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Y2 MSK > Rheumatoid And Other Inflammatory Arthritis > Flashcards

Rheumatoid And Other Inflammatory Arthritis Flashcards

1
Q

What are tendons?

A

Cords of strong fibrous collagen tissue attaching muscle to bone

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2
Q

What are ligaments?

A

Flexible fibrous connective tissue which connect two bones

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3
Q

What are the three key components of an synovial joint?

A

Articular capsule
Synovial membrane
Synovial fluid

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4
Q

What does synovium contain?

A

Macrophage-like phagocytic cells (type A synoviocyte) and fibroblast-like cells that produce hyaluronic acid (type B synoviocyte)
Type 1 collagen

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5
Q

What are type A synoviocytes

A

Macrophage-like pahogocytic cells

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6
Q

What are type 2 synoviocytes?

A

Fibroblast-like cells that produce hyaluronic acid

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7
Q

What type of fluid is synovial fluid, and what is it rich in?

A

Viscous fluid, rich in hyaluronic-acid

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8
Q

What type of collagen is articular cartilage composed of?

A

Type 2 collagen

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9
Q

What are the two components of articular cartilage?

A

Type 2 collagen and proteoglycans (aggrecan)

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10
Q

What is arthritis?

A

Disease of the joints

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11
Q

What are the two major divisions of arthritis?

A

Osteoarthritis (degenerative arthritis)
Inflammatory arthritis

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12
Q

What are two common features of osteoarhritis as seen on an x-ray?

A

Lack of joint space indicating loss of articular cartilage
Bony spurs (osteophyte)

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13
Q

What are the three causes of joint inflammation?

A

Infection
Crystal arthritis
Immune-mediated

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14
Q

What are two examples of crystal arthritis?

A

Gout, pseudo gout

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15
Q

What are three examples of immune mediated joint inflammation?

A

Rheumatoid arthritis
Seronegative spondyloarthropathies
Connective tissue disease

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16
Q

List two examples of infective joint inflammation

A

Septic arthritis, TB

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17
Q

Which of the three types of joint inflammation is due to primary inflammation?

A

Immune-mediated

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18
Q

Which two types of joint inflammation are caused by secondary inflammation in response to a noxious unit?

A

Infection
Crystal arthritis

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19
Q

Which type of joint inflammation is non-sterile?

A

Infective

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20
Q

What causes septic arthritis?

A

Bacterial infection of a joint - usually spread from the blood

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21
Q

What are the risk factors associated with septic arthritis?

A

Immunosupression, pre-existing joint damage, intravenous drug use

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22
Q

Why is septic arthritis a medical emergency?

A

If left untreated can rapidly destroy a joint

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23
Q

What is inflammation?

A

A physiological response to deal with injury or infection

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24
Q

What are the four manifestations of inflammation?

A

Rubor, calor, Dolor, tumour
Rubor = red, calor = heat, dolor = pain, tumor = swelling

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25
Q

What physiological changes occur in response to inflammation?

A

Increased blood flow
Migration of white blood cells into the tissues

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26
Q

What cellular changes occur as a response to inflammation?

A

Activation or differentiation of leukocytes

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27
Q

What molecular changes occur as a result of inflammation?

A

Cytokine production: TNF-alpha, IL1, IL6, IL17

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28
Q

Outline the clinical presentation of septic arthritis?

A

Acute red, hot, painful swollen joint
Usually only 1 joint is affected (mono arthritis)
Fever, patient often systemically unwell

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29
Q

Consider septic arthritis in any patient with …….

A

An acute painful, red, hot, swelling of a joint, especially is there is fever

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30
Q

How is septic arthritis diagnosed?

A

By joint aspiration, followed by sending sample for urgent gram stain and culture

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31
Q

What organisms commonly cause septic arthritis?

A

Staph.a , streptococci, gonococcus

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32
Q

What is different about septic arthritis that is caused by a gonococcus infection?

A

It often affect many joints (poly arthritis)
It is less likely to cause joint destruction

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33
Q

How is septic arthritis treated?

A

Surgical wash out (lavage) and intravenous antibiotics

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34
Q

What causes gout?

A

Deposition of monosodium urate (MSU)crystals in/around joints leading to inflammation

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35
Q

What risk factors are associated with gout?

A

Hyperuricaemia- high Uric acid levels

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36
Q

What causes hyperuricaemia?

A

Genetic tendency
Increased intake of purine rich foods
Increased cell turnover - chemotherapy
Reduced excretion - kidney failure
Increased alcohol intake

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37
Q

What causes pseudogout?

A

Deposition of calcium pyrophosphate dihydrate (CPPD) crystals leading to inflammation

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38
Q

What risk factors are associated with pseudogout?

A

Background osteoarthritis, elderly patients, inter current infection

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39
Q

What does the tissue deposition of MSU crystals lead to?

A

Gouty arthritis and/or Tophi (aggregated deposits of MSU in tissue)

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40
Q

Where do Tophi often develop?

A

Around hands, feet, elbows, ears

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41
Q

What are the clinical features of gout?

A

Abrupt onset, usually mono arthritis, joint red, warm, swollen and tender

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42
Q

Gouty arthritis most commonly affects which joint?

A

1st metatarsophalangeal joint of big toe - hallux

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43
Q

How is gout resolved?

A

Resolves spontaneously over 3-10 days

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44
Q

How does gout present on an x-ray?

A

Damage to joint - erosions

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45
Q

What is the key investigation for any acute mono arthritis?

A

Septic joint

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46
Q

What investigations are done in the diagnosis of gout - determining wether is gout or pseudogout

A

Needle inserted into joint and fluid aspirated - send to lab for microbiology and polarising light microscopy

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47
Q

What is the difference in shape and birefringence seen in gout vs pseudogout?

A

Gout = needle shape and negative birefringence
Pseudogout = brick shaped and positive birefringence

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48
Q

When assessing arthritis what are the key history and examination points?

A

Speed of duration
Worse or better with movement
Prolonged morning stiffness?
No. Of joints
Spinal involvement
Signs of inflammation

49
Q

How is gout managed in an acute attack?

A

Colchine, NSAIDS, steroids

50
Q

How is chronic gout managed?

A

Allopurinol

51
Q

How does allopurinol work?

A

Inhibits xanthine oxidase
Decreases uric acid production and decreases uric acid deposits in kidney

52
Q

What type of disease is RA?

A

Chronic autoimmune disease

53
Q

What is the primary site of pathology in RA?

A

Synovium

54
Q

What is synovitis?

A

Inflammation of the synovial membrane

55
Q

Where are synovium found?

A

Synovial joints, tenosynovium surrounding tendons, bursa

56
Q

What abnormality of the hand is characteristic of extensor tenosynovitis?

A

Incomplete extension of little and ring fingers

57
Q

How does the synovial membrane change in RA?

A

Synovium becomes a proliferated mass of tissue (pannus)

58
Q

What causes the synovium to become a proliferated mass of tissue (pannus) as seen in RA?

A

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

59
Q

Recruitment, activation and effector functions of inflammatory cells in RA is controlled by what?

A

Cytokine network - cytokine imbalance

60
Q

Does RA effect more men or women?

A

Women, 2:1 ratio

61
Q

The onset of RA is often at what age?

A

30-50s

62
Q

What are the key features of RA?

A

Poly arthritis
Pain, swelling and early morning stiffness
May lead to joint erosions on radiographs

63
Q

Which cytokine is dominant in the pathogenesis of RA?

A

TNF-alpha

64
Q

What is the name of the TNF-a inhibitor medication used in RA?
How does it work?

A

Inflixumab

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

65
Q

What are the actions of TNF-a in RA?

A

cytokine tumour necrosis factor-alpha (TNFα) is the dominant pro-inflammatory cytokine in the rheumatoid synovium• pleotropic actions are detrimental in this setting:• causes other inflammatory processes> other pro-inflammatory cytokines released like IL-1, IL-6> osteoclast activation> angiogenesis> chondrocyte activation• leads to the symptoms of rheumatoid arthritis:> bone erosion, pain, swelling, joint space narrowing

66
Q

What is the strongest genetic risk factor for RA?

A

HLA-DR

67
Q

What are the environmental risk factors associated with RA?

A

Smoking
Poor oral health
Porphyromonas gingivalis

68
Q

What are the most common affected joints in RA?

A

> Metacarpophalangeal joints (MCP)
Proximal interphalangeal joints (PIP)
Wrists, Knees, Ankles
Metatarsophalangeal joints (MTP)

69
Q

What are the common extra-articular features associated with RA?

A

Fever, weight loss
Subcutaneous nodules

70
Q

What are the 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

71
Q

What are subcutaneous nodules?

A

Feature of RA
• Central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue

72
Q

What is the most common site of subcutaneous nodules in RA?

A

Elbows

73
Q

Subcutaneous nodules are associated with_____

A

Severe disease
Extra-articular manifestations
Rheumatoid factor

74
Q

Rheumatoid factor is an autoantibody against which classification of antibody?

A

IgG

75
Q

What are the features of a healthy synovial membrane?

A

Healthy synovial membrane
• 1 to 3 cell layer that lines synovial joints
• Contains macrophage-like (type A synoviocyte) and fibroblast-like (type B synoviocyte) cells and type I collagen
• Functions include the maintenance of synovial fluid, the hyaluronate-rich viscous fluid within joint space

76
Q

Which type of arthritis: rheumatoid arthritis, osteoarthritis, septic arthritis, can cause anaemia?

A

RA

77
Q

Which type of arthritis: rheumatoid arthritis, osteoarthritis, septic arthritis, can cause an increase in RBC MCV?

A

None

78
Q

Which type of arthritis: rheumatoid arthritis, osteoarthritis, septic arthritis, can cause an increase in white blood cells (leucocytosis)

A

Septic arthritis

79
Q

Which type of arthritis: rheumatoid arthritis, osteoarthritis, septic arthritis, can cause an increased platelet count?

A

RA and septic arthritis

80
Q

Which type of arthritis: rheumatoid arthritis, osteoarthritis, septic arthritis, can cause a high ESR?

A

Usually in RA, sometimes in septic

81
Q

Which type of arthritis: rheumatoid arthritis, osteoarthritis, septic arthritis, causes an increased CRP?

A

RA and septic arthritis

82
Q

Which portion of the IgG does Rheumatoid factor recognise as its antigen?

A

Fc portion

83
Q

what type of antibody are rheumatoid factor?

A

Typically IgM

84
Q

What are the two key antibodies in RA?

A

Rheumatoid factor and ACPA - antibodies to citrullinated protein antigens

85
Q

Citrullination of peptides is mediated by enzymes termed:

A

Peptidyl arginine deiminases (PADs)

86
Q

What change do PADs enzymes cause?

A

Arginine to citrulline

87
Q

ACPAs predate first clinical symptoms of RA by a median of how many years?

A

4.5

88
Q

What are the radio graphic features of RA?

A

Soft tissue swelling
Peri-articular osteopenia
Bony erosions - in established disease

89
Q

Is an x-ray or ultrasound better for detecting synovitis?

A

Ultrasound

90
Q

What are the US changes seen in RA?

A

Synovial hypertrophy
Increased blood flow - Doppler signal

91
Q

What is the treatment goal for RA?

A

Prevent joint damage

92
Q

In order to prevent damage in RA, what is required?

A

Early recognition and diagnosis
Prompt initiation of treatment
aggressive pharmacological treatment

93
Q

What is the drug treatment for RA?

A

Disease-modifying anti-rheumatic drugs (‘DMARDs’) = drugs that control the disease process
1st line treatment:- methotrexate in combination with hydroxychloroquine or sulfasalazine
2nd line treatment:- Biological therapies offer potent and targeted treatment strategies

94
Q

What is the mechanism of methotrexate?

A

Inhibits dihydrofolate reductase

95
Q

what are the side effects associated with methotrexate?

A

Nausea
Hair loss
Fall in WCC
Abnormal liver function
Pneumonitis
Infection risk

96
Q

What are the four aims of use of biological therapies in RA?

A

Inhibition of TNF-a
B cell depletion
Modulation of T-cell co-stimulation
Inhibition of IL-6 signalling

97
Q

What biologic is used for B cell depletion in RA

A

Rituximab - antibody against CD20

98
Q

What biologic is used for modulation of T cell co-stimulation in RA?

A

Abatacept

99
Q

What is psoriasis?

A

An immune-mediated disease affecting the skin with characteristic scaly red plaques on extensor surfaces

100
Q

Why is psoriatic arthritis seronegative?

A

Rheumatoid factors are not present

101
Q

What is the dominant pathogenic pathways in psoriatic arthritis?

A

IL-17/IL-23

102
Q

What is reactive arthritis?

A

Sterile inflammation in joints following infection elsewhere in the body

103
Q

What are the common infections that cause reactive arthritis?

A

Urogenital - chlamydia trachomatis
Gastrointestinal - salmonella . Shigella

104
Q

What are the important extra-articular manifestations of reactive arthritis?

A

Enthesitis (tendon inflammation)
Skin inflammation
Eye inflammation

105
Q

Reactive arthritis can be the first manifestation of what two diseased?

A

HIV or hepatitis C

106
Q

Reactive arthritis commonly efffects young adults with _______

A

Genetic predisposition (HLA-B27) and environmental trigger

107
Q

Symptoms of reactive arthritis follow how many weeks after infection?

A

1-4 weeks

108
Q

What are the key differences between septic arthritis and reactive arthritis?

A

Synovial fluid culture - positive in septic
Antibiotic therapy - yes for septic
Joint lavage - yes for septic for large joints

109
Q

What is an example of inflammatory spondyloarthritis?

A

Ankylosing spondylitis (AS)

110
Q

What is ankylosing spondylitis?

A

Inflammation of the spine and sacro-iliac joints
Can also effect peripheral joints (entheses)

111
Q

Ankylosing spondylitis is associated with which gene?

A

HLA B27

112
Q

What is the presentation of ankylosing spondylitis?

A

• Lower back pain + stiffness
- Early morning
- Improves with exercise
• Reduced spinal movements
• Peripheral arthritis
• Plantar Fasciitis, Achilles Tendonitis
• Fatigue
• Back pain >3 months, <45 years is suggestive of possible Ank Spond

113
Q

What is seen in the bloods of someone with ankylosing spondylitis?

A

Normocytic anaemia
Raised CRP and ESR

114
Q

What is seen in the imaging of someone with ankylosing spondylitis?

A

Squaring vertebral bodies
romanus lesion
Erosion, sclerosis , narrowing SIJ
Bamboo spine (fusing together)
Bone marrow oedema

115
Q

What management is used for ankylosing spondylitis?

A

Physiotherapy NSAIDs

116
Q

What are the three seronegative spondyloarthropathies?

A

Ankylosing spondylitis
Psoaritic arthritis
Reactive arthritis

117
Q

Subchondral sclerosis with osteophytes affecting the DIPJ is a classic presentation of what?

A

Osteoarthritis

118
Q

loss of joint space in MCPJs with erosion and osteopenia are features of___

A

Rheumatoid arthritis

Y2 MSK (5 decks)

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