Rheumatoid Arthritis Flashcards

1
Q

What is rheumatology?

A

The medical specialty dealing with diseases of the musculoskeletal system

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2
Q

What are the components of synovial joints?

A

Two bones forming the join

Joint cavity with synovial fluid and cartilage on either side (type II cartilage)

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3
Q

What is Arthritis?

A

Disease of the joints

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4
Q

What are the 2 types of arthritis?

A
Osteoarthritis
Inflammatory arthritis (rheumatoid)
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5
Q

What is inflammation?

A

a physiological response to deal with injury or infection

However, excessive/inappropriate inflammatory reactions can damage the host tissues

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6
Q

How does inflammation clinically manifest?

A
Rubor
Dolor
Calor
Tumor
Loss of function
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7
Q

What are the physiological changes associated with inflammation?

A
  • Increased blood flow
    -Migration of white blood cells (leucocytes) into the tissues
    -Activation/differentiation of leucocytes
    -Cytokine production
    E.g. TNF-alpha, IL1, IL6, IL17
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8
Q

What are the two types of crystal arthritis?

A

Gout

Pseudogout

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9
Q

What is gout caused by?

A

syndrome caused by deposition of urate (uric acid) crystals -> inflammation

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10
Q

What is a risk factor for gout?

A

High uric acid levels (hyperuricaemia)

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11
Q

What causes hyperuricaemia?

A
Genetic tendency
Increased intake of purine rich foods
Reduced excretion (kidney failure)
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12
Q

What is pseudogout caused by?

A

a syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystal deposition crystals -> inflammation

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13
Q

What are the risk factors for pseudogout?

A

background osteoarthritis, elderly patients, intercurrent infection

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14
Q

What does gout cause?

A

Gouty arthritis
Tophi (aggregated deposits of MSU in tissue)
Extreme pain

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15
Q

What does gouty arthritis commonly affect?

A

Metatarsophalangeal joint of the big toe (‘1st MTP joint’)

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16
Q

What are the affects of gouty arthritis?

A

Abrupt onset
Extremely painful
Joint red, warm, swollen and tender
Resolves spontaneously over 3-10 days

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17
Q

What investigation is done in gout?

A

Joint aspiration – synovial fluid analysis

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18
Q

What is the management of gout?

A

Acute attack – colcihine, NSAIDs, Steroids

Chronic – allopurinol

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19
Q

What are synovial fluid samples examined for?

A

Pathogens
Crystals
Rapid Gram stain followed by culture and antibiotic sensitivity assays

Polarising light microscopy to detect crystals which can be seen in arthritis due to gout or pseudogut

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20
Q

What are the features of synovial fluid in gout?

A

Crystal - urate
Shape - needles
Polarizing light microscopy - negative

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21
Q

What are the features of synovial fluid in pseudogout?

A

Crystal - Calcium pyrophosphate dihydrate (‘CPPD’)

Shape - brick shaped

Polarizing light microscopy - positive

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22
Q

What are the immune mediated inflammatory joint diseases?

A

SLE
Rheumatoid arthritis
Vasculitis

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23
Q

What is the most common Immune-mediated inflammatory joint disease?

A

Rheumatoid arthritis

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24
Q

What is RA?

A

chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis
(inflammation of the synovial membrane) of synovial (diarthrodial) joints

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25
What is the pathogenesis of RA?
Synovial membrane is abnormal in rheumatoid arthritis: | The synovium becomes a proliferated mass of tissue (pannus
26
What is the dominant cytokine in RA?
TNF Alpha
27
How has the role of TNF alpha been proven?
validated by the therapeutic success of TNFα inhibition in this condition
28
How is TNF alpha inhibited
TNFα inhibition is achieved through parenteral administration (most commonly sub-cutaneous injection) of antibodies or fusion proteins
29
What are the key features of RA?
Polyarthritis - swelling of the small joints of the hand and wrists is common Symmetrical Early morning stiffness in and around joints May lead to joint damage and destruction - ‘joint erosions’ on radiographs
30
What are the extra-articular manifestation of RA?
Rheumatoid nodules | Others rare e.g. vasculitis, episcleritis
31
What might be detected in the blood in RA?
Rheumatoid factor Autoantibody against IgG - should really call this rheumatoid ‘antibody’ not ‘factor’
32
What is the joint pattern of involvement in RA?
Affects small and large joints, but particularly hands and feet Symmetrical Affects multiple joints (polyarthritis)
33
Which joints are most affected by RA?
``` Metacarpophalangeal joints (MCP) Proximal interphalangeal joints (PIP) Wrists Knees Ankles Metatarsophalangeal joints (MTP) ```
34
What are the effects of synovial inflammation?
joint synovitis tenosynovitis bursa
35
What are common extra-articular features?
Fever, weight loss | Subcutaneous nodules
36
What are less common extra-articular features?
vasculitis Ocular inflammation e.g. episcleritis Neuropathies Amyloidosis Lung disease – nodules, fibrosis, pleuritis Felty’s syndrome – triad of splenomegaly, leukopenia and rheumatoid arthritis
37
What are subcutaneous nodules?
Central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue Occur in ~30% of patients
38
What are subcutaneous nodules associated with?
Severe disease Extra-articular manifestations Rheumatoid factor
39
What is rheumatoid factors?
Antibodies that recognize the Fc portion of IgG as their target antigen typically IgM antibodies i.e. IgM anti-IgG antibody Positive in 70% at disease onset and further 10-15% become positive over the first 2 years of diagnosis
40
What are the second type of antibodies seen in RA?
Antibodies to citrullinated protein antigens
41
What are ACPA's?
highly specific for rheumatoid arthritis Anti-cyclic citrullinated peptide antibody ‘anti-CCP antibody’ Citrullination of peptides is mediated by enzymes termed: Peptidyl arginine deiminases (PADs)
42
What is the treatment goal in RA?
Prevent joint damage
43
What are the requirements regarding management?
Early recognition of symptoms, referral and diagnosis Prompt initiation of treatment: joint destruction = inflammation x time Aggressive treatment to suppress inflammation
44
What is the drug treatment in RA?
Disease-modifying anti-rheumatic drugs (‘DMARDs’) = drugs that control the disease process
45
What is the first line treatment for RA?
1st line treatment: | methotrexate in combination with hydroxychloroquine or sulfasalazine
46
What is 2nd line treatment for RA?
2nd line: Biological therapies offer potent and targeted treatment strategies New therapies include Janus Kinase inhibitors : Tofacitinib & Baricitinib
47
What drugs can be used short term?
Important roles for glucocorticoid therapy (prednisolone) but avoid long-term use because of side-effects.
48
What is important in the management of RA?
Multidisciplinary approach also important e.g. physiotherapy, occupational therapy, hydrotherapy, surgery
49
What are biologics?
Biological therapies are proteins (usually antibodies) that specifically target a protein such as an inflammatory cytokine
50
What are the main features with ankylosing spondylitis?
Seronegative spondyloarthropathy – no positive autoantibodies Chronic sacroillitis – inflammation of sacroiliac joints Results in spinal fusion – ankylosis Common demographic: 20-30yrs, M Associated with HLA B27
51
What is the clinical presentation of AS?
``` Lower back pain + stiffness Early morning Improves with exercise Reduced spinal movements Peripheral arthritis Plantar Fasciitis, Achilles Tendonitis Fatigue ```
52
What might you find on inspection in AS?
Hyperextended neck Loss of Lumbar lordosis Flexed hips and knees
53
What bloods are important in AS?
Normocytic anaemia Raised CRP, ESR HLA-B27
54
What imaging is done in AS?
X-rays | MRI
55
What would you look for on a MRI re AS?
Squaring Vertebral bodies, Romanus lesion Erosion, sclerosis, narrowing SIJ Bamboo Spine Bone Marrow Oedema
56
What is the management for AS?
Physiotherapy Exercise regimes NSAIDs Peripheral joint disease - DMARDs
57
What is psoriasis?
autoimmune disease affecting the skin (scaly red plaques on extensor surfaces eg elbows and knees)
58
What are the main features of psoriasis?
~10% of psoriasis patients also have joint inflammation Unlike RA, rheumatoid factors are not present (“seronegative”) Varied clinical presentations:
59
What is classical presentation of PA?
Classically asymmetrical arthritis affecting IPJs
60
How can PA clinically manifest?
- Symmetrical involvement of small joints (rheumatoid pattern) - Spinal and sacroiliac joint inflammation - Oligoarthritis of large joints - Arthritis mutilans
61
What investigations are done in PA?
X-rays of affected joints – pencil in cup abnormality MRI – sacroiliitis and enthesitis Bloods – no antibodies as seronegative
62
What is the management for psoriatic arhritis?
DMARDs – methotrexate Avoid oral steroids – risk of pustular psoriasis due to skin lesions
63
What is reactive arthritis?
Sterile inflammation in joints following infection especially urogenital (e.g. Chlamydia trachomatis) and gastrointestinal (e.g. Salmonella, Shigella, Campylobacter infections) infections
64
What are the extra-articular manifestations of reactive arthritis?
Enthesitis (tendon inflammation) Skin inflammation Eye inflammation
65
What can Reactive arthritis be a first manifestation of ?
HIV | Hep C
66
Who is reactive arthritis often seen in?
Commonly young adults with genetic predisposition (e.g. HLA-B27) and environmental trigger (e.g. Salmonella infection)
67
When does reactive arthritis occur?
Symptoms follow 1-4 weeks after infection and this infection may be mild
68
What is the management of reactive arthritis?
Condition is usually self-limiting – can be managed with NSAIDS or DMARDs if required
69
What is SLE?
a multi-system autoimmune disease Multi-site inflammation: can affect any almost any organ. Often joints, skin, kidneys, haematology. Also: lungs, CNS involvement
70
What is SLE associated with?
with antibodies to self antigens (‘autoantibodies’) | Autoantibodies are directed against components of the cell nucleus (nucleic acids and proteins)
71
What are the clinical tests for Lupus?
1. Antinuclear antibodies (ANA): High sensitivity for SLE but not specific. A negative test rules out SLE, but a positive test does not mean SLE. 2. Anti-double stranded DNA antibodies (anti-dsDNA Abs): High specificity for SLE in the context of the appropriate clinical signs
72
What are the epidemiological features of SLE?
F:M ratio 9:1 Presentation 15 - 40 yrs Increased prevalence in African and Asian ancestry populations Prevalence varies 4-280/100,000