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Pocket MSRA - Book 1 > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What are the key presenting features of OA?

A

Oligo-pauci-arthritis (<5 joints)
-can be asymmetrical
Joint stiffness worsens t/o day
Neuropathic pain

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2
Q

What are the key examination findings of OA?

A

Oligo-pauci-arthritis (<5 joints)
-can be asymmetrical
Crepitus
Muscle wasting
HerbeDen (DIPJ) and Bouchard (PIPJ) nodes

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3
Q

What are the key risk factors for OA?

A

Age
Obesity
Trauma

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4
Q

How should OA be treated?

A

Lifestyle/conservative w/ paracetamol –>
NSAIDs –>
Co-codamol –>
Intra-articular steroids –>
Joint replacement

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5
Q

What are the key risk factors for RA?

A

Smoking
FHx

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6
Q

What are the key presenting features of RA?

A

Poly-articular (>5 joints)
-symmetrical
DEFORMING
Early morning stiffness/pain improves w/ use
Constitutional sx

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7
Q

What are the key examination findings of RA?

A

Poly-articular (>5 joints)
-symmetrical
Boggy joints
Rheumatoid nodules
Joint deformity

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8
Q

What are the different patterns of RA?

A

Insidious (70%)
Acute (15%)
Constitutional (10%)
Palindromic (5%)

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9
Q

What are the systemic associations of RA?

A

ILD
Pleural effusion
Atherosclerosis
Anaemia
Mononeuritis multiplex + compression neuropathy
Scleritis & episcleritis
Felty syndrome
Lymphoma

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10
Q

What is Felty syndrome?

A

Triad of:
-RA
-Splenomegaly
-Neutropenia
Causes recurrent infections

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11
Q

What is a Swan-Neck deformity?

A

PIPJ hyperextended
DIPJ flexed

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12
Q

What is a Boutonniere deformity?

A

PIPJ flexed
DIPJ hyperextended

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13
Q

What is a Z-thumb?

A

MCPJ fixed flexion
PIPJ and DIPJ hyperextended

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14
Q

What is Jaccoud’s arthropathy?

A

Ulnar subluxation
-non-erosive

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15
Q

What is Vaughan-Jackson syndrome?

A

Inability to extend 5th finger 2o extensor tendon disruption on ulnar side
-seen in RA

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16
Q

What is arthritis mutilans?

A

Severe destructive joint disease
-seen in RA/PA

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17
Q

What % of patients w/ RA have a positive RF?

A

70%

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18
Q

What are the XR signs of arthritis?

A

Osteopenia
Cartilage loss
Space loss
Erosions
Subluxation

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19
Q

What is the management of RA?

A

Steroids AND DMARDs
-Methotrexate
-Hydroxychloroquine

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20
Q

How does PA present?

A

ANY joint pattern
Psoriatic rash
Tendon disease
Nail disease

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21
Q

What tendon problems are common in PA?

A

Achilles tendinitis
Golfer/tennis elbows
Plantar fasciitis
DACTYLITIS

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22
Q

What nail problems are common in PA?

A

Pitting
Onycholysis
Subungual hyperkeratosis
Dystrophy

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23
Q

What ix are indicated in PA?

A

ESR
XR (pencil-in-cup deformity)
SERONEGATIVE

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24
Q

What is the rx for PA?

A

NSAIDs
Methotrexate
AVOID STEROIDS - psoriatic flare
Sulfasalazine - if spinal
Ciclosporin +/- retinoids +/- anti-TNF +/- secukinumab +/- ustenkinumab - if severe

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25
Q

What are the key features of reactive arthritis?

A

Can’t see (uveitis)
Can’t pee (urethritis/cervicitis)
Can’t climb a tree (joint pain - usually monoarthropathy)
Rashes
Post infection

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26
Q

What mucocutaneous rashes are seen in reactive arthritis?

A

Keratoderma blenorrhagia
Circinate balanitis

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27
Q

What infections is reactive arthritis commonly associated with?

A

Salmonella
Chlamydia
Campylobacter
NOT GONORRHEA

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28
Q

What is the treatment for reactive arthritis?

A

Self-limiting
NSAIDs +/- steroid inj

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29
Q

What is ankylosing spondylitis?

A

Inflammation of sacro-iliac joints/spine
Typically affects young adult males who SMOKE

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30
Q

What are the HLA B-27 related arthritides?

A

Psoriatic
Reactive
Ankylosing Spondylitis

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31
Q

What are the key features of ank spond?

A

A’s
-achilles tendinitis
-ant uveitis
-aortitis (AR)
-apical pulmonary fibrosis
-acute pleural effusion
-ant. chest wall fusion
-associated colitis

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32
Q

How is ank spond investigated?

A

XR spine
-sacroillitis
-romano lesion
-syndesmophytes
-bamboo spine (end-stage)

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33
Q

What is the treatment for ank spond?

A

1 - Stop smoking, NSAIDs, PT
2 - Anti-TNFa
3 - Secukinumab

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34
Q

What are the crystal arthropathies?

A

Gout
Pseudogout

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35
Q

What are the risk factors for Gout?

A

CKD
Lifestyle - red meat, EtOH
Thiazides/thiazide-like (indapamide) precipitate attacks

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36
Q

How is gout diagnosed?

A

Joint aspiration
-negatively birefringent needles-shaped MSU crystals

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37
Q

How is gout treated?

A

Flare - NSAIDs, colchicine –> steroids
PPx - Allopurinol (not started during a flare but NOT stopped)

38
Q

What are the common s/e of Allopurinol?

A

Rashes (rarely SJS)
Somonlence
Vertigo
Ataxia

39
Q

What are the risk factors for Pseudogout?

A

M>W

40
Q

How is pseudogout investigated?

A

Joint aspirate
-rhomboid +ve birefringement
XR
-chondrocalcinosis

41
Q

How can pseudogout be distinguished from gout clinically?

A

Larger joints affected (shoulder, wrist, knee)
Attacks more prolonged but less painful

42
Q

How should pseudogout be treated?

A

NSAIDs, colchicine
Local injection

43
Q

How does septic arthritis present?

A

Red hot MONOArthropathy and unwell patient

44
Q

How should septic arthritis be ix and rx?

A

Joint aspirate
IV a/b
May need washout

45
Q

What are the s/e of Methotrextate?

A

Teratogenic
Requires folate replacement
Pneumonitis/ILD
GI upset
Bone marrow suppression
Hepatotoxicity

46
Q

What are the s/e of Sulphasalazine?

A

Bone marrow suppression (FBC)
Hepatotxic (LFTs)
Rash
MALE INFERTILITY

47
Q

What are the s/e of Hydroxychloroquine?

A

Bulls eye maculopathy
-yearly screening if >40 OR eye problems

48
Q

What are the s/e of Azathioprine?

A

Fever
Bruising
Hepatotoxicity (LFTs)
Bone marrow suppression (FBC)

49
Q

What are the s/e of Penicillamine?

A

Drug-induced SLE
Rash
Ulcers
Loss of taste
Proteinuria (Pr:Cr)
Bone marrow suppression (FBC)

50
Q

What are the s/e of Cyclophosphamide?

A

Skin pigmentation
MALE INFERTILITY
Haemorrhagic cystitis

51
Q

What are the s/e of Ciclosporin?

A

Bone marrow suppression (FBC)
Renal failure (hyperK, Cr, HTN, oedema)
Gingival hyperplasia

52
Q

What are the s/e of anti-TNFa?

A

Disseminated TB (screen before starting)
CHF
Sepsis
Demyelination

53
Q

What are the clinical criteria for SLE?

A

1 - Acute cutaneous (malar)
2 - Chronic cutaneous (discoid)
3 - Non-scarring alopecia
4 - Oronasal ulcers
5 - Arthritis (>2 joints)
6 - Serositis
7 - Renal (Type IV Nephritis)
8 - Neuropsychiatric
9 - Haemolytic anaemia
10 - Leukopenia
11 - Thrombocytopenia

54
Q

What are the immunological criteria for SLE?

A

1 - DCT +ve
2 - ANA
3 - Anti-DNA
4 - Anti-Smith
5 - Antiphospholipid
6 - Low C3/C4/CH50

55
Q

What medications can induce SLE?

A

Penicillamine
Isoniazide
Minocycline
Hydralazine
Phenytoin
Procainamide
Quinidine
Anti-TNFa

56
Q

What is the association between APS and SLE?

A

~1/3 of SLE have APS

57
Q

How does APS present?

A

Hypercoagulable state
-recurrent pregnancy loss
-DVTs/PEs
-Budd Chiari
-CVA

58
Q

How is APS treated?

A

Hydroxychloroquine
Azathioprine
Low-dose steroids
Anticoagulation

59
Q

How is SLE treated?

A

Avoid sunlight
Mild - NSAIDs, + HCQ
Mod - HCQ + low dose steroids +/- AZA/MTX
Severe - pulse steroids, mycophenolate, cyclophosphamide, biologics

60
Q

What are the risk factors for Sjogrens?

A

Female
Middle-age
Other autoimmune conditions

61
Q

How dose Sjogren’s present?

A

Sicca
Xerostomia
Dry vagina = thrush + dyspaerunia

62
Q

How is Sjogren’s investigated?

A

Anti-RNP
Anti-Ro/Anti-La (60%)
RhF (100%)
Biopsy of small salivary glands

63
Q

What are the complications of Sjogren’s?

A

B-cell marginal zone lymphoma
Neonatal lupus

64
Q

How is Sjogren’s treated?

A

NSAIDs
HCG

65
Q

What is the difference between Polymyositis and Dermatomyositis?

A

POLYmyositis - skin only
DERMATOmyositis - skin + skm involvement

66
Q

What are the presenting features of polymyositis/dermatomyositis?

A

Muscle
-b/l proximal weakness (esp. anti-grav muscles)
-tender
-waddling gait
Skin
-shawl sign
-heliotrope rash
-gottron’s papule
-linear erythema
-angioedema
-mechanic’s hand
-hyperaemic nail fold

67
Q

How are polymyositis/dermatomyositis treated?

A

Steroids
IVIG
Rituximab
Cyclophosphamide
SCREEN FOR CA

68
Q

What are the features of CREST syndrome?

A

CREST syndrome
-calcinosis
-raynauds
-eosophageal dysmotility
-sclerodactyly
-telangiectasia of face
Associated w/ pulm HTN

69
Q

What are the two main subtypes of systemic sclerosis?

A

Limited (CREST)
Diffuse

70
Q

What are the features of diffuse systemic sclerosis?

A

Skin tightening affecting neck/truck w/ early organ involvement
-ILD –> pulm HTN
-cardiac fibrosis
-GI dysmotility
-renal crisis

71
Q

How is systemic sclerosis treated?

A

Cyclophosphamide

72
Q

What are the two-types of anti-nuclear cytoplasmic antibody?

A

c-ANCA (GPA)
p-ANCA (MPA)

73
Q

What is the ddx for pulmonary-renal syndromes?

A

Wegener’s (GPA)
Microscopic polyangiitis (MPA)
Lupus
Goodpastures

74
Q

What are the presenting features of Wegener’s (GPA)?

A

Cavitating lung lesions
ENT/nasopharyngeal sx
Crescenteric rapid progressive glomerulonephritis
Arthralgia
Deafness

75
Q

What are the presenting features of MPA?

A

Pulm haemorrhage
Proteinuria
Purpura + vasculitic rash
Peripheral neuropathy
Polyarthralgia
Painful gut (mesenteric angina)

76
Q

What is Goodpastures disease?

A

Type IV Collagen a/b against glomerular basement membrane and lung collagen
–> rapid-onset crescenteric nephritis
–> pulm haemorrhage

77
Q

What is Churg-Strauss?

A

Eosinophilic granulomatosis w/ polyangiitis
-small-medium vessel vasculitis

78
Q

How does Churg-Strauss present?

A

Adult-onset asthma w/ nasal polypods
Eosinophilia –> pneumonia/cardiac involvement

79
Q

What is Cryoglobulinaemia?

A

Vasculitis caused by protein precipitation at low temps
-Type 1 (monoclonal IgG/M) = seen in MGUS
-Type 2 = hep C associated
-Type 3 = mixed polyclonal Ig disease

80
Q

What is polyarteritis nodosa?

A

Necrotising vasculitis affecting all organs EXCEPT lungs

81
Q

How does polyarteritis nodosa present?

A

Coronary - angina
Renal - AKI, HTN
SMA - mesenteric angina (post prandial colicky pain)
Skin ulcers, livedo reticularis
Neuro - mononeuritis multiplex
Myalgia
Sterile orchitis

82
Q

How is polyarteritis nodosa diagnosed?

A

Biopsy
Angiogram
-saccular microaneurysms w/ alternating fibrosis

83
Q

How is polyarteritis nodosa treated?

A

Mild –> AZA, MTX, MMF
Severe –> Cyclophosphamide
Stenting when inflammation settled

84
Q

What is Takayasu arteritis?

A

Large vessel vasculitis
Causes claudication sx in patients w/ no risk factors

85
Q

How is Takayasu arteritis diagnosed?

A

Radiological (MRA/CT-PET)

86
Q

How is Takayasu arteritis treated?

A

Pulse steroids
Cyclophosphamide
Stent when inflammation settled

87
Q

What is Giant cell/temporal arteritis?

A

Large vessel vasculitis
-predilection for extracranial branches of carotid artery

88
Q

How does GCA present?

A

Constitutional sx
Pulse-synchronous unilateral headache
Stiff, tender temp artery
Scalp tenderness w/ facial pain
Jaw/arm claudication
Vertigo/hearing loss
Amaurosis fugax/transient visual loss
PMR

89
Q

How is GCA diagnosed?

A

Clinical
High ESR
Temporal artery biopsy

90
Q

How is GCA treated?

A

Pulse steroids
Wean steroids until sx free at lowest dose

Pocket MSRA - Book 1 (7 decks)

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