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Core Conditions - Locomotor > Rheumatoid Arthritis (& other types) > Flashcards

Rheumatoid Arthritis (& other types) Flashcards

1
Q

What is rheumatoid arthritis?

A
  • a chronic, systemic inflammatory autoimmune disorder that primarily affects the joints
  • it can also manifest with extraarticular features
  • it is idiopathic with unknown aetiology
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2
Q

Who tends to be most affected by rheumatoid arthritis?

A
  • incidence is highest in women over 65 years of age
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3
Q

What are the risk factors for rheumatoid arthritis?

A
  • genetic disposition - associated with HLA-DR4 and HLA-DR1
  • environmental factors (e.g. smoking)
  • hormonal factors
    • premenopausal women are at the highest risk, suggesting a role of female sex hormones
  • infection
  • obesity
  • family history of RA
  • Remember “ a DRone with 4 propellers and 1 camera”*
  • it is associated with HLA-DR4 and HLA-DR1*
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4
Q

What is the pathophysiology involved in rheumatoid arthritis?

A
  • certain interstitial tissue proteins undergo a post-translational modification that involves conversion of arginine to citrulline
    • this is citrullination
  • citrullinated proteins are recognised as foreign by antigen-presenting cells that present them to CD4+ T-cells
  • activation of CD4+ T cells
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5
Q

How does activation of CD4+ T-cells result in inflammation?

A
  • IL-4 production, which leads to B-cell proliferation and differentiation
  • this leads to production of anticitrullinated peptide antibodies
  • this produces a type II and type III hypersensitivity reaction
  • CD4+ T cells then migrate to synovial joints and secrete cytokines (IFN-y & IL-17)
  • there is recruitment of macrophages and secretion of cytokines (TNF-a, IL-1, IL-16) which leads to inflammation and proliferation
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6
Q

How is there destruction of cartilage and bone in rheumatoid arthritis?

A
  • bouts of inflammation, angiogenesis and proliferation lead to production of proliferative granulation tissue with mononuclear inflammatory cells
  • this produces pannus and synovial hypertrophy
    • ​pannus is a growth of granulation tissue from the inflamed synovium into the joint space
    • it can destroy other intra-articular structures such as cartilage
  • this leads to invasion, progressive destruction and deterioration of cartilage and bone
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7
Q

What particular detectable antibodies are produced in rheumatoid arthritis and what does their presence suggest?

A
  • antibodies against the Fc portion of IgG are produced
  • these are called rheumatoid factors
  • they are produced to remove autoantibodies and immune complexes
  • individuals with positive RF are more likely to develop extraarticular manifestations
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8
Q

What are the articular manifestations of rheumatoid arthritis?

A
  • polyarthritis - multiple joints are affected
  • there is symmetrical pain and swelling of affected joints (also at rest)
  • morning stiffness (often > 30 minutes) that improves with activity
  • joint deformities
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9
Q

Which joints tend to be affected by rheumatoid arthritis?

Which joints are less commonly affected?

A
  • metacarpophalangeal joints (MCP)
  • proximal interphalangeal joints (PIP)
  • wrist joints and knee joints
  • the distal interphalangeal (DIP) joints tend NOT to be affected
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10
Q

What is “rheumatoid hand”?

What 3 deformities is this mainly associated with?

A

this typically manifests with one or more deformities:

  • swan neck deformity
    • PIP hyperextension and DIP flexion
  • boutonniere deformity
    • ​PIP flexion and DIP hyperextension
  • Hitchhiker thumb deformity (or Z deformity of thumb)
    • ​hyperextension of the interphalangeal joint with fixed flexion of the MCP joint
  • there may also be ulnar deviation of the fingers
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11
Q

What is the physical examination used in rheumatoid arthritis?

A

Gaenslen squeeze test

  • painful compression of hands (or feet) at the level of the MCP (or MTP) joint
  • a painful handshake is an early sign of arthritis
    • compression of the hand leads to lateral pressure on the synovial membrane of MCP joints
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12
Q

What are the constitutional symptoms associated with RA?

A
  • low-grade fever
  • myalgia (muscle aches)
  • malaise
  • fatigue
  • weight loss
  • night sweats
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13
Q

What are rheumatoid nodules and which areas of the body are affected by them?

A
  • they are nontender, firm, subcutaenous swellings (2mm - 5cm)
  • they commonly occur in areas exposed to higher pressure
    • e.g. extensor side of the forearm or bony prominences
  • they can also affect the lungs and tend to be bilateral and peripheral
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14
Q

What is Caplan syndrome?

A
  • rheumatoid pulmonary nodules that are accompanied by fibrosis and pneumoconiosis
  • pneumoconioses are restrictive ILDs associated with the inhalation of certain dusts
    • asbestosis and silicosis are the most common
  • this occurs in people with RA who have breathed in certain dusts or silica
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15
Q

What are the extraarticular manifestations of RA affecting the lungs and eye?

A

Lungs:

  • pleuritis (causing pleuritic chest pain)
  • pleural effusions
  • interstitial lung disease

Eyes:

  • keratoconjunctivitis sicca (“dry eye” disease)
  • scleritis
  • episcleritis
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16
Q

What is the consequence of RA affecting the endocrine and exocrine glands?

How does this present?

A

secondary Sjögren syndrome

  • autoimmune disease characterised by inflammatory destruction of the lacrimal and salivary glands
  • patients present with xerophthlamia (dry eyes) and xerostomia (dry mouth)
17
Q

What are the haematological extraarticular manifestations of RA?

A
  • normocytic anaemia as a result of anaemia of chronic disease
    • this can be normocytic or microcytic with elevated ferritin
    • mediated through hepcidin and cytokines
  • microcytic anaemia as a result of NSAIDs causing increased risk of GI bleeding, leading to iron-deficiency anaemia
  • macrocytic anaemia due to treatment with methotrexate decreasing folate levels
  • neutropenia
  • splenomegaly
  • lymphoma / large granular lymphocyte leukaemia
18
Q

what are the extraarticular manifestations of RA affecting the musculoskeletal system and the heart?

A

Musculoskeletal:

  • carpal tunnel syndrome
  • tenosynovitis and bursitis
    • tenosynovitis is inflammation of a tendon and its synovial sheath

Heart:

  • pericarditis and myocarditis
  • increased risk of MI, stroke, CHF & AF
19
Q

What are the vascular extraarticular manifestations of RA?

A
  • peripheral vasculitis, which manifests as livedo reticularis
    • reddish-blue discolouration of the skin in a net-like (reticular pattern) due to blood vessel spasm
  • Raynaud phenomenon
  • purpura
    • ​a purple-red nonblanchable cutaneous or mucosal lesion due to extravasation of blood into skin or mucous membranes
  • vasculitic ulcers
  • peripheral neuropathy
    • ​peripheral nerve damage characterised by distal sensory loss, burning sensation and/or weakness
20
Q

What criteria is used in the diagnosis of RA?

A

ACR criteria

  • there must be a score of 6 or more points + confirmed presence of synovitis in at least one typical joint
  • score is obtained by adding the points from each feature
21
Q

What are the nonspecific parameters that may be present in laboratory tests for RA?

A
  • raised inflammatory markers:
    • raised CRP and ESR which correlate with inflammatory activity
    • raised ferritin as an acute phase protein
    • possible leukocytosis and/or thrombocytosis
  • anaemia of chronic disease
22
Q

What are the 2 serology tests that can be done in the diagnosis of RA?

A

Anticitrullinated peptide antibodies (ACPA):

  • this is usually anti-CCP
  • this test has a specificity of >90%, allowing earlier detection of RA

Rheumatoid factor (RF):

  • IgM autoantibodies against the Fc region of IgG
  • present in 60-80% patients but low specificity, as it may be raised for other causes of chronic inflammation
23
Q

What is the typical X-ray performed to assess RA?

What are early and late radiological findings?

A
  • dorso-palmar X-ray of both hands
  • early changes include soft tissue swelling and juxta-articular demineralisation
  • late changes include joint space narrowing, erosions of cartilage and bone, general demineralisation and subchondral cysts
24
Q

What are subchondral cysts?

A
  • marginal erosions seen on imaging that correlate with pannus invasion of bone
  • they are fluid-filled spaces inside a joint
25
Q

How is disease activity of RA measured?

What is mild disease activity?

A
  • typically there are periods of minimal / no symptoms alternating with periods of increased disease activity
26
Q

What are the features of moderate disease activity?

A
27
Q

What are the characteristics of severe disease activity?

A
28
Q

What are the general measures in the treatment of RA?

A
  • encouraging regular physical activity
  • application of heat or cold packs as needed
    • heat reduces pain and relaxes muscles
    • cold will reduce swelling
      *
29
Q

What is the main source of acute anti-inflammatory therapy in RA and how long is it given for?

A

glucocorticoids

  • given until the onset of action of DMARD or as a long-term therapy for highly active RA
  • usually involves prednisolone systemically or via intra-articular injection
  • osteoporosis prophylaxis is needed by optimising calcium and vitamin D intake
30
Q

What is an alternative acute anti-inflammatory therapy used in RA that does not improve prognosis?

A
  • NSAIDs and selective COX-2 inhibitors provide symptomatic relief
  • comedication with a PPI is recommended as combining glucocorticoids with NSAIDs substantially increases risk of GI ulcers
31
Q

Who should not be given NSAIDs for symptomatic relief of RA?

A
  • patients > 60 years
  • impaired renal function
  • on antiplatelet agents or blood thinners
  • history of or active peptic ulcer disease
32
Q

What are DMARDs?

When should they be given to RA patients and what are the benefits?

A
  • disease-modifying antirheumatic drugs
  • they induce immunosuppression, leading to potential remission of RA
  • they should be given to anyone with RA, regardless of disease activity
  • DMARD therapy slows progression of disease, preserves joint function and limits RA complications
33
Q

Why are glucocorticoids still given initially with DMARD therapy?

A
  • DMARDs have a slow onset of action (6 weeks or more)
  • symptomatic treatment with glucocorticoids and/or NSAIDs is often required
34
Q

What is the drug of choice to use as a DMARD?

What must be checked before starting this, and what other medication is recommended?

A

methotrexate

  • check FBC and LFTs before starting
    • methotrexate can cause pancytopenia due to bone marrow suppression and hepatotoxicity
  • folic acid should be given 24-48 hours after taking methotrexate to minimise side effects
  • NSAIDs should not be taken on the same day as MTX as they can worsen side effects by inhibiting renal excretion
35
Q
A

Core Conditions - Locomotor (5 decks)

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