Self limiting short episodes of inflammatory arthritis with joint pain, stiffness and swelling typically affecting only a few joints. The episodes only last 1-2 days and then completely resolve. Having positive antibodies (RF and anti-CCP) may indicate that it will progress to full rheumatoid arthritis

24
Q

Joints affected in RA

A
  • Proximal Interphalangeal Joints (PIP) joints
  • Metacarpophalangeal (MCP) joints
  • Wrist and ankle
  • Metatarsophalangeal joints
  • Cervical spine
  • Large joints can also be affected such as the knee, hips and shoulders
  • DIP is never affected by rheumatoid arthritis as well as the Ips of the toes and the thoracolumbar spine
25
Q

Atlantoaxial subluxation

A

Occurs in the cervical spine. The axis (C2) and the odontoid peg shift within the atlas (C1). This is caused by local synovitis and damage to the ligaments and bursa around the odontoid peg of the axis and the atlas. Subluxation can cause spinal cord compression and is an emergency. This is particularly important if the patient is having a general anaesthetic and requiring intubation. MRI scans can visualise changes in these areas as part of pre-operative assessment.

26
Q

RA signs

A
  • Boggy synovium due to inflammation and swelling
  • Z shaped deformity of the thumb
  • Swan neck deformity- hyperextended PIP and flexed DIP
  • Boutonnieres deformity- hyperextended DIP and flexed PIP
  • Ulnar deviation of the fingers at the knuckle- MCP joint
27
Q

RA extra-articular manifestations

A
  • Pulmonary fibrosis with pulmonary nodules (Caplan’s syndrome)
  • Bronchiolitis obliterans (inflammation causing small airway destruction)
  • Felty’s syndrome (RA, neutropenia and splenomegaly)
  • Secondary Sjogren’s Syndrome (AKA sicca syndrome)
  • Anaemia of chronic disease
  • Cardiovascular disease
  • Episcleritis and scleritis
  • Rheumatoid nodules
  • Lymphadenopathy
  • Carpel tunnel syndrome
  • Amyloidosis
28
Q

Felty’s and caplan syndrome

A

Felty’s syndrome: Splenomegaly, Rheumatoid arthritis, Neutropenia. Can cause life threatening infections.

Caplans syndrome: Pulmonary fibrosis/lung nodules and rheumatoid arthritis. Normally due to exposure with coal

29
Q

RA investigations

A
  • Check rheumatoid factor
  • If RF negative, check anti-CCP antibodies
  • Bloods- Inflammatory markers such as CRP and ESR (non-specific), antibodies
  • X-ray of hands and feet
  • Ultrasound scan- to confirm synovitis
  • Bedside- urine dip
  • Joint aspiration if presenting with monoarthropathy
30
Q

Non-inflammatory causes of raised ESR

A

pregnancy, diabetes, ESRF, ageing, obesity and anaemia

31
Q

RA: x-ray changes

A
  • Soft tissue swelling
  • Periarticular osteopenia
  • Bony erosions
32
Q

RA diagnosis: points are scored based on

A
  • The joints that are involved (more and smaller joints score higher)
  • Serology (rheumatoid factor and anti-CCP)
  • Inflammatory markers (ESR and CRP)
  • Duration of symptoms (more or less than 6 weeks)
  • Scores are added up and a score greater than or equal to 6 indicates a diagnosis of rheumatoid arthritis.
33
Q

Das28 score

A

Based on the assessment of 28 joints and points are given for: swollen joints, tender joints, ESR/CRP score

34
Q

RA worse prognosis with

A
  • Younger age
  • Male
  • More joints and organs affected
  • Prescence of RF and anti-CCP
  • Erosions on x-ray
35
Q

RA management

A
  • Steroids- for flare ups
  • NSAID’s/ COX-2 inhibitors- risk GI bleeding so are co-prescribed with a PPI
  • Use minimal effective dose
36
Q

Disease modifying anti-rheumatic drugs (DMARD’s)

A
  • First line is monotherapy with methotrexate, leflunomide or sulfasalazine. Hydroxychloroquine can be considered in mild disease and is considered the “mildest” anti rheumatic drug.
  • Second line is 2 of these used in combination.
  • Third line is methotrexate plus a biological therapy, usually a TNF inhibitor.
  • Fourth line is methotrexate plus rituximab
  • Sulfasalazine and hydroxychloroquine are DMARDs in pregnancy
37
Q

RA biological therapy

A
  • Anti-TNF (adalimumab, infliximab, etanercept, golimumab and certolizumab pegol)
  • Anti-CD20 (rituximab)
  • Anti-IL6 (sarilumab)
  • Anti-IL6 receptor (tocilizumab)
  • JAK inhibitors (tofacitinib and baricitinib)
38
Q

Pathophysiology of RA

A
  • Autoimmune reaction
  • Body recognises own antigens on collagen as foreign
  • T cells, B cells and macrophages activated
  • T cells produce IFN‐γ (interferon gamma) and IL-17
  • Macrophages produce TNF alpha, IL-1 and IL-6
  • Inflammation causes proliferation of synovial cells
  • CARTILAGE DAMAGE, BONY DESTRUCTION AND DEFORMITY
39
Q

Pre-commencement on sDMARD’s

A
  • Warn about impact of DMARDs on fertility, pregnancy and delivery
  • Should be commenced from diagnosis
  • Baseline assessment: Height, weight, BP
  • Baseline Bloods: FBC, U&E, LFT, Albumin
  • Assessment of underlying co morbidities- respiratory/occult infection.
  • Vaccination –Flu and pneumococcal
40
Q

Hydroxychloroquine

A
  • Mechanism: Anti Malarial
  • Indications: RA, SLE, Mixed CTD
  • Route: PO
  • Dose: 200mg Bd for 3 months then od
  • Side effects: Nausea/retinal toxicity
  • Ophthalmology screening required, Safe in pregnancy
41
Q

Methotrexate

A
  • MoA: Folinic acid pathway
  • Indications RA/PSA, SLE, Limited scleroderma, Mixed CTD
  • Route: PO/SC
  • Dose:10-25 mg Once weekly
  • Side effects: GI side effects, pneumonitis, blood dyscrasias
  • Should not be co-prescribed with trimethoprim
  • Co-prescribed with Folic acid
  • Teratogenic
  • To reverse folinic acid rescue
42
Q

Azathioprine

A
  • MoA: Thiopurine pathway
  • Indications: Lupus, Scleroderma, Sjogrens, Mixed CTD, RA, PSA
  • Route: PO
  • Dosage:50mg -300 mg daily in divided doses
  • Side effects: GI side effects, myelosuppression, rarely agranulocytosis
  • TMPT levels if low then cap dose to 150 mg daily
  • Concomitant use of Allopurinol-increased risk of bone marrow suppression
  • Safe in pregnancy
43
Q

Sulfasalazine

A
  • Indications: RA, PSA
  • Route: PO
  • Dose: 500mg- 3g daily
  • Side effects: GI side effects, rash, low mood
  • Safe in pregnancy
44
Q

Leflunomide

A
  • Indications: non renal SLE. RA. PSA
  • Side effects: Transiently abnormal ALT, leucopenia and hypertension
  • Teratogenic- Consider stopping 2 years before conception/ if not cholestyramine washout
45
Q

sDMARD (synthetic DMARD’s) principles

A
  • During a serious infection, sDMARDs should be temporarily discontinued until the patient has recovered but not for minor cold
  • Dont stop before surgery but maybe if high risk
46
Q

bDMARD’s (biological DMARD’s) risk

A
  • Infection
  • Exacerbation of cardiac failure
  • Malignancy
  • Reactivation of TB, hepatitis B
  • Avoid live vaccines
  • (demyelination, SLE-like syndrome)
  • Examples: Adalimumab, Infilximab, Rituximab
47
Q

DMARD’s infection

A
  • Not initiated in active infection, check for infection while on biologics
  • Use Etarnercept and Abatacept in high risk patient
  • All patients screened for TB, HIV and Hepatitis before commencement of biologics
  • If active TB/latent TB, refer to Respiratory Physician
  • Malignancy: not commenced in active cancer. No conclusive evidence of increased risk of solid cancers but caution with risk of skin cancers. Caution in patients with previous malignancy
48
Q

Jak kinase inhibitors

A

Targeted synthetic DMARD’s. Similar efficacy and side effects/risks to bDMARD’s, oral.

49
Q

RA: treat to target approach

A
  • Advantages: reduce deformity, disability, impairement of function. Maintain independence/employment. Reduce pain, improve quality of life, economic benefit
  • Disadvantages: expensive, are we over treating, toxicity
50
Q

RA epidemiology

A
  • Commonest form of inflammatory arthritis
  • Symmetrical distribution of joint pain
  • More common in women, peaks 30-55
  • Multisystem autoimmune disease
  • Strong genetic component
51
Q

RA multisystem disease presentation

A
  • Synovial joints / tendons / ligaments
  • Skin (Rheumatoid nodules- tend to be on extensor aspect of joints)
  • Eyes (episcleritis / keratoconjunctivitis sicca)
  • Cardio-Pulmonary (pericarditis / rheumatoid nodules in lungs)
  • Splenomegaly- can cause neutropenia
  • Blood (anaemia of chronic disease)
  • Renal (amyloidosis and renal impairement)
  • Central / Peripheral nervous system (cervical spine / carpal tunnel)

Medicine year 4 CDM (44 decks)

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