Intro To Rheum P2 Flashcards

1
Q

What are the two ways you can classify joint?

A

Either by structure or function

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2
Q

What are the three different types of joints using structural classification?

A

Fibrous joints
Cartilaginous joints
Synovial joints

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3
Q

What are fibrous joints?

A

No space between the bones for example sutures in the skull

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4
Q

What are cartilaginous joints and an example?

A

Joints in which the bones are connected by cartilage such as in the spine

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5
Q

What are synovial joints and an example?

A

Joints Which have a space between the adjoining bones and the space is filled with synovial Fluid
E.g knees

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6
Q

What 3 categories can joints be classified into based of function?

A

Synarthroses (no movement)
Amphiarthroses (limited movement)
Diarthroses(free movement)

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7
Q

What does Synarthroses mean?

A

No movement joints

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8
Q

What does Amphiarthroses mean?

A

Limited movement of joints

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9
Q

What does Diarthroses mean?

A

Free movement of the joint

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10
Q

What is this?

A

Synovium membrane

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11
Q

What is this?

A

Articular cartilage

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12
Q

What is this?

A

Joint cavity containing synovial fluid

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13
Q

What does the Synovium contain

A

Type one collagen
Type A &B synoviocytes

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14
Q

What does articular cartilage contain?

A

Type 2 collagen
Aggrecan

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15
Q

What is cartilage composed of?

A

Chondrocytes and extracellular matrix

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16
Q

What is the most relevant proteoglycan present in Cartilage?

A

Aggrecan

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17
Q

What are the three main categories of autoimmune arthritis?

A

Rheumatoid arthritis
Seronegative arthritis
lupus and related disorders

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18
Q

What extra articular diseases can occur in rheumatoid arthritis?

A

Subcutaneous nodules
Lung disease
Ocular inflammation
Vasculitis
Neuropathies
Felty’s syndrome

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19
Q

What does this image show and what condition shows this feature?

A

Episcleritis seen in rheumatoid arthritis

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20
Q

What is feltys syndrome?

A

A rare condition characterised by the triad of splenomegaly, leukopenia and RA

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21
Q

What is splenomegaly?

A

Enlarged spleen

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22
Q

What does this image show?

A

Rheumatoid/subcutaneous nodules

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23
Q

What do subcutaneous/rheumatoid nodules contain?

A

Central area of fibrinoid necrosis (dead tissue) surrounded by histiocytes (macrophages)

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24
Q

Describe the pathogenesis of rheumatoid arthritis?

A
  • in RA, elevated TNF- alpha levels
  • causes neovascularisation lymphangiogenesis + production of inflammatory cells
  • Synovium = inflamed
  • It proliferates it form a mass of tissue = pannus 
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25
Q

What factors cause the synovium to proliferate and form a pannus?

A

Neovascularisation (in growth of new blood vessels)
Lymph angiogenesis
Inflammatory cells

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26
Q

What is the dominant cytokine in rheumatoid arthritis?

A

TNFa (tumour necrosis factor -alpha)

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27
Q

What does TNF-a do in RA?

A

Bone erosion
Pain,joint swelling
Joint space narrowing

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28
Q

What would the blood test findings be in a px with RA (Hb, MCV, WCC, PLT, ESR, CRP)?

A
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29
Q

What 2 auto antibodies are seen in RA?

A

Rheumatoid factor
Antibodies to citrullinated proteins antigens (ACPA)

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30
Q

How do we detect rheumatoid factor?

A

Use IgM antibodies against that recognise the Fc portion of IgG (autoantibody)
Essentially use an antibody against an antibody

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31
Q

Why is the presence of rheumatoid factor only indicative of rheumatoid arthritis not diagnostic?

A

Has a very low specificity
If px has negative result def doesn’t have RA
BUT if has positive, may not necessarily have it

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32
Q

What is citrullination? 

A

A type of post-transcriptional modification where AA arginine is converted into AA citrulline

33
Q

What enzyme mediates the citrullination of peptides?

A

Peptidyl arginine deiminases

34
Q

Why is the presence of CCP a useful marker of RA?

A

It’s highly specific, hence if you have it you are very likely to have rheumatoid arthritis

35
Q

What 3 imaging techniques can you do in RA?

A

X-ray
Ultrasound
MRI

36
Q

How useful are X rays in diagnosing RA?

A

Can only see severe forms of RA with X Ray
Harder to pick up early stages of RA

37
Q

How useful is an ultrasound detecting rheumatoid arthritis?

A

V good at picking up earlier stages of condition
Can see:
Synovial hypertrophy, Increased blood flow and erosions

38
Q

What is a Doppler signal and how does this relate to RA?

A

Shows blood flow through tissue during ultrasound. Seen in early stages of RA

39
Q

What are the 3 main groups of medication RA patients can use?

A

Glucocorticoids (steroids)
NSAIDs
DMARDS (disease modifying anti rheumatic drugs)

40
Q

Why are steroids used in rheumatoid arthritis?

A

Reduce inflammation but only used in short term

41
Q

Why are steroids only used in the short term and what major condition can it lead to?

A

Have really bad side effects such as Cushing syndrome

42
Q

What is the 1st line treatment regime of RA

A

short course of steroids
DMARD (methotrexate & another one)

43
Q

What is the main DMARD used in RA?

A

methotrexate

44
Q

How does methotrexate work?

A

Inhibits dihydrofolate reductase
Is immunosuppressive

45
Q

What is the 2nd line treatment regime for RA

A

biologicals such as anti-TNF-a

46
Q

What do DMARDS tend to be

A

Immunosuppressive

47
Q

What are biological therapies?

A

Proteins (usually antibodies) that specifically target a protein such as an inflammatory cytokine

48
Q

What are 4 things biological therapies can target to treat RA?

A
  1. Inhibit TNF-a
  2. Deplete B cell
  3. Modulation of T cell costimulation
  4. Inhibit IL-6 signalling
49
Q

What does the ‘seronegative’ mean in seronegative arthritis?

A

Blood doesn’t have rheumatoid factor or CCP, but patient still has arthritis

50
Q

What is psoriatic athritis?

A

Arthritis that occurs when you have psoriasis

51
Q

Is rheumatoid factor present in psoriatic arthritis?

A

No - it’s a seronegative arthritis

52
Q

What are some of the clinical presentations of psoriatic arthritis?

A

Varied clinical presentations, but classically asymmetrical arthritis affecting interphalangeal joints

53
Q

What is reactive arthritis?

A

Sterile inflammation in joints following infection elsewhere in the body

54
Q

What are the common infections that cause reactive arthritis?

A

Urogenital
Gastrointestinal
HIV
Hep C

55
Q

What are some important extra-articular manifestations of reactive arthritis?

A

Enthesitis (tendon inflammation)
Skin inflammation
Eye inflammation

56
Q

What type of arthritis is seen as a manifestation of HIV or HEP C infection?

A

Reactive arthritis

57
Q

Which HLA makes you more predisposed to reactive arthritis?

A

HLA -B27

58
Q

How long after infection does reactive arthritis symptoms begin to show?

A

1-4 weeks post infection

59
Q

What is inflammatory spondyloarthritis?

A

Inflammation of spine and sacroiliac joints
Peripheral joints such as entheses an also be affected

60
Q

What is a classical example of inflammatory spondyloarthritis?

A

Ankylosing spondylitis

61
Q

What are the the extra articular manifestations of inflammatory spondyloarthritis? (4 A’s)

A

Anterior uveitis
Apical lung fibrosis
Aortitis
Amyloidosis

62
Q

What does this image show and which type of arthritis is this seen in?

A

Anterior uveitis
Seen in inflammatory spondyloarthritis

63
Q

What is ankylosing spondylitis characterised by?

A

Enthesitis (inflammation of the entheses - where tendon/ligament join to bone)

64
Q

Which HLA gene is strongly associated with ankylosing spondylitis?

A

HLA-B27

65
Q

What 3 cytokines have a key role in the pathophysiology of ankylosing spondylitis?

A

TNF-A
IL-17
IL-23

66
Q

What is a key clinical feature of ankylosing spondylitis?

A

Loss of spinal movement

67
Q

What happens if ankylosing spondylitis is left untreated

A

Spinal Enthesitis -> bone growths between vertebrae -> spinal fusion -> loss of spinal movement

68
Q

What sign does this MRI show and what condition is this ?

A

Shiny corners - seen in ankylosing spondylitis

69
Q

How is ankylosing spondylitis managed?

A

Combination of physiotherapy and
Pharmolologicals

70
Q

What are the 1st line drugs used in ankylosing spondylitis?

A

NSAIDS

71
Q

what is the mechanism of action of NSAIDS

A

inhibits COX 1 &2 hence inhibits prostaglandin production, reducing inflammation and pain

72
Q

What are some key side effects of NSAIDS

A

Peptic ulcers and asthma exacerbation

73
Q

Why is asthma exacerbated by NSAIDS.?

A

As NSAIDs inhibit conversation of arachidonic acid into prostaglandins, more arachidonic acid is converted into leukotrienes which causes bronchoconstriction

74
Q

What is the 2nd line treatment option for ankylosing spondylitis?

A

Biological therapies

75
Q

What are the biological therapies used in treating ankylosing spondylitis ?

A

Monoclonal antibodies
Anti-TNF-A
Anti-IL17

76
Q

What is lupus (sle)

A

A multi-system autoimmune disease

77
Q

Which organ is particularly affected by SLE?

A

Kidneys, leads to renal failure

78
Q

What clinical tests can be used to diagnose SLE

A

usually detect autoantibodies such as:
Antinuclear antibodies
Anti double stranded DNA antibodies

79
Q

What type of rash is this and in which condition do you commonly see this in?

A

Malar/ butterfly rash seen in SLE