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Rheumatology > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What is RA?

A

Inflammatory Arthritis

Autoimmune condition that causes chronic inflammation of the synovial lining of the joints, tendon sheaths and bursa

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2
Q

What is the typical distribution of RA?

A

Tends to be symmetrical

Affects multiple joints

Symmetrical polyarthritis

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3
Q

Who gets RA?

A

Three times more common in women

Most often develops in middle age

FH increases risk

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4
Q

Genetic associations with RA

A

HLA DR4 (a gene often present in RF positive patients)

HLA DR1 (a gene occasionally present in RA patients)

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5
Q

What is Rheumatoid Factor?

A

Autoantibody presenting in around 70% of RA patients

Targets the Fc portion of the IgG antibody

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6
Q

What are Cyclic citrullinated peptide antibodies (anti-CCP antibodies)

A

Autoantibodies

More sensitive and specific to rheumatoid arthritis than rheumatoid factor

Often pre-date the development of RA - indication patient will go on to develop RA

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7
Q

How does RA present?

A

Symmetrical distal polyarthropathy
Typically the wrist, ankle, MCP and PIP (very rarely DIP) joints in the hands

Joint:

Pain
Swelling
Stiffness

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8
Q

Onset of RA

A

Can be very rapid (i.e. overnight) or over months to years

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9
Q

Associated systemic symptoms of RA (4)

A

Fatigue

Weight loss

Flu like illness

Muscles aches and weakness

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10
Q

Pain in RA - rest/activity

A

Improves with activity

Worse after rest

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11
Q

What is atlantoaxial subluxation?

A

Axis (C2) and the odontoid peg shift within the atlas (C1)

Caused by local synovitis and damage to the ligaments and bursa around the odontoid peg

Can cause spinal cord compression

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12
Q

Hand signs in RA (5)

A

Boggy joints

Z shaped deformity to the thumb

Swan neck deformity (hyperextended PIP with flexed DIP)

Boutonnieres deformity (hyperextended DIP with flexed PIP)

Ulnar deviation of the fingers at the knuckle (MCP joints)

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13
Q

Extra-articular Manifestations (11)

A

Pulmonary fibrosis with pulmonary nodules (Caplan’s syndrome)

Bronchiolitis obliterans (inflammation causing small airway destruction)

Felty’s syndrome (RA, neutropenia and splenomegaly)

Secondary Sjogren’s Syndrome (AKA sicca syndrome)

Anaemia of chronic disease

Cardiovascular disease

Episcleritis and scleritis

Rheumatoid nodules

Lymphadenopathy

Carpel tunnel syndrome

Amyloidosis

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14
Q

Investigations in RA

A

Check rheumatoid factor

If RF negative, check anti-CCP antibodies

Inflammatory markers such as CRP and ESR

X-ray of hands and feet

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15
Q

Xray changes in RA (4)

A

Joint destruction and deformity

Soft tissue swelling

Periarticular osteopenia

Boney erosions

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16
Q

Diagnosis

A

Based on:

Joints that are involved (more and smaller joints score higher)

Serology (rheumatoid factor and anti-CCP)

Inflammatory markers (ESR and CRP)

Duration of symptoms (more or less than 6 weeks)

17
Q

What is DAS28?

A

Disease Activity Score
Assessment of 28 joints

Swollen joints

Tender joints

ESR/CRP result

18
Q

What is HAQ?

A

Health Assessment Questionnaire

Measures functional ability
NICE recommend using this at diagnosis to check the response to treatment

19
Q

What worsens the prognosis of RA? (5)

A

Younger onset

Male

More joints and organs affected

Presence of RF and anti-CCP

Erosions seen on xray

20
Q

Treatment during flare ups

Monitoring treatment

A

NSAIDs/COX-2 inhibitors - minimal effective dose
(PPI)

CRP and DAS28 is used to monitor the success of treatment

21
Q

First line treatment

A

Disease Modifying Anti-Rheumatic Drugs (DMARDs)

Methotrexate
Leflunomide
Sulfasalazine

(Hydroxychloroquine used in mild disease)

22
Q

Second third and fourth line treatment

A

2nd - 2 1st line used in combination

3rd - methotrexate plus a biological therapy, usually a TNF inhibitor

4th - methotrexate plus rituximab

23
Q

Treatment in pregnancy

A

Sulfasalazine and hydroxychloroquine

24
Q

Biologics used in RA

A

Anti-TNF (adalimumab, infliximab, etanercept, golimumab and certolizumab pegol)
Anti-CD20 (rituximab)

Anti-IL6 (sarilumab)
Anti-IL6 receptor (tocilizumab)
JAK inhibitors (tofacitinib and baricitinib)

25
Q

How does methotrexate work?

A

Interferes with the metabolism of folate
Suppresses certain components of the immune system

Folic acid 5mg also prescribed

26
Q

SE of Methotrexate (5)

A

Mouth ulcers and mucositis

Liver toxicity

Pulmonary fibrosis

Bone marrow suppression and leukopenia (low white blood cells)

It is teratogenic (mothers and fathers)

27
Q

How does Leflunomide work?

A

immunosuppressant

Interfering with the production of pyrimidine (important component of RNA and DNA)a

28
Q

SE of Leflunomide (7)

A

Mouth ulcers and mucositis

Increased blood pressure

Rashes

Peripheral neuropathy

Liver toxicity

Bone marrow suppression and leukopenia (low white blood cells)

It is teratogenic

29
Q

How does sulfasalazine work?

A

Immunosuppressive
Anti-inflammatory

Appears to be safe in pregnancy

30
Q

SE of sulfasalazine

A

Temporary male infertility (reduced sperm count)

Bone marrow suppression

31
Q

SE of Hydroxychloroquine

A

Nightmares

Reduced visual acuity (macular toxicity)

Liver toxicity

Rash

32
Q

What is TNF?

A

Cytokine involved in stimulating inflammation

33
Q

SE of Anti-TNF drugs

A

Vulnerability to severe infections and sepsis

Reactivation of TB and hepatitis B

34
Q

Action of rituximab

A

Targets the CD20 protein on the surface of B cells

Causes destruction of B cells

35
Q

SE of rituximab (5)

A

Vulnerability to severe infections and sepsis

Night sweats

Thrombocytopenia (low platelets)

Peripheral neuropathy

Liver and lung toxicity

36
Q

Unique SE of drugs used in RA

A

Methotrexate: pulmonary fibrosis

Leflunomide: Hypertension and peripheral neuropathy

Sulfasalazine: Male infertility (reduces sperm count)

Hydroxychloroquine: Nightmares and reduced visual acuity

Anti-TNF medications: Reactivation of TB or hepatitis B

Rituximab: Night sweats and thrombocytopenia

Rheumatology (11 decks)

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