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Rheumatoid Arthritis Flashcards

1
Q

What is Rheumatology? Which parts of the MSK system does it include?

A

The medical specialty dealing with diseases of the musculoskeletal system including:

Joints = where 2 bone meets
Tendons = cords of strong fibrous collagen tissue attaching muscle to bone
Ligaments = flexible fibrous connective tissue which connect two bones
Muscles
Bones

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2
Q

What are the components of a synovial joint?

A

2 bones meet

Joint cavity lined by the synovium containing the synovial fluid

Articular cartilage on either side

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3
Q

What is the synovium? What is it made of?

A

Synovium = connective tissue that lines the inside of the joint capsule

1-3 cell deep lining containing macrophage-like phagocytic cells (type A synoviocyte) and fibroblast-like cells that produce hyaluronic acid (type B synoviocyte)

Type I collagen

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4
Q

What is the synovial fluid made up of?

A

Hyaluronic acid-rich viscous fluid

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5
Q

What is the articular cartilage made up of?

A

Type II collagen

Proteoglycan (aggrecan)

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6
Q

What is the main joint disease?

A

Arthritis = disease of the joints

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7
Q

What are the 2 types of arthritis?

A

Osteoarthritis = degenerative arthritis

Inflammatory arthritis = main type is called rheumatoid arthritis, but also includes reactive arthritis, psoriatic arthritis, ankylosing spondylitis and more

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8
Q

What is inflammation?

What happens if there is too much inflammation?

A

Inflammation = a physiological response to deal with injury or infection

Excessive/inappropriate inflammatory reactions = damage to the host tissues

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9
Q

How does excessive inflammation manifest as clinically?

A
  1. RED (rubor)
  2. PAIN (dolor)
  3. HOT (calor)
  4. SWELLING (tumor)
  5. LOSS OF FUNCTION
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10
Q

What are the physiological changes at the site of 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

Specific cytokines e.g. TNF-a, IL1, IL6, IL17 = important for targetting medications (biologics) at these as treatment options

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11
Q

What are the 3 main types of inflammatory arthritis that cause joint inflammation?

A
  1. Crystal arthritis
    - Gout
    - Pseudogout
  2. Immune-mediated (“autoimmune”)
    - Rheumatoid arthritis
    - Seronegative spondyloarthropathies
    - Connective tissue diseases
  3. Infection
    - Septic arthritis
    - Tuberculosis (TB)
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12
Q

What are the 2 types of crystal arthritis?

A

Gout = tissue deposition of monosodium urate (MSU) crystals occurs as a result of hyperuricaemia –> inflammation

Pseudogout = deposition of calcium pyrophosphate dihydrate (CPPD) crystal deposition crystals –> inflammation

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13
Q

What are risk factors / causes for gout?

A

High uric acid levels (hyperuricaemia) = risk factor for gout

Causes of hyperuricaemia:
Genetic tendency
Increased intake of purine rich foods
Reduced excretion (kidney failure)

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14
Q

What are some risk factors for pseudogout?

A

Background osteoarthritis
Elderly patients
Intercurrent infection

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15
Q

What is acute gout? How does acute gout present clinically?

A

Acute gout - inflammatory arthritis due to deposition of MSU crystals leading to fouty arthritis and/or tophi (aggregated deposits of MSU in tissue)

Presents clinically as:
Abrupt onset
Extremely painful 10/10 
Joint looks red, warm, swollen, and tender
Resolves spontaneously over 3-10 days
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16
Q

Which joint is most affected in gouty arthritis?

A

1st MTP (metatarsophalangeal) joint i.e. the big toe

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17
Q

What is seen on an x-ray (radiograph) image of gout?

A

Black parts on the bones called ‘rat bite’ erosions

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18
Q

How can gout and pseudogout be investigated?

A

Joint aspiration - for synovial fluid analysis and to rule out septic arthritis

Not always possible - depends on size and site of the joint

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19
Q

How can gout be managed?

A

Acute = colcihine (anti-inflammatory drug), NSAIDs, steroids

Chronic = alopeuranol (works to reduce uric acid formation in the body)

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20
Q

How is synovial fluid examined from the joint aspiration?

A

Some of the sample is rapid Gram stain followed by culture and antibiotic sensitivity assays to check for septic arthritis

Some of the sample is analysed under polarising light microscopy to detect crystals which can be seen in arthritis due to gout or pseudogut

  • Gout = needle shaped crystals; negative birefringence
  • Pseudogout - brick shaped cyrstals, positive birefringence
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21
Q

What are some other immune mediated inflammatory joint diseases?

A

RA - rheumatoid arthritis

Lupus / SLE

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22
Q

What is rheumatoid arthritis (RA)?

A

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

23
Q

What is the pathogenesic of RA?

A 
Synovial membrane is abnormal - so synovium becomes proliferated mass of tissue due to:
Neovascularisation
Lymphangiogenesis
inflammatory cells:
- Activated B and T cells
- Plasma cells
- Mast cells
- Activated macrophages

Recruitment and activation of these cells is controlled by the cytokine network - excess of pro-inflammatory VS lack anti-inflammatory cytokines = ‘cytokine imbalance’
Leads to inflammation

24
Q

What is the main / dominant cytokine in RA?

A

TNF-alpha = most dominant cytokine in RA

Shown this is dominant due to biologic medications that inhibit TNFa
Which have been proven to be very effective
= TNFa is a strong pro-inflammatory esp. in RA as it recruits other cytokines / interleukins

25
How does TNFa cause painful symptoms in RA?
When TNFa is recruited - it causes: proinflammatory cytokine release, chemokine release, hepcidin induction, endothelial activation, leukocyte accumulation, angiogenes, chondrocyte activation, oesteoclast activation etc. Leading to: Synovitis --> joint inflammation and selling --> bone erosion --> joint space narrowing
26
What are the key features of RA seen clinically?
Chronic arthritis: - Polyarthritis - swelling of the smeall joins fo the hands and wrists is common - Symmetrical - Early morning stiffness in and around joints - May lead to joint damage and destruction - 'joint erosions' on radiographs Extra-articular disease can occur = - Rheumatoid nodules - appear on the skin - Others rare e.g. vasculitis, episcleritis (eyes) ``` Rheumatoid factor (RF) may be detected in blood - RF = autoantibody against IgG ```
27
What is a key investigation for RA?
Blood test = elevated CRP, high levels of RF USS - look for swelling X-ray - look for bone erosions
28
Whta is the pattern of joint involvement for RA?
Symmetrical Affects multiple joints (polyarthritis) Affects small and large joints, but particularly hands and feet ``` Commonest affected joints: Metacarpophalangeal joints (MCP) Proximal interphalangeal joints (PIP) Wrists Knees Ankles Metatarsophalangeal joints (MTP) ```
29
Where is the primary site of inflammation in RA? Where else in RA can there be inflammation?
RA = synovial inflammation so: Primarily = synovium is inflammed e.g. in the proximal interphalageal joints (ITPJs) But inflammation can also spread to: Tenosynovium = surrounding tendons Bursa (lubricated fluid-filled thin sac located between bone and surrounding soft tissue)
30
What are the common and uncommon extra-articular features of RA?
Common = Fever, weight loss Subcutaneous nodules Uncommon = Vasculitis Ocular inflammation e.g. episcleritis Neuropathies Amyloidosis Lung disease – nodules, fibrosis, pleuritis Felty’s syndrome – triad of splenomegaly, leukopenia and rheumatoid arthritis
31
What are subcutaenous nodules? How do the subcutaneous nodules appear in RA?
Central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue Occur in 30% of patients but generally associated with severe disease, extra-auricular manifestations, and rheumatoid factor
32
What is a key investigation for RA?
2 types of antibodies are found in the blood of RA patients: 1. Rheumatoid factor = Immunoglobulin M (IgM) autoantibodies against the Fc fragment of immunoglobulin G (IgG) are called rheumatoid factors (RFs) i.e. IgM anti-IgG antibody Positive in 70% of patient at disease onset, and further 10-15% over the first 2 years of diagnosis 2. Anti-cyclic citrullinated peptide antibody ‘anti-CCP antibody' = antibodies against citrulinated peptides - highly specific for rheumatoid arthritis ---- What are citrulinated peptides mediated by? An enzyme called peptidyl arginine deiminase (PAD) = works by converting arginine to citrulline
33
How is RA managed clinically? What is the treatment goal and what does this require?
Treatment goal = prevent joint damage Requires = Early recognition of symptoms, referral and diagnosis Prompt initiation of treatment: joint destruction = inflammation x time Aggressive treatment to suppress inflammation Patient is then given drug treatment(s)
34
What are the drug treatments given for RA?
DMARDS = disease-modifying anti-rheumatic drugs = drugs that control the disease process Glucocorticoid therapy e.g. prednisolone is avoided long term, so DMARDS are given instead as they can be used long term 1st line treatment = Methotrexate in combination with hydroxychloroquine or sulfasalazine 2nd line treatment = biologics e.g. new therapies include Janus Kinase inhibitors: Tofacitinib & Baricitinib Multidisciplinary approach also important e.g. physiotherapy, occupational therapy, hydrotherapy, surgery
35
What are the different available / emerging biological therapies and when are they used?
Usually given to those with severe RA Biological therapies offer potent and targeted treatment strategies Biological therapies are proteins (usually antibodies) that specifically target a protein such as an inflammatory cytokine 1. Inhibition of tumour necrosis factor-alpha (‘anti-TNF’) - antibodies (infliximab, and others) - fusion proteins (etanercept) 2. B cell depletion - Rituximab – antibody against the B cell antigen, CD20 3. Modulation of T cell co-stimulation - Abatacept - fusion protein - extracellular domain of human cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) linked to modified Fc (hinge, CH2, and CH3 domains) of human immunoglobulin G1 4. Inhibition of interleukin-6 signalling - Tocilizumab (RoActemra) – antibody against interleukin-6 receptor. - Sarilumab (Kevzara) – antibody against interleukin-6 receptor.
36
What x-ray findings may be found in RA?
Affects MCPJs in hands (knuckles) May see bony erosions if RA has progressed enough Ulnar rotation / tilt of fingers Some osteoporosis at the joints
37
What are the differences in the x-rays of RA VS OA?
RA = affects MCP joints more (knuckles), also loss of joint space but mainly knuckles, also see some osteoporosis of the joints and bony erosions (black areas on the bone) OA = distal joints = almost no joint space
38
What other conditions can cause inflammatory arthritis other than rheumatoid causes?
Seronegative = Reactive arthritis Ankylosing spondylitis (AS) Psoriatic arthritis Seropositive = SLE
39
What are the features of ankylosing spondilitis (AS)?
Seronegative = no positive autoantibodies Anklylosis = spinal fusion Characterised by chronic sacroillitis – inflammation of sacroiliac joints Commonly found in males between 20-30 years Associated with HLA B27
40
What is the clinical presentation of AS?
Lower back pain + stiffness - Early morning - Improves with exercise Reduced spinal movements Peripheral arthritis Inflammation of other connective tissue e.g. plantar fasciitis, achilles tendonitis Fatigue Back pain >3 months, <45 years is suggestive of possible AS
41
What investigations are ordered for suspected AS?
Bloods = Normocytic anaemia Raised CRP, ESR HLA-B27 ``` Imaging = X-Ray MRI - Squaring Vertebral bodies, Romanus lesion - Erosion, sclerosis, narrowing SIJ - Bamboo Spine - Bone Marrow Oedema ```
42
What is the management for AS?
Phsyiotherapy = improvement with exercise Pain medications = usually NSAIDS as they also reduce the inflammation Exercise regimes Peripheral joint disease = prescribe DMARDs
43
What is psoriatic arthritis and what are its features?
Psoriasis = autoimmune skin disease Psoriasis presents clinically as scaly red plaques on extensor surfaces e.g. elbows and knees) But 10% of these patients also have joint inflammation Also seronegative - no positive autoantibodies
44
What is the clinical presentation of Psoriatic athritis?
Varied clinical presentations - classicially asymmetrical arthritis affecting the IPJs (interphalangeal joints) But can also manifest as: - Symmetrical involvement of small joints (rheumatoid pattern) - Spinal and sacroiliac joint inflammation - Oligoarthritis of large joints - Arthritis mutilans
45
What are the investigations conducted for psoriatic arthritis?
Blood test = analyse to make sure it is not rheumatoid arthritis (RA) - check for autoantibodies; psoriatic arthritis = seronegative X-ray of affected joints = pencil in cup abnormality MRI of affected joints = sacrolitis and enthesitis
46
What are the management options for psoriatic arthritis?
Avoid oral steroids as skin psoriasis becomes worse with these But long-term = DMARDs e.g. methotrexate
47
What is reactive arthritis? What are its features?
Sterile inflammation in joints following infection especially urogental (e.g. Chlamydia trachomatis) and/or GI gastrointestinal (e.g. Salmonella, Shigella, Campylobacter) infections
48
What are some extra-auricular manifestations of reactive arthritis?
Enthesitis (tendon inflammation) Skin inflammation Eye inflammation
49
What demographic does reactive arthritis affect? How may it present clinically?
Reactive arthritis may be first manifestation of HIV or hepatitis C infection Commonly young adults with genetic predisposition (e.g. HLA-B27) and environmental trigger (e.g. Salmonella infection) Symptoms follow 1-4 weeks after infection and this infection may be mild Condition is usually self-limiting – can be managed with NSAIDS or DMARDs if required
50
Reactive VS septic arthritis?
Reactive arthritis is distinct from infection in joints (septic arthritis) As reactive arthritis is STERILE and septic arthritis is NOT
51
What is SLE (systemic lupus erythematous)?
Lupus = a multi-system autoimmune disease Multi-site inflammation: can affect any almost any organ. Often joints, skin, kidneys, haematology Also: lungs, CNS involvement Associated with antibodies to self antigens (‘autoantibodies’) Autoantibodies are directed against components of the cell nucleus (nucleic acids and proteins)
52
What clinical investigations are suitable for suspected SLE in patients?
Blood test for autoantibodies - 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.
53
What demographic is SLE found in?
F:M ratio 9:1 Presentation 15 - 40 yrs Increased prevalence in African and Asian ancestry populations Prevalence varies 4-280/100,000
54
What are some other connective tissue diseases?
Systemic Sclerosis Myositis Sjogrens syndrome Mixed connective tissue disease

Y2 - BRS - MSK (10 decks)

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