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BRS 1b > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Which type of macrophages reside within the synovium?

A

Type A synoviocytes

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2
Q

Which cells produce hyaluronic acid within the synovium?

A

Fibroblast-like cells (Type B)

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3
Q

Which extracellular matrix protein is prevalent within the synovial fluid?

A

Hyaluronic acid

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4
Q

Which proteoglycan predominates within the articular cartilage?

A

Aggrecan

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5
Q

Name an example of degenerative arthritis?

A

Osteoarthritis

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6
Q

What is inflammation?

A

Inflammation is a physiological process in response to alleviate injury or infection. An excessive/inappropriate inflammatory reaction can be deleterious to the host

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7
Q

What are the 5 features of inflammation?

A 
Red (Rubor)
Pain (Dolor)
Hot (Calor)
Swelling (Tumour)
Loss of function (Functio Laesio)
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8
Q

In response to an infection/injury what role doe pro-inflammatory mediators and cytokines have?

A

Increase vascular flow and inflammatory cell recruitment in tissue

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9
Q

Which cytokines are released during inflammation?

A

• TNF-alpha, IL-I, IL-6, IL-17.

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10
Q

What type of crystals form in gout?

A

urate crystals

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11
Q

What is gout?

A

Gout is a syndrome characterised by hyperuricaemia and deposition of urate crystals - Acute flares of inflammatory arthritis.
• Tophi around the joints and potential joint destruction
• Affects the first toe (podagra), foot, ankle, knee, fingers, wrist and elbow.

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12
Q

What are the manifestations of gout?

A

Tophi around the joints and potential joint destruction

Affects the first toe (Podagra), foot, ankle, knee, fingers, wrist and elbow

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13
Q

What is podagra?

A

Gout affecting the first toe

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14
Q

Which type of foods result in an increased risk in developing gout?

A

Purine rich foods

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15
Q

What are the three main causes for gout?

A 
Genetic tendency 
Increased intake of purine rich foods
Reduced excretion (Kidney failure)
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16
Q

How do gout crystals triggers an acute inflammatory response?

A

Interact with undifferentiated phagocytes within the joint, releasing TNF-alpha and iL-8 (Neutrophil chemoattractant)

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17
Q

Which chemoattractant molecule is responsible for the recruitment of neutrophils in gout?

A

IL-8 causing neutrophilic synovitis

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18
Q

Which immune cell is associated with gout synotivits?

A

neutrophil

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19
Q

What are the symptoms of gout?

A

• Rapid onset severe pain (10+ severity)
• Joint stiffness
• Joint red, warm, swollen and tender
• Tophi – Aggregated deposits of urate monosodium urate crystals
• Foot joint distribution (Metatarsophalangeal joint)
• Swelling and joint effusion
• Gouty arthritis
N.B: Resolves spontaneously over 3-10 days.

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20
Q

How severe is gout pain?

A

10+ severity

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21
Q

What are tophi?

A

Aggregated deposits of urate monosodium urate crystals

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22
Q

How quickly does gout resolve?

A

Resolves spontaneously within 3-10 days.

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23
Q

Which crystals are associated with psuedogout?

A

Calcium pyrophosphate crystals within the joint space

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24
Q

What are the risk factors for developing pseudogiout?

A

Background osteoarthritis
Elderly patients
intercurrent infection

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25
Q

What types of erosions are seen in patients with pseduogout?

A

Rat bite erosions

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26
Q

What are the first line investigations for gout?

A

Arthrocentesis with synovial fluid analysis (joint aspiration)

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27
Q

What WBC is expected in patients with gout?

A

WBC > 2 x 10^9/L

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28
Q

How are crystals detected in gout?

A

Polarising light microscopy to detect crystals

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29
Q

What happens to synovial fluid samples?

A

Examined for patients - rapid gram stain followed by culture and antibiotic sensitivity assays

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30
Q

What shaped crystals are gout?

A

Needle shaped

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31
Q

What shaped crystals are found in pseudogout?

A

brick-shaped

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32
Q

What are the birefringence of gout crystals?

A

Negative

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33
Q

What are the birefringence of pseudogout crystals?

A

Positive

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34
Q

What is rheumatoid arthritis?

A

Rheumatoid arthritis is a chronic autoimmune condition that manifests as pain, stiffness, and symmetrical synovitis (inflammation of the synovial membrane) of synovial (diarthrodial) joints.
• Inflamed synovial membrane
• Increased angiogenesis (neovascularisation)
• Cellular hyperplasia
• Influx of inflammatory cells (Activated B & T cells, plasma cells, mast cells and activated macrophages)  Invade the synovial lining.

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35
Q

Which cytokines are prevalent within rheumatoid arthritis?

A

TNF-alpha
IL-1
IL-6

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36
Q

What is the function of the synovial membrane?

A

To include the maintenance of the synovial fluid, the hyaluronate rich viscous fluid within the joint soace

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37
Q

What is the dominant pro-inflammatory cytokine found within the rheumatoid synovium?

38
Q

The inhibition of TNF-alpha, results in the blockage of which cytokines?

A

IL-1, IL-6 and IL-8

GM-CSF

39
Q

Which cells produce TNF-alpha?

A

Macrophages

40
Q

What is polyarthritis?

A

Polyarthritis: Swelling of the small joints of the hand and wrists (MCP, PIPs and MTP joints).

41
Q

What are the presentations of chronic rheumatoid arthritis?

A 
Polyarthritis
Symmetrical pattern
Early morning stiffness in and around joints
Joint erosions on radiography 
Ulnar deviation
42
Q

Why does ulnar deviation occur in rheumatoid arthritis?

A

Due to inflammation of the MCP joints, causes the fingers to become dislocated. As the tendons pull on the dislocated joints, the fingers tend to drift towards the ulnar side.

43
Q

Where are rheumatoid nodules typically seen?

A

On the extensor surfaces of tendons

44
Q

What are the cutaneous manifestations of vasculitis?

A

Palpable purpura

45
Q

Which eye inflammatory dysfunction is seen in rheumatoid?

A

Episcleritis

46
Q

Which factor is seen in the serum for patients with Rheumatoid arthritis?

A

Rheumatoid factor

47
Q

what is rheumatoid factor?

A

An autoantibody against IgG

48
Q

What joints are commonly affected in RA?

A 
MCPs
PIPs
Wrists
Knees
Ankles
MTP
49
Q

What is extensor tenosynovitis?

A

note swelling is not above either the wrist or MCP joints.
-Patient has incomplete extension of the little and ring fingers (cannot stick the fingers straight) – consistent with extensor damage by the tenosynovitis.

50
Q

What are the common extra-articular feature seem in rheumatoid arthritis?

A

Fever
Weight loss
Subcutaneous nodules: Central area of fibrinoid necrosis surrounded by histocytes and peripheral layer of connective tissue

51
Q

What are subcutaneous noduels?

A

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

52
Q

What are the uncommon extra-articular features found in rheumatoid arthritis?

A
  • Vasculitis – Small vessel disease with characteristic palpable purpura.
  • Ocular inflammation e.g episcleritis
  • Neuropathies
  • Amyloidosis
  • Lung disease – nodules, fibrosis, pleuritis.
  • Felt’s syndrome – Triad of splenomegaly, leukopenia and rheumatoid arthritis.
53
Q

What is Felt’s Syndrome?

A

Triad of splenomegaly, leukopenia and rheumatoid arthritis

54
Q

Which autoantibodies are found in rheumatoid arthritis?

A

Rheumatoid factor

Anti-CCP

55
Q

What is rheumatoid factor?

A

Antibodies that recognise the Fc region of IgG as their target antigen

56
Q

What are anti-ccp antibodies?

A

Antibodies to citrullinated peptides are highly specific for rheumatoid arthritis

57
Q

Citrullination of peptides is mediated by which enzymes?

A

Peptidyl arginine deiminases (PADs)

58
Q

What is the treatment goal for rheumatoid arthritis?

A

Prevent joint pain

59
Q

What is the first line drug treatment for patients with rheumatoid arthritis?

A

Methotrexate in combinations with hydroxychloroquine or sulfasalazine

60
Q

What type of drug is methotrexate?

A

A disease modifying anti rheumatic drug

61
Q

What are the 2nd line treatment for rheumatoid arthritis?

A

Biological therapies

-Janus kinase inhibitors

62
Q

What is the purpose of glucocorticoid therapy in patients with rheumatoid arthritis?

A

Short term relief for acute exacerbation, howevere, avoid long-term use due to side effects

63
Q

What are the four methods of biological therapies in rheumatoid arthritis?

A

Inhibition of tumour necrosis factor (Anti-TNF-alpha)
B-cell depletion
Modulation of T-cell co stimulation
Inhibition of interleukin- signalling

64
Q

What is the function of inflixmab?

A

Antibodies targeted against anti-TNF-Alpha

65
Q

What is the function of rituixmab?

A

An antibody targeted against the B-cell antigen, CD20

66
Q

What is the function of abatacept fusion protein?

A

Abatacept- fusion protein – extracellular domain of human cytotoxic T-lymphocyte associated antigen 4 (CTLA-4) linked to modified Fc (hinge, CH2, and H3 domains) of human immunoglobulin G1.

67
Q

What is ankylosing spondylitis?

A

Seronegative spondyloarthropathy - no positive autoantibodies

68
Q

Are autoantibodies found in ankylosing spondylitis??

69
Q

What is the consequence of ankylosing spondylitis?

A

Spinal fusion

70
Q

What is ankylosis?

A

Spinal fusion

71
Q

What is the common demographic of ankylosing spondylitis?

A

20-30 years. Male

72
Q

which gene is associated with ankylosing spondylitis?

A

HLA-B27 gene

73
Q

what are the clinical presentations of ankylosing spondylitis?

A 
Lower back pain, and stiffness
Early morning and improves with exercise (chronic back pain for more than 3 months)
Reduced spinal movements
Peripheral arthritis
Plantar fasciits, Achilles tendonitis
Fatigue
74
Q

What is visible in patients with ankylosing spondylitis (posture)?

A

Hyperextended neck
Loss of lumbar lordosis
Flexed hips and knees

75
Q

What investigations are conducted in patients with ankylosing spondylitis?

A

Normocytic anaemia
Raised CRP, ESR
HLA-B27

76
Q

What is the management for ankylosing spondylitis?

A

Physiotherapy
Exercise regimes
NSAIDs
DMARDs - peripheral joint disease

77
Q

What imaging is conducted in patients with ankylosing spondylitis?

A

X-rays

MRIs

78
Q

What abnormal manifestations are seen in patients with ankylosing spondylitis?

A
  • Squaring Vertebral bodies, Romanus lesions
  • Erosion, sclerosis, narrow SIJ
  • Bamboo spine
  • Bone marrow oedema
79
Q

What is psoriatic arthritis?

A

Psoriasis is an autoimmune disease affecting the skin (scaly red plaques on extensor surfaces – elbows & knees).
• ~10% of psoriasis patients also have joint inflammation
• Unlike RA, rheumatoid factors are not present (seronegative).
Classically asymmetrical arthritis affecting IPJs.

80
Q

Are there any auto-antibodies associated with psoriatic arthritis?

A

seronegative, therefore no

81
Q

Which joints are mainly affected in psoriatic arthritis?

A

Sacro-illiac joints

IPJs

82
Q

What are the manifestations of psoriatic arthritis?

A
  • Symmetrical involvement of small joints (Rheumatoid pattern)
  • Spinal and sacroiliac inflammation
  • Oligoarhtiris of large joints
  • Arthritis mutilans
83
Q

What distinctive X-ray finding is found in psoriatic arthritis?

A

Pencil in cup deformity

84
Q

What is the management for psoriatic arthritis?

A

DMARDs- methotrexate

85
Q

What is reactive arthritis?

A

Sterile inflammation in joints following infection, especially urogenital, and gastrointestinal

86
Q

What are the extra-articular manifestations of reactive arthritis?

A

Enthesis (tendon inflammation)
skin inflammation
eye inflammation

87
Q

What immunocompromised disease is associated with reactive arthritis?

A

HIV or hepatitis C

88
Q

Which gene is associated with reactive arthritis?

89
Q

what is SLE?

A

Lupus = A multi-system autoimmune disease manifesting as multi-site inflammation that affects a number of organs.
• Associated with auto-antibodies -directed against components of the cell nucleus (nucleic acids and proteins).

90
Q

What autoantibodies are associated with SLE?

A

• Antinuclear antibodies (ANA) – high sensitivity for SLE but not specific.
A negative test rules out SLE, but a positive test does not diagnose SLE.

  • Anti-double stranded DNA antibodies (Anti-dsDNA Abs)
  • High specific for SLE in the context of the appropriate clinical signs.

BRS 1b (62 decks)

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