Rheumatoid Arthritis Flashcards
What is rheumatoid arthritis?
Chronic, systemic autoimmune condition that causes chronic inflammation of the synovial lining of the joints, tendon sheaths and bursa. It is a symmetrical polyarthritis.
Discuss the pathophysiology of rheumatoid arthritis
- Citrullination of self antigens
- These citrullinated self antigens are then recognised by T & B cells which can produce the following antibodies:
- Rheumatoid factor (autoantibodies against Fc portion of IgG) and anti-CCP (anti citrullinated cyclic peptide)
- These antibodies can then stimulate macrophages and fibroblasts causing the release of TNF-alpha dn activation of inflammatory cascade
- Inflammatory cascade leads to proliferation of synoviocytes; this results in synoviocytes growing over cartilage and therefore restircting nutrient supply to cartilage leading to cartilage damage
- Activated macrophages also stimulate osteoclast differentiation resulting in bone damage
What two autoantibodies are involved in RA?
Which is more sensitive and specific to RA?
- Rheuamatoid factor (autoantibody to Fc portion of IgG) and Anti-CCP (anti-citrullinated cyclic peptide antibodies)
- Anti-CCP is more specific to RA
Anti-CCP antibodies often pre-date the development of RA and give an indication that the pt will develop RA at some point; true or false?
True
State some risk factors for rheumatoid arthritis
- Female sex
- Family history
- Smoking
Who/in what individuals does rheumatoid arthritis usually present in?
- Most commonly develops in middle aged females
- 3x more common in women
Compare pain from inflammtory athritis with pain from mechanical arthritis
Inflammatory arthritis
- Worse after rest
- Improves with activity
Mechanical arthritis
- Worse with activity
- Improves with rest
State the symptoms/typical presentation of rheumatoid arthritis
Typically presents with symmetrical distal polyarthropathy (e.g. small joints of hands & feet, wrist and ankles- but may also affect larger joints like knees, shoulder & elbows); key joint symptoms:
- Pain
- Swelling
- Stiffness (usually morning stiffness, >30mins)
Associated systemic symptoms:
- Fatigue
- Weight loss
- Flu-like illness
- Muscle aches & weakness
Discuss the onset of RA i.e. is it sudden or does it take a long time?
Onset can be very rapid (e.g. overnight) or over months to years
Which joints does RA typically affect?
- PIPJ
- MCPJ
- MTPJ
- Wrist & ankle
- Cervical spine
- Large joints can also be affected e.g. knee, hips, shoulders
Which joints are almost never affected by RA?
DIPJ
*If these are enlarged and painful most likely Herbenden’s nodes due to OA
State what you might find in the hands on clinical examination of someone with rheumatoid arthritis?
- “Boggy” feeling when palpating around joints
- Z shaped deformity to thumb
- Swan neck deformity
- Boutonnieres deformity
- Ulnar deviation of fingers at MCP/knuckles
Describe and explain how the following develop:
- Swan neck deformity
- Boutonniere’s deformity
Swan neck deformity
-
Hyperextension of PIPJ, flexion of DIPJ
- PIPJ: tissues on palmar aspect of PIPJ become lax as a result of synovitis causing an imbalnce of forces
- DIPJ: elongation or ruputure of insertion of extensor digitorum into base of proximal phalanx
Boutonniere’s deformity
-
MCPJ and DIPJ are hyperextended and PIPJ is flexed
- Inflammation in PIPJ lead to lenghthening or rupture of central slip of extensor digitorum as it inserts onto base of middle phalanx on . Lateral bands slip down sides fo fingers and now act as flexors- instead of extensors- and now also hyperextend DIPJ
State what you might find, other than findings in hands, on clinical examination of someone with RA?
- Fine crackles (Caplan’s syndrome)
- Splenomegaly (Felty’s syndrome)
- Dry eyes, dry mouth, lymphadenopathy (secondary Sjogren’s)
- Conjunctival pallor (anaemia of chronic disease)
- Episcleritis & scleritis
- Lymphadenopathy
- Rheumatoid nodules- most common at elbow
State some extra-articular manifestations of RA
- Caplan’s syndrome (pulmonary fibrosis with pulmonary nodules)
- Bronchiolitis obliterans (inflammation causing small airway destruction)
- Felty’s syndrome (RA, neutropenia, splenomegaly)
- Secondary Sjogren’s syndrome
- Anaemia of chronic disease
- Cardiovascular disease
- Episcleritis & scleritis
- Lymphadenopathy
- Carpel tunnel syndrome
- Amyloidosis
To help you remember extra-articular manifestations of RA you can think of the 3CAPS; state these
- Carpel tunnel syndrome
- Cardiac risk elevated
- Cord compression (atlanto-axial subluxation)
- Anaemia
- Amyloidosis (rare due to improved treatment)
- Arteritis (rare due to improved treatment)
- Pericarditis
- Pleural disease
- Pulmonary disease( e.g. bronchiectasis, fibrosis)
- Sjogren’s syndrome
- Scleritis/episcleritis
- Splenic enlargement (with neutropenia & RA= Felty’s syndrome)
The diagnosis of RA is largely clinical; true or false?
True (although we do some investigations to support diagnosis)
What diagnostic criteria is used to diagnose RA?
Describe this criteria
American college of Rheumatology (ACR)/EULAR critera. A score >/= to 6 is required for definitive diagnosis:
- Joints that are involved (more and smaller joints= higher score) 0-5
- Serology (RF and anti-CCP) 0-3
- Inflammtory markers (CRP & ESR) 0-1
- Druation of symptoms > or < 6 weeks 0-1
*Highest possible score=10
What investigations would you do for someone with suspected rheumatoid arthritis, include:
- Bedside
- Bloods
- Imaging
*Where appropriate, justify each
Bedside
Bloods
- Rheumatoid factor
- Anti-CCP
- FBC: may show normocytic anaemia
- CRP, ESR
Imaging
- Ultrasound: can be used to confirm synovitis
- X-ray of hands & feet: may show changes in established disease. USS or MRI more sensitive in early disease (RECCOMENDED BY NICE IN ALL PTS WITH SUSPECTED RA)
NOTE: other investigations may be required; guided by hhistory and exam e.g. may need pulmonary function tests, HRCT chest if lung involvement suspected
State 4/5 things you may see on x-ray of pt with RA
*Asking for cardinal signs of RA on x-ray
- Joint space narrowing
- Periarticular/juxta-articular osteopenia
- Marginal bony erosions
- Subluxation & gross deformity
- (soft tissue swelling)
What scoring system can we use to monitor disease activity and response to treatment in RA; describe what is included in this scoring system
DAS28 Score
Based on the assessment for 28 joints and points given for:
- Swollen joints
- Tendor joints
- ESR/CRP result
Help you assess severity of disease and also response to treatment.
What questionnaire can be used to measure functional ability?
When do NICE reccomend you use it?
- Health assessement qeustionnaire
- Use at diagnose to check response to treatment (compare results)
Discuss the general management of rheumatoid arthritis
*NOTE: not asking for specific drugs
Management of acute flares & symptom control:
- Steroids (oral, IM or intra-articular) **STEROIDS MOST OFTEN USED
- NSAIDs with PPI
Management to slow progression/improve long term outcomes
- DMARDs
- If disease still severe, consider combination of 2 DMARDs
- If disease still severe consider methotrexate plus a biological therapy
Multidisciplinary team management
- Doctor, specialist nurse, physio, OT, psychology, podiatry
What biologics can we use in RA?
Often use ANTI-TNF biologics such as infliximab, adalimumab, etanercept. Can also use rituximab
Discuss the different DMARDs we can use in RA
- Methotrexate *Usually used first
- Leflunomide
- Sulfasalazine
- Hydroxychloroquine: can be used in mild disease- it is considered the mildest anti-rheumatic drug
State the first, second, third & fourth line therapy for RA (not referring to acute treatment- referring to long term treatment)
-
First line= monotherapy with DMARD
- Methotrexate, leflunomide, sulfasalazine, hydroxychloroquine
- NICE 2018 guidance states to use DMARD with bridging corticosteroid as initial step
- Second line= dual therapy with DMARDs
- Third line= methotrexate + a biological therapy (usually anti-TNF biologic)
- Fourth line= methotrexate + rituximab (anti-CD20)
Which DMARDs would you use in pregnancy?
Sulfasalazine and hydroxychloroquine
*NOTE: symptoms often improve in pregnancy probably due to higher natural production of steroids
Orthopaedic surgery is no longer an important part of management in pts with RA; true or false?
True, now that DMARDs & biologics are used pts are less likely to progress to stage where they need surgery
For methotrexate, state:
- Mechanism of action
- How it is administered
- What else must be prescribed (if it is being taken for reasons other than malignancy)
- Side effects
- Interferes with metabolism of folate and supresses certain components of immun system
- Injection or tablet once a week
- 5mg folic acid once a week (take diff day to methotrexate)
- ADRs:
- Mouth ulcers
- Mucositis
- Pulmonary fibrosis
- bone marrow supression
- Teratogenic
For leflunomide, state:
- Mechanism of action
- ADRs
- Inhibits dihydroorotate dehydrogenase and hence inhibits production of pyrimidine which is an important component of RNA and DNA
- ADRs
- Mouth ulcers
- Mucositis
- Hypertension
- Peripheral neuropathy
- Liver toxicity
- Bone marrow supression
- Teratogenic
For hydroxychloroquine, state:
- Mechanism of action
- ADRs
- Interferes with toll-like receptors disrupting antigen presentation and increasing pH of lysosomes in immune cells
- ADRs:
- Nightmares
- Reduced visual acuity
- Liver toxicity
- Skin pigmentation
For sulfasalazine, state:
- Mechanism of action
- ADRs
- Sulfasalazine is combination of 5-aminosalicyclic acid and sulfapyridine. Mechanism of action not clear but it is thought that is is related to folate metabolism
- ADRs:
- Temporary male infertility
- Bone marrow supression
For rituximab, state:
- Mechanism of action
- ADRs
- Monoclonal antibody that targets CD20 protein on surface of B cells causing destruction of B cells
- ADRs:
- Immunosupression
- Night sweats
- Thrombocytopenia
- Peripheral neuropathy
- Lung & liver toxicity
State mechanism of action of following anti-TNF drugs:
- Infliximab & adalimumab
- Etanercept
- Infliximab & adalimumab: monoclonal antibodies to TNF
- Etanercept: protein that binds TNF to the Fc portion of IgG and reduced its activty
All of DMARDs & biolgoics are immunosupressants; true or false?
True
What monitoring is required when using DMARDs & biologics long term- why?
- FBCs: all are immunosupressants so need to check cell counts
- LFTs: can cause hepatotoxicity
Discuss some complications of RA
- Atlantoaxial subluxation (axis and odontoid peg shift within the atlas due to damage to ligaments and bursa. Can cause spinal cord compression and this is an emergenc)
- Increased risk of coronary artery disease
- Interstitial lung disease
- Carpal tunnel syndrome
Discuss the prognosis of RA, include what makes prognosis worse
Varies between pts; some pts have mild, remitting disease and some have progressive severe disease. Prognnosis is worse if:
- Younger onset
- Male
- More joints & organs affected
- Presence of RF and anti-CCP
- Erosions seen on x-ray
