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RACP 2024 > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What medications are effective for osteoarthritis?

A

NSAIDs
Duloxetine (SNRI)
Intra-articular glucocorticoids

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2
Q

What is fibromyalgia and its clinical features?

A

Central nociplastic pain disorder

Chronic widespread pain
Allodynia
Fatigue
Fibrofog
Sleep disturbance
Mood disturbance
Sensory sensitivity
Medication intolerance
Altered interoception

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3
Q

How is fibromyalgia managed non-pharmacologically?

A

Movement practice (exercise)
Attention to sleep
Cognitive therapy

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4
Q

What medications can be used in the management of fibromyalgia?

A

TCAs
Gabapentinoids
SNRIs
Tramadol

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5
Q

How is rotator cuff disease diagnosed?

A

Clinically, no role for imaging

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6
Q

How is rotator cuff disease managed?

A

Non-invasively with time, PT and NSAIDs

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7
Q

How is greater tronchateric pain diagnosed?

A

Clinically, features of maximal tenderness over greater trochanter, positive Trendelenberg test

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8
Q

How is greater trochanter pain managed?

A

PT and analgesia
No evidence to support gluco-corticoid injection

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9
Q

What conditions are associated with yellow nail syndrome? How is it managed?

A

Chronic resp illness, lymphoedema, rarely RA, malignancy, immunodeficiency

Treatment includes Vit E, zinc, itraconazole (speeds up nail growth not antifungal activity)

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10
Q

What is the classical appearance of mycosis fungiodes?

A

Poikilodermatous patches= (hypopigmentation, hyperpigmentation, telangiectasias and atrophy) in bathing suit distribution

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11
Q

What are histological features of neutrophilic dermatoses?

A

Diffuse neutrophilic infiltrates in absence of identifiable infection

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12
Q

What are clinical feature of Sweet Syndrome (acute febrile neutrophilic dermatosis) and how is it treated?

A

Fevers, infiltrated plaques +/- bullae on head and neck
Associated with AML, IBD
Treated with high dose oral prednisolone and treatment of underlying condition

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13
Q

What is the treatment for vitiligo?

A

Topical steroids or tacrolimus

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14
Q

What HLA types are associated with DRESS to anti-retrovirals?

A

HLA-B5701 and abacavir
HLA-B3505 and nevirapine

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15
Q

How is lipoatrophy associated with anti-retrovirals for HIV treated?

A

Switching to non-thymidine agents (didanosine, lamivudine, zalcitabine)
Pravastatin

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16
Q

What medications are commonly associated with SJS and TENS?

A

Allopurinol, NSAIDs, antibiotics, anti convulsants

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17
Q

What is the key difference between SJS and TENS?

A

BSA involved
< 10% = SJS
> 10% = TENS

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18
Q

What HLA type is associated with SJS/TEN and carbamazepine?

A

HLA-B*1502, Han Chinese esp in Taiwan

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19
Q

How is SJS/TEN managed?

A

Admission to ICU or Burns unit
Fluids
DVT prophylaxis
IVIg 1g/kg/day for 3 days

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20
Q

What immunological tests are associated with dermatomyositis?

A

ANA, anti-Jo1, anti-p55/140 (cancer), anti-Mi2

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21
Q

What are the two types of axial apodyloarthritides?

A
  1. Axial spondyloarthritis: involves spin and sacroiliac joints
  2. Peripheral spondyloarthritis: involve peripheral joints or entheses or dactylitis
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22
Q

How is axial spondyloarthrtitis classified?

A

3 months of inflammatory back pain and age of onset < 45
AND
Sacroilitis on imaging + 1 feature of axial spondyloarthrtitis
OR
HLA-B27 positive and 2 other features of axial spondyloarthrtitis

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23
Q

What are clinical features of axial spondyloarthrtitis?

A

-inflammatory back pain
- arhtritis
- enthesitis
- uveitis
- dactylitis
- psoriasis
- crohn’s/colitis
- good response to NSAIDs
- family history of SpA
- HLA-B27
- raised CRP

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24
Q

What is the diagnostic criteria for peripheral apondyloarthritis?

A

Peripheral arthritis and/or enthesitis and/or dactylitis
AND
1 non-joint SpA feature
OR 2 other joint SpA features

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25
Q

What is inflammatory back pain?

A
  • age onset < 40
  • insidious onset
  • improves with exercise
  • no improvement with rest
  • pain at night (2nd half of night)
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26
Q

What are key features in the pathophysiology of axial spondyloarthrtitis?

A
  • genetic susceptibility (HLA-B27)
  • IL-23 binding to T-cells resulting in IL-17 production
  • IL-17 can also result from chronic gut or skin inflammation
  • IL-17 acts on epithelial, endothelial and fibroblasts resulting in synovitis
  • IL-7 can act on osteoclasts resulting in bone erosion
  • new bone forms at sties of mechanical stress (SIJ, vertebrae)
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27
Q

What is the most common extra-articular manifestation of axial spondyloarthrtitis?

A

Anterior uveitis

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28
Q

Does MRI or x-ray findings of sacroiliitis have a greater association with axial spondyloarthrtitis?

A

X-ray has likelihood ratio of 20 (MRI = 9)

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29
Q

What % of HLA-B27+ individuals develop axial spondyloarthrtitis?

A

5%

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30
Q

What are MRI features of axial spondyloarthrtitis?

A

Subchondral bone marrow oedema on STIR = active inflammation

Erosions, sclerosis, ankolysis, fatty lesions on T1 = post inflammatory

Synovitis, enthesitis

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31
Q

What is the treatment for axial spondyloarthrtitis?

A

1st line:
- NSAIDs
- PT
- if has primarily peripheral disease can consider DMARDs (sulfasalazine, methotrexate) or local steroids (DMARDs have no effect for axial disease)

2nd line: failed 12/52 of therapy
- TNFa blocker: adalimumab, certolizumab pegol, etanercept, golimumab, infliximab
- IL-17 blocker: secukinumab
- JAK inhibitor: tofacitinib, upadacitinib

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32
Q

What are predictors of response to biologic therapy in axial spondyloarthrtitis?

A
  • shorter disease duration
  • younger age
  • high baseline inflammatory markers
  • worse inflammation on MRI
  • less functional impairment at baseline
  • HLA-B27+
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33
Q

What biologics for axial spondyloarthrtitis should be avoided in IBD?

A
  • secukinumab
  • etanercept
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34
Q

What biologic should be used for axial spondyloarthrtitis if IBD or uveitis present?

A

TNFa mAb: adalimumab, certolizumab pegol, golimumab, infliximab
NOT etanercept in IBD

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35
Q

What is the diagnostic criteria for psoriatic arthritis?

A

Peripheral or axial arthritis or anthesitis + 3 points from:
- Current skin psoriasis (2 pts)
- Prior or FHx of skin psoriasis (1 pt)
- dactylitis (1 pt)
- nail changes (1 pt)
- RF negative (1pt)
- juxta-articular new bone on x-ray (1 pt)

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36
Q

What are the five distinct patterns of joint involvement of psoriatic arthritis?

A
  1. Asymmetric oligoarthritis (most common)
  2. Symmetric polyarthritis
  3. Spondyloarthritis (assymetrical, asymptomatic)
  4. DIPJ with nail disease (pitting oncholysis)
  5. Arthritis mutilans (shortening of bone)
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37
Q

In what disease do you see a pencil in cup deformity?

A

Psoriatic arthritis (arthritis mutilans)

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38
Q

How is psoriatic arthritis treated?

A
  • NSAIDs
  • intra-articular steroids (not usually systemic)
  • If peripheral: methotrexate, sulfasalazine, leflunomide
  • Anti-TNFa: adalimumab, certolizumab pegol, etanercept, golimumab, infliximab
  • Anti-IL-17: secukinumab, ixekizumab
  • Anti-p40 subunit IL-12/23 = ustekinumab
  • Anti-p19 subunit IL-23: guselkumab
  • JAKi: tofacitinib, upadacitinib (Axial involvement)
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39
Q

What DMARD has activity for all manifestations of psoriatic arthritis?

A

TNFi
(not etanercept for IBD or uveitis)

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40
Q

What are the safety considerations for JAKi?

A
  • VTE
  • major CV events
  • malignancy (haem, lung)
  • shingles risk
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41
Q

What are clinical features of reactive arthritis?

A

Sterile arthritis following a remote infection 1-4/52 prior

Asymmetric, oligoarticular, lower limb
Enthesitis
Dactylitis
Sacro-iliitis

Extra-articular:
- skin: keratoderma blenorrhagica, circinate balanitis, mouth ulcers
- ocular: conjunctivitis, uveitis
- genito-urinary: aseptic urethritis, cervicitis, prostatisit
- constitutional symptoms

Classic triad: arthritis/urethritis/conjunctivitis

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42
Q

What organisms have been associated with reactive arthritis?

A

Chlamydia trachomatis
Shigella spp
Salmonella spp
Campylobacter
Yersinia

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43
Q

How is reactive arthritis treated?

A
  • treat underlying infection
  • NSAIDs
  • IA steroids
  • systemic steroids if unwell
  • Sulfasalazine for chronic symptoms
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44
Q

How should IBD associated apondyloarthritis be treated?

A
  • caution with NSAIDs
  • Sulfasalazine, anti-TNF or IL-23 blockade for peripheral joints
  • Anti-TNF for axial

(avoid IL-17 blockade and entanercept)

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45
Q

What are the 3 pillars of systemic sclerosis?

A
  • autoimmunity
  • vasculopathy
  • interstitial fibrosis
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46
Q

What are clinical features of diffuse cutaneous systemic sclerosis?

A
  • Raynauds (short history)
  • Rapid onset skin changes leading to contractures
  • skin of trunk and proximal limbs
  • tendon friction rubs
  • constitutional symptoms
  • early onset organ involvement (lung, kidney)
  • Scl-70 antibodies (ILD)
  • anti-RNA polymerase III antibodies (renal crisis)
  • ANA with nucleolar pattern
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47
Q

What are clinical features of limited cutaneous systemic sclerosis?

A

Previously CREST
Calcinosis
Raynauds (years)
Oesophageal dysmotility
Skin changes (upper limb and face)
Telangiectasia
Anticentromere antibodies

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48
Q

What is the most common cause of death in systemic sclerosis?

A

Pulmonary fibrosis

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49
Q

What therapies are indicated for the treatment of skin thickening in systemic sclerosis?

A

-Methotrexate (2nd line is mcyophenylate, cyclophosphamide)
- PT
- OT

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50
Q

How should ILD be screened for in systemic sclerosis?

A
  • All patients get PFTs and HRCT at baseline
  • diffuse get serial PFTs every 3-4 months for 3-5 years the annually
  • limited get annual
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51
Q

How should ILD be treated in systemic sclerosis?

A
  • mycophenylate (2nd line is cyclophosphamide)
  • anti fibrotic = nintedanib
  • tocilizumab if systemic inflammation
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52
Q

What type of pulmonary hypertension occurs in systemic sclerosis?

A

Type 1 = due to vascular remodelling
Type 2 = due to left heart dysfunction from myocardial involvement
Type 3 = due to ILD
Type 4 = due to antiphospholipid antibodies

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53
Q

What is the most common cause of pulmonary hypertension on systemic sclerosis?

A

Pulmonary artery hypertension (type 1)

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54
Q

What indicates a role for right heart catheter study to evaluate for pulmonary hypertension in systemic sclerosis?

A

DLCO <70% predicted + FVC/DLCO > 1.8
OR
proBNP > 210

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55
Q

What are features of a sclerodermic renal crisis?

A
  • abrupt onset of hypertension
  • normal urine sediment/mild proteinuria
  • progressive renal failure
  • can be triggered by corticosteroids
  • onion skin appearance on histology

Severe:
- microangiopathic haemolytic anaemia + thrombocytopenia
- heart failure and flash pulmonary oedema
- blurred vision (retinopathy)
- headache, fever, malaise
- encephalopathy, seizure
- pericardial effusion

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56
Q

How is scleroderma renal crisis treated?

A
  • ACEi (captopril)
  • IV nitroprusside if CNS involvement
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57
Q

How is Raynaud’s treated?

A
  • treat underlying cause (cryoglobulinaemia)
  • cold avoidance
  • smoking cessation
  • caffeine cessation
  • hand skin cares
  • keeping warm during procedures
  • nifedipine (2nd line = ARB, sildenafil)
  • severe = IV prostacyclin
58
Q

How should rheumatological digital tip ulcers be treated?

A
  • cold avoidance
  • vasodilator therapy (IV iloprost, sildenafil, bosentan)
  • analgesia
  • wound care
59
Q

How should rheumatological PIP ulcers be treated?

A

wound care

60
Q

How should calcinosis be managed?

A

wound care/debridement if ulcerate

61
Q

How should critical digital ischaemia be managed?

A
  • urgent admission
  • establish and treat cause
  • IV prostaglandin
62
Q

How is faecal incontinence treated in systemic sclerosis?

A
  • exclude overload
  • stool firming + laxatives
63
Q

What are indciations for HSCT in systemic scleroderma?

A

No smokers non responsive to standard treatment:
- diffuse in first 5 years with moderate organ involvement
- limited with progressive visceral involvement

64
Q

What are the 4 types of idiopathic inflammatory myopathies?

A
  • polymyositis
  • dermatomyositis
  • inclusion body myositis
  • immune mediated necrotising myopathy
65
Q

What are the shared features of idiopathic inflammatory myopathies?

A

Proximal skeletal muscle weakness
Immune mediated muscle inflammation or necrosis

66
Q

What is the pattern of muscle weakness in dermatomyositis and polymyositis?

A

Symmetrical proximal muscles weakness:
- deltoids, hip flexors, neck flexors
- diaphargmatic and intercostals
- striated muscle of upper 1/3 of oesophagus

67
Q

What rashes can be seen in dermatomyositis?

A
  • gotron’s papules (scaling + erythema over hand joints)
  • shawl sign (photodistributed poikiloderma)
  • helitrope rash
  • v sign
  • periungal erythema, ragged cuticles
68
Q

What is the significance of MDA-5 antibodies in dermatomyositis?

A
  • can be amyopathic
  • higher risk for ILD
  • increased risk of malignancy
69
Q

What are clinical features of inclusion body myositis?

A
  • insidious onset of asymmetric muscle weakness
  • quads often involved
  • distal > proximal
  • muscle atrophy
  • elevated CK
  • less responsive to steroids
70
Q

What feature differentiates statin myopathy from immune mediated?

A

Myopathy persisting despite statin withdrawal suggests immune mechanism
Statins are recognised trigger for immune mediated necrotising myopathy (anti-HMGCR antibodies)

71
Q

What key immune mechanisms contribute to dermatomyositis?

A

Autoantibodies activate complement, deposits in vasculature and mediate capillary necrosis, perivascular inflammation and perfasicular atrophy

72
Q

What key immune mechanisms contribute to polymyositis

A

CD8 T-cell responses against molecules

73
Q

What immune mechanisms contribute to inclusion body myositis?

A

Accumulation of antigens due to protein misfolding drives KLRG1+T-cell responses
Plasma cells make anti-cN1A antibodies

74
Q

What is the key immune cell in immune mediated necrotising myopathy?

A

Macrophages

75
Q

What are histopathological features of the following:
- dermatomyositis
- polymyositis
- inclusion body myositis
- immune mediated necrotising myopathy

A

dermatomyositis:
- perifasicular mononuclear cells
- perifasicular atrophy

polymyositis:
- lymphocytic invasion into myofibre

inclusion body myositis:
- vacuoles rimmed with basophilic granules

immune mediated necrotising myopathy:
- muscle fibre necrosis with sparse inflammatory infiltrate

76
Q

What are immunhistochemistry features of:
- dermatomyositis
- Anti-synthetase syndrome
- inclusion body myositis
- immune mediated necrotising myopathy

A

dermatomyositis:
- MxA positive
- MAC deposited in endomysial capillaries
- perifasicular MHC-I
- MHC-II negative

Anti-synthetase syndrome:
- MxA negative
- MHC-II on myofibres
- perfasicular MAC deposition

inclusion body myositis:
- p62 positive
- CD8 infiltrate
- KLRG1 positive

immune mediated necrotising myopathy:
- p62 positive in sarcoplasm
- diffuse MAC deposition

77
Q

Which anti-synthetase antibody is associated with mechanics hands?

A

Anti-Jo-1

78
Q

What malignancies are associated with dermatomyositis and polymyositis?

A

DM: cervix, lung, ovaries, pancreas, bladder, CRC, stomach, NHL
PM: lung, bladder, NHL

79
Q

How are dermatomyositis, polymyositis and immune mediated necrotising myositis treated?

A
  • high dose steroids (80 mg/day) tapered over 1 year
  • azathioprine
  • methotrexate
  • rituximab
80
Q

How is inclusion body myositis treated?

A

Limited response to steroids
IVIg for dysphagia

81
Q

What are clinical features of giant cell arteritis?

A
  • systemic vasculitis of medium and large arteries
  • affects age > 50
82
Q

What is the most common cause of vision loss in GCA?

A

Anterior ischaemic optic neuropathy (due to occlusion of posterior ciliary arteries, is not pathognomic)

83
Q

What are the 4 clinical patterns of GCA?

A
  1. isolated cranial (headache, jaw claudication, scalp tenderness) = most common
  2. Symptomatic large vessel vasculitis (claudication, pulseless limb) +/- cranial
  3. isolated fever/inflammation
  4. Isolated PMR with vasculitis on imaging
84
Q

What test has the best utility for diagnosing GCA?

A

CRP > 20 + platelet > 300

85
Q

What are ultrasound features of giant cell arteritis?

A

Halo sign
Luminal narrowing

86
Q

How is GCA treated?

A
  • visual symptoms: 1 g IV methylpred for 3/7, followed by 40-60 mg/day pred and tapered 15-20 mg/day over 2-3 months then tapered over 1 year
  • if no visual symptoms 40-60 mg/day pred
  • tocilizumab for large vessel only
87
Q

What are clinical features of PMR?

A
  • aching, stiffness around, neck, shoulder and hips
  • prolonged morning stiffness (key)
  • normal muscle strength but limited by pain
  • over 50 y/o
88
Q

How is PMR treated?

A
  • prednisolone 15-25 mg/day for 4 weeks then wean by 2.5 mg every 2 weeks, then by 1 mg/month
  • expect response in 48 hours
89
Q

What are radiographical features of atypical femoral fractures?

A
  • fracture line originates at lateral cortex, is transverse in orientation and becomes oblique as it progresses medially
  • localised periosteal or endosteal thickening/flat cortex at fracture site
90
Q

How are atypical femoral fractures managed?

A
  • stop bisphosphonates and other anti-resorptives (can use teriparatide)
  • continue calcium/Vit D
  • investigate for secondary cause of osteoporosis and underlying metabolic bone disease
  • surgical repair
  • muscle strenghthening exercises
91
Q

What is the leading cause of death in myositis?

A

CV disease
(accelerated atherosclerosis, myocarditis)

92
Q

What antibodies are associated with myocarditis?

A

SRP
MDA-5
Jo-1
PL12
Ro
Antimichondrial antibodies

93
Q

What are single gene defects associated with SLE?

A
  • complement deficiencies: C1q, C4A and B, C2
  • TREX1 gene mutations
  • TLR7 gene mutation
94
Q

What drugs can induce lupus?

A

Hydralazine (high risk)
Procainamide (high risk)
etanercept
infliximab
interferon-alpha
minocycline
isoniazid
rifampin
phenytoin
penicillamine
quinidine
phenytoin
methyldopa
chlorpromazine
carbamazepine
ethosuximide
propylthiouracil
sulfasalazine
Diltiazem

95
Q

What are the 3 main types of lupus rashes?

A

Acute (non-scarring):
- malar rash (spares nasolabial folds)
- diffuse erythema of skin
- photosensitivity

Subacute:
- annular, papulosquamous or both
- photosensitivie

Chronic:
- discoid lupus, can scar

96
Q

How is SLE arthritis different to RA arthritis?

A

SLE typically non erosive and non deforming, synovial effusions uncommon and smaller

97
Q

What is Jaccoud’s arthropathy?

A

Rare part of lupus
Tenosynovitis, RA- like swan-neck deformity and ulnar deviation (no erosion on X-ray) and deformity reducible

98
Q

What is the most common cardiac presentation of SLE?

A

Pericarditis

99
Q

What is the most common valvular lesion associated with SLE?

A

Mitral regurgitation

100
Q

What is Libman Sacks endocarditis?

A

Verrucous sterile valvular lesions typically on edge of aortic, mitral and tricuspid valves
Seen in SLE

101
Q

How should antiphospholipid syndrome associated with SLE be managed?

A
  • hydroxychloroquine has anti-thrombotic effect
  • aspirin as prophylaxis
  • lifelong warfarin after first unprovoked venous or any arterial event
    (DOACs shown in meta-analysis to be inferior to warfarin)
102
Q

What SLE antibodies are high risk for neuropsychiatric lupus?

A

antiphospholipid antibodies
Anti-ribosomal p antibodies
Anti neuronal antibodies

103
Q

What CSF features support a diagnosis of neuropsychiatric lupus?

A
  • raised WCC, elevated protein, low glucose
  • oligoclonal bands
  • anti-dsDNA, anti-neuronal and anti-ribosomal p antibodies
104
Q

What auto-antibodies are associated with neonatal lupus?

A

anti-Ro
anti-La
(risk of complete heart block 16-26/40)

105
Q

What SLE autoantibodies are associated with renal involvement?

A

Anti-Sm
Anti-dsDNA

106
Q

What lab measures can be used to measure SLE disease activity?

A

ESR > CRP
Increased anti-dsDNA
Low C3/C4
(not ANA)

107
Q

What are the benefits of hydroxychloroquine for SLE?

A
  • decrease flares
  • decrease organ damage
  • improve survival
  • improve mycophenylate response in lupus nephritis
  • improve cholesterol profile
  • anti-thrombotic

Immunomodulatory NOT immunosuppressive

108
Q

What is the major side effect of hydroxychloroquine?

A

Retinal toxicity

109
Q

When is a renal biopsy indicated in SLE?

A
  • increased serum Cr without alternate cause
  • confirmed proteinuria > 1.0 g/24h
  • At least 2 episodes in short time period of : proteinuria > 0.5g/24h AND haematuria OR cellular casts
110
Q

How is lupus nephritis treated?

A
  • Immunosuppression for class III, IV and V (not for I, II or VI) = induction with IV pulsed steroids AND mycophenylate OR cyclophosphamide, maintenance = mycophenylate or azathioprine
  • ACEi if proteinuria > 0.5g/day
  • Aim BP < 130/80
  • statin for LDL > 2.6
  • Plasma exchange for thrombotic microangiopathy
111
Q

What are contraindications to pregnancy in SLE?

A
  • severe pulmonary hypertension (>50)
  • severe restrictive lung disease (FVC < 1L)
  • advanced renal insufficiency
  • advanced heart failure
  • prior severe pre eclampsia or HELLP
  • stroke in last 6/12
  • severe disease flare in 6/12
112
Q

How can lupus nephritis be distinguished from pre-eclampsia in pregnancy?

A
  • haematuria/active urinary sediment = SLE
  • low complement = SLE
  • Anti-dsDNA level raised in SLE
  • raised liver enzymes and uric acid = pre-eclampsia
113
Q

Is hydroxychloroquine safe in pregnancy? What immunosupresants are safe?

A

Yes
Azathioprine

114
Q

What autoantibodies are associated with rheumatoid arthritis?

A
  • RF (anti-IgG Fc) = more severe + extr-articular
  • ACPA (anti-citrullinated proteins = post-translational modification) = severe + destructive, associated interstitial and CV
  • anti-PAD4
    -anti-CarP
115
Q

What is RS3PE syndrome?

A

Pattern of RA:
- remitting, seronegative, symmetric synovitis with pitting oedema
- hand or foot oedema
- tenosynovitis
- good response to glucocorticoids
- paraneoplastic

116
Q

What is the swan neck deformity of rheumatoid arthritis?

A

Subluxation of lateral bands of extensor tendons resulting in volar herniation of PIP and and flexion of DIP

117
Q

What is the boutinniere deformity of RA?

A

Rupture of PIP through extensor tendon due to tenosynovitis resulting in PIP flexion and DIP extension

118
Q

What sort of pleural effusion is associated with rheumatoid arthritis?

A

Exudate (very low glucose, raised protein : LDH, low complement and low pH)

119
Q

What is felty syndrome?

A

Extra-articular manifestation of seropositive rheumatoid arthritis:
-splenomegaly
- leukopenia
- lower limb ulcers
- hyperpigmentation
- bone marrow hyperplasia

120
Q

What cancers are associated with RA?

A
  • lung cancer
  • lymphoma
121
Q

What are radiographic features of RA?

A
  • periarticular soft tissue swelling
  • juxta-articular osteoporosis
  • marginal erosions
  • joint space narrowing
  • symmetric involvement
  • deformities
122
Q

What is the most effective DMARD for RA?

A

Methotrexate

123
Q

What is the mechanism of action of leflunomide?

A

Inhitis dihydroorate hehydrogenase (enzyme in pyrimidine synthesis, required for T-cell activation)

124
Q

Can patients on biologic DMARDs have live vaccines?

A

No

125
Q

Which patient group with RA should be started on biologics?

A
  • adverse prognostic markers (autoantibodies, high disease activity, radiographic damage)
  • failed 2 course with conventional DMARD
    (not first line)
126
Q

What is the mechanism of action of abatacept?

A

binds to the costimulatory molecules CD80 and CD86 on antigen-presenting cells (APC), thereby blocking interaction with CD28 on T cells

127
Q

What biologics are used for the treatment of RA?

A

TNFi:
- infliximab
- adalimumab
- golimumab
- certolizumab (lacks Fc, safe in pregnancy)
- entancercept (soluble TNF receptor)

Abatacept (CD80 CD86)

Rituximab (anti-CD20)

Tocilizumab (anti-IL-6R)

JAKi:
- tofacitinib
- baricitinib
- upadacitinib

128
Q

When should RA drugs be tapered?

A
  • when in remission for at least 6 months and should maintain therapeutic dose on at least 1 DMARD
  • prefer ceasing sulfasalazine over hydroxychloroquine
  • prefer ceasing methotrexate over biologic
129
Q

What is the cause of gout?

A

Immune response to precipitation of monosodium urate crystals in and around joint space

130
Q

How is uric acid formed in humans and what level defines hyperuricaemia?

A

End product of purine catabolism, conversion of xanthine to urate by xanthine oxidase

> 0.4 mmol/L

131
Q

What are the two x-linked recessive syndromes associated with gout due to impaired purine salvage?

A
  1. Lesch-Nyhan: complete HGPRT1 deficiency
  2. Kelley-Seegmiller: partial HGPRT1 deficiency
132
Q

What is the most common cause of hyperuricaemia?

A

Under-excretion of urate (20% GIT, majority renal) due to transporter mutation or CKD or drugs (diuretics, aspirin)

133
Q

Where in the glomerulus is urate reabsorbed and secreted?

A

Proximal tubule

134
Q
A
135
Q

How do gout crystals appear under polarised light microscopy?

A

intracellular needle-shaped negatively birefringent

136
Q

How is an acute flare of gout managed?

A

NSAID or Prednisone or colchicine +/- intra-articular steroid

137
Q

What are the two classes of urate lowering therapy?

A
  1. xanthine oxidase inhibitors:
    - allopurinol
    - febuxostat
  2. uricosuric agents = inhibit URAT1 and GLUT9 in proximal tubule
    - probenecid
    - benzbromarone
138
Q

What is the serum urate target in gout?

A

< 0.36 (< 0.3 if severe recurrent flares)

139
Q

What are clinical features of allopurinol hypersensitivity syndrome?

A
  • desquamating rash, fever, eosinophilia, end organ damage
  • HLAB*5801 (Han Chinese, Thai)
  • increased risk with concomitant thiazide use
140
Q

When should an underlying primary metabolic disorder in CPPD be investigated for?

A

In. patients presenting < 55 years

141
Q

What are features of CPPD in synovial fluid analysis?

A
  • raised WCC, 90% neuts
  • rhomboid/rod-shaped crystals
  • weak positive bifringence with polarised light
142
Q

How is CPPD managed?

A

NSAIDs, prednisone, corticosteroid injection

RACP 2024 (15 decks)

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