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BRS > intro to rheumatology > Flashcards

intro to rheumatology Flashcards

1
Q
  • What are the structural and functional classification of fibrous joints?
A

Structural - No space between bones. E.g. sutures in skull, syndesmosis (sheet of connective tissues) in tibia and fibula.

Functional classification - Synarthroses (generally allow no movement) and amphiarthroses (allow very limited movement)
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2
Q
  • What are the structural and functional classification of cartilaginous joints?
A

Structural - Joints in which bone are connected by cartilage. E.g. joints between spinal vertebrae

Functional classification - Synarthroses (generally allow no movement) and amphiarthroses (allow very limited movement)
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3
Q
  • What are the structural and functional classification of synovial joints?
A

Structural classification - Have a space between the adjoining bones (synovial cavity) filled with synovial fluid.

Functional classification - Diarthroses (Allow for free movement)
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4
Q
  • What are the components of a synovial joint and describe each of them?
A

Synovium - 1-3 cell deep lining containing macrophage-like phagocytic cells (type A synoviocyte)

   - fibroblast-like cells that produce hyaluronic acid (type B synoviocyte).
   - Type I collage also present. 

Synovial fluid - Hyaluronic acid-rich viscous fluid. 

Articular cartilage - Type II collagen + Proteoglycan (aggrecan)
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5
Q
  • What is cartilage composed of?

- Describe the blood supply of cartilage and why is this important?

A

Specialised cells → Chondrocytes
ECM: Water, collagen and proteoglycans (mainly aggrecan)

Avascular (no blood supply)
Means that cartilage heals poorly after injury.

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6
Q
  • What is aggrecan and what is it characterised by?
A

Proteoglycan possessing many chondroitan sulphate and keratin sulphate chains

Characterised by ability to interact with hyaluronan (HA) to form large proteoglycans
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7
Q
  • What is arthritis broadly speaking?

- What are the 2 major divisions of arthritis?

A

Disease of joints

    Osteoarthritis (Degenerative arthritis) 
    Inflammatory arthritis (main type is rheumatoid arthritis)
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8
Q
  • What are the pathological changes of osteoarthritis?
A

Cartilage being worn out and bony remodelling

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9
Q
  • Outline the epidemiology and onset of osteoarthritis.
A

Epidemiology - more prevalent as age increases

 - more likely if you've had previous joint trauma
 - people who have jobs involving heavy manual labour are more prone to it. 

Onset - Gradual, slowly progressive disorder.
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10
Q
  • Which joints are affected typically in osteoarthritis?
A

Joints of hand - DIP, PIP, first CMC

Spine

Weight-bearing joints of lower limbs - especially knees and hips, first MTP (metatarsophalangeal joint)
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11
Q
  • What signs and symptoms are associated with osteoarthritis?
A

Joint pain - worse with activity, better with rest

Joint crepitus - creaking, cracking grinding sound on moving affected joint. 

Joint instability (giving way) 

Joint enlargement (e.g. Heberden's and Bouchard's Nodes)

Joint stiffness after immobility 

Limitations of range of motion
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12
Q

What is the difference between Heberden’s and Bouchard’s nodes

A
  1. Heberden’s Nodes → Osteophytes at DIP joints.

2. Bouchard’s Nodes → Osteophytes at PIP joints.

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13
Q
  • List the radiographic features of osteoarthritis.
A

Joint space narrowing

Subchondral bony sclerosis (increased white appearances on xray)

Osteophytes (bone spurs)

Subchondral cysts
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14
Q
  • What are the physiological, cellular and molecular changes that occur in inflammation?
A

Increased blood flow

Migration of WBCs (leucocytes) into tissues

Activation/differentiation of leucocytes 

Cytokine production (E.g. TNF-alpha, IL-1,16 and  17 - Important ones for joint disease)
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15
Q
  • What are the causes of joint inflammation?
A

Infection - Septic arthritis, TB

Crystal arthritis - Gout and pseudo-gout 

Immune-mediated (autoimmune) - Rheumatoid arthritis, psoriatic arthritis, reactive arthritis, SLE
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16
Q
  • What are the causes of joint inflammation?
A

Infection - Septic arthritis, TB

Crystal arthritis - Gout and pseudo-gout 

Immune-mediated (autoimmune) - Rheumatoid arthritis, psoriatic arthritis, reactive arthritis, SLE
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17
Q
  • What causes septic arthritis?

- What are the risk factors of septic arthritis?

A

Bacterial infection of a joint (usually caused by haematogenous spread)

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

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18
Q
  • Why is septic arthritis classified as a medical emergency?
A

Untreated, septic arthritis can rapidly destroy a joint.

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19
Q
  • How many joints are usually affected in septic arthritis?

- What is the main exception?

A

1 (mono-arthritis)

Gonococcal septic arthritis - often affects multiple joints (polyarthritis); it is less likely to cause joint destruction.

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20
Q
  • When should you consider septic arthritis for a patient?
A

Any patient with an acute painful, red, hot swelling of a joint, especially if there is a fever.

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21
Q
  • What technique can you use to diagnose septic arthritis?
A

Joint aspiration (then send sample for urgent gram stain and culture)

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22
Q
  • What bacteria are commonly responsible for septic arthritis?
A

Staphylococcus aureus, Streptococci, Gonococcus

23
Q
  • How can you treat septic arthritis?
A

Surgical wash-out (lavage) and IV antibiotics

antibiotics do not work on their own- penetrate joint and pus poorly
so drainage of joint is needed

24
Q
  • When does crystal arthritis occur?
A

Results when crystals deposit in the joint triggering an inflammatory reaction.

(2 main types → Gout and pseudogout)
25
Q
  • What is gout caused by?

- What is hyperuricaemia?

A

Deposition of urate (uric acid) crystals → Inflammation

High uric acid levels in blood → Risk factor for gout (not everyone who has high levels will have develop attacks of gout)
26
Q
  • What are the causes of hyperuricaemia?
A

Genetic tendency

Increased uptake of purine rich foods (Purine gets broken down into uric acid → Beer drinkers particularly vulnerable).

Reduced excretion (kidney failure) of uric acid

High production of uric acid, purines

Diet high in red meat, shellfish, anchovies, organ meat

Dehydration, alcohol consumption decreases clearance of uric acid

27
Q
  • What is pseudo-gout?

- What are the risk factors of pseudo-gout?

A

Syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystals → Crystals lead to inflammation.

Background osteoarthritis, elderly patients, intercurrent infection.
28
Q
  • What are the clinical features of gout?
A

Typically presents with an acute mono-arthritis- rapid onset. First MTP joint (big toe) is the most commonly affected joint (Podagra)

Other joints affected → joints in foot, ankle, knee, wrist, finger and elbow are most frequently affected. 

Crystal deposits (tophi) developing around hands, feet, elbows and ears. → Yellowish appearance
29
Q
  • What X-ray results indicates Gout?
A

Juxta-articular ‘rat bite’ erosions at MTPJ of the great toe. → Strong indicator of Gout (CA)

30
Q
  • The diagnosis of crystal arthritis is made by aspirating fluid from affected joint and examining under a microscope using polarised light. What would you see for gout and pseudo-gout?
A

Gout - needle-shaped crystals with -ive birefringence.

Pseudo-gout - rhomboid shaped crystals with +ive birefringence.
31
Q
  • What is the most common immune-mediated inflammatory disease and explain what this condition is?
A

Rheumatoid arthritis (RA) - chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis of synovial (diarthroidal) joints.

32
Q

What are the features of chronic arthritis in rheumatoid arthritis?

A
  • Polyarthritis - swelling of small joints of hand and wrists.
    • Symmetrical
    • Early-morning stiffness in and around joints (gradually eases up as patient starts moving); Lasts more than 30 minutes
    May lead to joint damage and destruction - ‘joint erosions’ on radiographs.
33
Q

What are examples of Extra-articular disease in Rheumatoid arthritis

A

Rheumatoid nodules - hard lumps under skin

Other rare e.g. vasculitis, episcleritis (type of inflammation of eye)

34
Q
  • What is the pattern of joint involvement in rheumatoid arthritis and what are the most commonly affected joints?
A 
Symmetrical 
    Polyarthritis 
    Affects small and large joints, but particularly hands and feet.
    Commonest affected joints 
      - MCP 
      - PIP 
      - Wrists 
      - Knees 
      - MTP
35
Q

What may be detected in the blood of those with RA

A

Rheumatoid ‘factor’ may be detected in blood of patients

Autoantibody against IgG
36
Q
  • The primary site of pathology for rheumatoid arthritis is in the synovium (inflammation occurs here). What 3 things does this include?
A

Synovial joints

Tenosynovium surrounding tendons - swelling not over joints or wrist

Bursa (fluid-filled sacs that provide lubrication to allow easy movement)
37
Q
  • What are the common features of rheumatoid arthritis? (not joint based)
A

Common
- Fever, weight loss

  - Subcutaneous nodules
38
Q

What are uncommon extra-articular features of RA

A

Uncommon

  - Vasculitis 
  - Ocular inflammation - episcleritis 
  - Neuropathies 
  - Amyloidosis 
  - Lung disease - nodules, fibrosis, pleuritis (inflammation of pleura which are the lining of the lungs) 
  - Felty's Syndrome - triad of splenomegaly, leukopenia and RA
39
Q

What is the clinical significance of Rheumatoid Nodules?

A

Ulnar border of forearm is a typical position where these might be detected

Presence confirms diagnosis of rheumatoid arthritis as it is invariably associated with rheumatoid factor.

40
Q
  • Describe a healthy synovial membrane?

- What is its function?

A

1-3 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.
41
Q
  • In the rheumatoid arthritis the synovium becomes a proliferated mass of tissue (pannus) due to what?
A

Neovascularisation - formation of blood vessels

Lymphangiogenesis - formation of lymph vessels 

Inflammatory cells → activated B and T cells, plasma cells, mast cells and activated macrophages. (There is an excess of pro-inflammatory vs. anti-inflammatory cytokines (CYTOKINE IMBALANCE)
42
Q
  • What cytokine is the dominant pro-inflammatory cytokine in the rheumatoid synovium?
  • What does this cytokine do that causes a person to develop rheumatoid arthritis?
A

TNF-alpha

TNF-alpha has an affect on multiple process contributing to inflammatory response and destruction of the joint in the long term.

  • such as increase in cytokines
  • increase in chemokines
  • angiogenesis
  • osteoclast activating
  • chondrocyte activation
43
Q
  • How is inhibition of TNF- alpha cytokine achieved?
A

Through parenteral administration (most commonly sub cutaneous injection) of either antibodies or fusion proteins.

44
Q
  • What are the 2 types of autoantibodies that are found in blood of patients with rheumatoid arthritis and explain their mechanisms?

.

A

Antibodies to citrullinated protein antigens (ACPA)

 - ACPAs are highly specific for rheumatoid arthritis (Anti-cyclic citrullinated peptide antibody - anti-CCP Ab)
 - Citrullination is mediated by enzymes termed peptidyl arginine deaminase (PADs). Convert arginine to citrulline

Rheumatoid factor 

 - Antibodies that recognise the Fc portion of IgG as their target antigen. 
 - Typically IgM antibodies i.e. IgM anti-IgG antibody.
45
Q
  • What is the overall treatment goal for rheumatoid arthritis and what does this goal therefore require?
A

Treatment goal - Prevent joint damage.

This requires early recognition of symptoms and referral from GP to a rheumatologist, prompt initiation of treatment (joint destruction gets worse with time) and AGGRESSIVE treatment to suppress inflammation.
46
Q
  • What is the difference between the causes of joint space narrowing in rheumatoid and osteoarthritis?
A

In osteoarthritis this is the primary abnormality whereas in rheumatoid arthritis it is caused by secondary damage due to synovitis.

47
Q
  • What is psoriatic arthritis?
  • Are rheumatoid factors present in patients with psoriatic arthritis?
  • What is the classical clinical presentation of psoriatic arthritis?
A

Autoimmune disease affecting skin (scaly red plaques on extensor surfaces)

No; they are seronegative 

Classically asymmetrical arthritis affecting IPJs
48
Q
  • What else can psoriatic arthritis manifest as other than the classical presentation?
A

Symmetrical involvement of small joints (rheumatoid pattern)

Spine and sacroiliac joint inflammation 

Oligoarthritis of large joints 

Arthritis mutilans
49
Q
  • What is reactive arthritis?
A

Sterile inflammation in joints following injection especially urogenital (e.g. Chlamydia trachomatis) and GI (salmonella, Shigella, Campylobacter infections)

50
Q
  • What are the important extra-articular manifestations of reactive arthritis?
A

Enthesitis (another form of tendon inflammation)

Skin inflammation 

Eye inflammation
51
Q
  • Reactive arthritis may be the first manifestation of what 2 infections?
A

HIV and Hep-C infection

52
Q
  • How long do symptoms follow for reactive arthritis after infection?
A

1-4 weeks after infection

53
Q
  • What is SLE?
A

Multi-system autoimmune disease. Autoantibodies are directed against components of the cell nucleus (nucleic acids and proteins).

Can affect almost any organ - often joints (get pain), skin, kidneys, haematology, lungs and CNS.
54
Q
  • What are the clinical tests for SLE?
A

Antinuclear antibodies (ANA) - high sensitivity for SLE but not specific. Negative test rules out SLE, but positive doesn’t mean patient has SLE.

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

BRS (41 decks)

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