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BRS > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

How many joints does oligoarthritis affect?

A

2-4 joints

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2
Q

How many joints does polyarthritis affect?

A

5+

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3
Q

What are the two types of arthritis?

A

Degenerative joint disease and inflammatory joint disease.

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4
Q

Signs on inflammation?

A

Red, Pain, Hot, Swelling and loss of function.

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5
Q

Two types of secondary joint inflammation?

A

Infection and crystal arthritis.

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6
Q

Type of primary joint inflammation?

A

Immune mediated.

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7
Q

Example of non sterile inflammation of joint?

A

Infection of joint.

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8
Q

Example of sterile inflammation of joint?

A

Crystal arthritis and immune mediated arthritis.

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9
Q

What causes septic arthritis?

A

Bacterial infection of joint.

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10
Q

Symptoms of septic arthritis?

A

Acute onset. Inflammation symptoms of joint. Monoarthritis. Fever.

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11
Q

How do you diagnose septic arthritis?

A

Joint aspiration to get bacteria sample. Gram stain and culture done.

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12
Q

Treatment of septic arthritis?

A

Surgical washout and iv antibiotics.

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13
Q

Risk factors of septic arthritis?

A

Immunosupressed and IV drug use.

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14
Q

What is an exception for septic arthritis that displays different symptoms?

A

Gonococcal septic arthritis causes polyarthritis.

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15
Q

2 types of crystal arthritis?

A

Gout and pseudogout.

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16
Q

What causes gout?

A

Deposition of monosodium urate crystals around joints. This results in inflammation.

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17
Q

What is a key risk factor for gout?

A

High uric acid levels.

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18
Q

What causes hyperuricemia?

A

Genetic tendency, increase intake of high purine foods and reduced excretion due to kidney failure.

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19
Q

What causes pseudogout?

A

Deposition of calcium pyrophosphate dihydrate crystals around joints which results in inflammation.

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20
Q

What are the symptoms of gout?

A

Acute onset, monoarthritis and formation of tophi.

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21
Q

What are tophi?

A

Stone deposits on skin.

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22
Q

Gout biomarkers?

A

High CRP and high serum urate.

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23
Q

What is a definitive test for crystal arthritis?

A

Synovial fluid analysis.,

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24
Q

How is synovial fluid analysed?

A

Use of microscopy and polarising light microscopy.

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25
Q

Shape of gout crystal?

A

Needle shaped.

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26
Q

Shape of pseudogout crystal?

A

Brick shaped.

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27
Q

Birefringerence test result for gout?

A

Negative.

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28
Q

Birefringerence test result for pseudogout?

A

Positive.

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29
Q

What may you administer to treat gout?

A

Non steroidal anti inflammatory drugs. Use of glucocorticoids.

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30
Q

What may you prescribe to treat chronic gout?

A

Xanthine oxidase inhibitor.

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31
Q

Lifestyle changes for chronic gout?

A

Avoid purine rich foods.

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32
Q

How does a xanthine oxidase inhibitor help treat chronic gout?

A

Reduces serum urate levels by inhibiting purine metabolism.

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33
Q

How are osteoarthritis different to rheumatoid arthritis?

A

Osteoarthritis is a gradual onset. OA worsens with movement. There is joint enlargement in OA but no swelling. RA has morning stiffness.

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34
Q

How is OA different on an Xray to rheumatoid arthritis?

A

OA has osteophytes and has subchondral sclerosis (increased whiteness at joint). RA can have osteopenia and bony erosions.

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35
Q

What is subchondral sclerosis?

A

Thickening of bone below cartilage surface.

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36
Q

What are the 3 types of joints?

A

Fibrous joints, cartilaginous joints and synovial joints.

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37
Q

What is a fibrous joint and give an example

A

No space between bones such as sutures in skull.

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38
Q

What is a cartilaginous joint and give an example

A

Joints in which the bones are connected by cartilage such as joints between spinal vertebrae.

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39
Q

What is a synovial joint and give an example

A

Have synovial cavity between adjoining bones that is filled with synovial fluid. Knee joint.

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40
Q

What is the proteoglycan in articular cartilage?

A

Aggrecan.

41
Q

What is a main compound present in synovial fluid?

A

Hyaluronic acid.

42
Q

What is the synovium made up of?

A

Type 1 collagen. Synoviocytes.

43
Q

What is the main reason to why cartilage doesn’t heal well?

A

Cartilage is avascular (lacks blood supply).

44
Q

What is cartilage composed of?

A

Chondrocytes and ECM.

45
Q

What is ECM made up of?

A

Water, collagen and proteoglycans.

46
Q

What is the main proteoglycan in the ECM of cartilage?

A

Aggrecan.

47
Q

What can happens to the two bones in a joint if there is a loss of articular cartilage in OA?

A

Bone in contact with bone.

48
Q

What structure in the joint does rheumatoid arthritis affect?

A

Synovium.

49
Q

Describe the pattern of joint involvement in rheumatoid arthritis

A

Polyarthritis and symmetrical.

50
Q

What joints does rheumatoid arthritis commonly affect?

A

Joints in hands, wrists and feet.

Metacarpophalangeal joints (MCP)
Proximal interphalangeal joints (PIP)
NOT distal interphalangeal joints
Metatarsophalangeal joints (MTP)

51
Q

What are common extra articular features present in a rheumatoid arthritis patient?

A

Fever, weight loss. Subcutaneous nodules.

52
Q

What are some uncommon extra articular features present in a rheumatoid arthritis patient?

A

Vasculitis and episcleritis.

53
Q

What causes proliferation of the synovium into a mass of tissue in rheumatoid arthritis?

A

Neovascularisation, lymphangiogenesis and recruitment of inflammatory cells. Excess of pro inflammatory cytokines.

54
Q

What is the dominant pro inflammatory cytokine in rheumatoid arthritis? How does it cause symptoms of rheumatoid arthritis?

A

Tumour necrosis factor alpha. Osteoclast activation, chondrocyte activation which results in production of MMP and pro inflammatory cytokine release.

55
Q

Example of TNF-alpha inhibitor?

A

Adalimumab.

56
Q

Rheumatoid arthritis biomarkers?

A

Normocytic anaemia (low Hb but normal MCV). Raised platelets, raised ESR and CRP.

57
Q

What biomarker can differentiate septic arthritis from rheumatoid arthritis?

A

Raise white blood cell count in septic arthritis but normal in rheumatoid arthritis.

58
Q

What are the two main biomarkers for septic arthritis?

A

Raise white cell count and CRP.

59
Q

What class of antibody is rheumatoid factor?

A

IgM.

60
Q

What are the two self antigens targeted in rheumatoid arthritis?

A

Fc portion of IgG antibodies. Citrullinated proteins.

61
Q

What are the two types of autoantibodies in rheumatoid arthritis?

A

Rheumatoid factor and anti-CCP antibody (anti-cyclic citrullinated protein antibody).

62
Q

What is the most specific test for rheumatoid arthritis?

A

Anti-CCP antibody test.

63
Q

When do bony erosions present in RA?

A

Later on in disease once its fully established.

64
Q

Why is ultrasound better that xrays for RA?

A

Synovium can be visualised better.

65
Q

What would you seen in the ultrasound of a joint in a rheumatoid arthritis patient?

A

Thickening of the synovium. Increased blood flow due to neovascularisation of synovium (doppler ultrasound) and erosions (IF RA IS ESTABLISHED).

66
Q

1st line treatment for rheumatoid arthritis?

A

Glucocorticoids and DMARDs (disease modifiying anti rheumatic drugs).

67
Q

Example of a disease modifying anti rheumatic drug?

A

Methotrexate.

68
Q

2nd line treatment for rheumatoid arthritis?

A

Biologics such as JAK inhibitors (Janus kinase inhibitors).

69
Q

Mechanism for how methotrexate works?

A

Acts as a folate antagonist by inhibiting dihydrofolate reductase.

70
Q

Side effects of methotrexate?

A

Abnormal liver function and fall in white cell count.

71
Q

Examples of biological therapies for rheumatoid arthritis?

A

Anti TNF alpha, antibody against B cell antigen or CD20, antibody against IL-6 receptor, blocking of T cell co stimulation proteins.

72
Q

What is seronegative arthritis?

A

When you have inflammatory joint disease symptoms but don’t have rheumatoid factor or anti ccp.

73
Q

Types of seronegative arthritis?

A

Psoriatic arthritis, reactive arthritis, ankylosing spondylitis and IBD associated arthritis.

74
Q

Presentation of psoriatic arthritis

A

Scaly red plaques on extensor surfaces (elbows and knees). Asymmetrical pattern of joint involvement. Usually affects interphalangeal joints.
Doesn’t affect MCPJ’s unlike RA.

75
Q

What is reactive arthritis?

A

Sterile inflammation of joint following infection elsewhere in the body.

76
Q

What type of infections usually cause reactive arthritis?

A

Urogenital (chlamydia) and gastrointestinal (salmonella).

77
Q

What extra articular features might be present in reactive arthritis?

A

Enthesistis (inflammation where tendon or ligament attached to bone), skin inflammation and eye inflammation.

78
Q

What serious infections can trigger reactive arthritis?

A

HIV or Hepatitis C infection.

79
Q

What test can you do to see if someone is more likely to develop reactive arthritis?

A

HLA-B27

80
Q

What is HLA-B27?

A

MHC I class molecule.

81
Q

How does ankylosing spondylitis present?

A

Inflammation of spine. Inflammation of sacro iliac joints. Enthesistis

82
Q

Extra articular features in ankylosing spondylitis?

A

4 A’S. Anterior uveitus (iris), Apical lung fibrosis, aortitis (inflammation of aorta), amyloidosis.

83
Q

What is Enthesitis

A

Inflammation where tendon or ligament joins bone.

84
Q

What is a big risk factor for ankylosing spondylitis?

A

HLA-B27 positive.

85
Q

Main cytokines involved in ankylosing spondylitis?

A

TNF alpha, IL-17 and IL-23.

86
Q

Untreated ankylosing spondylitis can lead to what?

A

Bone growth between adjacent vertebrae leading to spinal fusion.

87
Q

What diagnostic imaging technique is used for ankylosing spondylitits?

A

MRI.

88
Q

Lifestyle changes to improve ankylosing spondylitis?

A

Physiotherapy and exercise.

89
Q

First line treatment for ankylosing spondylitis?

A

NSAID’s

90
Q

How do NSAID’s work?

A

Reduce inflammation by blocking COX1 and COX2 resulting in inhibition of prostaglandin production.

91
Q

Risks of NSAID’s

A

Can make asthma worse. Peptic ulcer.

92
Q

Second line treatments for ankylosing spondylitis?

A

Biologics such as anti TNF alpha and anti IL17.

93
Q

Why do NSAID’s cause asthma to get worse?

A

Increased production of leukotrienes which cause bronchoconstriction.

94
Q

Autoantibodies in SLE (systemic lupus erythematous) target what?

A

Nucleic acids and other cell nucleus proteins.

95
Q

Key symptom present in SLE (systemic lupus erythematous)?

A

Butterfly rash.

96
Q

Two types of autoantibodies produced in SLE that can be measured in the blood?

A

Antinuclear antibodies and anti-double stranded DNA antibodies.

97
Q

What is a big risk factor for SLE (systemic lupus erythematous)?

A

Sex (Women are a lot more likely to get it).

98
Q

Which of the two autoantibodies is more specific for SLE?

A

Anti-double stranded DNA antibodies.

99
Q

Where does gout usually occur?

A

Big toe.

BRS (52 decks)

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