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Year 2 - Musculoskeletal (DP) > Clinical (Weeks 1+2) > Flashcards

Clinical (Weeks 1+2) Flashcards

1
Q

What genes are associated with a susceptibility to RA?

A

HLA DR4

HLA DR1

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2
Q

What cells invade the synovium in RA?

A

Macrophages
Fibroblasts
Multinucleated giant cells

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3
Q

What is the basic process behind RA?

A
  1. Synovial expansion
  2. Invasion of bone
  3. Erodes bone and cartilage
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4
Q

Articular symptoms of RA?

A

Joint pain
Morning stiffness
Joint swelling

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5
Q

Extra-articular manifestations of RA

A 
Respiratory:
     - Effusions
     - Fibrosis
     - Nodules
Rheumatoid nodules on extensor surfaces
Ocular involvement:
     - Keratoconjunctivitis
     - Episcleritis
     - Uveitis
     - Nodular scleritis
Increased CVS morbidity and mortality
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6
Q

What hand joint is not affected by RA?

A

DIP

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7
Q

What pattern of joint involvement is seen in RA?

A

Symmetrical

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8
Q

How is RA defined by the EULAR/ACR Classification?

A 
Synovitis in >/=1 joint
Absence of better diagnosis
Achievement of >/=6/10 of:
     - Number and site of affected joints (0-5)
     - Serological abnormality (0-3)
     - Increased CRP/ESR (0-1)
     - Symptom duration (0-1)
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9
Q

What is the best autoantibody to test for to aid in the diagnosis of RA?

A

Anti-CCP (Cycli citrullinated peptide) Antibody

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10
Q

Does a patient need to be Rheumatoid Factor positive (RhF) to have RA?

A

No

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11
Q

What chronic haematological change may be seen in RA?

A

Anaemia

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12
Q

What x-ray changes are seen in RA?

A

Osteopaenia:
- Loss of joint space
- Periarticular erosions
Soft tissue swelling

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13
Q

What late complications can be seen in RA?

A 
Infection
Cervical myelopahy secondary to:
     - Atlanto-axial/Subaxial subluxation
ILD
Peripheral neuropathy
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14
Q

What comorbidities is RA associated with?

A

Severe infections
CVS mortality
Lymphoma

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15
Q

What genetic factor is a poor prognostic factor in RA?

A

HLA DR4 positive

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16
Q

How soon must treatment be begun in RA to prevent irreversible damage?

A

Within 3 months

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17
Q

What are the principles of RA treatment?

A

DMARDs
Steroids to cover lag phase
Frequent reviews

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18
Q

Give examples of DMARDs and when they might be used?

A

1st line - Methotrexate
2nd line and in pregnancy - Sulphasalazine
Hydroxychloroquine
Leflunamide

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19
Q

What four approaches to biologic therapy can be used in RA and give examples of drugs in each class?

A 
TNF-alpha inhibition:
     - Infliximab
     - Adalimumab
     - Etanercept
B cell depletion:
     - Rituximab
Disruption of T cell co-stimulation:
     - Abatecept
Interleukin inhibition:
     - Anankira (IL-1)
     - Tocilizumab (IL-6)
(Jak-2 inhibitors)
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20
Q

What is the pathogenesis of OA?

A

Loss of matrix (Collagen ii with chondrocytes embedded)
Cytokine release:
- IL-1
- TNF-alpha
- Metalloproteinases
- Prostaglandins from chondrocytes
Surface fibrosis and attempted repair -> Oestophytes

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21
Q

How are localised and generalised idiopathic OA defined

A 
Localised:
     - Hands
     - Feet
     - Knee
     - Hip
     - Spine
Generalised is >/= 3 sites involved
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22
Q

What are some secondary causes of OA?

A 
Previous injury
RA
Genetic
Acromegaly
Crystal arthropathy
Perthes
SUFE
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23
Q

Risk factors of OA

A 
Age
Female
Obesity
Job
Injury/Sports
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24
Q

When is pain typically present in OA?

A

During exercise

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25
Q

How long does morning stiffness last in OA?

A

Less than 30 minutes

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26
Q

What might be found on examination of a patient with OA?

A

Crepitus
Bony enlargements
Joint tenderness and effusion

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27
Q

What can lumbar spine OA result in?

A

Spinal stenosis

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28
Q

Where does hip OA pain radiate to?

A

Groin/back

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29
Q

OA at what site can result in genu valgum and a Baker’s cyst?

A

Knee

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30
Q

What are some features of OA in the hand?

A

Heberden’s nodes (DIP OA)
Bouchard’s nodes (PIP OA)
Thumb base squaring (CMC OA)

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31
Q

Sterotypical x-ray features of OA?

A 
Loss of joint space
Osteophyte formation
Subchondral sclerosis
Subchondral cysts
(LOSS)
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32
Q

Define the grades of OA according to the Kellgren-Lawrence scale?

A 
Grade 0:
     - No findings
Grade 1:
     - Minute osteophytes
Grade 2:
     - Definite osteophytes
     - Unimpaired joint space
Grade 3:
     - Definite osteophytes
     - Moderate loss of joint space
Grade 4:
     - Definite osteophytes
     - Severe space loss and sclerosis
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33
Q

What are the main non-pharmacological treatments of OA?

A

Physiotherapy
Weight loss
Exercise

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34
Q

What pharmacological treatments are prescribed in OA?

A 
Analgesia:
     - Paracetamol
     - Topicals
NSAIDs
Pain modulators:
     - TCAs
     - Gabapentin
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35
Q

What intra-articular medications can be used in OA?

A

Steroids

Hyaluronic acid

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36
Q

Surgical treatments of OA

A

Arthroscopic washout
Soft tissue trimming
Joint replacement

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37
Q

What causes gout?

A

Uric acid crystals

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38
Q

Is gout more common in men or women?

A

Men

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39
Q

What results in increased urate production?

A 
Enzyme defects
Psoriasis
Haemolytic disorders
Alcohol
High purine diet (red meat, seafood)
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40
Q

What results in decreased urate excretion?

A 
Renal impairment
Volume depletion
Hypothyroidism
Diuretics
Cytotoxics
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41
Q

True or false; Blood uric acid can be normal in acute gout?

A

True

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42
Q

What joint is the most common site of acute gout?

A

1st MTP (Podagra)

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43
Q

What is chronic tophaceous gout associated with?

A

Diuretics

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44
Q

What is the best diagnostic investigation for gout?

A

Polarised microscopy:

 - Negatively birefringent
 - Needle shaped crystals
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45
Q

What appearance will gout show on x-ray?

A

Erosive arthritis features

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46
Q

How do we treat an acute flare of gout?

A

NSAIDs
Steroids
Colchicine

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47
Q

How can we prevent gout?

A

Xanthine oxidase inhibitors:

 - Allopurinol
 - Febuxostat
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48
Q

How do we use allopurinol?

A

Start 2-4 weeks after acute
Continue use during future acute flares
Titrate dose up until serum urate

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49
Q

What causes psuedogout?

A

Deposition of calcium pyrophosphate crystals

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50
Q

What does pseudogout cause?

A

Calcinosis:

 - Deposition of calcium in cartilage and soft tissue
 - No inflammation
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51
Q

How does pseudogout appear on polarised micropscopy?

A

Mildly positive birefringement

Envelope-shaped crystals

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52
Q

What is pseudogout associated with?

A 
Hyperparathyroidism
Hypothyroidism
Amyloidosis
Haemochromatosis
Gout
Trauma
Ageing
Haemosiderosis
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53
Q

A 54 year old female prevents with reduced shoulder movement, that is painful and tender to touch. There is hydroxyapatite in the synovial fluid. How would we treat this?

A

Milwaukee shoulder:

 - NSAIDs
 - Intra-articular steroids
 - Physiotherapy
 - Arthroplasty
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54
Q

How could we differentiate between soft tissue rheumatism and fibromyalgia?

A

Fibromyalgia is a more generalised pain

Soft tissue rheumatism is confined to one site

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55
Q

What genetic syndromes are associated with joint hypermobility?

A

Marfan’s

Ehlers Danlos

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56
Q

How do we measure joint hypermobility?

A

Modified Beighton Score

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57
Q

When do we treat joint hypermobility?

A

If there is arthralgia or permature OA

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58
Q

What is the female to male ratio in SLE?

A

F:M is 9:1

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59
Q

What does SLE stand for?

A

Systemic Lupus Erythematosus

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60
Q

What populations is SLE most common in?

A

Asians
African-Americans
Afro-Caribbeans
Hispanic Americans

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61
Q

What population is SLE least common in?

A

African blacks

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62
Q

What is the environmental aetiology of SLE?

A

Smoking
UV light
Silica dust

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63
Q

What infection can trigger SLE?

A

EBV

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64
Q

Order these steps in the pathogenesis of SLE:

  • B+T cells stimulated
  • Loss of immune regulation
  • Autoantibodies made
  • Increase in defective apoptosis
  • Immune complexes
  • Nuclear material persists -> Acts as autoantigens
  • Autoimmunity due to extended exposure to nuclear and intraceullar proteins
A
  1. Loss of immune regulation
  2. Increase in defective apoptosis
  3. Nuclear material persists -> Acts as autoantigens
  4. Autoimmunity due to extended exposure
  5. B+T cells stimulated
  6. Autoantibodies made
  7. Immune complexes
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65
Q

Where do the immune complexes in SLE gather and what does this cause?

A 
In blood vessel walls:
     - Skin
     - Kidneys
Complement release -> Neutrophils release enzymes
Damage to basement membrane results
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66
Q

Are complement levels high or low in SLE?

A

Low

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67
Q

What are some of the distinguishing cutaneous features of SLE?

A 
Photosensitivity
Malar 'butterfly' rash:
     - Spares labial-nasal fold
Discoid LE
Subacute cutaneous lupus
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68
Q

What deforming arthropathy can be seen in SLE?

A

Jaccoud’s arthritis

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69
Q

What pulmonary features can be present in lupus?

A 
Pleurisy -> Pleuritis
Effusion
PE
Pulmonary hypertension
Fibrosis (diffuse) -> ILD
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70
Q

What cardiac features can be present in SLE?

A

Pericarditis
Cardiomyopathy -> MI
Libman-Sachs endocarditis

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71
Q

What haematological conditions can be seen in lupus?

A

Lymphadenopathy
Leukopaenia
Anaemia
Thrombocytopaenia

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72
Q

Why are patients with lupus more susceptible to infections?

A

Decreased complement
Impaired cell mediated immunity
Defective phagocytosis
Poor Ab response

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73
Q

What is the most specific autoantibody in lupus?

A

Anti-double stranded DNA antibody (Anti-DNA)`

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74
Q

What other antibodies can also be present in SLE?

A 
Anti-ENA:
     - Anti-Ro
     - Anti-Sm
     - Anti-RNP
Anti-ANA
75
Q

What autoantibody is associated with the cutaneous manifestations and congenital heart block and neonatal LE?

A

Anti-Ro

76
Q

What autoantibody is associated with the CNS manifestations in SLE?

A

Anti-Sm

77
Q

What is prescribed to every SLE patient?

A

NSAIDs
Simple analgesia
Hydroxychloroquine

78
Q

How is hydroxychloroquine effective in SLE?

A

Reduces arthritis

Reduces cutaneous and constituional symptoms

79
Q

A patient with severe disease and diffuse glomerulonephritis presents to A&E. There is extensive organ involvement and they are known to have SLE. What steroids would we prescribe?

A

High dose prednisolone:

- 1mg/kg/day IV

80
Q

What classes as a small dose of steroids in SLE and what can this treat?

A

15mg prednisolone daily

Rashes, arthritis and serositis

81
Q

What immunosuppressant used in SLE is safe in pregnancy?

A

Azathioprine

82
Q

How do we define mild SLE?

A

Cutaneous and MSK involvement only

83
Q

How do we treat mild SLE?

A

HCQ
Topical steroid
NSAIDs

84
Q

How do we treat moderate SLE?

A

Oral steroids
Azathioprine
Methotrexate

85
Q

How do we define severe SLE?

A

Renal, CNS and severe Haem involvement

86
Q

How do we treat severe SLE?

A

IV steroids
Cyclophosphamide
Rituximab

87
Q

A 29 year old woman presents with a purple mottled discolouration on her lower limbs. She has suffered from migraines for the past year. She has noted that she has bruised easily and has suffered regular nosebleeds. She also suffered a miscarriage at 28 weeks.

A

Anti-Phospholipid syndrome

88
Q

What features in a patient’s history may suggest anti-phospholipid syndrome?

A

Pregnancy loss with no explanation 10-34 weeks

3 losses with no explanation

89
Q

Having at least one of the following, on two occasions >/= 12 weeks apart is diagnostic of what:

 - Positive anti-cardiolipin Ab
 - Lupus anticoagulant activity
 - Anti-Beta2-glycoprotein
A

Anti-Phospholipid syndrome

90
Q

What is the treatment of anti-phospholipid syndrome?

A

Lifelong warfarin
If pregnancy loss:
- Aspirin and heparin during pregnancy

91
Q

A patient presents with a swelling in front of her left ear. She notes eye and mouth dryness for the last 5 months. She has been feeling very fatigued.

A

Sjogren’s syndrome

92
Q

What causes Sjogren’s syndrome?

A

Lymphocyte infiltration of exocrine glands

93
Q

What is the name given to the ocular dryness cause by Sjogren’s?

A

Keratoconjunctivitis sicca

94
Q

What is the diagnostic test of Sjogren’s?

A

Schirmer test:

- Normal result is >10mm of water

95
Q

Which of the following is not associated with Sjogren’s?

 - Lymphoma
 - Arthralgia
 - Raynaud's
 - Pulmonary hypertension
 - ILD
A

Pulmonary hypertension

96
Q

What is pilocarpine

A

A parasympathomimetic used to increase salivation

97
Q

What autoantibodies are associate with Sjogrens?

A

ANA

Anti-Ro

98
Q

What is CREST syndrome and what does it stand for?

A 
Limited Systemic Sclerosis
Calcinosis
Raynaud's
Esophageal dysmotility
Sclerodactyly (Hands)
Telangiectasias
99
Q

How soon are skin changes seen in diffuse systemic sclerosis?

A

Within one year of Raynaud’s (Trunk and limbs - Not just hands like in limited)

100
Q

What organs can be involved in diffuse systemic sclerosis?

A 
Renal
Pulmonary
GI
MSK
CVS
101
Q

How do we treat systemic sclerosis?

A 
Raynauds:
     - Calcium channel blockers
     - Iloprost
     - Bosentan
Renal:
     - ACE inhibitors
GI:
     - PPIs
ILD:
     - Cyclophosphamide
102
Q

What autoantibodies are associated with each type of systemic sclerosis?

A

Limited - Anti-Centromere

Diffuse - Anti-Scl-70

103
Q

What are the following major criteria of?

 - Raynauds
 - Arthralgia
 - Myositis
 - Sclerodactyly
 - Pulmonary hypertension
 - ILD
A

Mixed Connective Tissue Disease

104
Q

Anti-RNP autoantibodies are seen in what condition?

A

Mixed Connective Tissue Disease

105
Q

A 43 year old woman presents complaining of difficult climbing the stairs. You note a rash around her eyes and a rash over her scapulae. She has also noted difficulty swallowing.

A

Dermatomyositis

106
Q

What is Gottron’s sign and what is it seen in?

A

Erythematous scaling:
- Symmetrical
- Over MCP and IP joints
Seen in dermatomyositis

107
Q

What malignancies are increased in polymyositis and dermatomyositis?

A 
Ovarian
Breast
Gastric
Lung
Bladder
Colon
108
Q

What features of a patient’s PMHx may be present in polymyositis?

A

Diabetes

Thyroid disease

109
Q

What autoantibodies are present in polymyositis/dermatomyositis?

A

ANA

Anti-Jo-1

110
Q

What is seen in electromyography in polymositis patients?

A

Increased fibrillations
Abnormal motor potentials
Repetitive discharges

111
Q

How is polymyositis treated?

A 
Steroids
Azthioprine
Methotrexate
Ciclosporin
IV Ig
112
Q

A 61 year old man presents with wrist, finger and leg weakness over the last month.

A

Inclusion body myositis

113
Q

What is the difference in creatinin kinase levels between polymyositis and inclusion body myositis?

A

CK higher in PM

114
Q

What will a muscle biopsy show in inclusion body myositis?

A

Inclusion bodies

115
Q

A 73 year old woman presents with difficult climbing stairs and brushing her hair. She also notes morning stiffness that lasts about two hours. She says her symptoms improve throughout the day.

A

Polymyalgia Rheumatica

116
Q

What is polymyalgia rheumatica associated with?

A

Giant cell arteritis

117
Q

How do we treat polymyalgia rheumatica?

A

15mg prednisolone daily for 18 months

118
Q

A patient presents with pain on chewing and vision problems. They have also experience a temporal headache and pain on brushing her hair.

A

Giant cell arteritis

119
Q

What is the definitive diagnostic technique of GCA?

A

Temporal artery biopsy

Also increased ESR/PV/CRP

120
Q

Treatment options for GCA

A 
No vision problems:
     - 40mg prednisolone
Vision problems:
     - 60mg prednisolone
(for 2 years)
121
Q

What CVS problems is GCA associated with?

A

Aortic aneurysm

Aortic dissection

122
Q

What is the commonest cause of chronic MSK pain in women?

A

Fibromyalgia

123
Q

Spondyloarthropathies are usually seen in individuals positive for what?

A

HLA-B27

124
Q

What are the four subgroups of spondyloarthropathies?

A

Ankylosing spndylitis
Psoriatic arthritis
Reactive arthritis/Reiter’s syndrome
Enteropathic arthritis

125
Q

When is mechanical back pain worst?

A

On exertion

At the end of the day

126
Q

When is inflammatory back pain worst?

A

With rest

In the morning - Stiffness

127
Q

What are some common features that all spondyloarthropathies present?

A 
Sacroiliac and spine involvement
Enthesitis:
     - Inflammation at tendon insertion
               > Achilles tendinitis
               > Plantar fasciitis
Dactylitis:
     - 'Sausage digits' (Inflammation of the whole digit)
128
Q

What is the typical joint pattern in spondyloarthropathies?

A

Oligoarticular
Asymmetric
Mainly lower limb

129
Q

What sites are commonly by extra-articular manifestations in spondyloarthropathies?

A

Eyes:
- Anterior uveitis
- Conjunctivitis
Mucous membranes

130
Q

Sacroiliitis is the hallmark of what spondyloarthropathy?

A

Ankylosing spondylitis

131
Q

Is ankylosing spongylitis more common in men or women?

A

Men

132
Q

What are the Modified New York Criteria for Ankylosing Spondylitis?

A
  1. Limited lumbar movement
  2. Lower back pain for 3 months:
    • Improves with exercise
    • Not relieved by rest
  3. Reduced chest expansion
  4. Bilateral (Grade 2-4) sacroiliitis on x-ray
  5. Unilateral (Grade 3-4) sacroiliitis on x-ray
    Define as AS is criterion 4 or 5 plus 1,2 or 3
133
Q

Why is ankylosing spondylitis called the ‘A’ disease?

A 
Axial arthritis
Anterior uveitis
Aortic regurgitation
Amyloidosis/IgA Nepropathy
Achilles tendonitis
plAntar fasciitis
134
Q

What is the main examination test for ankylosing spondylitis?

A

Modified Schober’s Test:

 - 5cm line below posterior superior iliac crest
 - 10cm line above PSIC
 - Ask patient to bend forward
 - Normal distance >/= 20cm
 - Less than 18cm is AS
135
Q

What x-ray features are seen in ankylosing spondylitis?

A

Sacroilitis
Syndesmophytes:
- Bony growths from within ligaments
- Bridge intervertebral disc
- Result in a late ‘Bamboo spine’ on AP view

136
Q

Treatment of ankylosing spondylitis

A 
Physiotherapy
NSAIDs
DMARDs if peripheral joint involvement
Anti-TNF (If BASDAI >4)
Surgery
137
Q

Does a patient need to have psoriasis to suffer from psoriatic arthritis?

A

No

138
Q

What nail features are seen in psoriatic arthritis?

A

Pitting

Onycholysis

139
Q

What is the most severe subgroup of psoriatic arthritis?

A

Arthritis mutilans (aggressive and destructive)

140
Q

What is the hallmark x-ray feature of psoriatic arthritis?

A

‘Pencil-in-cup’ appearance of DIP

141
Q

What common infections result in reactive arthritis?

A 
GU:
     - Chlamydia
GI:
     - Salmonella
     - Shigella
     - Yersinia
142
Q

What is Reiter’s syndrome?

A

Can’t see, can’t pee, can’t bend the knee:

 - Uveitis
 - Urethritis
 - Arthritis
143
Q

How do we treat reactive arthritis?

A

Steroids

DMARDs

144
Q

True of false; The joint aspirate in reactive arthritis is not sterile?

A

False. It is usually sterile

145
Q

What mucocutaneous features can be seen in reactive arthritis?

A 
Keratoderma blennorrhagicum:
     - Vesiculopustular
     - Yellow/brown
     - Soles and palms
Circinate balantis:
     - Painless
     - Serpiginous dermatitis
     - Glans penis
Painless oral ulcers
Hyperkeratotic nails
146
Q

A 29 year old man presents with loose stools with mucus present. He has noticed weight loss over the last 6 months. The sole of his left foot is very painful. There are some painful ulcers on his buccal surfaces. He has noticed his knees and lower back have been stiff and painful when he is at rest.

A

IBD with enteropathic arthritis

147
Q

What will an USS of an enteropathic arthritis show?

A

Synovitis

Tenosynovitis

148
Q

What can trigger a secondary vasculitis?

A 
Infection
Drugs
Toxins
Inflammatory conditions
Cancer
149
Q

Give two examples of large-vessel vasculitidies

A

Takayasu arteritis

GCA

150
Q

Give two examples of medium-vessel vasculitidies

A

Polyarteritis nodosa

Kawasaki disease

151
Q

What two categores can small-vessel vasculitidies be divided into? Give examples of each

A 
Immun-complex mediated:
     - Henoch-Schonlein vasculities (IgA)
     - Cryoglobulinaemic vasculitis
     - Hypocomplementeric urticarial vasculitis
ANCA-Associated (AAV):
     - Microscopic polyangiitis
     - GPA (Wegener's)
     - EGPA (Churg-Strauss)
152
Q

What populations are large-vessel vasculitidies most common in?

A
153
Q

What are large-vessel vasculitidies characterised by?

A

Granulomatous infiltration of vessel walls

154
Q

What are common examination findings in large-vessel vasculitidies?

A 
Carotid bruit
BP difference at extremities
Claudication
Carotodynia
Hypertension
155
Q

What lesions are seen in temporal artery biopsies in GCA patients?

A

Skip lesions

156
Q

What might MRI/CT scans show in GCA patients?

A

Vessel wall thickening
Stenosis
Aneurysm
Increased metabolism

157
Q

What populations is Kawasaki disease seen in?

A

Kids younger than 5 years old

158
Q

What is the most concerning complication of Kawasaki disease?

A

Coronary Aneurysm

159
Q

What types of lesions are seen in polyarteritis nodosa and where are they typically found?

A

Necrotising lesions

Located at vessel bifurcations

160
Q

What body sites do medium-vessel vasculitidies tend to affect?

A

Skin
Gut
Kidneys

161
Q

What infection is medium-vessel vasculitidies associated with?

A

Hep B

162
Q

A 40 year old man presents complaining of regular nosebleeds and mouth ulcers. He also says he has experienced periods of deafness.

A

GPA

163
Q

In what populations is GPA most common in?

A

Northern Europeans
Males
35-55 year olds

164
Q

What ENT features are seen in GPA?

A 
Sinusitis
Nasal crusting
Epistaxis
Mouth ulcers
Sensorineural defects
Otitis media
Deafness
'Saddle nose'
165
Q

What other systems are affected by GPA?

A 
Renal:
     - Necrotising glomerulonephritis
CNS:
     - Mononeuritis multiplex
     - Sensorimotor polyneuropathy
     - CN palsies
Ophthalmology:
     - Conjunctivitis/Uveitis
     - CN ii vasculitis
     - Proptosis
166
Q

A 41 year old man presents which shortness of breath and a runny nose. On examination you note wheeze and expiratory rhonchi.

A

EGPA/Churg-Strauss

167
Q

On blood testing, what would expect in EGPA?

A

Increased peripheral blood eosinophil count

168
Q

True or false: Mononeuritis multiplex is common in EGPA?

A

True

169
Q

What are the two types of ANCA and what staining patterns are seen?

A 
Cytoplasmic ANCA (c-ANCA):
     - Uniform staining
     - No interlobular accentuation
Perinuclear ANCA (p-ANCA):
     - Perinuclear staining
     - Nuclear expansion
170
Q

What conditions are associated with each kind of ANCA?

A 
c-ANCA:
     - GPA (Wegener's)
p-ANCA:
     - EGPA (Churg-Strauss)
     - Microscopic polyangiitis
171
Q

What is PR3?

A

The specific c-ANCA antigen seen in GPA

172
Q

What is MPO and what is it more positive in, EGPA or MPA?

A

Myeloperoxidase (p-ANCE antigen)

MPA

173
Q

How do we classify localised AAV?

A

Upper or lower respiratory tract disease

174
Q

How do we classify early systemic AAV?

A

Without organ or life threatening disease

175
Q

How do we classify generalised AAV?

A

Renal disease (Creatinine

176
Q

How do we classify systemic AAV?

A 
Renal disease (Creatine > 500micrograms/dL)
Other vital organ failure
177
Q

How do we classify refractory AAV?

A

Progressive disease

Unresponsive to steroids and cyclophosphamide

178
Q

How do we treat localised and early systemic AAV?

A

Methotrexate/Azathioprine

Plus steroids

179
Q

How do we treat generalised and systemic AAV?

A 
1st line:
     - Cyclophosphamide + steroids
          OR
     - Rituximab + steroids
Plasma exchange if creatinine > 500
180
Q

How do we treat refractory AAV?

A

IV Ig + Rituximab

181
Q

A 5 year old boy presents with a purple rash on his lower limbs and buttocks. He has been complaining of “on and off” abdominal pain. His mother noticed some blood in his stool. Two weeks ago he had a URTI.

A

Henoch-Schonlein Purpura

182
Q

What infections can precede Henoch-Schonlein purpura?

A

URTI
Pharyngeal
GI

183
Q

How do we treat and monitor Henoch-Schonlein purpura?

A

Usually self-limiting

Perform urinalysis

Year 2 - Musculoskeletal (DP) (16 decks)

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