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mbbs y5 > Medicine - Rheumatology > Flashcards

Medicine - Rheumatology Flashcards

1
Q

risk factors for OA?

A

NAME?

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2
Q

LOSS: XR changes seen in OA?

A

NAME?

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3
Q

presentation of OA?

A
  • joint pain- joint stiffness- worsened by activity - joint deformity- atlantoaxial subluxation of C-spine- reduced ROM
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4
Q

commonly affected joints in OA?

A
  • hips- knees- sacro-iliac joints - DIPs- MCP of thumb- wrist- C-spine
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5
Q

hand signs in OA?

A
  • herberden’s nodes at DIPs (never seen in RA)- bouchard’s nodes at PIPs- squaring at base of thumb- weakened grip- reduced ROM
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6
Q

how is OA diagnosed?

A
  • clinical diagnosis if >45 and these 2 present:- activity-related joint pain- no morning stiffness (or lasts <30 mins)
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7
Q

management of OA?

A

NAME?

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8
Q

describe the 3 steps in analgesia for OA

A
  1. PO paracetamol / topical NSAIDs / topical capsaicin 2. PO NSAIDs + PPI (omeprazole for gut) 3. opiates (codeine, morphine)
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9
Q

what is RA?

A

inflammatory, symmetrical polyarthritis

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10
Q

genetic associations for RA?

A
  • HLA DR4| - HLA DR1
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11
Q

antibodies found in RA?

A
  • anti-CCP (gold standard)| - RF in 70%
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12
Q

presentation of RA?

A
  • joint pain, swelling, stiffness- onset can be as fast as overnight or take months-years- typically MCPs and PIPs of hands affected (DIP-sparing)- fatigue- weight loss- flu-like illness- muscle aches and weakness- short duration if palindromic rheumatism- atlantoaxial subluxation
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13
Q

what is palindromic rheumatism? when would you worry?

A
  • short, self-limiting episode of inflamm arthritis| - when anti-CCP present in blood (almost definitely goes on to develop RA)
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14
Q

what is atlantoaxial subluxation? what is the main complication?

A
  • axis (C2) and atlas (C1) fuse together| - spinal cord compression
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15
Q

hand signs in active RA?

A
  • “boggy” feeling synovium around joints- Z-shaped deformity of thumb- swan neck deformity - boutonnieres deformity- ulnar deviation at MCP joints
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16
Q

describe swan neck deformity

A
  • hyperextended PIP| - flexed DIP
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17
Q

describe boutonnieres deformity

A
  • hypextended DIP| - flexed PIP
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18
Q

systemic signs of RA?

A
  • caplan’s syndrome- bronchiolitis obliterans - felty syndrome (RA, neutropenia and splenomegaly)- sjogren’s syndrome - anaemia of chronic disease- CVD- eye signs- rheumatoid nodules- lymphadenopathy- carpel tunnel syndrome- amyloidosis
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19
Q

what is caplan’s syndrome? where is it seen?

A
  • pulmonary fibrosis with pulmonary nodules| - RA
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20
Q

triad of felty syndrome?

A

NAME?

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21
Q

eye signs of RA? hint: everything inflamed af

A

NAME?

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22
Q

investigations in RA?

A
  • bloods (RF, anti-CCP, CRP, ESR)- XR hands - XR feet - USS shows synovitis
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23
Q

X-ray changes seen in RA?

A

NAME?

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24
Q

why should patients with persistent synovitis be referred? when does it become urgent?

A
  • to rule out RA| - when symptoms have persisted >3m or small joints of hands / feet affected
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25
Q

scoring system used in RA diagnosis? how is it calculated? hint: it u

A
  • disease activity score 28 (DAS28) - looks at tenderness / swelling in 28 joints - takes ESR and CRP into account too
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26
Q

what is the health assessment questionnaire (HAQ) used for? when is it used?

A
  • to measure functional ability in RA| - done at diagnosis to monitor response to treatment
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27
Q

factors indicating a poor prognosis in RA?

A

NAME?

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28
Q

management of RA?

A

NAME?

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29
Q

describe the DMARD ladder in RA?

A
  • 1st line: monotherapy with methotrexate / leflunomide / sulfasalazine / hydroxychloroquine (mild)- 2nd: add another one of above- 3rd: methotrexate + TNF inhibitor (e.g. infliximab)- 4th: methotrexate + CD20 inhibitor (rituximab)
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30
Q

examples of TNF inhibitors? important side effect of these?

A

NAME?

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31
Q

how is methotrexate prescribed? what gets co-prescribed?

A
  • IM / SC injection or weekly tablet| - 5mg folic acid to be taken weekly, but on a different day
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32
Q

side effects of DMARDs?

A

NAME?

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33
Q

unique SE of methotrexate?

A

pulmonary fibrosis

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34
Q

unique SEs of leflunomide?

A
  • HTN| - peripheral neuropathy
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35
Q

unique SE of sulfasalazine?

A

reduces sperm count in men

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36
Q

unique SEs of hydroxychloroquine?

A
  • nightmares| - reduced visual acuity
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37
Q

which underlying diseases could be reactivated by anti-TNF therapy?

A
  • TB| - hep B
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38
Q

unique SEs of rituximab?

A
  • night sweats| - thrombocytopenia
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39
Q

what is psoriatic arthritis (PsA)? which group of conditions is it in?

A
  • an inflammatory arthritis associated with psoriasis| - one of the seronegative spondyloarthropathies
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40
Q

what % of psoriasis patients also have PsA?

A

up to 20%

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41
Q

signs of PsA?

A

NAME?

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42
Q

describe onycholysis

A

nail coming off the nail bed

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43
Q

which conditions might be associated with PsA?

A

NAME?

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44
Q

screening tool for PsA? who gets it?

A
  • psoriasis epidemiological screening tool (PEST)| - all psoriasis patients
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45
Q

X-ray changes seen in PsA?

A

NAME?

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46
Q

what is arthritis mutilans? which body part is affected? key finding?

A

NAME?

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47
Q

management of PsA?

A
  • similar to RA- NSAIDs for pain- DMARDs- anti-TNFs- last line: ustekinumab (targets IL-12 and IL-23)
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48
Q

pathophysiology of reactive arthritis? old name for this?

A
  • synovitis in joints in response to recent infection| - reiter syndrome
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49
Q

presentation of reactive arthritis?

A

NAME?

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50
Q

useful acronym for reactive arthritis presentation?

A

can’t see can’t pee can’t climb a tree

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51
Q

key differential of reactive arthritis?

A

septic arthritis

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52
Q

common infective triggers of reactive arthritis?

A

NAME?

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53
Q

management of reactive arthritis?

A
  • ABx according to local guidelines until septic arthritis ruled out, then:- NSAIDs- steroid injections at joint- systemic steroids if multiple joints affected
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54
Q

investigations for reactive arthritis? why are these done?

A

NAME?

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55
Q

prognosis in reactive arthritis?

A
  • very good| - most resolve in 6 months and never recur
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56
Q

mortality rate in septic arthritis?

A

10%

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57
Q

which procedure increases the risk of septic arthritis?

A

joint replacement

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58
Q

presentation of septic arthritis?

A
  • typically only 1 joint affected- hot, red, swollen joint- stiffness- reduced ROM- systemic: fever, lethargy, sepsis
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59
Q

most common infective organism in septic arthritis?

A

staph aureus

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60
Q

bacterial causes of septic arthritis?

A

NAME?

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61
Q

differentials for septic arthritis?

A

NAME?

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62
Q

management of septic arthritis? which ABx would you choose?

A
  • empirical IV ABx initially - continued for 3-6 weeks - e.g. flucloxacillin + rifampicin 1st line - vancomycin if penicillin allergy / MRSA / prosthetic joint- joint aspirate for staining, microscopy, culture and sensitivities - then tailor ABx to sensitivities
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63
Q

what is ankylosing spondylitis? which group is it in?

A

NAME?

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64
Q

what groups the seronegative spondyloarthropathies together?

A

all linked to HLA B27 gene

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65
Q

which conditions come under seronegative spondyloarthropathies?

A

NAME?

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66
Q

typical demographic affected by ankylosing spondylitis?

A
  • young male in teens / 20s| - M:F = 3:1
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67
Q

presentation of ankylosing spondylitis?

A

NAME?

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68
Q

key complication in ankylosing spondylitis?

A

vertebral fractures

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69
Q

non-spinal signs of ankylosing spondylitis?

A
  • systemic (weight loss, fatigue)- chest pain (from costovertebral joints)- plantar fasciitis, achilles tendonitis (from enthesitis)- dactylitis - anaemia - anterior uveitis- aortitis- heart block - restrictive lung disease- pulmonary fibrosis in 1%- IBD
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70
Q

X-ray findings in ankylosing spondylitis?

A
  • X-ray of spine shows:- “bamboo spine” (all fused together) - squaring of vertebral bodies- subchondral sclerosis and erosions - syndesmophytes - ossification - fusion of facet, sacroiliac and costovertebral joints
71
Q

useful test to assess spine mobility in ankylosing spondylitis?

A
  • schober’s test - mark 2 points on lumbar spine and see how much they move apart on lumbar flexion - if difference is <20cm, this is restricted
72
Q

investigations for ankylosing spondylitis?

A

NAME?

73
Q

what does MRI spine show early on in ankylosing spondylitis?

A
  • bone marrow oedema| - comes up before any x-ray changes do
74
Q

drug management for ankylosing spondylitis?

A
  • NSAIDs- steroids - anti-TNF (etanercept) or infliximab - last line: secukinumab (anti IL-17)
75
Q

non-drug management of ankylosing spondylitis?

A

NAME?

76
Q

what is SLE?

A

inflammatory autoimmune connective tissue disease

77
Q

leading causes of death in SLE patients?

A
  • CVD| - infection
78
Q

antibodies found in SLE?

A

antinuclear antibodies

79
Q

presentation of SLE? hint: there’s a lot

A
  • non-specific- fatigue- weight loss- joint pain, non-erosive arthritis- muscle pain- fever- malar rash- lymphadenopathy- splenomegaly - SOB- pleuritic chest pain- mouth ulcers- hair loss- raynaud’s phenomenon
80
Q

describe the skin changes seen in SLE

A
  • photosensitive malar rash- made worse by sunlight - “butterfly” distribution across nose and cheekbones
81
Q

investigations and findings in SLE?

A
  • autoantibodies (ANA present in 85%)- FBC (anaemia of chronic disease)- C3 and C4 (low in active disease)- CRP and ESR (raised in active disease)- immunoglobulins (raised)- urine protein : creatinine ratio - renal biopsy
82
Q

why are urinalysis and renal biopsy done as SLE investigations?

A

to check for lupus nephritis

83
Q

which antibodies are most specific to SLE? what does this mean?

A
  • anti-double stranded DNA (anti-dsDNA)- anyone who doesn’t have SLE is very unlikely to have these antibodies - 2nd most specific are anti-Smith
84
Q

which condition is associated with anti-Ro and anti-La antibodies?

A

sjogren’s syndrome

85
Q

which condition might develop secondary to SLE?

A

antiphospholipid syndrome

86
Q

complications of SLE?

A

NAME?

87
Q

pregnancy complications associated with SLE?

A

NAME?

88
Q

2 neuro complications of SLE?

A
  • optic neuritis| - transverse myelitis
89
Q

psych complication of SLE?

A

psychosis

90
Q

1st line treatments for SLE?

A
  • hydroxychloroquine (1st line where mild)- NSAIDs- prednisolone- sun cream for rash
91
Q

when are immunosuppressants and biological therapies used in SLE? give some examples

A

NAME?

92
Q

main types of med used in SLE?

A

NAME?

93
Q

typical demographic affected by discoid lupus erythematosus (DLE)?

A
  • female- aged 20-40- dark skinned- smoker
94
Q

prognosis of DLE?

A
  • 5% go on to develop SLE| - rarely progresses to SCC
95
Q

distribution of skin lesions in DLE?

A

NAME?

96
Q

describe the presentation of lesions in DLE?

A

NAME?

97
Q

what skin changes can DLE cause?

A

NAME?

98
Q

how is DLE diagnosed?

A

usually done clinically, but can be confirmed with skin biopsy

99
Q

management of DLE?

A

NAME?

100
Q

what is systemic sclerosis?

A

autoimmune inflammatory, fibrotic connective tissue disease

101
Q

distribution of skin lesions in systemic sclerosis?

A

all over

102
Q

what are the 2 main patterns of disease in systemic sclerosis?

A
  • limited cutaneous (CREST syndrome)| - diffuse cutaneous
103
Q

CREST: features of limited cutaneous systemic sclerosis?

A
  • Calcinosis- Raynaud’s phenomenon - oEsophageal dysmotility - Sclerodactyly - Telangiectasia
104
Q

features of diffuse cutaneous systemic sclerosis?

A

CREST plus: - heart: HTN, CAD- lungs: pulmonary HTN, pulmonary fibrosis- kidneys: glomerulonephritis, scleroderma renal crisis

105
Q

what is calcinosis? where is it typically found?

A
  • calcium deposits under the skin| - fingertips
106
Q

where is oesophageal dysmotility seen? describe some features

A

NAME?

107
Q

features of scleroderma renal crisis?

A
  • severe HTN| - renal failure
108
Q

antibodies found in systemic sclerosis?

A
  • antinuclear antibodies- anti-centromere antibodies (limited)- anti-Scl-70 antibodies (diffuse)
109
Q

investigation done in raynaud’s phenomenon to rule out systemic sclerosis?

A

nailfold capillaroscopy

110
Q

non-medical management of systemic sclerosis?

A
  • stop smoking- skin stretching - emollients- gloves (raynaud’s)- physiotherapy for joints- OT
111
Q

medical management of systemic sclerosis?

A
  • nifedipine (for raynaud’s)- PPIs, metoclopramide (for GI signs)- analgesia (joint pain)- ABx (skin infections)- antihypertensives
112
Q

distribution of joint pain and stiffness in polymyalgia rheumatica (PMR)?

A

NAME?

113
Q

which condition is PMR strongly associated with?

A

GCA

114
Q

describe PMR

A

inflammatory condition causing pain and stiffness in certain joints

115
Q

typical demographic affected by PMR?

A

Caucasian women aged >50

116
Q

NICE criteria for diagnosing PMR?

A

the following present for >2 weeks:- bilateral shoulder pain- bilateral pelvic girdle pain- pain worse on movement- pain interfering with sleep- 45 mins or more of morning stiffness

117
Q

other, non-diagnostic features of PMR?

A

NAME?

118
Q

differentials of PMR?

A

NAME?

119
Q

investigations in PMR? hint: mostly to rule out differentials

A
  • ESR, plasma viscosity and CRP all raised (inflammation)- FBC, UEs, LFTs to rule out other causes- Ca (raised in hyperPT / cancer, low in osteomalacia)- serum protein electrophoresis (myeloma)- CK (myositis)- rheumatoid factor (RA)- ANA (SLE)- anti-CCP (RA)- urinary bence jones protein (myeloma)- CXR (lung abnormalities)
120
Q

treatment of PMR?

A
  • 15mg prednisolone per day for a week- if no improvement after 1 week, PMR ruled out- there should be a 70% improvement in 3-4 weeks - if this is the case, start a reducing regime - more severe: refer to rheum
121
Q

DON’T stop: advice for patients on long-term steroids?

A
  • DON’T: they should not stop taking steroids suddenly because of risk of adrenal crisis- Sick day rules: reduce dose if feeling ill- Treatment card: carry it - Osteoporosis: consider bisphosphonates, Ca and vit D to prevent this- PPI: consider omeprazole for stomach lining protection
122
Q

what is giant cell arteritis (GCA)?

A

systemic vasculitis which affects the medium and large arteries

123
Q

which condition is GCA strongly associated with?

A

PMR

124
Q

key complication of GCA?

A

vision loss

125
Q

presentation of GCA?

A

NAME?

126
Q

nature of headache in GCA?

A

NAME?

127
Q

which systemic signs may be seen in GCA?

A

NAME?

128
Q

how is GCA diagnosed?

A
  • clinical presentation - ESR >50mm/h (raised)- temporal artery biopsy findings
129
Q

investigations in GCA?

A
  • bloods (raised ESR and CRP, FBC may show anaemia + thrombocytosis)- temporal artery biopsy - LFTs (raised ALP)- duplex USS of temporal artery
130
Q

what is found on temporal artery biopsy in GCA?

A

multinucleated giant cells

131
Q

what is found on duplex USS of the temporal artery in GCA?

A

hypoechoic halo sign

132
Q

management of GCA?

A
  • start high-dose steroids before confirming diagnosis- 40-60mg pred per day- aspirin 75mg (decreases vision loss / stroke risk)- PPI for gastric protection
133
Q

why should high-dose steroids be started before a diagnosis of GCA is confirmed?

A

to reduce risk of permanent vision loss

134
Q

which antibodies are found in antiphospholipid syndrome?

A
  • lupus anticoagulant- anticardiolipin antibodies- anti-beta-2 glycoprotein I antibodies
135
Q

key complication in women with antiphospholipid syndrome?

A

recurrent miscarriage

136
Q

describe the pathophysiology of antiphospholipid syndrome

A

NAME?

137
Q

which condition can antiphospholipid syndrome occur secondary to?

A

SLE

138
Q

complications of antiphospholipid syndrome? hint: 3 of them are pregnancy-related

A

NAME?

139
Q

rash seen in antiphospholipid syndrome? what does it look like?

A
  • livedo reticularis| - purple lace like rash, makes skin look mottled
140
Q

what is Libmann-Sacks endocarditis? which conditions is it seen in?

A
  • non-bacterial vegetations on mitral valve| - SLE and antiphospholipid syndrome
141
Q

how is antiphospholipid syndrome diagnosed?

A
  • Hx of thrombosis / recurrent pregnancy complications| - PLUS: presence of any of the 3 antibodies
142
Q

management of antiphospholipid syndrome?

A
  • long-term warfarin (aim for INR 2-3) to prevent VTE- LMWH (enoxaparin) + aspirin in pregnancy to reduce complication risk- remember NO warfarin in pregnancy!
143
Q

eye signs seen in RA?

A

NAME?

144
Q

key features of sjogren’s syndrome?

A

dry mucous membranes:- dry eyes- dry mouth- dry vagina

145
Q

which conditions might sjogren’s syndrome occur secondary to?

A
  • SLE| - RA
146
Q

which antibodies are associated with sjogren’s syndrome?

A
  • anti-RO| - anti-La
147
Q

which condition is the schirmer test used to diagnose? what does this involve?

A
  • sjogren’s syndrome- putting a dry folded piece of paper under the lower eyelid- wait 5 mins - measure distance travelled by tears - 15mm in healthy adult- <10mm in sjogren’s
148
Q

management of sjogren’s syndrome?

A

NAME?

149
Q

complications of sjogren’s syndrome? hint: all relate to areas of dryness

A

NAME?

150
Q

which other organs might be affected in sjogren’s?

A

NAME?

151
Q

which types of vasculitis affect small vessels?

A
  • HSP- eosinophilic granulomatosis with polyangiitis - microscopic polyangiitis- wegener’s granulomatosis
152
Q

which types of vasculitis affect medium-sized vessels?

A

NAME?

153
Q

which types of vasculitis affect large vessels?

A
  • GCA| - takayasu’s arteritis
154
Q

presentation of vasculitis? hint: there’s a LOT

A

NAME?

155
Q

blood tests and findings in vasculitis?

A
  • CRP and ESR (raised)| - ANCA (positive)
156
Q

in which conditions will p-ANCA be positive?

A
  • microscopic polyangiitis| - eosinophilic granulomatosis with polyangiitis
157
Q

in which condition will c-ANCA be positive?

A

wegener’s granulomatosis

158
Q

management of vasculitis?

A

NAME?

159
Q

describe the pathophysiology of HSP

A

there are IgA deposits in certain blood vessels which give symptoms in the affected areas

160
Q

which demographic is most commonly affected by HSP?

A

children under 10

161
Q

4 classic features of HSP?

A
  • purpura- joint pain- abdo pain (for first few days)- renal impairment (IgA nephritis in 50%)
162
Q

prognosis of HSP?

A
  • most fully recover in 4-6 weeks - 1 in 3 have it again within 6 months - 1% get ESRF
163
Q

key finding on bloods in eosinophilic granulomatosis with polyangiitis?

A

raised eosinophils on FBC

164
Q

presentation of wegener’s granulomatosis?

A

NAME?

165
Q

CXR findings in wegener’s granulomatosis?

A
  • consolidation| - often mistaken for pneumonia!
166
Q

which infection is polyarteritis nodosa most associated with? which others might it be associated with?

A
  • hep B| - HIV, hep C
167
Q

features of polyarteritis nodosa?

A

NAME?

168
Q

describe livedo reticularis. which condition is it seen in?

A
  • mottled, purple, lacy rash| - polyarteritis nodosa
169
Q

typical demographic affected by kawasaki disease?

A

children under 5

170
Q

features of kawasaki disease?

A
  • persistent high fever for >5 days- erythematous rash- bilateral conjunctivitis - redness and desquamation of soles of palms / soles- strawberry tongue
171
Q

key complication of kawasaki disease?

A

coronary artery aneurysm

172
Q

treatment of kawasaki disease?

A
  • aspirin| - IV immunoglobulins
173
Q

which named arteries are mainly affected in takayasu’s arteritis? what does it cause?

A

NAME?

mbbs y5 (27 decks)

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