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Year 2 Clinical > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

Definition?

A

SYMMETRICAL, inflammatory arthritis, mainly affecting the PERIPHERAL, synovium joints; if untreated, it can lead to joint damage and irreversible deformities (erosion), resulting in loss of function and increased morbidity and mortality

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2
Q

Occurrence?

A
  • Can affect both sexes but WOMEN are affected 3X

* Can affect any age group

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3
Q

Other problems assoc. ?

A

Increased CV risk

Damage to nerves

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4
Q

Cause and triggers?

A

Antigen is unknown but it is HLA-DR4 mediated

Potential triggers inc. infections, stress and CIGARETTE SMOKING

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5
Q

Variability?

A

Severity and course depend on genetic factors and the presence of auto-antibodies (like anti-CCP, which increases severity and progression)

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6
Q

Examples of affected joints?

A 
Any joints lined with synovium (AKA synovial membrane), e.g:
• Hand and wrist 
• Elbows
• Shoulders
• TMJs
• Knees
• Hips
• Ankles
• Feet 
• Joints of C1/C2
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7
Q

Pathogenesis of RA?

A

Unknown antigen is presented to a naive T cell; this leads to eventual macrophage activation

Cytokines have a variety of effects, inc. B cell activation leading to auto-antibody production

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8
Q

How does joint destruction occur?

A

Cytokines cause osteoclast activation, which resorb bone and cause erosion and inhibition of cartilage cells

Synovial cells cause neovascularisation; this results in PANNUS formation (a fibrovascular tissue over the joint surfaces) which increases the blood supply and allows recruitment of more inflammatory cells

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9
Q

Two main types of inflammation in RA?

A

Synovitis

Tenosynovitis (as synovium also lines tendon sheaths and this can cause tendon rupture)

Both cause SWELLING and PAIN

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10
Q

Early RA definition? Importance?

A

Less than 2 years since symptoms onset; the first 3 months is the therapeutic window of opportunity, as the disease process can be modified and established disease can be prevented

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11
Q

Current classification criteria for RA?

A

PICTURE 2

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12
Q

Why is arthritis of < 6 weeks not awarded a point?

A

This may have been self-limiting; RA is chronic

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13
Q

What does diagnosis of RA involve?

A
  • History and clinical examination
  • Routine blood testing for anaemia of chronic disease, raised platelets
  • Inflammatory markers (CRP, ESR/plasma viscosity)
  • Auto-antibodies
  • Imaging (X-ray, US scan, MRI)
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14
Q

Clinical features of RA?

A
  • Prolonged morning stiffness (>30 mins), due to increased synovial fluid viscosity
  • Inv. of small joints of hands and feet (RA often spares the distal interphalangeal joints)
  • Symmetric distribution
  • Positive compression tests of MCP and MTP joints (if there is pain on compression/ squeezing)
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15
Q

Variable clinical presentation of RA?

A
  • PIP, MCP, wrist and MTP synovitis
  • Monoarthritis at the start but this EVENTUALLY progresses to symmetric polyarthritis
  • Tenosynovitis and trigger finger (defect in tendon causes a finger to jerk or snap straight when the hand is extended)
  • Carpal tunnel syndrome (compression of median nerve due to swelling)
  • Polymyalgia rheumatica (inflammation of muscles around the shoulders, neck and hips)
  • Palindromic rheumatism (rare episodic form of RA, where symptoms disappear between attacks; 50% progress to full RA)
  • Systemic symptoms (due to systemic inflammation), e.g: weight loss, night sweats
  • Poor grip strength
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16
Q

What is one of the first manifestations of RA?

A

Extensor carpi ulnaris tenosynovitis

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17
Q

Auto-antibodies in RA?

A

Not all patients have these so a -ve result does not rule out RA:
• Rheumatoid factor, i.e: rheumatoid IgM
• To cyclic cirtullinated peptide (anti-CCP antibodies)

Both have a moderate sensitivity but anti-CCP has a much higher specificity

18
Q

Describe the presence of anti-CCP antibodies

A

Can be present several years prior to articular symptoms and are assoc. with current/previous smoking; they remain +ve despite treatment

They are more likely to be assoc. with EROSIVE DAMAGE

19
Q

Advantages and disadvantages of plain X-rays in RA?

A

Advantages:
Cheap and reproducible

Disadvantage:
Absence of findings in early disease

20
Q

Signs of RA on X-ray?

A
  • Soft tissue swelling
  • Erosions
  • Loss of the joint space
  • Periarticular osteopaenia (loss of bone density around the joint)
21
Q

Locations that often shows first RA changes on X-ray?

A

5th MTP joint

Ulnar styloid

22
Q

Advantages of US scan?

A

Increased sensitivity for synovitis in early disease and this is superior to examination

Detects more MCP erosions than plain X-ray, in early RA

Useful in making treatment changes

23
Q

Advantages of MRI scans?

A
  • Bone marrow oedema on MRI is assoc. with inflammatory joint disease and may be a forerunner of erosion
  • Integrity of tendons can be assessed
  • Can distinguish synovitis from effusions
  • Can detect erosions earlier
  • Can be used to monitor disease activity
24
Q

Disadvantages of MRI scans?

A

Limited by cost

25
Q

What scoring system is used to assess disease activity?

A

DAS 28 - assesses 28 joints; how many are tender and how many are swollen?

26
Q

Interpreting DAS28 scores?

A

> 5.1 : active disease

  1. 2- 5.1 : moderate disease
  2. 6-3.2 : low disease activity

< 2.6 : remission

27
Q

What is the aim of RA treatment?

A

Push the patient into remission

28
Q

Management of RA?

A

Early treatment with disease-modifying, anti-rheumatic drugs (DMARDs)

Use of NSAIDs and steroids as adjuncts only (bridging therapy), as DMARDs can take 6 weeks to work)

Patient education

29
Q

Reason for steroid use?

A

Improve RA symptoms and reduce radiological evidence of damage

30
Q

How are steroids used?

A

Short, sharp courses in combo with a DMARD (not to be used solitarily)

Can be given orally/injections/IM

31
Q

Examples of DMARDS?

A

• Methotrexate
• Sulfasalazine
• Hydroxychloroquine (does not prevent erosions)
These can be given as triple therapy

  • Leflunomide
  • Gold injections, penicillaemina, azathioprine, etc
32
Q

RA treatment pyramid?

A

PICTURE 3

33
Q

Describe methotrexate use

A

Start at 15 mg/week with rapid escalation, with a max of 25 mg/week

Folic acid must be given 24 hrs after MTX dose

34
Q

How is palindromic RA treated?

A

Hydroxychloroquine

35
Q

Risks with methotrexate?

A

Allergic reaction

Pneumonitis

Bone marrow suppression

Hepatotoxicity

36
Q

Cautions with methotrexate?

A

Advise effective contraception

Regular blood tests

Avoid in patient with pre-existing lung disease, as pneumonitis on top of another disease would have a higher mortality; do a base-line CXR

Avoid Sulfasalazine in septrin allergy and G6PD deficiency

37
Q

Examples of biologic agents?

A

Anti-TNF agents: Infliximab, Etanercept, Adalimumab,
Certolizumab, Golimumab

T-cell receptor blocker: Abatacept

B cell depletor: Rituximab

IL-6 blocker: Tocilizumab

JAK 2 inhibitors: Tofacitinib

38
Q

Guidelines for use of biologic agents?

A

Used if there is a failure to respond to 2 DMARDs, inc. Methotrexate and DAS28 > 5.1, on two occasions 4 weeks apart

Methotrexate therapy is CO-PRESCRIBED

Must screen for latent or active TB, Hep B/C, HIV, Varicella zoster

Avoid live attenuated vaccines

39
Q

What is remission?

A

Absence of signs and symptoms of significant inflammatory arthropathy

40
Q

Complications of untreated RA?

A

Joint damage and deformities:
Boutonniere deformity of thumb
Ulnar deviation of MCP joints
Swan-neck deformity of fingers

Atlanto-axial subluxation (C1 and C2 are linked by the odontoid process and bones can move excessively and compress the spinal cord; if the person has neck pain, do an X-ray

PICTURE 4

Year 2 Clinical (119 decks)

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