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Zero to Finals: Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

risk factors for OA?

A
  • obesity
  • ageing
  • occupation
  • trauma
  • being female
  • FHx
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2
Q

LOSS: XR changes seen in OA?

A
  • Loss of joint space
  • Osteophytes
  • Subarticular sclerosis
  • Subchondral cysts
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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
  • advise to lose weight
  • physiotherapy
  • occupational therapy
  • orthotics
  • analgesia
  • intra-articular steroid injections
  • hip / knee replacements
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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
  • RA
  • neutropenia
  • splenomegaly
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21
Q

eye signs of RA? hint: everything inflamed af

A
  • scleritis
  • episcleritis
  • keratitis (inflamed cornea)
  • keratoconjunctivitis sicca (dry conjunctiva and cornea)
  • cataracts (due to steroids)
  • retinopathy (due to chloroquine)
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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
  • joint destruction
  • joint deformity
  • soft tissue swelling
  • periarticular osteopenia
  • bony erosions
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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
  • being male
  • younger onset
  • more joints / organs affected
  • RF / anti-CCP antibodies present
  • erosions on XR
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28
Q

management of RA?

A
  • steroids for initial presentation and acute flare ups
  • DMARDs, following ladder
  • surgery
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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
  • adalimumab
  • infliximab
  • immunosuppression
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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
  • mouth ulcers
  • liver toxicity
  • leukopenia (due to bone marrow suppression)
  • teratogenic
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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
  • psoriatic plaques on skin
  • nail pitting
  • onycholysis
  • dactylitis
  • enthesitis
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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
  • conjunctivitis
  • anterior uveitis
  • aortitis (inflamed aorta)
  • amyloidosis
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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
  • periostitis
  • ankylosis
  • osteolysis
  • dactylitis
  • pencil-in-cup appearance
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46
Q

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

A
  • most severe form of PsA
  • osteolysis of joints in fingers, causes skin to fold over
  • “telescopic finger”
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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
  • hot, red, swollen joint
  • bilateral conjunctivitis
  • anterior uveitis
  • circinate balanitis
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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
  • any cause of gastroenteritis
  • chlamydia is most common STI preceding this
  • gonorrhoea more likely to cause gonococcal septic arthritis
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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
  • joint aspiration
  • gram staining, culture and sensitivity
  • to rule out septic arthritis
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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
  • staph aureus (commonest)
  • gonococcus
  • strep pyogenes (and other group A streptococci)
  • H. influenza
  • E. coli
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61
Q

differentials for septic arthritis?

A
  • reactive arthritis
  • gout
  • pseudogout
  • haemoarthrosis
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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
  • inflammatory arthritis affecting spine, causing stiffness and pain
  • seronegative spondyloarthropathies
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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
  • ankylosing spondylitis
  • IBD-related (enteropathic) arthritis
  • reactive arthritis
  • psoriatic arthritis
  • undifferentiated spondylitis
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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
  • lower back pain
  • lower back stiffness
  • sacroiliac pain
  • pain worsened by rest, improves on movement
  • pain may wake patient at night, gets better throughout day
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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
  • bloods (CRP, ESR)
  • HLA B27 gene test
  • X-ray of spine and sacrum
  • MRI spine
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
  • physiotherapy
  • exercise
  • stop smoking
  • bisphosphonates for any osteoporosis
  • surgery for joint deformities
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
  • CVD
  • infection
  • anaemia of chronic disease
  • leukopenia, neutropenia, thrombocytopenia
  • pericarditis
  • pleuritis
  • interstitial lung disease, then pulmonary fibrosis
  • lupus nephritis
  • neuropsychiatric SLE
  • recurrent miscarriage
  • VTE
87
Q

pregnancy complications associated with SLE?

A
  • recurrent miscarriage
  • IUGR
  • pre-eclampsia
  • pre-term labour
88
Q

2 neuro complications of SLE?

A
  • optic neuritis

- transverse myelitis

89
Q

psych complication of SLE?

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
  • when it is either anti-inflammatory resistant or more severe
  • immunosuppressants: methotrexate, azathioprine, tacrolimus
  • biologics: rituximab, belimumab
92
Q

main types of med used in SLE?

A
  • anti-inflammatories
  • immunosuppressants
  • biological therapies
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
  • face
  • ears
  • scalp
96
Q

describe the presentation of lesions in DLE?

A
  • inflamed
  • dry
  • erythematous (red)
  • patchy
  • crusty
  • scaly
97
Q

what skin changes can DLE cause?

A
  • lesions
  • scarring alopecia
  • hyper or hypopigmented scars
98
Q

how is DLE diagnosed?

A

usually done clinically, but can be confirmed with skin biopsy

99
Q

management of DLE?

A
  • sun protection
  • topical steroids
  • intralesional steroid injections
  • hydroxychloroquine
100
Q

what is systemic sclerosis?

A

autoimmune inflammatory, fibrotic connective tissue disease

101
Q

distribution of skin lesions in systemic sclerosis?

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
  • seen in systemic sclerosis
  • swallowing difficulties
  • acid reflux
  • oesophagitis
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
  • shoulders
  • pelvic girdle
  • neck
113
Q

which condition is PMR strongly associated with?

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
  • systemic (weight loss, fatigue, fever, low mood)
  • upper arm tenderness
  • carpal tunnel syndrome
  • pitting oedema
118
Q

differentials of PMR?

A
  • OA, RA
  • SLE
  • myositis
  • cervical spondylitis
  • adhesive capsulitis (of both shoulders)
  • thyroid dysfunction
  • osteomalacia
  • fibromyalgia
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?

124
Q

key complication of GCA?

A

vision loss

125
Q

presentation of GCA?

A
  • headache
  • scalp tenderness on brushing hair
  • jaw claudication
  • blurred / double vission
  • systemic signs
  • irreversible painless complete vision loss
126
Q

nature of headache in GCA?

A
  • severe
  • unilateral
  • affects temple and forehead
127
Q

which systemic signs may be seen in GCA?

A
  • fever
  • muscle aches
  • fatigue
  • loss of appetite / weight
  • peripheral oedema
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
  • antiphospholipid antibodies interfere with the clotting cascade
  • pt is in hypercoagulable state
  • thrombosis occurs
137
Q

which condition can antiphospholipid syndrome occur secondary to?

138
Q

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

A
  • VTE (DVT, PE)
  • arterial thrombosis
  • recurrent miscarriage
  • stillbirth
  • pre-eclampsia
  • Libmann-Sacks endocarditis
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
  • keratoconjunctivitis sicca (most common)
  • episcleritis (red, no pain)
  • scleritis (red and painful)
  • corneal ulceration
  • keratitis
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?

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
  • artificial tears and saliva
  • vaginal lube
  • hydroxychloroquine to halt progression
149
Q

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

A
  • corneal ulcers
  • dental cavities
  • sexual dysfunction
  • oral or vaginal candidiasis
150
Q

which other organs might be affected in sjogren’s?

A
  • lungs (pneumonia, bronchiectasis)
  • lymph nodes (NHL)
  • nerves (peripheral neuropathy)
  • vessels (vasculitis)
  • kidneys (renal impairment)
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
  • polyarteritis nodosa
  • eosinophilic granulomatosis with polyangiitis
  • kawasaki disease
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
  • purpura, non-blanching
  • joint / muscle pain
  • peripheral neuropathy
  • renal impairment
  • GI disturbance (diarrhoea, abdo pain, bleeding)
  • anterior uveitis + scleritis
  • HTN
  • systemic (fever, weight loss, fatigue, anorexia, anaemia)
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
  • specialist referral
  • steroids (prednisolone, hydrocortisone)
  • immunosuppressants (cyclophosphamide, methotrexate)
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
  • nosebleeds
  • crusty nasal secretions
  • hearing loss
  • sinusitis
  • O/E saddle shaped nose (perforated nasal septum)
  • cough
  • wheeze
  • haemoptysis
  • glomerulonephritis
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
  • renal impairment
  • stroke
  • MI
  • livedo reticularis rash
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
  • aorta and pulmonary arteries
  • they swell and aneurysms form
  • may become blocked
  • “pulseless disease”

Zero to Finals: Medicine (11 decks)

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