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Yr3 Medicine- Rheumatology > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What is rheumatoid arthritis?

A

Chronic, systemic autoimmune condition that causes chronic inflammation of the synovial lining of the joints, tendon sheaths and bursa. It is a symmetrical polyarthritis.

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2
Q

Discuss the pathophysiology of rheumatoid arthritis

A
  • 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
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3
Q

What two autoantibodies are involved in RA?

Which is more sensitive and specific to RA?

A
  • Rheuamatoid factor (autoantibody to Fc portion of IgG) and Anti-CCP (anti-citrullinated cyclic peptide antibodies)
  • Anti-CCP is more specific to RA
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4
Q

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?

A

True

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5
Q

State some risk factors for rheumatoid arthritis

A
  • Female sex
  • Family history
  • Smoking
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6
Q

Who/in what individuals does rheumatoid arthritis usually present in?

A
  • Most commonly develops in middle aged females
  • 3x more common in women
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7
Q

Compare pain from inflammtory athritis with pain from mechanical arthritis

A

Inflammatory arthritis

  • Worse after rest
  • Improves with activity

Mechanical arthritis

  • Worse with activity
  • Improves with rest
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8
Q

State the symptoms/typical presentation of rheumatoid arthritis

A

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
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9
Q

Discuss the onset of RA i.e. is it sudden or does it take a long time?

A

Onset can be very rapid (e.g. overnight) or over months to years

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10
Q

Which joints does RA typically affect?

A
  • PIPJ
  • MCPJ
  • MTPJ
  • Wrist & ankle
  • Cervical spine
  • Large joints can also be affected e.g. knee, hips, shoulders
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11
Q

Which joints are almost never affected by RA?

A

DIPJ

*If these are enlarged and painful most likely Herbenden’s nodes due to OA

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12
Q

State what you might find in the hands on clinical examination of someone with rheumatoid arthritis?

A
  • “Boggy” feeling when palpating around joints
  • Z shaped deformity to thumb
  • Swan neck deformity
  • Boutonnieres deformity
  • Ulnar deviation of fingers at MCP/knuckles
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13
Q

Describe and explain how the following develop:

  • Swan neck deformity
  • Boutonniere’s deformity
A

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
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14
Q

State what you might find, other than findings in hands, on clinical examination of someone with RA?

A
  • 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
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15
Q

State some extra-articular manifestations of RA

A
  • 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
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16
Q

To help you remember extra-articular manifestations of RA you can think of the 3CAPS; state these

A
  • 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)
17
Q

The diagnosis of RA is largely clinical; true or false?

A

True (although we do some investigations to support diagnosis)

18
Q

What diagnostic criteria is used to diagnose RA?

Describe this criteria

A

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

19
Q

What investigations would you do for someone with suspected rheumatoid arthritis, include:

  • Bedside
  • Bloods
  • Imaging

*Where appropriate, justify each

A

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

20
Q

State 4/5 things you may see on x-ray of pt with RA

*Asking for cardinal signs of RA on x-ray

A
  • Joint space narrowing
  • Periarticular/juxta-articular osteopenia
  • Marginal bony erosions
  • Subluxation & gross deformity
  • (soft tissue swelling)
21
Q

What scoring system can we use to monitor disease activity and response to treatment in RA; describe what is included in this scoring system

A

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.

22
Q

What questionnaire can be used to measure functional ability?

When do NICE reccomend you use it?

A
  • Health assessement qeustionnaire
  • Use at diagnose to check response to treatment (compare results)
23
Q

Discuss the general management of rheumatoid arthritis

*NOTE: not asking for specific drugs

A

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
24
Q

What biologics can we use in RA?

A

Often use ANTI-TNF biologics such as infliximab, adalimumab, etanercept. Can also use rituximab

25
Q

Discuss the different DMARDs we can use in RA

A
  • Methotrexate *Usually used first
  • Leflunomide
  • Sulfasalazine
  • Hydroxychloroquine: can be used in mild disease- it is considered the mildest anti-rheumatic drug
26
Q

State the first, second, third & fourth line therapy for RA (not referring to acute treatment- referring to long term treatment)

A
  • 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)
27
Q

Which DMARDs would you use in pregnancy?

A

Sulfasalazine and hydroxychloroquine

*NOTE: symptoms often improve in pregnancy probably due to higher natural production of steroids

28
Q

Orthopaedic surgery is no longer an important part of management in pts with RA; true or false?

A

True, now that DMARDs & biologics are used pts are less likely to progress to stage where they need surgery

29
Q

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
A
  • 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
30
Q

For leflunomide, state:

  • Mechanism of action
  • ADRs
A
  • 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
31
Q

For hydroxychloroquine, state:

  • Mechanism of action
  • ADRs
A
  • 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
32
Q

For sulfasalazine, state:

  • Mechanism of action
  • ADRs
A
  • 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
33
Q

For rituximab, state:

  • Mechanism of action
  • ADRs
A
  • 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
34
Q

State mechanism of action of following anti-TNF drugs:

  • Infliximab & adalimumab
  • Etanercept
A
  • Infliximab & adalimumab: monoclonal antibodies to TNF
  • Etanercept: protein that binds TNF to the Fc portion of IgG and reduced its activty
35
Q

All of DMARDs & biolgoics are immunosupressants; true or false?

A

True

36
Q

What monitoring is required when using DMARDs & biologics long term- why?

A
  • FBCs: all are immunosupressants so need to check cell counts
  • LFTs: can cause hepatotoxicity
37
Q

Discuss some complications of RA

A
  • 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
38
Q

Discuss the prognosis of RA, include what makes prognosis worse

A

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

Yr3 Medicine- Rheumatology (18 decks)

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