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BRS 5 Musculoskeletal > 1b Rheumatoid And Other Inflammatory Arthritis > Flashcards

1b Rheumatoid And Other Inflammatory Arthritis Flashcards

1
Q

What is the synovium?

A

1-3 cell deep lining containing macrophage-like phagocytic cells (type A synoviocyte) and fibroblast-like cells that produce hyaluronic acid (type B synoviocyte)

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2
Q

What enables the synovial fluid to be viscous?

A

It is rich in hyaluronic acid

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3
Q

What type of collagen makes up the articular cartilage?

A

Type 2 collagen

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4
Q

What proteoglycan plays a large role in the articular cartilage?

A

Aggreca

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5
Q

What are the two main divisions of arthritis?

A

Osteoarthritis and rheumatoid arthritis

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6
Q

What are the key characteristics of OA?

A

lack of joint space
loss of articular cartilage
bony spurs - osteophyte

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7
Q

What are the two infectious causes of joint inflammation?

A

Septic arthritis and tuberculosis

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8
Q

What are the two forms of crystal arthritis?

A

gout
pseudogout

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9
Q

What are the two sterile inflammatory processes which can occur in joints?

A

Crystal arthritis
Immune mediated “autoimmune”

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10
Q

What causes septic arthritis?

A

Bacterial infection of a joint (usually caused by spread from the blood)

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11
Q

What are the risk factors for septic arthritis?

A

immunosuppressed, pre-existing joint damage, intravenous drug use (IVDU)

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12
Q

Describe the typical presentation of a joint with septic arthritis?

A

Acute red, hot, painful swollen joint

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13
Q

How many joints are commonly affected in septic arthritis?

A

mono-arthritis

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14
Q

What common symptom will patients with septic arthritis present with?

A

Fever

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15
Q

How is septic arthritis diagnosed?

A

Joint aspiration - send sample for urgent gram stain and culture

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16
Q

What are the common organisms which cause septic arthritis?

A

Staphylococcus aureus, Streptococci, Gonococcus

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17
Q

in what way is gonococcal septic arthritis an exception?

A
  • effects multiple joints (polyarthritis)
  • less likely to cause joint destruction
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18
Q

What is the treatment for septic arthritis?

A

Surgical wash out - lavage and intravenous antibiotics

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19
Q

What is gout caused by?

A

Deposits of monosodium urate (uric acid)

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20
Q

What are some causes of gout?

A

Genetic tendency
Increased intake of purine rich foods
Increased cell turn over eg chemotherapy
Reduced excretion (kidney failure)

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21
Q

What is the main risk factor for gout?

A

hyperuricaemia

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22
Q

What is pseudogout caused by?

A

deposition of calcium pyrophosphate dihydrate crystals

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23
Q

What are the risk factors for pseudogout?

A

background osteoarthritis, elderly patients, intercurrent infection

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24
Q

What are tophi?

A

aggregated deposits of MSU in tissue): often develop around hands, feet, elbows, and ears) – in other tissues

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25
Q

Describe the clinical features of gout?

A

Abrupt onset, usually monoarthritis

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26
Q

Which joint is most commonly affected by gout? What is it called?

A

Big toe 1st MTPJ (metatarsophalangeal joint) most commonly affected

(podagra)

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27
Q

What is a key investigation to do for any acute monoarthritis?

A

synovial fluid analysis

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28
Q

What is the shape of the crystals in GOUT vs PSUEDOGOUT?

A

Gout = needle shaped
Pseudogout = rhomboid / brick shaped

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29
Q

What is the Birefringence for GOUT vs PSUEDOGOUT?

A

gout = negative
pseudogout = positive

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30
Q

What is the primary site of inflammation in RA?

A

synovium

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31
Q

What is synovitis?

A

inflammation = of the synovial membrane

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32
Q

What are the three locations the synovium are found at?

A

Synovial joints
Tenosynovium
Bursa

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33
Q

What is extensor tenosynovitis?

A

inflammation of the tenosynovium surrounding tendons

  • shows as patieng having incomplete extension of the little and ring finger
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34
Q

What are the key features of rheumatoid arthritis?

A

chronic condition
- poly arthritis
- pain swelling and early morning stiffness in and around the joints
- may lead to joint damage and destruction = seen as joint erosions on the radiographs

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35
Q

What is detected in the blood of patients with RA?

A

auto-antibodies

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36
Q

How is the contribution between genetics and the environment estimated?

A

look at the concordance of a trait in monozygotic and dizygotic twins

If the concordance rate for monozygotic twins > dizygotic twins, this indicates a genetic component.

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37
Q

What is the largest genetic risk factor for Rheumatoid Arthritis?

A

Strongest genetic risk factor = HLA-DR

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38
Q

Describe the pattern of joint involvement in Rheumatoid arthritis?

A

Symmetrical

Affects multiple joints (polyarthritis)

Affects small and large joints, but particularly hands, wrists and feet

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39
Q

What are the most common joints to be affected by RA?

A

Metacarpophalangeal joints (MCP)
Proximal interphalangeal joints (PIP)

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40
Q

What are the common extra-articular features of RA

A

Fever, weight loss
Subcutaneous nodules

41
Q

What are the uncommon extra-articular features of RA?

A

Lung disease – nodules, fibrosis, pleuritis
Ocular inflammation e.g. episcleritis
Vasculitis
Neuropathies
Felty’s syndrome – triad of splenomegaly, leukopenia and rheumatoid arthritis
Amyloidosis = chronic inflammation causing increase in amyloid P

42
Q

What is a subcutaenous nodules which is seen in RA?

A

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

43
Q

What is a rheumatoid nodule?

A

nodule found on the ulnar border of the forearm where you might detect nodules - if they are present confirms the diagnosis of RA and is invariably associated with RF

44
Q

What does the synovium become in RA?

A

proliferated mass of tissue (pannus) due to neovascularisation
lymphangiogenesis
inflammatory cell infiltration

45
Q

What immune cells are found in the synovium in RA?

A

activated B and T cells
plasma cells
mast cells
activated macrophages

46
Q

Describe the cytokine balance in RA?

A

Inbalance = more pro-inflammatory then anti-inflammatory

47
Q

What are the pro inflammatory cytokines which are important in RA?

A

TNF Alpha
IL-1

48
Q

What are the anti-inflammatory cytokines which are seen in RA?

A

IL-10, IL - 1 receptor antagonist

49
Q

What is the dominant pro-inflammatory cytokine in RA?

A

The cytokine tumour necrosis factor-alpha (TNFα) is the dominant pro-inflammatory cytokine in the rheumatoid synovium

50
Q

How do osteoclasts effect RA?

A

they increase bone resorption and bone erostion

51
Q

How do synoviocytes contribute to RA?

A

increase joint inflammation which leads to painful swelling

52
Q

How do chondrocytes contribute to RA?

A

Lead to cartilage deposition which results in joint space narrowing

53
Q

What is the name of the anti-TNF drugs?

A

infliximab and adalimumab

54
Q

What happens to haemaglobin levels in RA?

A

lowered - this is because the bone marrow gets depressed so haemaglobin is low

55
Q

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

A

Rheumatoid factor and antibodies to citrullinated protein antigens

56
Q

What are rheumatoid factor antibodies?

A

Antibodies which recognise the Fc portion of the IgG as their target antigen = they are typically IgM antibodies

57
Q

What mediates the citrullination of peptides?

A

Peptidyl arginine deiminases (PADs)

58
Q

What causes the citrullination of proteins in the lung epithelium?

A

smoking

59
Q

antibodies to citrullinated peptides are highly specific for…

A

RA

60
Q

What are the radiographic features of RA?

A

Soft tissue swellin
Peri-articular osteopenia
Bony Erosions

61
Q

What are the ultrasound changes which occur in RA?

A

Synovial thickening
Increased blood flow
may detect erosions which are not seen on a plain X ray

62
Q

What are DMARDs?

A

(disease-modifying anti-rheumatic drugs) =
drugs that control the disease process (usually immunosuppressive)

63
Q

What is the first line regime in the treatment of RA?

A

IM or short course of oral steroids
Start combination DMARD therapy (usually Methotrexate + hydroxychloroquine &/or sulfasalazine)

64
Q

What is the second line regime in the treatment of RA?

A

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

65
Q

How do steroids work?

A

Glucocorticoids bind the glucocorticoid receptor (GR)
GR resides in cytoplasm
On binding by glucocorticoids, steroid-GR complex translocates to the nucleus and binds DNA response elements, affecting transcription

66
Q

What is the main bad side effect of glucocorticoids?

A

Cushings

67
Q

What is the key DMARD?

A

Methotrexate

68
Q

How does methotrexate work?

A

Inhibits dihydrofolate reductase (”folate antagonist”)
Immunosuppressive/anti-inflammatory

69
Q

What are the side effects of Methotrexate?

A

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

70
Q

What is the biologic responsible for B cell depletion?

A

Rutiximab - antibody against the B cell antigen, CD20

71
Q

What is the biologic used to block IL-6 signalling?

A

Tocilizumab (RoActemra) – antibody against interleukin-6 receptor.
Sarilumab (Kevzara) – antibody against interleukin-6 receptor.

72
Q

What is psoriatic Arthritis?

A

Psoriasis is an immune-mediated disease affecting the skin
Scaly red plaques on extensor surfaces (eg elbows and knees)

73
Q

What is the dominant pathogenic pathway in psoriatic arthritis?

A

Dominant pathogenic pathway is interleukin-17/interleukin-23
(IL17-IL23)

74
Q

Are rheumatoid factors present in psoratic arthritis?

A

no

75
Q

What is the typical presentation of psoriatic arthritis?

A

Classically asymmetrical arthritis affecting IPJs

76
Q

What are the other possible manifestations of Psoriatic Arthritis?

A

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

77
Q

what is reactive arthritis?

A

Sterile inflammation in joints following infection elsewhere in the body

Common infections is urogenital and gastrointestinal

78
Q

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

A

Enthesitis (tendon inflammation)
Skin inflammation
Eye inflammation

79
Q

What might be the first manifestation of HIV or Hepatitis C infection?

A

Reactive arthritis may be first manifestation of HIV or hepatitis C infection

80
Q

Who is reactive arthritis commonly seen in?

A

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

81
Q

What are the key differences between septic and reactive arthritis?

A

Septic - synovial fluid culture positive, need Abx theapry and joint lavage

reactive - sterile and no Abx, no lavage

82
Q

What is inflammatory spondyloarthritis?

A

Anklosing spondylitis - primary inflammation of the spine and the sacroiliac joints

83
Q

What are the extra-articular manifestations of SpA?

A

Peripheral joints, esp. tendon insertions (entheses), can also be affected
Extra-articular manifestations including anterior uveitis (iritis)

84
Q

What are the three autoimmune causes of RA?

A

Rheumatoid arthritis

Seronegative spondyloarthropathies

Connective tissue disease

85
Q

What is seen on an X ray of a patient with gout?

A

Juxta-articular ‘rat bite’ erosions at MTPJ of great toe

86
Q

What is the treatment for an acute attack of gout?

A

Colchicine - tubulin disruption, less preferred to NSAIDs and steroids

NSAIDs

Steroids

87
Q

What is the management of chronic case of gout?

A

Allopurinol - xanthine oxidase inhibitors reducing production of uric acid in the body

88
Q

In rheumatoid arthritis, what causes the synovium to become pannus?

A

Neovascularisation - growth of new blood vessels

Lymphangiogenesis - new lymphatic vessel formation

Inflammatory cells

Activated B and T cells

Plasma cells

Mast cells

Activated macrophages

89
Q

What is the biological therapy causing B cell depletion?

A

Rituximab - antibody against B cell antigen CD20

90
Q

What are the 2 biological therapies inhibiting IL-6 signalling?

A

Tocilizumab (RoActemra) – antibody against interleukin-6 receptor

Sarilumab (Kevzara) – antibody against interleukin-6

-

91
Q

What are 5 common clinical presentations of AS?

A

Lower back pain + stiffness

Early morning

Improves with exercise

Reduced spinal movements

Peripheral arthritis

Plantar fasciitis, achilles tendonitis

Fatigue

92
Q

What is the relevance of doing a U&E in rheumatological diseases (give examples)?

A

They can affect the kidneys.

E.g. SLE → lupus nephritis; Vasculitis → glomerular nephritis; chronic inflammation in poorly controlled inflammatory disease → high levels of serum amyloid A (SAA) protein → SAA deposits in organs (AA amyloidosis; can happen in the kidneys)

93
Q

Compare the radiographic changes seen in RA and OA.

A

RA: Joint space narrowing, osteopenia and body erosions

OA: Joint space narrowing, Osteophytes and subchondral sclerosis

94
Q

What are osteophytes at the DIPJs and PIPJs termed respectively?

A

DIPJs - Heberden’s nodes

PIPJs - Bouchard’s nodes

95
Q

Which type of arthritis is worse in the morning, and doesn’t generally improve?

A

RA

OA is bad in morning but improves with movement

96
Q

What is the pattern of joint involvement in RA and OA?

A

RA - symmetric, bilateral
OA - random and asymmetric

97
Q

Which are the two most common joints to be effected in RA?

A

PIP and MCP

98
Q

Describe the difference in joint swelling seen in RA and OA?

A

RA - red, hot effusion
OA - bony

BRS 5 Musculoskeletal (13 decks)

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