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Inflammatory arthritis Flashcards

1
Q

What is the definition of rheumatoid arthitis?

A

Insidious (v slow onset so as not be noticed), symmetrical arthritis, with swollen and painful joints > 6 weeks

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2
Q

Autoimmune rheumatic diseases - name 6

A 
RA
Seronegative spondylo-arthropaties
Chronic arthritis in childre
SLE
Systemic sclerosis
Sjogren's syndrome
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3
Q

RA - female:male ratio?

A

3:1

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4
Q

What age does RA normally begin?

A

20-50

Generally young adults. Premenopausal women.

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5
Q

What is the evidence for the immune system’s role in RF

A

Identification of RF (an anti IgG AB present in >80% patients). Most of these ABs are IgM subtype. High levels of RF associated with RA.

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6
Q

How is FR linked to prognosis?

A

High elves of FR = worse prognosis

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7
Q

Other than RF, what else is normally raise in RA?

A

Anti - CCP

Inflammation signs - raised ESR, CRP, (platelets)

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8
Q

What is anchor treatment for RA?

A

Methotrexate

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9
Q

Consider sensitivity and specificity re. RF vs anti-CCP

A

Anti-CCP is v specific (if you have it, you definitely have RA), but less sensitive (found in 60% patients, while 75% patients with RA have RF present)

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10
Q

4 hand deformities associated with RA?

A

Swan neck deformity (finger - DIP hyperflexed, PIP hyperextended)
Boutonnier (DIP hyperextended, PIP flexed)
Z thumbs
Ulnar deviation

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11
Q

What is a clinical skin feature of RA? NB - v rare

A

Vasculitic lesions

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12
Q

Clinical eye feature of RA?

A

Scleritis/uveitis

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13
Q

Lung feature of RA? (4)

A

Fibrosing alveolitis
Effusions
Pleuritis
Caplan’s syndrome - occurs when there is: RA + pneumoconiosis (occupational restrictive lung disease) = intrapulmonary nodules

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14
Q

What can be found on the bony prominences in RA?

A

Rheumatoid nodules (inflammatory granulomatous lesions, espec subcutaneous)

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15
Q

Where else can rheumatoid nodules occur? (not on bony prominences)

A

Lung pleura (Caplan’s?)

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16
Q

What time of day is RA stiffness worst?

A

Morning

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17
Q

Which joints are most commonly affected in RA (pain and swelling)?

A

MCP, POP, MTP, wrists, ankles, elbows.

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18
Q

Disorder of the blood associated with RA?

A

Vasculitis

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19
Q

XR features of RA?

A

Erosion at the margins of a joint
Bone not covered by cartilage
Decr joint space
Soft tissue inflammation

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20
Q

High percentage of RA patients is associated with which particular genetics?

A

HLA-DR4 subtype

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21
Q

What is Felty’s syndrome? Triad? Which genotype is it associated with? Which extra-articular manifestation is is particularly associated with?

A

Aggressive complication of RA. Triad of RA, splenomegaly and neeutropenia
HLA-DR4 (an aggressive RA genotype)
Vasculitis

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22
Q

RA therapy against which immune cells has proved effecctive?

A

T cells

B cells

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23
Q

Which cytokine has proved pivotal in RA, both directly and indirectly?

A

TNF

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24
Q

MHC polymorphism is related to which kind of immune cell?

A

T cellss

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25
Q

RA susceptible individual tend to be at risk of what more generally?

A

Persistant inflammation

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26
Q

Deposits of __ trigger free radical production and so are important in RA pathogenesis

A

Iron

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27
Q

5 main categories of current treatments?

A 
NSAIDs
Steroids
DMARDs
Anti - cytokines (e.g. anti TNF)
Anti CD20
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28
Q

Which sorts of joints tend to be affected in RA?

A

Small joints

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29
Q

Systemically, what is often foudn in RA?
Blood?
Lymph?

A

Anaemia

Lymphadenopathy

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30
Q

What is the effect of NSAIDs on prognosis?

A

None. But good for symptom relief (better than opiates and paracetamol)

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31
Q

Most common polyarthropathy in UK? What percentage of adults affected?

A

RA

1%

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32
Q

Which of the COX enzymes is inducible? Which compound does COX act on? What is its stimulus? What does it cause?

A

COX - 2
Arachidonic acid
Inflammatory stim –> inflammation via positive feedback

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33
Q

How do NSAIDs act pharmacologically?

A

Inhibit COX enzymes

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34
Q

What is the reason for the main side effects of NSAIDs?

  • GI (ulcers, haemorrhage etc)
  • Renal (nephrotoxicity etc)
A

Inhibit production of prostaglandins
GI: PGs inhibit gastric acid production os have protective effect on mucosa
Renal: PGs cause renal vasodilatation —> creatinine clearance

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35
Q

How often is the hip involved in rheumatoid arthiritis?

A

Rarely

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36
Q

What feature is unique to RA compared to other inflammatory arthritises?

A

Nodules:

- dermis, periosteum (pressure sites), lungs, heart

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37
Q

What lifestyle habit is associated with incr RA risk?

A

Smoking

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38
Q

How do B cells make rheumatic factor, despite it being an autoantibody?

A

T cell help

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39
Q

What diagnosis (RA is a differential), should you consider first when a young woman presents with symmetrical synovitis of pip and MCP?

A

SLE

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40
Q

What sort of presentation has the worst prognosis?

A

Gradual

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41
Q

4 big side effects of methotrexate? What should you do to prevent some of these? Who must you be very careful about giving it to?

A

BM suppression - PANCYTOPAENIA (so must monitor v closely)
Mouth ulcers (Rx folic acid)
Tetarogenic - is actually an abortificant, so be careful with woomen of repro age
Pneumonitis

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42
Q

Hydroxychloroquine is another DMARD used in RA, main side effect?

A

Retinal damage

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43
Q

Other main DMARD (not methotrexate) used to treat RA?

A

Sulphasalazine

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44
Q

Sulphasalazine:
1 common SE
1 rare (but serious side effect)
1 SE in males

A

Nausea
Neutropaenia
Azoospermia

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45
Q

How do you achieve best effects with DMARDs?

A

Use a combo of the 3 big ones

46
Q

If combo of DMARDs doesnt work, what is the first biological you would try? Give an example.

A

Anti TNFa drug e.g. Infliximab

47
Q

2nd line biological? How does it work?

A

Rituximab. Deplete B cells.

48
Q

What is the big risk of biologicals? (there are lots, just name one that you should screen for/consider prophylaxis of)

A

Reactivation of TB

49
Q

When are steroids useful in RA?

A 
Serious complication (eg vasculitis)
Low dose while introducing DMARDs
Flares that need rapid resolution
50
Q

Before being started on biologicals, a patient needs:
__ occasions of active disease, __ month(s) apart
Not responded to at least __ DMARDs for __ months

A

2
1
2
6

51
Q

When is RA stiffness worst?

A

Morning

52
Q

5 features of seronegative spondyloarthropathies

  • where does it affect (3)
  • antibodies?
  • genetics?
A 
Axial inflammation (spinal and sacroiliac)
Assymetrical peripheral arthritis
Inflammation of enthesis
Absence of RF (seronegative)
Strong association with HLA - B27
53
Q

5 seronegative spondyloarthropathies

A 
Ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis
Post-dysenteric reactive arthritis
Enteropathic arthritis
54
Q

Who does ankylosing spondylitis mainly affect? (age, sex)

A

Young adults

Men (more frequent and more severe)

55
Q

How do AS patients present present history wise?

A

Increasing pain and morning stiffness in the lower back and buttocks

56
Q

What does inspection of the spine reveal in AS?

A

Loss of lumbar lordosis and increased kyphosis

Limitation of lumbar spine mobility in both sagittal and frontal planes.

57
Q

How do you demonstrate reduced spinal flexion?

A

Schober test - mark made at 5th lumbar spinous process and 10cm above, on bending forward, the distance should increase to >15cm in normal individuals

58
Q

Ankylosing spondylitis

Articular:

  • foot features (2)
  • chest features. Why? (2)

Extra articular:

  • eyes
  • heart
  • lungs
A

Achilles tendinitis, plantar fasciitis
Tenderness around chest wall (and also pelvis). Reduced chest expansion due to involvement of costovertebral joint
Anterior uveitis
Aortic incompetence and cardiac conduction defects
Apical lung fibrosis

59
Q

What do each of the following tests reveal in ankylosing spondylitis?
- bloods

  • MRI
A

Raised ESR and CRP

Sacroiliitis before it is seen on X-ray

60
Q

Ankylosing spondylitis xray

Erosion and ___ of the margins of the ___ joint –> ___ (immobility and consolidation of the joint)
Spinal column - blurring of the upper or lower vertebral rims at the thoracolumbar junction caused by an ___ at the insertion of the ___ ___.
This heals with new bone resulting in bony spurs (___).
Progressive calcification of the ___ ___ and ___ eventually produce ‘___ ___’.

A 
Sclerosis
Sacroiliac
Ankylosis
Enthesitis
Intervertebral ligaments
Syndesmophytes
Interspinous ligaments
Syndesmophytes
Bamboo spine
61
Q

What is a syndesmophyte?

A

A bony growth originating inside a ligament

62
Q

At what point does ankylosing spondylitis become irreversible?

A

Syndesmophyte formation

63
Q

Drugs for ankylosing spondylitis:

  • pain, when are they taken?
  • methotrexate: where is it helpful and also not helpful?
  • most effective drug class for treating both spinal and peripheral joint inflammation?
A

NSAIDs, at night
Helpful for peripheral arthritis but not spinal disease
TNFalpha blocking drugs

64
Q

In what percentage of patients with psoriasis does arthritis occur? What feature of psoriasis is particularly associated with arthritis?

A

20%

Nail disease

65
Q

4 types of psoriatic arthritis?

A

Asymmetrical involvement of the small joints of the hand, incl distal interphalangeal joints
Symmetrical seronegative polyarthritis resembling RA
Arthritis mutilans, severe form with destruction of small hand and foot bones
Sacroiliitis - unilateral or bilateral

66
Q

What do the following investigations reveal in psoriatic arthritis?

  • bloods
  • Xrays
A

Nothing really, ESR often normal

‘Pencil in cup’ deformity in IPJs

67
Q

Why do ‘pencil in cup’ deformities come about?

A

Bone erosion - pointy appearance

Articulating bone = concave

68
Q

How do you treat psoriatic arthritis?

  • normally
  • local synovitis
  • severe cases
A

NSAIDs and analgesia
Intra-articular corticosteroid injections
Methotrexate or anti TNFalphas

69
Q

What is reactive arthritis? What precedes it? What drives it?

A

A sterile synovitis following a GI infection or STI

Bacterial antigens persist in the inflamed synovium

70
Q

What can cause the GI infections that precede reactive arthritis? (4 organisms)

A

Shigella, Salmonella, Yersinia, Campylobacter

71
Q

What STIs can precede reactive arthritis?

  • male
  • female (2 organisms)
A

Urethritis (non-specific)

Cervicitis - Chlamydia trachomatis or Ureaplasma urealyticum

72
Q

Which joints are particularly affected in reactive arthritis? what pattern?

A

Lower limb joints

Asymmetrical

73
Q

What to the skin lesions in reactive arthritis resemble?

A

Psoriasis

74
Q

What other features are there with reactive arthritis?

  • eyes
  • enthesitis (2)
  • ___ syndome
  • spine?
A

Anterior uveitis
Achilles tendonitis, plantar fasciitis
Reiter’s
Sacroiliitis and spondylitis

75
Q

What is the triad found with Reiter’s syndrome

A

Urethritis, reactive arthritis, conjunctivitis

76
Q

Reactive arthritis:

  • bloods
  • synovial fluid?
A

ESR raised in acute stage

Sterile but with high neutrophil count

77
Q

What is normally use to treat reactive arthritis (2)?
If the infection persists?
In cases that relapse (they normally don’t) (3)

A

NSAIDs, local corticosteroid injection,
ABx
Methotrexate/sulphasalazine and antiTNFa

78
Q

What conditions is enteropathic arthritis associated with?

A

Ulcerative colitis/Chrohn’s. Normally parallels activity of the IBD.

79
Q

Which joints does enteropathic arthritis affect? (2 options)

A
  • large joint mono arthritis
    OR
  • asymmetrical oligo-arthritis
80
Q

What is gout caused by?

A

Hyperuricaemia and intra-articular sodium urate crystals

81
Q

Who does gout affect?

- gender? age?

A

10x more common in men than women
Rarely before young adulthood (if it does occur, generally due to enzyme deficiency)
Rarely in pre-menopausal females

82
Q

How does hyperuricaemia come about?

A

Overproduction of uric acid or renal undexcretion

83
Q

Where does uric acid come from?

A

Breakdown of purines

84
Q

4 different gout syndromes?

A

Acute gout
Chronic polyarticular gout
Chronic tophaceous gout
Urate renal stone formation

85
Q

What can precipitate an attack of acute gout? (4)

A

Dietary excess
Alcohol excess
Dehydration
Diuretic

86
Q

Where does gout normally begin?

A

Big toe

87
Q

What is the most important condition to rule out in monoarthritis?

A

Septic arthritis

88
Q

What colour are tophi?

They are found particularly in the skin and around joints, which body parts are affected particularly?

A

White

Fingers, ear, Achilles’ tendon

89
Q

What does joint fluid microscopy reveal in gout affected joints?

A

Needle shaped crystals which are negatively birefringent under polarized light

90
Q

When does serum urate levels determined gout diagnosis? What is the problem generally using serum urate levels?

A

When plasma levels are in lower half of normal range

When urate crystalises during an acute attack, the serum plasma level is often normal

91
Q

What is first line gout treatment? 2nd line? And?

A

NSAIDs
Colchine
Cortiocosteroids

92
Q

What are problems with using Colchine and what are its side effects?

A

Narrow therapeutic window

Side effects - diarrhoea, abdo pain, multiorgan failure

93
Q

How do you prevent future gout attacks?

A

Reduce serum uric acid levels

  • obese patients should lose weight
  • alcohol consumption reduced
  • drugs like thiazides and salicylates should be withdrawn
94
Q

3 example of purine riich foods?

A

Offal
Fish/shellfish
Spinach

95
Q

What main drug is given to prevent future gout? How does it work?

A

Allopurinol

Reduces serum urate levels by inhibiting xanthine oxidase (enzyme involved in xanthine oxidase

96
Q

When you start someone on allopurinol, why do you give them NSAIDs and Colchine for 4 weeks before and after?

A

Allopurinol can trigger an acute attack

97
Q

What is pseudogout?

A

Deposition of calcium pyrophosphate dihydrate (CPPD) in articular cartilage and periarticular tissue.

98
Q

Why does pseudogout resemble gout?

A

Shedding of crystals into the joint –> acute synovitis

99
Q

How is pseudogout different from gout in terms of who gets it?

A

More common in elderly women

100
Q

How is pseudogout diff from gout in terms of where it affects?

A

Knee or wrist

101
Q

What conditions is gout associated with in young people?(4)

A

Haemochromoatosis
Hyperparathyroidism
Wilson’s disease
Alkaptonuria (black/brown depostion in cartilage etc)

102
Q

What does joint fluid microscopy of pseudogout show?

A

Small brick-shaped pyrophosphate crystals which positively birefringent under polarized light

103
Q

What is key xray finding of pseudogout? What is it?

A

Chondrocalcinosis.

That is the deposition of CDDH crystals

104
Q

What might blood results show in pseudogout?

A

Raised WBC count

105
Q

What is treatment of pseudogout?

A

Joint aspiration with NSAIDs or colchine

Injection of local corticosteroids

106
Q

Why does gout start in the big toe? (2)

A

MTPJ - lots of pressure (so more prone to osteoarthritis), coldest part of body

107
Q

Why is gout so hot?

A

It is NEUTROPHILIC inflammation

108
Q

Why is gout more common in men? (2)

A

Boozing (and meat)

Testosterone poss has an effect

109
Q

Why is gout systemic?

A

It is caused by urate in the blood

110
Q

Which drugs impair excretion of uric acid (2)?

A

Thiazide diuretics

Low dose aspirin

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