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Z Year 2 BRS MSK > Introduction to Rheumatology > Flashcards

Introduction to Rheumatology Flashcards

1
Q

What is rheumatology?

A

medical specialty dealing with diseases of the musculoskeletal system

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2
Q

What are joints?

A

where 2 bone meets

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3
Q

What are tendons?

A

cords of strong fibrous collagen tissue attaching muscle to bone

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4
Q

What are ligaments?

A

flexible fibrous connective tissue which connect two bones

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5
Q

What are the components of a synovial joint?

A
  1. Bone
  2. Joint cavity containing synovial fluid
  3. Articular carilage
  4. Bone
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6
Q

What is synovium?

A
  1. 1-3 cell deep lining containing macrophage-like phagocytic cells (type A synoviocyte) and fibroblast-like cells that produce hyaluronic acid (type B synoviocyte)
  2. Type I collagen
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7
Q

What is synovial fluid?

A

Hyaluronic acid-rich viscous fluid

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8
Q

What is articular cartilage?

A
  1. Type II collagen

2. Proteoglycan (aggrecan)

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9
Q

What is arthritis?

A

disease of the joints

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10
Q

What are the two main divisions of arthritis?

A
  1. Osteoarthritis (degenerative arthritis)

2. Inflammatory arthritis (main type rheumatoid)

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11
Q

What is inflammation?

A
  • a physiological response to deal with injury or infection

- aexcessive/inappropriate inflammatory reactions can damage the host tissues

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12
Q

How does inflammation manifest?

A
  1. RED (rubor)
  2. PAIN (dolor)
  3. HOT (calor)
  4. SWELLING (tumor)
  5. LOSS OF FUNCTION
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13
Q

What are the Physiological, cellular and molecular changes in inflammation?

A
  1. Increased blood flow
  2. Migration of white blood cells (leucocytes) into the tissues
  3. Activation/differentiation of leucocytes
  4. Cytokine production
    E.g. TNF-alpha, IL1, IL6, IL17
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14
Q

What are the causes of joint inflammation?

A
  1. Crystal arthritis
  2. Immune mediated (“autoimmune”)
  3. Infection
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15
Q

What are examples of crystal arthritis?

A
  1. Gout

2. Pseudogout

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16
Q

What are the examples of immune-mediated joint inflammation?

A

E.g.

  1. Rheumatoid arthritis
  2. Seronegative spondyloarthropathies
  3. Connective tissue diseases
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17
Q

What are examples of infection that causes joint inflammation?

A
  1. Septic arthritis

2. Tuberculosis

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18
Q

What is gout?

A

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

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19
Q

What is a high risk factor for gout?

A

High uric acid levels (hyperuricaemia)

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20
Q

What are the causes of hyperuricaemia?

A
  1. Genetic tendency
  2. Increased intake of purine rich foods
  3. Reduced excretion (kidney failure)
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21
Q

What is pseudogout?

A

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

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22
Q

What are the risk factors of pseudogout?

A
  1. background osteoarthritis
  2. elderly patients
  3. intercurrent infection
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23
Q

What is a good example of arthritis?

A

acute gout

24
Q

What does a disease in which tissue deposition of monosodium urate (MSU) crystals occurs as a result of hyperuricaemia and lead to?

A
  • Gouty arthritis

* Tophi (aggregated deposits of MSU in tissue)

25
Q

What does gouty arthritis usually affect?

A

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

26
Q

What are the symptoms of gouty arthritis?

A
  • Abrupt onset
  • Extremely painful
  • Joint red, warm, swollen and tender
27
Q

When does gout resolve?

A

spontaneously over 3-10 days

28
Q

What are the investigations for gout?

A

oint aspiration – synovial fluid analysis

29
Q

What is the management for an acute attack of gout?

A

colcihine, NSAIDs, Steroids

30
Q

What is the management for chronic gout?

A

allopurinol

31
Q

How is synovial fluid examined?

A
  1. Rapid Gram stain followed by culture and antibiotic sensitivity assays
  2. Polarising light microscopy to detect crystals which can be seen in arthritis due to gout or pseudogu
32
Q

What is the crystal like the the synovial fluid of gout and psuedogout?

A
  • gout: urate

- pseudogout: CPPD

33
Q

What is the shape like the the synovial fluid of gout and psuedogout?

A
  • gout: needle

- pseudogout: brick shaped

34
Q

What is the birefringence (polarizing light microscopy) l like the the synovial fluid of gout and psuedogout?

A
  • gout: negative

- pseudogout: positive

35
Q

What is the most common form of immune mediated inflammatory joint disease?

A

rheumatoid arthritis (RA)

36
Q

What is RA?

A

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

37
Q

What happen to the synovium in rheumatoid arthritis?

A

a proliferated mass of tissue (pannus)

38
Q

Why does the synovium change?

A
  1. Neovascularisation
  2. Lymphangiogenesis
  3. Inflammatory cells:
39
Q

What inflammatory cells are involved in RA?

A
  1. activated B and T cells
  2. plasma cells
  3. mast cells
  4. activated macrophages
40
Q

How are these changes to synovium in RA controlled?

A
  1. Recruitment, activation and effector functions of these cells is controlled by a cytokine network
  2. There is an excess of pro-inflammatory vs. anti-inflammatory cytokines (‘cytokine imbalance’)
41
Q

What is in a healthy synovial membrane?

A
  • 1-3 cell layer than lines synovial joints

- contains macrophage-like (type A synoviocyte) and fibroblast-like (type B synoviocyte) cells and type 1 collagen

42
Q

What is the function of a healthy synovial membrane

A
  • Maintenance of the synovial fluid

- the hyaluronate rich viscous fluid within joint space

43
Q

What does TNF alpha do in RA?

A

detrimental role

44
Q

How is RA controlled?

A

TNF alpha inhibitors

45
Q

How is TNF alpha inhibition achieved?

A

parenteral administration (most commonly sub-cutaneous injection) of antibodies or fusion proteins

46
Q

What is the dominant pro-inflammatory cytokine in Rheumatoid synovium?

A

cytokine tumour necrosis factor-alpha (TNF alpha)

47
Q

What does TNF alpha come from?

A

activated macrophage

48
Q

What does TNF alpha do?

A
  1. Pro-inflammatory cytokine release (including Il-1, Il-6, Il-23 and GM-CSF)
  2. Hepicidin induction: acute phase response
  3. PGE2 production
  4. Osteoclast activation: bone resorption
  5. Chonrdocyte activation:
    - metalloproteinase production
    - cartilage destruction
  6. Angiogenesis
  7. Leukocyte accumulation: induction/maintenance of HLA class II expression
  8. Endothelial cell activation: upregulation of E-selectin and VCAM-1, Leukocyte accumulation
  9. Chemokine release (including RANTES, MCP-1, IL-8 and SDF-1, leukocyte acitvation)
49
Q

When are the key features of RA chronic arthritis?

A
  1. Polyarthritis - swelling of the small joints of the hand and wrists is common
  2. Symmetrical
  3. Early morning stiffness in and around joints
  4. May lead to joint damage and destruction - ‘joint erosions’ on radiographs
50
Q

When can extra-articular disease can occur?

A
  • Rheumatoid nodules

* Others rare e.g. vasculitis, episcleritis

51
Q

How can rheumatoid ‘factor’ be detected in blood?

A

Autoantibody against IgG - should really call this rheumatoid ‘antibody’ not ‘factor’

52
Q

What is the pattern of joint involvement in RA?

A
  1. Symmetrical
  2. Affects multiple joints (polyarthritis)
  3. Affects small and large joints, but particularly hands and feet
53
Q

What is commonest affected joint in RA?

A
  1. Metacarpophalangeal joints (MCP)
  2. Proximal interphalangeal joints (PIP)
  3. Wrists
  4. Knees
  5. Ankles
  6. Metatarsophalangeal joints (MTP)
54
Q

Where is the primary site of pathology in RA?

A

In the synovium

55
Q

What does the synovium include?

A
  1. synovial joints
  2. tenosynovium surrounding tendons
  3. bursa
56
Q

What synovial joints are affected in RA?

A

proximal inter-phalangeal joint synovitis

Z Year 2 BRS MSK (18 decks)

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