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BRS Phase 1b > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is Rheumatology?

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 main 2 types of joint disease?

A

Osteoarthritis

Inflammatory arthritis

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3
Q

How does inflammation manifest?

A

RED (rubor)

  1. PAIN (dolor)
  2. HOT (calor)
  3. SWELLING (tumor)
  4. LOSS OF FUNCTION
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4
Q

What physiological changes underpin 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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5
Q

What are the 3 main causes of joint inflammation?

A

Crystal arthritis - gout, pseudo gout

Immune mediated - rheumatoid arthritis, seronegative spondyloarthropathies, connective tissue disease

Infection - Septic arthritis, TB

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6
Q

What happens in gout?

A

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

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7
Q

What is a major risk factor for gout?

A

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

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8
Q

What are the causes of gout?

A 
Genetic tendency
Increased intake of purine rich foods
Reduced excretion (kidney failure)
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9
Q

What happens in pseudo gout?

A

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

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10
Q

What are the risk factors for Pseudogout?

A

background osteoarthritis, elderly patients, intercurrent infection

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11
Q

What can gout lead to?

A

Gouty arthritis

Tophi (aggregated deposits of MSU in tissue)

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12
Q

Where does gout typically affect?

A

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

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13
Q

How does gout present?

A

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

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14
Q

What investigations are done for gout?

A

Joint aspiration, synovial fluid analysis

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15
Q

What is the management for gout?

A

Acute attack – colcihine, NSAIDs, Steroids

Chronic – allopurinol

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16
Q

What are the characteristics of gout crystals under polarising light microscopy?

A

urate crystals
needle shape
negative Birefringence

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17
Q

What are the characteristics of pseudo gout crystals under polarising light microscopy?

A

Calcium pyrophosphate dihydrate CPPD crystals
Brick shaped
positive Birefringence

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18
Q

What is the most common immune mediated inflammatory joint disease?

A

Rheumatoid arthritis

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19
Q

Define Rheumatoid arthritis

A

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

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20
Q

What is the pathogenesis of Rheumatoid arthritis?

A

Synovial membrane is abnormal in rheumatoid arthritis:
The synovium becomes a proliferated mass of tissue (pannus) due to:

Neovascularisation
Lymphangiogenesis
inflammatory cells:
activated B and T cells
plasma cells
mast cells
activated macrophages

Recruitment, activation and effector functions of these cells is controlled by a cytokine network
There is an excess of pro-inflammatory vs. anti-inflammatory cytokines (‘cytokine imbalance’)

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21
Q

What is the role of TNF-alpha in RA?

A

The cytokine tumour necrosis factor-alpha (TNFα) is the dominant pro-inflammatory cytokine in the rheumatoid synovium
Its pleotropic actions are detrimental in this setting:

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22
Q

How was TNF-alphas role in RA validated?

A

arthritis validated by the therapeutic success of TNFα inhibition in this condition

TNFα inhibition is achieved through parenteral administration (most commonly sub-cutaneous injection) of antibodies or fusion proteins

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23
Q

What are the Key features of Rheumatoid Arthritis?

A

Chronic arthritis
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

Extra-articular disease can occur
Rheumatoid nodules
Others rare e.g. vasculitis, episcleritis

Rheumatoid ‘factor’ may be detected in blood
Autoantibody against IgG - should really call this rheumatoid ‘antibody’ not ‘factor’

24
Q

What is the pattern of joint involvement in RA?

A

Symmetrical

Affects multiple joints (polyarthritis)

Affects small and large joints, but particularly hands and feet

25
Q

What are the commonest affected joints in RA?

A 
Metacarpophalangeal joints (MCP)
Proximal interphalangeal joints (PIP)
Wrists 
Knees
Ankles
Metatarsophalangeal joints (MTP)
26
Q

What are the primary sites of pathology in RA?

A

Synovial joints
Tenosynovium
Bursa

27
Q

What are some common extra-articular features in RA?

A

Fever, weight loss

Subcutaneous nodules

28
Q

What are some uncommon extra-articular features of RA ?

A

vasculitis
Ocular inflammation e.g. episcleritis
Neuropathies
Amyloidosis
Lung disease – nodules, fibrosis, pleuritis
Felty’s syndrome – triad of splenomegaly, leukopenia and rheumatoid arthritis

29
Q

How do subcutaneous nodules occur in RA?

A 
Central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue
Occur in ~30% of patients
Associated with:
Severe disease
Extra-articular manifestations
Rheumatoid factor
30
Q

What are the two types of Antibodies found in the blood of RA patients?

A

Rheumatoid factor

Antibodies to citrulinated protein antigens ACPA

31
Q

What is Rheumatoid factor?

A

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

32
Q

What are ACPA?

A

Antibodies to citrullinated peptides are 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)

33
Q

What is the management for RA?

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

Drug treatment:
Disease-modifying anti-rheumatic drugs (‘DMARDs’) = drugs that control the disease process

34
Q

What is 1st line treatment for RA?

A

methotrexate in combination with hydroxychloroquine or sulfasalazine

35
Q

What is 2nd line treatment for RA?

A

Biological therapies offer potent and targeted treatment strategies
New therapies include Janus Kinase inhibitors : Tofacitinib & Baricitinib

Important roles for glucocorticoid therapy (prednisolone) but avoid long-term use because of side-effects.

Multidisciplinary approach also important e.g. physiotherapy, occupational therapy, hydrotherapy, surgery

36
Q

What are Biological therapies?

A

Biological therapies are proteins (usually antibodies) that specifically target a protein such as an inflammatory cytokine

37
Q

What are biological therapies used in RA Management?

A
  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.
38
Q

What is Ankolysing spondylitis?

A

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

39
Q

What is the clinical presentation of ankolysing Spondylitis?

A 
Lower back pain + stiffness
Early morning
Improves with exercise
Reduced spinal movements
Peripheral arthritis
Plantar Fasciitis, Achilles Tendonitis
Fatigue
40
Q

What bloods are done for AS?

A

Normocytic anaemia
Raised CRP, ESR
HLA-B27

41
Q

What imaging is done in AS?

A 
X-Ray
MRI
Squaring Vertebral bodies, Romanus lesion
Erosion, sclerosis, narrowing SIJ
Bamboo Spine 
Bone Marrow Oedema
42
Q

What is the management for AS?

A

Physiotherapy
Exercise regimes
NSAIDs
Peripheral joint disease - DMARDs

43
Q

What is Psoriasis?

A

Psoriasis is an autoimmune disease affecting the skin (scaly red plaques on extensor surfaces eg elbows and knees)

~10% of psoriasis patients also have joint inflammation

44
Q

What is different in psoriatic arthritis compared to RA?

A

Unlike RA, rheumatoid factors are not present (“seronegative”)

45
Q

What are the clinical presentations of Psoriatic arthritis?

A

Classically asymmetrical arthritis affecting IPJs

But also can manifest as:

  • Symmetrical involvement of small joints (rheumatoid pattern)
  • Spinal and sacroiliac joint inflammation
  • Oligoarthritis of large joints
  • Arthritis mutilans
46
Q

What investigations should be done for psoriatic arthritis?

A

X-rays of affected joints – pencil in cup abnormality
MRI – sacroiliitis and enthesitis

Bloods – no antibodies as seronegative

47
Q

What is the management of Psoriatic arthritis?

A

DMARDs – methotrexate

Avoid oral steroids – risk of pustular psoriasis due to skin lesions

48
Q

What is Reactive arthritis?

A

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

49
Q

What are important extra-articular manifestations in Reactive arthritis?

A

Enthesitis (tendon inflammation)
Skin inflammation
Eye inflammation

50
Q

What can reactive arthritis be a first manifestation of?

A

HIV or HepC infection

51
Q

Who is affected by reactive arthritis?

A

Commonly young adults with genetic predisposition (e.g. HLA-B27) and environmental trigger (e.g. Salmonella infection)

52
Q

When do you get symptoms of reactive arthritis?

A

1-4 weeks after infection( may be mild infection).

53
Q

What is the treatment for Reactive arthritis?

A

Condition is usually self-limiting – can be managed with NSAIDS or DMARDs if required
Reactive arthritis is distinct from infection in joints (septic arthritis)

54
Q

What happens in Systemic Lupus Erythematous SLE?

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)

55
Q

What autoantibodies can be helpful in SLE diagnosis?

A
  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.
56
Q

What is the epidemiology of SLE?

A

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

BRS Phase 1b (80 decks)

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