RA Flashcards

1
Q

How does inflammatory arthritis present?

A

Inflammatory arthritis (IA) may present fairly acutely usually within weeks or a few months.

It is typically worse in the morning and associated with > 30 minutes of morning stiffness. It improves with exercise/ as the day goes on.

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2
Q

What are the differentials for IA?

A
Connective tissue disease 
Vasculitis 
RA
Ankylosing spondylitis 
Psoriatic arthritis 
Reactive arthritis 
IBD arthritis
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3
Q

When is IA more likely to be due to vasculitis or CTD?

A

In vasculitis/ CTD expect systemic features (weight loss, anorexia, fever, sweats, lethargy) and multisystem involvement.

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4
Q

When is RA more likely to be the cause of the PC?

A

The presence of a family history makes RA more likely as it has a strong genetic component.

The patient is at an age when this frequently presents. It, typically affects the small joints of hands, feet and wrists in a symmetrical distribution as in this case.

Dry eyes suggests Sjogren’s syndrome which is commonly associated with rheumatoid arthritis.

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5
Q

How does psoriatic arthritis present?

A

Psoriatic arthritis can take many forms e.g. polyarthritis, oligoarthritis, but is usually asymmetrical.

It may be associated with other features such as dactylitis and tendonitis.

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6
Q

What is arthritis mutilans?

A

The term “arthritis mutilans” refers to an extremely severe form of psoriatic arthritis characterised by resorption of bones and the consequent collapse of soft tissue.

When this affects the hands, it can cause a phenomenon sometimes referred to as “telescoping fingers.” Similar changes can occur in the feet. It is not seen in RA.

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7
Q

How does reactive arthritis present?

A

It usually affects younger patients and presents with an asymmetric oligoarthritis shortly after infection with an enteropathic or genitourinary organism.

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8
Q

How does OA present?

A

Non- inflammatory/ Osteoarthritis (OA) is usually insidious in onset, sometimes over years.

It involves < 30 minutes of morning stiffness and is typically worsened by activity and worse towards the end of the day.

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9
Q

How does septic arthritis present?

A

With an acute history- onset over hours/days - infection should be considered. This is particularly the case for monoarthritis and oligoarthritis.

Look for underlying risk factors such as diabetes and immunosuppression.

Also, there are likely to be systemic features such as sweats and fevers and the patient is likely to feel generally unwell.

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10
Q

How does gout present?

A

Gout/ Pseudogout should be considered with an acute history. Risk factors for gout include a family history of gout, and purine consumption.

Pseudogout is more likely in elderly patients with underlying osteoarthritis.

Acute attacks of gout often affects the first metatarsophalangeal joint

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11
Q

Which questions should you ask to determine if pain and swelling of the hands is due to IA?

A

When did your symptoms start?

Did they start suddenly or build up gradually?

Do your symptoms typically vary throughout the day?

When are they at their worst?

What happens if you exercise?

How do you feel first thing in the morning?

Do your joints ever feel stiff? If so for how long?

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12
Q

What does boggy swelling indicate?

A

“Boggy” swelling feels similar to when you squash a grape and is suggestive of synovitis which occurs in IA. In OA swelling is bony in nature.

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13
Q

What is RA?

A

Rheumatoid arthritis (RA) is a common chronic inflammatory autoimmune disease characterised by an inflammation of the synovial joints leading to joint and periarticular tissue destruction, as well as a wide variety of extra-articular features.

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14
Q

Why is it important to diagnose RA in its early stages?

A

Suppression of inflammation in the early stages of the disease can result in substantial improvements in long-term outcomes.

There is evidence that the first 12-week period of the disease is immunologically distinct and represents a unique opportunity to influence the progress of the disease.

Once mechanical damage has occurred, pain and joint deformity often require aids and appliances and, eventually, surgery.

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15
Q

What is the pathophysiology of RA?

A

In RA, the synovium becomes inflamed and thickened and proliferative synovitis (pannus) can be seen. Angiogenesis occurs enabling movement of leucocytes from the blood to the synovial tissues.

The intima contains greatly increased numbers of inflammatory cells including macrophages, fibroblasts, T-cells, B-cells and plasma cells. The synovial fluid becomes a fibrinous inflammatory exudate, containing many neutrophils.

Local release of matrix-degrading enzymes and mediators of inflammation may damage the adjacent cartilage and result in the formation of erosions.

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16
Q

What are the risk factors for RA?

A

RA results from an interaction between genetic susceptibility and environmental factors, including high birth weight, smoking, silica exposure, alcohol abstention, obesity, diabetes mellitus, rheumatoid factor, and anti-citrullinated protein (CCP) antibody.

Smoking is an important risk factor.

HLA DR4 and DR1 are associated, especially with severe disease.

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17
Q

What is the challenge for GPs with the presentation of RA?

A

The challenge for GPs is to recognise early symptoms and refer early. The presentation can be very variable. Constitutional symptoms (eg, profound fatigue, influenza-like symptoms, fever, sweats and weight loss) are common.

18
Q

How does RA present?

A

Arthritis:
Usually starts as an insidious symmetrical polyarthritis, often with nonspecific systemic symptoms.

RA can affect any synovial joint but typically affects the small joints of the hands and the feet. It is usually bilateral and symmetrical in distribution.

More joints are affected with the progression of the disease.

Joint inflammation produces characteristic changes: heat and sometimes redness, swelling, pain, stiffness (especially in the early morning or after inactivity), progressive joint destruction and loss of joint function.

Pain, swelling, muscle wasting and damage to joints result in progressive deformity, disability and handicap.

Tendon sheaths have synovial linings and inflammation of these can result in tendon rupture.

19
Q

What is palindromic rheumatism?

A

Palindromic rheumatism is a rare form of inflammatory arthritis.

Attacks of joint pain and swelling are similar to rheumatoid arthritis, but the joints return to normal between attacks.

Patients with palindromic rheumatism may later develop rheumatoid arthritis.

20
Q

What are the signs of rheumatoid arthritis?

A

Shoulders, elbows and hips are less commonly affected.

Hand deformities, including ulnar deviation, swan neck and Boutonnière’s deformity of the fingers, Z deformities of thumbs and piano key deformity of the wrist.

The characteristic features of the hands in patients with RA are subluxation of the metacarpophalangeal joints, radial deviation of the wrist joint and ulnar deviation of the fingers.

Muscle wasting and tendon rupture.

Cervical complications (instability of the cervical spine).

21
Q

What is swan-neck deformity?

A

Swan-neck deformity (proximal interphalangeal joint hyperextension with concurrent distal interphalangeal joint flexion) occurs in patients with RA, but may also follow trauma or be congenital.

22
Q

What is boutonniere deformity?

A

Boutonnière deformity (flexion of the proximal interphalangeal joint accompanied by hyperextension of the distal interphalangeal joint) can result from tendon laceration, dislocation, fracture, osteoarthritis or RA.

23
Q

What is the percentage of patients with RA with extra-articular features?

A

40%

24
Q

What are the extra-articular features seen in RA?

A

Eyes: secondary Sjögren’s syndrome, scleritis and episcleritis.
Scleromalacia performans- occurs where there is rupture of the globe due to weaking of the scleral layer.
Skin: leg ulcers especially in Felty’s syndrome (association of rheumatoid factor positive rheumatoid arthritis, neutropenia and splenomegaly). Rashes, nail fold infarcts.
Rheumatoid nodules: these are common, and may occur in the eyes, may be subcutaneous, and may be in the lung, heart and occasionally the vocal cords.
Neurological: peripheral nerve entrapment, atlanto-axial subluxation, polyneuropathy, mononeuritis multiplex.
Respiratory system: pleural involvement, pulmonary nodules, pulmonary fibrosis, obliterative bronchiolitis, Caplan’s syndrome.
Cardiovascular system: cardiovascular disease, pericardial involvement, valvulitis and myocardial fibrosis, immune complex vasculitis.
Kidneys: rare, including analgesic nephropathy, amyloidosis.
Liver: mild hepatomegaly and abnormal transaminases are common.
Other: thyroid disorders, osteoporosis, depression, splenomegaly and susceptibility to infections.

25
Q

What are the differentials of RA?

A
Viral arthritis 
Reactive arthritis 
Psoriatic arthritis 
Ankylosing spondylitis 
IBD 
SLE 
Scleroderma 
Polymyalgia rheumatica 
Gout 
OA
Septic arthritis 
Fibromyalgia
26
Q

What is the ACR criteria?

A

ACR criteria is used for RA diagnosis

The criteria should be used for patients who have at least 1 joint with clinical synovitis (swelling) or with the synovitis not better explained by another disease.

This criteria uses joint involvement (0-5), serology such as RF and ACPA (0-3), acute phase reactants such as CRP and ESR (0-1) and duration of symptoms (0-1)

A score of 6 or more out of 10 is diagnostic of RA

27
Q

What are the non-specific investigations done for RA?

A

ESR, CRP and plasma viscosity: usually raised but may be normal.

FBC: normochromic, normocytic anaemia and reactive thrombocytosis are common in active disease. Raised ferritin but low serum iron concentration and total iron-binding capacity.

LFTs: mild elevation of alkaline phosphatase and gamma GT.

Antinuclear antibody: positive in SLE and related conditions; also in up to 30% of RA patients and weakly positive in up to 10% of the normal population.

Uric acid/synovial fluid analysis: excludes polyarticular gout.

Urinalysis: microscopic haematuria/proteinuria may suggest connective tissue disease.

TFTs as thyroid disease may present with joint pain.

28
Q

What are the specific investigations done for RA?

A

Rheumatoid factor in people with suspected RA who are found to have synovitis on clinical examination.

Anti-cyclic citrullinated peptide (anti-CCP) antibodies in an individual with suspected RA.

X-ray the hands and feet early in the course of the disease in people with persistent synovitis in these joints.

29
Q

Which antibody is more specific in RA?

A

If the patient is negative for rheumatoid factor, and there is a need to decide about starting combination therapy. Anti-CCP has been found to be more specific than rheumatoid factor in RA and may be more sensitive in erosive disease.

Rheumatoid factor: positive in 60-70% of patients (and 5% of the normal population).

30
Q

What does the X-ray show in RA?

A

X-rays may show soft tissue swelling, periarticular osteopenia, loss of joint space (uniform), erosions and deformity.

31
Q

Why might a patient with RA be anaemic?

A

Anaemia may be seen due to Felty’s syndrome (anaemia, leucopaenia and enlarged spleen), pernicious anaemia (people with autoimmune condition are more likely to have a second autoimmune condition) and autoimmune haemolytic anaemia.

32
Q

When should you refer a patient with RA?

A

NICE advises referral for specialist opinion any adult with suspected persistent synovitis of undetermined cause. Refer urgently if any of the following apply:

  • The 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 onset of symptoms and seeking medical advice.

Do not avoid referring urgently any person with suspected persistent synovitis of undetermined cause whose blood tests show a normal C-reactive protein (CRP) and ESR or a negative rheumatoid factor.

The window of opportunity in which disease-modifying drugs can prevent joint damage is only a few months.

33
Q

What is DAS28?

A

In people with recent-onset active RA, measure CRP and key components of disease activity (using a composite score such as DAS28) monthly until treatment has controlled the disease to a level previously agreed with the person with RA.

The DAS28 is a measure of disease activity in RA.

34
Q

How is the DAS28 score calculated?

A

The score is calculated by a complex mathematical formula, which includes the number of tender and swollen joints (out of a total of 28 - shoulders, elbows, wrists, metacarpophalangeal joints, proximal interphalangeal joints and the knees), the ESR, and the patient’s ‘assessment of global health’. A DAS28 score greater than 5.1 implies active disease, less than 3.2 - well-controlled disease, and less than 2.6 – remission

35
Q

What is the management of RA?

A

Screen for comorbid conditions such as osteoporosis, depression and CVD.
Non-drug management:
-RA patients should have easy access to physiotherapy, occupational therapy, psychological services and podiatry. There should be regular review, particularly with physiotherapy and occupational therapy.
-Exercise reduces bone loss in postmenopausal women with RA

Drug management
-NSAIDs when control of pain or stiffness is inadequate.
Offer PPI and lowest effective dose for NSAIDs
Review risk factors for adverse events regularly.
-Short-term treatment with glucocorticoids may be used for managing flares in adults with recent-onset or established disease to rapidly decrease inflammation.
-In adults with established RA, long-term treatment with glucocorticoids may be continued.
-Short-term bridging treatment with glucocorticoids may be used when starting a new conventional DMARD
-DMARDs
-Biologics
-Surgery

36
Q

When should long-term treatment with glucocorticoids be considered in RA?

A

when:
The long-term complications of glucocorticoid therapy have been fully discussed; and
All other treatment options (including biological and targeted synthetic DMARDs) have been offered.

37
Q

What are examples of DMARDs?

A

First-line treatment with cDMARD monotherapy using oral methotrexate, leflunomide or sulfasalazine should be started as soon as possible and ideally within three months of onset of persistent symptoms.

Hydroxychloroquine can be used for first-line treatment as an alternative to oral methotrexate, leflunomide or sulfasalazine for mild or palindromic disease.

38
Q

When are biologics indicated in the management of RA?

A

Biological therapies (cytokine modulators) have been shown to be effective in the treatment of RA, including patients resistant to methotrexate. The following are approved for treatment of RA:

  • Tumour necrosis factor (TNF) inhibitors: adalimumab, certolizumab pegol, etanercept, golimumab, infliximab.
  • Anti-interleukin-1 therapy: anakinra.
  • T-cell co-stimulator modulator: abatacept.
  • Anti-CD20 therapy: rituximab.
  • Anti-interleukin-6 receptor therapy: tocilizumab.

NICE recommends that in addition to low-dose glucocorticoids, two trials of six months of traditional DMARD monotherapy or combination therapy (at least one including methotrexate) should fail to control symptoms or prevent disease progression before a biological therapy be recommended.

39
Q

What is discussed in the annual review of a person with RA?

A

Assess disease activity and damage

Check for development of co-morbidities

Assess for complications such as vasculitis and disease of the cervical spine.

Assess the need for surgery

Review effectiveness and adverse effects of medication.

40
Q

What are the complications of RA?

A
Adverse effects on work and social life
Depression 
Vasculitis
PE, pulmonary fibrosis 
Pericarditis, MI, myocarditis 
Lymphadenopathy
Neuropathy 
Felty’s syndrome- RA plus splenomegaly and neutropenia 
Amyloidosis 
Anaemia 
Carpal tunnel syndrome 
Osteoporosis 
Tendon rupture
41
Q

What are the drug complications of RA?

A

Gastrointestinal: mainly due to the adverse effects of NSAIDs.

Increased risk of infection: glucocorticoids and immunosuppressants.

Liver toxicity: methotrexate-related.

Malignancy: particularly TNF-alpha inhibitor-related (increased risk of skin cancer).

Osteoporosis: low-dose glucocorticoid use. RA also increases the risk of osteoporosis in the absence of glucocorticoid use.

42
Q

Which factors are associated with a worse prognosis of RA?

A

Age younger than 30 years, male.
Insidious onset.
Extra-articular manifestations, a large number of involved joints, systemic symptoms, persistent anaemia of chronic disease.
HLA-DRB1*04/04 genotype, a high serum titre of autoantibodies (eg, rheumatoid factor, anti-CCP), raised levels of complement C1q.
Early X-ray evidence of bone erosions.
RA that remains persistently active for longer than one year.