Rheumatoid Arthritis Flashcards

1
Q

What are rheumatoid factors?

A

An IgM antibody that works against IgG antibodies
Line vasculature (e.g. spleen) and attach to passing antibodies
Seen in old age, chronic infections and rheumatoid arthritis

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2
Q

Why should rheumatoid factors not be used as a routine screening tool?

A

Rheumatoid factors seen in population anyway particularly with ageing (seen in 10-25% of people over 70)
Should only be used if history indicates rheumatoid arthritis (joint pain alone does not indicate rheumatoid!)

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3
Q

What clinical features in a history could indicate rheumatoid arthritis?

A

Often young to middle age females (20-50 years)
Pain and stiffness in joints
Gradual or sudden onset
Usually bilateral (hands, feet and other joints)
Genetic link (family member with RA)
Smoking increases risk

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4
Q

What is the ‘S’ factor?

A

Indicators of RA:
Stiffness (>30 mins in morning)
Swelling
Squeeze (pain or tenderness when squeezing joint)

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5
Q

Which genes are linked to rheumatoid arthritis?

A

HLA-DR4

HLA-DR1

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6
Q

What is the classic distribution of rheumatoid arthritis?

A

Hands/ fingers
Ankles/ toes
Knees

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7
Q

What are the symptoms of rheumatoid arthritis?

A

Joint aching and stiffness (esp. hands and feet)
Early morning stiffness (improves within couple of hours normally)
Systemic symptoms e.g. fatigue, weight loss, anorexia, anaemia, low-grade fever

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8
Q

What hand deformities can present in rheumatoid arthritis?

A

Fusiform swelling
Ulna deviation
Swan neck deformities
Boutonniere deformities

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9
Q

What extra-articular manifestations can appear in rheumatoid arthritis?

A

Cardiac (e.g. pericarditis, valve problems, atherosclerosis, ischaemic heart disease)
Pulmonary (e.g. pleural effusions, pulmonary fibrosis)
Blood (e.g. anaemia)
Bones (e.g. osteoporosis)
Skin (e.g. leg ulcers, vasculitis)
Neurological (e.g. nerve compression)
Eyes (e.g. scleritis, xerophthalmia)

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10
Q

What can be done in rheumatoid arthritis to minimise the chance of developing ischaemic heart disease?

A
Address risk factors e.g. smoking, high cholesterol, obesity 
Treat hypertension (if present)
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11
Q

What is the pathogenesis of rheumatoid arthritis?

A
  1. T-cell mediated immune response
  2. Inflammatory response
  3. Release of cytokines (TNF, IL-1)
  4. Pannus formation (caused by angiogenesis of synovium and synovial proliferation)
  5. Release of enzymes (e.g. protease) and PGs resulting in cartilage breakdown
  6. Synovial joint destruction
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12
Q

What blood test results would we expect to see in a patient with rheumatoid arthritis?

A
FBC: anaemic
ESR/ CRP: moderately raised
Rheumatoid factor: raised
Anti CCP: positive
ALP: raised
Albumin: decreased
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13
Q

Why can people with rheumatoid arthritis develop anaemia?

A

Active disease (anaemia of chronic disease)
Blood loss
Drugs can suppress bone marrow
Felty’s syndrome (rare complication of rheumatoid arthritis causing splenomegaly)

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14
Q

What would we expect to see in imaging of patients with rheumatoid arthritis?

A

LESS:

Loss of joint space
Erosions (“punched out” areas of bone)
Soft tissue swelling
Sublaxation (causing ulna deviation and swan neck deformities, can also be seen at atlantoaxial joint in cervical spine)

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15
Q

What analgesia should be used to manage pain in rheumatoid arthritis?

A
1st line: Paracetamol 
2nd line: NSAIDs + paracetamol 
3rd line: Weak opioid (e.g. codeine)
4th line: Moderate opioid (e.g. tramadol) 
5th line: Strong opioid (e.g. morphine)
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16
Q

What is the current strategy for treating RA?

A

1st line: disease-modifying anti-rheumatic drugs [Methotrexate + Sulfasalazine in combination]

+ NSAIDS
+ Corticosteroids (e.g. prednisolone) short term

2nd line: Biologic therapies

17
Q

How do corticosteroids work to treat RA?

A

Inhibition of transcription factors leading to reduced transcription of cytokine genes (e.g. interleukins and TNF) which leads to reduced clonal proliferation of T helper cells

18
Q

How does Methotrexate work to treat RA?

A

Inhibits DNA synthesis by inhibiting folate pathway

Reduces lymphocyte proliferation

19
Q

What anti-proliferative drugs are used in RA managament?

A

Methotrexate

Azathioprine

20
Q

What immunomodulators are used in RA management?

A

Sulfasalazine

21
Q

How does Azathioprine work to treat RA?

A

Inhibits DNA synthesis by inhibiting purine pathway

Reduces lymphocyte proliferation

22
Q

How does Sulfasalazine work to treat RA?

A

Mechanism unclear

? Possible COX inhibition

23
Q

What are the potential side effects of anti-proliferative drugs?

A

Increased risk of infection
Teratogenic (should avoid in pregnancy!)
GI symptoms (e.g. mouth ulcers, nausea, diarrhoea)
Hair loss

24
Q

What biologic agents can be used in RA management?

A

Monoclonal antibody therapy (MAb):
Anti TNFa (infliximab)
Anti CD20 on B cells (rituximab)

25
Q

What are the problems with biologic agents?

A

Infliximab and Rituximab must be given by IV infusion (time consuming for patient and NHS)
Expensive
Use of biosimilar agents (not identical so efficacy and side effects may be different - unknown until tested)

26
Q

How does Infliximab work?

A

Binds to and blocks pro-inflammatory function of TNFa

27
Q

How does Rituximab work?

A

Depletion of B cells