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Finals Revision > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is the commonest seropositive inflammatory condition?

A

Rheumatoid arthritis

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2
Q

Who is RA common in?

A

Women aged 35-50, genetic association

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3
Q

What is the pathophysiology of RA?

A

Autoimmune destruction of the synvoium ultimately leading to joint destruction

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4
Q

How does RA present?

A

Symmetrical swollen stiff joints, worse in the morning, better after use

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5
Q

What are signs of RA?

A

Symmetrical synovitis, pain, lymphadenopathy, lung fibrosis, pleural effusion, Raynauds, carpal tunnel, episcleritis, scleritis

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6
Q

What antibodies are positive in RA?

A

Rf +ve

Anti CCP +ve

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7
Q

What does an x-ray in RA show?

A

Soft tissue swelling, bony erosions, subluxation, destruction, peri-articular osteopenia

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8
Q

How is disease monitored in RA?

A

DAS28 score

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9
Q

When should DMARDs be initiated in RA?

A

Within 3 months of onset

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10
Q

What DMARDs are used in RA normally?

A

Methotrexate and sulphasalazine

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11
Q

What drugs are used for flare ups in RA?

A

Steroids

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12
Q

What drugs may be used for symptomatic relief in RA?

A

NSAIDs

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13
Q

What can be used if DMARDs do not work well?

A

Biologics (e.g. Anti-TNF)

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14
Q

What are the 4 seronegative arthropathies?

A

Ankylosing spondylitis
Psoriatic arthritis
Enteropathic arthritis
Reactive arthritis

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15
Q

What are the seronegative arthropathies characterised by?

A

Inflammation and/or arthritic disease of the spine

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16
Q

Who commonly gets ankylosing spondylitis?

A

Males aged 20-40

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17
Q

What are symptoms of ankylosing spondylitis?

A

Lower back pain, stiffness of insidious onset, worse in mornings, improves with exercise

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18
Q

What are signs of ankylosing spondylitis?

A

Loss of spinal movement - reduced lateral flexion and forward flexion, reduced chest expansion. Question mark spine - loss of lumbar lordosis and increased thoracic kyphosis

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19
Q

What are some associated features of ankylosing spondylitis?

A

Anterior uveitis, achilles tendonitis, pulmonary fibrosis, amyloidosis,

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20
Q

What will investigations show in Ank Spond?

A

Raised ESR and CRP

HLA B27 +ve

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21
Q

What does an x-ray in ank spond show?

A

Sacroilitis, squaring of lumbar vertebrae, bamboo spine

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22
Q

What is the management of ank spond?

A

Physiotherapy/exercise
NSAIDs
DMARDs - only useful in peripheral joint disease
Anti-TNFs reserved for if severe

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23
Q

How many people with psoriasis have psoriatic arthritis?

A

30%

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24
Q

How does psoriatic arthritis present?

A

Asymmetrical oligoarthritis. Rheumatoid like. Spondylitis. Dactilitis. Pitting and onycholysis of the nails

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25
Q

What is the management of psoriatic arthritis?

A

Treated the same as RA - DMARDs, NSAIDs, steroids, anti-TNFs

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26
Q

What is enteropathic arthritis?

A

Inflammatory arthritis inolving peripheral joints and occasionally spine in patients with IBD

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27
Q

How does enteropathic arthritis present?

A

Asymmetrical large joint oligoarthritis

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28
Q

How is enteropathic arthritis managed?

A

Immunosuppressive drug that manages both IBD and arthritis

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29
Q

What is reactive arthritis?

A

An arthritis occurring in response to infection in another part of the body

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30
Q

What infections does reactive arthritis commonly occur in?

A

STIs (chlamydia, gonorrhoea) or GI infections (salmonella)

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31
Q

How does reactive arthritis present?

A

Develops within 4 weeks of getting infection. Lasts around 4-6 months. Large joint oligoarthritis. Also get balanitis, conjunctivitis, urethritis etc

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32
Q

What is the triad of Reiters syndrome?

A

Arthritis, Conjunctivitis, Urethritis

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33
Q

How is reactive arthritis managed?

A 
Treat underlying infection
Symptomatic relief (IA/IM steroids)
Occasionally DMARDs in chronic cases
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34
Q

What are connective tissue diseases?

A

Multisystem disorders that cause organ pathology

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35
Q

What is systemic lupus erythematosus?

A

Chronic autoimmune condition which presents highly variably. More common in women

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36
Q

What is the pathogenesis of SLE?

A

Immune system dysregulation leading to immune complex formation and deposits

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37
Q

What are constitutional symptoms of SLE?

A

Fever, fatigue, weight loss

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38
Q

What are MSK symptoms of SLE?

A

Arthralgia, myalgia, inflammatory arthritis

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39
Q

What skin manifestations are seen in SLE?

A

Malar rash, photosensitivity, discoid lupus, oral/nasal ulceration, Raynauds

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40
Q

What are renal manifestations in SLE?

A

Lupus nephritis

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41
Q

What are respiratory manifestations of SLE?

A

Pleurisy, pleural effusion, pneumonitis, PE, pulmonary hypertension, ILD

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42
Q

What are cardiac manifestations of SLE?

A

Pericarditis, effusion, accelerated IHD

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43
Q

What are GI manifestations of SLE?

A

Autoimmune hepatitis, pancreatitis, mesenteric vasculitis

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44
Q

What investigations do you do for SLE?

A

FBC - anaemia, leucopenia, thrombocytopenia
Immunology
Urinalysis (for GN)
Imaging for organ involvement

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45
Q

What antibodies are positive in SLE?

A

ANA
Anti-DsDNA (key one)
Anti-Sm, Anti Ro, Anti La, Anti-RNP, complement

46
Q

How is SLE managed?

A

Hydroxychloroquine, NSAIDs, Azaithioprine, Mycophenolate

IV steroids and biologics if severe

47
Q

How is SLE monitored?

A

Anti-DsDNA and complement
Urinalysis
Evaluation of cardiac risk

48
Q

What is sjogrens syndrome?

A

Autoimmune disorder causing lymphocytic infiltration of exocrine glands, resulting in dry mucosal surfaces

49
Q

What are features of sjogrens?

A

Keratoconjuncitivis sicca, dry mouth, vaginal dryness, arthralgia, raynauds, myalgia, sensory polyneuropathy

50
Q

What investigations are done for sjogrens syndrome?

A

Immunology, schirmers test, tissue biopsy

51
Q

What does immunology show in sjogrens?

A

Anti-Ro/Anti-La positive

RF +ve ANA +ve

52
Q

How is sjogrens syndrome managed?

A

Symptomatic relief - lubricating eye drops, saliva replacement
Hydroxychloroquine for arthralgia and fatigue

53
Q

What is systemic sclerosis?

A

Condition characterised by hardened skin and collagen deposition in connective tissues

54
Q

How does systemic sclerosis present?

A

Raynauds, skin sclerosis, sclerodactyly, finger tip atrophy, telangactasia, calcinosis, pulmonary fibrosis, hypertension, dysphagia, malabsorption, arthritis, myositis

55
Q

What is limited systemic sclerosis?

A

Skin involvement of face and limbs and minimal organ involvement (CREST syndrome)

56
Q

What is diffuse systemic sclerosis?

A

Skin changes on trunk and diffuse organ involvement

57
Q

What antibodies are positive in systemic sclerosis?

A

Anti-centromere (limited)

Anti-scl-70 (diffuse)

58
Q

How is systemic sclerosis treated?

A

Raynauds = calcium channel blockers
Renal involvement = ACE inhibitors
GI upset = PPIs
ILD = cyclophosphamide

59
Q

What is mixed connective tissue disease?

A

Condition featuring a mixture of different symptoms from other connective tissue diseases

60
Q

What antibody is positive in mixed connective tissue disease?

A

Anti-RNP

61
Q

What is antiphospholipid syndrome?

A

Autoimmune condition presenting as recurrent thrombosis and fetal loss

62
Q

How does antiphospholipid syndrome present?

A

Recurrent thrombosis, fetal loss, migraine, livedo reticularis

63
Q

What immunology is positive in antiphospholipid syndrome?

A

Positive Anti-cardiolipin antibodies

64
Q

How is anti-phospholipid syndrome managed?

A

Anti-coagulation (only if have had thrombosis not just if positive antibodies)

65
Q

What is gout?

A

Crystal arthropathy characterised by deposition of urate crystals within a joint

66
Q

What causes gout?

A

Increased uric acid due to dietary purines (seafood, red meat), alcohol excess, diuretics, leukaemia, CKD

67
Q

How does gout present?

A

Acute monoarthropathy, usually 1st MTP. Intensely red hot and swollen

68
Q

What does light microscopy show in gout?

A

Negatively birefringent needle shaped crstals

69
Q

What may be seen on x-ray in gout?

A

Joint effusion, punched out lesions, soft tissue tophi

70
Q

How is gout treated acutely?

A

NSAIDs, corticosteroids, colchicine (if NSAIDs contraindicated)

71
Q

How is gout treated prophylactically?

A

Allopurinol

72
Q

How long after an acute gout attack should allopurinol be started?

A

2 weeks after

73
Q

What is pseudogout?

A

Crystal arthropathy caused by deposition of calcium pyrophosphate

74
Q

What are causes of pseudogout?

A

Old age, OA, diabetes, hypothyroidism, hyperparathyroidism, haemochromatosis, Wilsons disease

75
Q

How does pseudogout present?

A

Monoarthropathy, red hot swollen joint, usually larger joints than gout e.g. knee

76
Q

What does light microscopy show in pseudogout?

A

Positively birefringent rhomboid shaped crystals

77
Q

How is pseudogout treated?

A

Analgesia, NSAIDs, steroids

78
Q

What is polymyalgia rheumatica?

A

Common inflammatory condition of unknown aetiology of the elderly

79
Q

How does PMR present?

A

Subacute onset of symmetrical proximal myalgia of the hip and shoulder girdles and accompanying morning stiffness

80
Q

What do investigations show in PMR?

A

Raised inflammatory markers (CRP, PV, ESR)

Normal CK

81
Q

How is PMR managed?

A

Low dose steroids should show a dramatic response

82
Q

What is PMR associated with?

A

Giant cell arteritis

83
Q

How does GCA present?

A

Visual disturbance, headache, scalp tenderness, jaw claudication

84
Q

What is polymyositis?

A

Inflammatory muscle condition causing symmetrical proximal muscle weakness

85
Q

What is the pathogenesis of polymyositis?

A

T cell mediated process against muscle antigens

86
Q

How does polymyosisits present?

A

Symmetrical proximal weakness, insidious onset, often noticed when doing particular activities e.g. walking up and down stairs

87
Q

What do investigations show in polymyosisits?

A

Raised inflammatory markers (ESR, CRP, PV)
Raised CK
EMG abnormal
Muscle biopsy shows irregular findings

88
Q

What antibodies are seen in polymyositis?

A

Anti-Jo-1

89
Q

How is polymyositis managed?

A

Steroids and immunusuppressants

90
Q

What should all patients with polymyositis be investigated for?

A

Underlying malignancy (25%)

91
Q

What are the cutaneous manifestations in dermatomyositis?

A

V shaped chest rash
Heliotrope rash
Gottrons papules

92
Q

What are side effects of methotrexate?

A

Interstitial pneumonitis
Myelosuppression
Liver cirrhosis

93
Q

What are side effects of sulphasalazine?

A

Rashes
Oligospermia
Interstitial lung disease

94
Q

What are side effects of hydroxychloroquine?

A

Retinopathy

Corneal deposits

95
Q

What is side effect of Gold?

A

Proteinuria

96
Q

What are the side effects of penicillamine?

A

Proteinuria

Exacerbation of myaesthenia gravis

97
Q

What are side effects of biologics (e.g. infliximab, rituximad, etanacept)?

A

Reactivation of TB

98
Q

What does methotrexate + trimethoprim cause?

A

Marrow aplasia

99
Q

What does azaithioprine + allopurinol cause?

A

Bone marrow suppression

100
Q

What is Feltys syndrome?

A

RA
Neutropenia
Splenomegaly

101
Q

Which rheumatoid drug should patients with an allergy to aspirin not take?

A

Sulphasalazine

102
Q

What Schobers test result is indicative of Ankylosing spondylitis?

A

<5cm

103
Q

What condition is cANCA +ve?

A

Wegners granulomatosis

104
Q

What condition is pANCA +ve?

A

Churgg-Strauss

105
Q

What is found in Takyasu’s vasculitis?

A

Upper limb claudication, absent upper limb pulses, ESR raised

106
Q

What is found in Buergers disease?

A

Occlusions of lower limbs, absent distal pulses, tortuous corkscrew shaped collateral vessels on angiography

107
Q

‘pencil in cup appearance’

A

Psoriatic arthritis

108
Q

What antibodies are associated with drug induced lupus?

A

Antihistone

109
Q

What type of hypersensivity reaction is lupus?

A

Type 3

110
Q

What are the classic features of Bechets disease?

A

Oral ulcers, genital ulcers, anterior uveitis, arthritis,

Finals Revision (22 decks)

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