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BRS Year 2 > Rheumatoid Arthritis > Flashcards

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 hyperuricemia (from breakdown of purines) –> inflammation

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

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13
Q

What are risk factors / causes for gout?

A

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

Causes of hyperuricemia:
Genetic tendency
Increased intake of purine rich foods (e.g. wild game, red meat, sea food, organ meat)
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? What should you particularly look at?

A

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

Presents clinically as:
Abrupt onset
Extremely painful 11/10 
Joint looks red, warm, swollen, and tender (classic signs of inflammation)
Resolves spontaneously over 3-10 days

Look at their diet: are they eating foods high in purines?

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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 (normally this is unnecessary as clinical observations along with bloods are very characteristic)

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 = allopurinol (xanthine oxidase inhibitors- 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

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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
Q

How does TNFa cause painful symptoms in RA?

A

When TNFa is recruited - it causes:
proinflammatory cytokine release, chemokine release, hepcidin induction (inhibits iron transport), endothelial activation, chondrocyte activation, osteoclast activation, leukocyte accumulation, angiogenesis, etc.

Leading to:
Synovitis –> bone reabsorption, joint inflammation and cartilage degradation -> bone erosion, pain and joint swelling, joint space narrowing

26
Q

What are the key features of RA seen clinically?

A

Chronic arthritis:

  • Polyarthritis - swelling of the small joints of 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
Q

What is a key investigation for RA?

A

Blood test = elevated CRP, high levels of RF
USS - look for swelling
X-ray - look for bone erosions

28
Q

Whta is the pattern of joint involvement for RA?

A

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
Q

Where is the primary site of inflammation in RA?

Where else in RA can there be inflammation?

A

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
Q

What are the common and uncommon extra-articular features of RA?

A

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
Q

What are subcutaenous nodules? How do the subcutaneous nodules appear in RA?

A

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
Q

What is a key investigation for RA?

A

2 types of antibodies are found in the blood of RA patients:

  1. Rheumatoid factor =
    Immunoglobulin M (IgM) autoantibodies against the Fc portion 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
Q

How is RA managed clinically? What is the treatment goal and what does this require?

A

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
Q

What are the drug treatments given for RA?

A

DMARDS = disease-modifying anti-rheumatic drugs = drugs that control the disease process

Glucocorticoid therapy e.g. prednisolone is avoided long term, however do provide quick inflammatory relief (IM methylprednisolone, Oral prednisolone or IV if very bad)

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
Q

What are the different available / emerging biological therapies and when are they used?

A

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 - made up off the 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
Q

What x-ray findings may be found in RA?

A

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
Q

What are the differences in the x-rays of RA VS OA?

A

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
Q

What other conditions can cause inflammatory arthritis other than rheumatoid causes?
(seropositive and seronegative)

A

Seronegative =
Reactive arthritis
Ankylosing spondylitis (AS)
Psoriatic arthritis

Seropositive =
SLE

39
Q

What are the features of ankylosing spondylitis (AS)?

A

Seronegative = no positive autoantibodies
Ankylosis = spinal fusion
Characterised by chronic sacroiliitis – inflammation of sacroiliac joints

Commonly found in males between 20-30 years
Associated with HLA B27

Patient may present with:

  • Hyperextended neck
  • Loss of lumbar lordosis
  • Flexed hips and knees
40
Q

What is the clinical presentation of AS?

A

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
Q

What investigations are ordered for suspected AS?

A

Bloods =
Normocytic anaemia
Raised CRP, ESR
HLA-B27

Imaging =
X-Ray
MRI
- Squaring Vertebral bodies, Romanus lesion (white on corner of vertebrae)
- Erosion, sclerosis, narrowing scaro-iliac joint
- Bamboo Spine
- Bone Marrow Oedema

42
Q

What is the management for AS?

A

Phsyiotherapy = improvement with exercise
Pain medications = usually NSAIDS as they also reduce the inflammation
Exercise regimes
Peripheral joint disease = prescribe DMARDs

43
Q

What is psoriatic arthritis and what are its features?

A

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
Q

What is the clinical presentation of Psoriatic athritis?

A

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
Q

What are the investigations conducted for psoriatic arthritis?

A

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 = sacroiliitis (inflammation of sacroiliac joint) and enthesitis (inflammation of where ligament/tendon attaches to bone- enesthesis)

46
Q

What are the management options for psoriatic arthritis?

A

Avoid oral steroids as skin psoriasis becomes worse with these

But long-term = DMARDs e.g. methotrexate

Also:
IV steroids
Biologics: Secukinumab (target TH-17), Ustekinumab (target IL-23), anti-TNF-a, JKI

47
Q

What is reactive arthritis? What are its features?

A

Sterile inflammation in joints following infection especially urogental (e.g. Chlamydia trachomatis) and/or GI gastrointestinal (e.g. Salmonella, Shigella, Campylobacter) infections

48
Q

What are some extra-auricular manifestations of reactive arthritis?

A

Enthesitis (tendon inflammation)
Skin inflammation
Eye inflammation

49
Q

What demographic does reactive arthritis affect? How may it present clinically?

A

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 (normally resolves spontaneously) – can be managed with NSAIDS or DMARDs if required

50
Q

Reactive VS septic arthritis?

A

Reactive arthritis is distinct from infection in joints (septic arthritis)

As reactive arthritis is STERILE and septic arthritis is NOT

51
Q

What is SLE (systemic lupus erythematous)?

A

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
Q

What clinical investigations are suitable for suspected SLE in patients?

A

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
Q

What demographic is SLE found in?

A

F:M ratio 9:1
Presentation 15 - 40 yrs
Increased prevalence in African and Asian ancestry populations
Prevalence varies 4-280/100,000

54
Q

What are some other connective tissue diseases?

A

Systemic Sclerosis
Myositis
Sjogrens syndrome
Mixed connective tissue disease

55
Q

What is chronic gout?

A

Repeated episodes of inflammation and pain due to gout

BRS Year 2 (110 decks)

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