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MUSCULOSKELETAL AND RHEUMATOLOGY 2 > INTRODUCTION TO RHEUMATOLOGY > Flashcards

INTRODUCTION TO RHEUMATOLOGY Flashcards

1
Q

What is rheumatology?

A

Specialty dealing with diseases of the musculoskeletal system including joints, tendons, ligaments, muscles and bones

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2
Q

What is the synovium and what makes it up?

A

1-3 cell deep lining containing phagocytic cells and fibroblast=like cells that make hyaluronic acid

Type 1 collagen

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3
Q

What is synovial fluid?

A

Hyaluronic acid-rich viscous fluid contained in the synovial joint cavity

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4
Q

What is articular cartilage made of?

A

Type II collagen

Proteoglycan (aggrecan)

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5
Q

What are the 2 divisions of arthritis?

A 
Osteoarthritis (degenerative arthritis)
Inflammatory arthritis (RA is main type)
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6
Q

What are the clinical signs of inflammation?

A 
Rubor
Dolor
Calor
Tumor
Loss of function
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7
Q

What are the physiological/cellular and molecular changes in inflammation

A

Increased blood flow
Migration of leukocytes into the tissues
Activation/differentiation of leukocytes
Cytokine production (TNF-alpha, IL1…)

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8
Q

What are the 3 causes of inflammatory arthritis?

Name examples for each

A

Crystal arthritis:

  • Gout
  • Pseudogout

Immune-mediated (autoimmune):
- Rheumatoid arthritis
- Seronegative spondyloarthropathies e.g. ankylosing
spondylitis
- Connective tissue diseases e.g. SLE, psoriatic arthritis

Infection:

  • Septic arthritis
  • Tuberculosis
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9
Q

What is gout and what are its risk factors?

A

Syndrome caused by deposition of monosodium urate (MSU)(uric acid) crystals in joint causing inflammation

Hyperuricaemia increases risk of gout:

  • Genetic tendency
  • Increased intake of purine rich foods
  • Reduced excretion
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10
Q

What is pseudogout and what are its risk factors?

A

Syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystals causing inflammation

Risk factors:

  • Background osteoarthritis
  • Elderly patients
  • Intercurrent infection
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11
Q

How does gouty arthritis present?

A

Commonly monoarthritic 1st MTP joint (big toe) - podagra
Tophi - crystals in subcutaneous locations
Sudden onset
Extremely painful
Red, warm, swollen and tender
Resolves spontaneously over 3-10 days

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12
Q

What does an xray of a patient with gout typically show?

A

Juxta-articular rat bite erosions at the MTP joint of big toes if chronic

Usually in acute gout - looks normal

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13
Q

How can you investigate a patient suspected with gout?

A

Joint aspiration for synovial fluid analysis of crystals

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14
Q

How is gout managed?

A

Acute attack - colchicine, NSAIDs, steroids

Chronic - allopurinol

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15
Q

What does a synovial fluid examination involve?

A

Rapid Gram stain followed by culture and antibiotic sensitivity assays

Polarising light microscopy to detect crystals

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16
Q

What do the crystals in a patient with gout/pseudogout look like under polarising light microscopy?

A

Gout - Needle shaped with negative birefringence

Pseudogout - Brick shaped with positive birefringence

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17
Q

What is the most common autoimmune inflammatory joint disease?

A

Rheumatoid arthritis

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18
Q

What is rheumatoid arthritis?

A

Chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis of synovial joints

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19
Q

What is synovitis?

A

Inflammation of synovial membrane

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20
Q

What is the pathogenesis of rheumatoid arthritis?

A

Idiopathic

Neovascularisation
Lymphangiogenesis
Inflammatory cells - T/B, plasma, mast cells and macrophages

All causing synovium to become a proliferated mass of tissue (pannus)

Recruitment, activation of these cells controlled by cytokine network (cytokine imbalance of excess pro-inflammatory vs anti-inflammatory) - TNF-alpha has a major role and can be targeted in therapy via antibodies/fusion proteins

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21
Q

What cell is the main producer of TNF alpha

A

Activated macrophages in rheumatoid synovium

22
Q

How does rheumatoid arthritis present?

A 
Chronic polyarthritis (> 6 weeks)
Swollen small joints of hand and wrist common
Symmetrical
Early morning stiffness in and around joints
Joint erosions on radiographs

Extra-articular features (rheumatoid nodules…)

Rheumatoid factor may be detected in blood

23
Q

Which joints are most commonly affected in rheumatoid arthritis?

A 
MCP joints
PIP joints
MTP joints
Wrists
Knees
Ankles
24
Q

What is the primary site of pathology in RA and what can this cause?

A

Synovium

Synovitis of synovial joints
Extensor tenosynovitis (tenosynovium surrounding tendons)
Olecranon bursitis (bursa)
25
Q

List the extra-articular features that might be seen in a patient with RA

A

Fever
Weight loss
Rheumatoid nodules

Uncommon:

  • Vasculitis
  • Ocular inflammation
  • Neuropathies
  • Amyloidosis
  • Lung disease
  • Felty’s syndrome
26
Q

What are rheumatoid nodules?

A

Subcutaneous nodules with central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue

Occurs in ~ 30% patients and associated with severe disease and rheumatoid factor

27
Q

What are the 2 autoantibodies that are found in RA patients?

A

Rheumatoid factor

Antibodies to citrullinated protein antigens (ACPA)

28
Q

What is rheumatoid factor?

A

Typically IgM antibodies that bind to Fc portion of IgG as their target antigen (IgM anti-IgG antibody)

Positive in 70% at disease onset and further 10-15% over the first 2 years

29
Q

What are antibodies to citrullinated protein antigens (ACPA)?

A

AKA anti-cyclic citrullinated peptide antibody (anti-CCP antibody)

30
Q

What is the citrullination of peptides mediated by?

A

Peptidyl arginine deaminases (PADs)

31
Q

Describe the management of a patient with RA

A

Aggressive treatment as early as possible to prevent joint damage

Drugs:

  • DMARDs
  • Glucocorticoids (prednisolone) but avoid long-term use

1st line: methotrexate with hydroxychloroquine/sulfasalazine

2nd line: Biological therapies e.g. Janus Kinase inhibitors (Tofacitinib, Baricitinib)

Multidisciplinary too e.g. physiotherapy, occupational therapy, hydrotherapy, sugery

32
Q

What are DMARDs?

A

Disease modifying anti-rheumatic drugs

Drugs which control the disease process

33
Q

What are the different ways biological therapies work for RA?

A
  1. Anti-TNF alpha (Infliximab - antibody, fusion proteins)
  2. B cell depletion (Rituximab - antibody against CD20)
  3. T cell co-stimulation modulation (Abatacept)
  4. Inhibition of IL-6 signalling (Tocilizumab, Sarilumab)
34
Q

What is ankylosing spondylitis?

A

Form of seronegative spondyloarthropathy so no positive autoantibodies. Causes chronic sacroillitis (inflammation of sacroiliac joints) and results in ankylosis (spinal fusion)

35
Q

What antigen/gene is ankylosing spondylitis associated with?

A

HLA B27 on leukocytes

36
Q

What is the common demographic of ankylosing spondylitis?

A

20-30 year old men

37
Q

How does ankylosing spondylitis present clinically?

A

Lower back pain and stiffness (early morning and improves with exercise)
Reduced spinal movements
Poor posture (hyperextended neck, no lumbar lordosis, flexed hip and knees)
Peripheral arthritis
Plantar fasciitis, achilles tendonitis
Fatigue

38
Q

What investigations can you do for ankylosing spondylitis and what would the results be?

A

Bloods:

  • Normocytic anaemia
  • Raised CRP, ESR
  • HLA B27 +ve
  • no rheumatoid factor

Imaging:

  • X-ray
  • MRI (squaring vertebral bodies, romanus lesion, erosion, sclerosis, narrowing SIJ, bamboo spine, bone marrow oedema)
39
Q

What is the management for ankylosing spondylitis?

A

Physiotherapy
Exercise regimes
NSAIDs
DMARDs for peripheral joints disease

40
Q

What is psoriatic arthritis?

A

Joint inflammation associated with 10% of psoriasis patients. Seronegative

41
Q

How does psoriatic arthritis present?

A

Classically asymmetrical arthritis affected IPJs

But can also:
Symmetrical involvement of small joints (rheumatoid pattern)
Spinal and sacroiliac joint inflammation
Oligoarthritis of large joints
Arthritis mutilans

These are the 5 types of psoriatic arthritis

42
Q

What investigations can be done for psoriatic arthritis and what can be seen?

A

Bloods:
- Seronegative

Imaging:

  • X-ray (pencil in cup abnormality)
  • MRI (sacroiliitis and enthesitis)
43
Q

What is the management for psoriatic arthritis?

A

DMARDs - methotrexate

Avoid oral steroids as risk of pustular psoriasis

44
Q

What is reactive arthritis?

A

Sterile inflammation in joints following infection elsewhere especially urogenital and GI

May be first manifestation of HIV or hepatitis C infection

45
Q

How does reactive arthritis present?

A 
Joint inflammation
Extra-articular manifestations:
- Enthesitis
- Skin inflammation
- Eye inflammation

Symptoms usually 1-4 weeks after infection

46
Q

How is reactive arthritis managed?

A

Symptoms are usually self limiting

Can be managed with NSAIDs or DMARDs if needed

47
Q

What is the common demographic of reactive arthritis?

A

Young adults with genetic predisposition (e.g. HLA B27) and environmental trigger (infection)

48
Q

What is SLE and its pathology?

A

System Lupus Erythmatous

Multi system autoimmune inflammation which can affect almost any organ and joints. Autoantibodies against cell nucleus components (nucleic acids and proteins)

49
Q

What clinical tests for autoantibodies in SLE be done diagnostically?

A

Antinuclear antibodies (ANA);

  • High sensitivity for SLE but not specific
  • -ve rules out SLE but +ve doesn’t mean SLE

Anti-double stranded DNA antibodies (anti-dsDNA Abs):
- High specificity for SLE but in context of appropriate clinical signs

50
Q

What is the epidemiology of SLE?

A

F:M 9:1
15-40 years old
Increased prevalence in african and asian populations

MUSCULOSKELETAL AND RHEUMATOLOGY 2 (5 decks)

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