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02F > 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
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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
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72
Q

investigations for ankylosing spondylitis?

A
  • bloods (CRP, ESR)
  • HLA B27 gene test
  • X-ray of spine and sacrum
  • MRI spine
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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?

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
  • 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?

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
  • 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?

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
  • 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?

A

PMR

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?

A

SLE

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?

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
  • 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”
174
Q 
what is behcets disease?
Gene association 
Features 
Test 
Management
A

multisystem disorder arising from inflammation of arteries and veins
HLA b51

Oral ulcers, genital ulcers, anterior uveitis
thrombophlebitis and deep vein thrombosis
arthritis
neurological involvement (e.g. aseptic meningitis)
GI: abdo pain, diarrhoea, colitis
erythema nodosum

Clinical diagnosis and pathergy test

Steroids, colchine and immunosupressants

175
Q 
WHat is gout?
RF
Joints affected
DIagnosis 
Management 
Prophylaxis
A

crystal arthroapthy associated with hight uric crystals, deposiitng in joints

Male
Obesity
High purine diet (e.g. meat and seafood)
Alcohol
Diuretics
Existing cardiovascular or kidney disease
Family history

Base of the big toe (metatarsophalangeal joint)
Wrists
Base of thumb (carpometacarpal joints)

Aspirated fluid will show:

No bacterial growth
Needle shaped crystals
Negatively birefringent of polarised light
Monosodium urate crystals

NSAIDs (e.g. ibuprofen) are first-line
Colchicine second-line
Steroids can be considered third-line

Allopurinol is a xanthine oxidase inhibitor used for the prophylaxis of gout. It reduces the uric acid level.

176
Q

What is pseudogout?
Diagnosis
Management

A 
Pseudogout is a crystal arthropathy caused by calcium pyrophosphate crystals aka chondrocalcinosis 
Aspiration 
Calcium pyrophosphate crystals
Rhomboid shaped crystals
Positive birefringent of polarised light
management 
NSAIDs
Colchicine
Joint aspiration
Steroid injections
Oral steroids
177
Q

What is pseudogout?
Diagnosis
Management

A 
Pseudogout is a crystal arthropathy caused by calcium pyrophosphate crystals aka chondrocalcinosis 
Aspiration 
Calcium pyrophosphate crystals
Rhomboid shaped crystals
Positive birefringent of polarised light
management 
NSAIDs
Colchicine
Joint aspiration
Steroid injections
Oral steroids
178
Q

What is pagets disease of bone?
Presentation

Investigations
Management

A

Pagets disease of bone increased bone turnover as a result of excess activity of osteoblasts and osteoclasts

Bone pain
Bone deformity
Fractures
Hearing loss can occur if it affects the bones of the ear

Xray
bone enlargement and deformity
“Osteoporosis circumscripta” describes well defined osteolytic lesions that appear less dense compared with normal bone
“Cotton wool appearance” of the skull describes poorly defined patchy areas of increased density (sclerosis) and decreased density (lysis)
“V-shaped defects” in the long bones are V shaped osteolytic bone lesions within the healthy bone

Raised ALP normal calcium and phosphate

Bisphosphonates are the main treatment. They are generally very effective. They interfere with osteoclast activity and seem to restore normal bone metabolism. They improve symptoms and prevent further abnormal bone changes.

Other measures include:

NSAIDs for bone pain
Calcium and vitamin D supplementation, particularly whilst on bisphosphonates
Surgery is rarely required for fractures, severe deformity or arthritis

179
Q 
What is osteoporosis and osteopenia 
RF 
FRAX?
BMD
z and t score 
Management
A

osteoporosis severe reduction in bone density, osteopenia less sevre reduction in bone density

Older age
Female
Reduced mobility and activity
Low BMI (<18.5 kg/m2)
Rheumatoid arthritis
Alcohol and smoking
Long term corticosteroids. NICE suggest the risk increases significantly with the equivalent of more than 7.5mg of prednisolone per day for more than 3 months)
Other medications such as SSRIs, PPIs, anti-epileptics and anti-oestrogen

The FRAX tool gives a prediction of the risk of a fragility fracture over the next 10 years. This is usually the first step in assessing someone’s risk of osteoporosis.

It involves inputting information such as their age, BMI, co-morbidities, smoking, alcohol and family history. You can enter a result for bone mineral density (from a DEXA scan) for a more

Risk of. a major osteoporotuic fracrture and hip fracture

Bone mineral density (BMD) is measured using a DEXA scan, which stands for dual-energy xray absorptiometry. DEXA scans are brief xray scans that measure how much radiation is absorbed by the bones, indicating how dense the bone is. The bone mineral density (BMD) can be measured at any location on the skeleton, but the reading at the hip is key for the classification and management of osteoporosis.

Z scores represent the number of standard deviations the patients bone density falls below the mean for their age. T scores represent the number of standard deviations below the mean for a healthy young adult their bone density is.

More than -1

Normal

-1 to -2.5

Osteopenia

Less than -2.5

Osteoporosis

Less than -2.5 plus a fracture

Severe Osteoporosis

Activity and exercise
Maintain a healthy weight
Adequate calcium intake
Adequate vitamin D
Avoiding falls
Stop smoking
Reduce alcohol consumption
Bisphopsphonates
180
Q 
What is osteoporosis and osteopenia 
RF 
FRAX?
BMD
z and t score 
Management
A

osteoporosis severe reduction in bone density, osteopenia less sevre reduction in bone density

Older age
Female
Reduced mobility and activity
Low BMI (<18.5 kg/m2)
Rheumatoid arthritis
Alcohol and smoking
Long term corticosteroids. NICE suggest the risk increases significantly with the equivalent of more than 7.5mg of prednisolone per day for more than 3 months)
Other medications such as SSRIs, PPIs, anti-epileptics and anti-oestrogen

The FRAX tool gives a prediction of the risk of a fragility fracture over the next 10 years. This is usually the first step in assessing someone’s risk of osteoporosis.

It involves inputting information such as their age, BMI, co-morbidities, smoking, alcohol and family history. You can enter a result for bone mineral density (from a DEXA scan) for a more

Risk of. a major osteoporotuic fracrture and hip fracture

Bone mineral density (BMD) is measured using a DEXA scan, which stands for dual-energy xray absorptiometry. DEXA scans are brief xray scans that measure how much radiation is absorbed by the bones, indicating how dense the bone is. The bone mineral density (BMD) can be measured at any location on the skeleton, but the reading at the hip is key for the classification and management of osteoporosis.

Z scores represent the number of standard deviations the patients bone density falls below the mean for their age. T scores represent the number of standard deviations below the mean for a healthy young adult their bone density is.

More than -1

Normal

-1 to -2.5

Osteopenia

Less than -2.5

Osteoporosis

Less than -2.5 plus a fracture

Severe Osteoporosis

Activity and exercise
Maintain a healthy weight
Adequate calcium intake
Adequate vitamin D
Avoiding falls
Stop smoking
Reduce alcohol consumption
Bisphopsphonates
181
Q

osteomalacia

A

02F (18 decks)

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