Rheumatology: Inflammatory Arthritis Flashcards

1
Q

Rheumatoid arhthritis - examination findings [4]

A
  • Soft-tissue swelling over the joints with tenderness.
  • Joint deformities: swan-neck and boutonniere in the fingers, Z-thumb, ulnar deviation at the MCP
    joints, radial deviation of the wrist joint, over-riding and hammer toes.
  • Rheumatoid nodules (~20% of patients):
    ◆ Firm, mobile and usually over pressure points.
    ◆ Consist of fibrinoid necrosis and palisading histiocytes.
  • Muscle weakness (due to disuse atrophy), tenosynovitis and bursitis.
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2
Q

Rheumatoid arthritis Investigations

A
  • Synovial fluid analysis
    Bloods
  • FBC: normochromic, normocytic or hypochromic microcytic anaemia, thrombocytosis, neutropenia associated with Felty’s syndrome
  • Inflammatory markers (ESR and CRP): elevated, especially in acute flares.
  • Auto-antibodies (RF and anti-CCP): anti-CCP has greater sensitivity and specificity than RF. Anti-
    CCP can be detected several years prior to onset of RA
  • Renal, liver and bone biochemistry: to exclude other pathologies and prior to institution of medical
    treatments.

Radiology

  • Plain film radiography.
  • Joint US examination.
  • MRI of small joints of the hands and feet may help (e.g. peri-articular osteopaenia, erosions, joint
    space narrowing), where plain films and US have been unremarkable.
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3
Q

Rheumatoid arhtritis extra-articular manifestations

skin, bone, haema, resp, cardio, ocular, renal, neuro

A
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4
Q

Rheumatoid arhtritis

Poor prognostic indicators [4]

A
  • Presentation- insiduous onset, constitutional sx, poor functional state at 1y, social deprivation, high disease activity score on presentation.
  • Demographic- female, smoking
  • Biochemical - high inflammatory markers, shared epitope HLA-DRB*04 cluster. RF positivity with high titres (especially IgA RF) and anti-CCP.
  • Radiological- early erosions
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5
Q

Synovial fluid in RA

A
  • Inflammatory diseases may show yellow or green with decreased viscosity
  • High WCC - neutrophilia, lymphocytosis
  • Glucose may be low in RA as it is in bacterial infections.
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6
Q

RA Definition

A

Chronic autoimmune systemic illness

characterised by symmetrical peripheral arthritis

and other systemic features

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7
Q

RA diagnosis needs a score of x according to 2010 EULAR Classification

A

6 OR MORE out of 10

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8
Q

4 sub-categories of RA Classification/Criteria

In each sub-category, what would score high pointing to a dx of RA?

A

Joint Involvement (poly + small joints)

Serology (RF +ve, ACPA +ve)

Acute phase reactants (raised)

Duration of symptoms 6w

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9
Q

Epidemiology of RA

Gender

Prevalence

Peak age of onset

But may occur at any age from ____

A

F:M 3:1

1% of population

4th or 5th decade

But may occur at any age from 16 y

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10
Q

Aetiology RA

Genetic - closest association with specific amino acid sequences at positions ____ of _____

What are the susceptibility genes?

Environmental factors (2)

A

Genetic - closest association with specific amino acid sequences at positions 70-74 of DRb1

HLA DR1 and HLA DR4

Environmental factors:

Smoking

Chronic infection - peri-odontal disease

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11
Q

Pathogenesis RA

3 stages

A

Rheumatoid factor binding to IgG forming immune complexes

Not easily cleared

Activate complement - further inflammation

Activation of macrophages

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12
Q

RA Symptoms 4

A

Pain

Swelling

Loss of function

Systemic symptoms

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13
Q

Symptoms RA

  • Systemic symptoms
    • Non-specific (3)
A

Fatigue

Weight loss

Anemia

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14
Q

Which types of malignancy have higher incidence assoc with RA

A

Leukemia and Lymphoma

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15
Q

DAS28 score - how does it relate to RA?

What score represents clinical remission?

What score indicates eligibility for biology therapy

A

DAS28 score – monitor disease activity (disease activity score)

DAS<2.4 represents clinical remission

DAS>5.1 represents eligibility for biologic therapy

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16
Q

4 modes of management of RA

A

NSAIDS

DMARDS

Biologics

Corticosteroids

17
Q

Name 4 DMARDs used in RA

Whats the gold standard DMARD drug

A

Methotrexate

Sulfasalazine

Hydroxychloroquine

Leflunomide

18
Q

Name 5 drugs under ‘Biologics’ category of RA MX

A

TNF-alpha inhibitors Etanercept

IL-1 inhibitors Anakinra

IL-6 inibitors Tocilizumab

Anti-B cell therapy - Rituximab

Anti-T cell therapies - Abatacept

19
Q

What are the extra-articular manifestations of RA? [4]

A

Extra-articular

  • Rheumatoid nodules
  • Increased risk of atherosclerosis
  • Interstitial lung fibrosis
  • Pleural effusions (SOB)
20
Q

What is Felty’s syndrome? Why can it be dangerous?

A

Triad of:

RA

Splenomegaly

Granulocytopenia

Can lead to life-threatening infections

21
Q

X-ray of RA

Early [3]

Late [3]

A

soft tissue swelling, juxta-articular osteopenia, loss of joint space

Late changes: bony erosions, subluxation, complete carpal destruction

L – loss of joint space
E – erosions
S – soft tissue swelling
S – soft bones (osteopenia)

22
Q

What finding would you see on FBC

A

Increased platelets

23
Q

DMARDs

Indications for prescribing [1]

How long before patient should expect symptomatic benefit [1]

Best results with? [3]

SE [3]

How to counter this side effect [1]

A

Should be started within 3 months of persistent symptoms

Can take 6-12w for symptomatic benefit

DMARD monotherapy +/- a short-course of bridging prednisolone (NICE, 2018)

SE: immunosupression, pancytopenia, neutropenic sepsis so regular FBC monitoring

24
Q

DMARDs side effects

Methotrexate [3]

Sulfasalazine [3]

Leflunomide [4]

Hydroxychloroquine [1]

A

Methotrexate - pneumonitis, oral ulcers, hepatotoxicity

Sulfasalazine - rash, decreased sperm count, oral ulcers

Leflunomide - teratogenicity, oral ulcers, increased BP, hepatotoxicity

Hydroxychloroquine - Bull’s eye retinopathy

25
Q

Biologics

First line? When is this indicated? [2]

Second line? [2]

Third line? [2]

A
  1. TNF alpha inhibitors - after failure of 2 DMARDs and DAS28>5.1
  2. Anti B-cell therapy - after failure of DMARDs and TNF alpha inhibitor
  3. IL6 inhibitior - after failure of TNF alpha and anti-B cell therapy
26
Q

SE profile of biologics [5]

A

Serious infection eg reactivation of TB, Hep B

Worsening heart failure

Hypersensitivity

Blood disorders

Reversible SLE-type illness may evolve

27
Q

Palindromic RA

Presentation of joint inflammation [2]

A

Episodic and sequential moving from one joint to another

Hours-days then symptom-free periods that last days-months

28
Q

MOA Methotrexate

A
  • a competitive inhibitor of dihydrofolate reductase (DHFR), DHFR catalyses the conversion of dihydrofolate to the active tetrahydrofolate.
  • Folate is needed for nucleoside thymidine production (required for DNA synthesis) and for purine and pyrimidine base biosynthesis.
  • In RA, methotrexate has further inhibitory actions on T- and B-cell function.
29
Q
  • Biologic DMARD use mandates a careful screening process prior to treatment initiation including screening for:
A

◆ Mycobacterial infections: if active, requires treatment. Prophylactic anti-TB therapy for those with potential latent disease (e.g. past history of TB or abnormal CXR).
◆ Hepatitis B and C and HIV: hepatitis B vaccination is offered to high risk patients. Influenza and pneumococcal vaccinations given prior to biologic DMARDs (unless contraindicated).
◆ Malignancy: caution is warranted in patients with previous malignancy and premalignant conditions
(e.g. Barrett’s oesophagus, cervical dysplasia). The risk for specific skin cancers (e.g. malignant melanoma) should be discussed, and preventative skin care and surveillance offered.
Anti-tumour necrosis factor (TNF) treatment must be discontinued if malignancy is confirmed.

30
Q

Anti-TNF therapy is contraindicated in patients with:

A

◆ Multiple sclerosis and used with caution with other demyelinating diseases.
◆ NYHA grade 3 or 4 cardiac failure (see Table 3.39) and used with caution in patients with mild
cardiac failure (NYHA grade  or 2).

31
Q

Which HLA is RA associated with?

A

DR4

Especially Felty’s syndrome

32
Q

What is Felty’s syndrome?

A

RA
Splenomegaly
Neutropaenia

33
Q

Psoriatic arthritis

Genetic factors [3]

A
  • Family history of psoriasis or psoriatic arthritis (PsA) in 40% of patients.
  • Increased frequency of psoriasis and PsA in monozygotic and dizygotic twins.
  • Increased frequency of HLA-B13, B17, B27, B38, B39, DR4, DR7 and Cw6.
34
Q

Psoriatic Arhtiritis

Which genetic association may be protective

A

◆ HLA B22 may be protective.