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cortext > rheumatology > Flashcards

rheumatology Flashcards

1
Q

arthropathy definition

A

disease of a joint

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2
Q

arthritis definition

A

inflammation of a joint

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3
Q

arthralgia definition

A

pain in a joint

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4
Q

seropositive condition

A

auto-antibodies present in serum

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5
Q

anti-CCP antibody

A

rheumatoid arthritis

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6
Q

anti-nuclear antibody

A

SLE, Sjorgen’s syndrome, systemic sclerosis, mixed connective tissue disease, autoimmune liver disease

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7
Q

anti-double stranded DNA antibody

A

SLE

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8
Q

anti-Sm

A

SLE

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9
Q

anti-Ro

A

SLE, Sjorgen’s syndrome

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10
Q

anti-La

A

Sjorgen’s syndrome

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11
Q

anti-centromere antibody

A

systemic sclerosis (limited)

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12
Q

anti-Scl-70 antibody

A

systemic sclerosis (diffuse)

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13
Q

anti-RNP antibody

A

SLE, MCTD, myositis

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14
Q

anti-cardiolopin antibody and lupus anti-coagulant

A

anti-phospholipid syndrome

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15
Q

anti-neutrophil cytoplasmic antibody (ANCA)

A

small vessel vasculitis (GPA, EGPA, MPA)

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16
Q

osteoarthritis X-ray signs (LOSS)

A

loss of joint space osteophytes sclerosis subchondral cysts

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17
Q

the four groups of inflammatory arthropathies

A

seropositive, seronegative, infectious and crystal deposition arthropathies

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18
Q
A

osteoarthritis

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19
Q
A

inflammatory spondylitis

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20
Q
A

psoriatic arthritis

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21
Q
A

rheumatoid arthritis

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22
Q

is RA more common in men or women?

A

women

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23
Q

joints most commonly affected by RA

A

small joints of the hands and feet

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24
Q

what role does the pannus play in the pathogenesis of RA?

A

an inflammatory pannus forms and then attacks and denudes the articular cartilage leading to joint destruction

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25
Q

features of inflammatory arthritis

A

joint pain with associated swelling

morning stiffness

improvement of symtpoms with exercise

synovitis on examination

raised imflammatory markers

extra-articular symptoms

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26
Q

clinical features of RA

A

symmetrical synovitis, pain, morning stiffness, early involvement of hands and feet

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27
Q

why is the DIP joint not commonly affected in RA?

A

because RA only affects synovial joints, and the DIP is so small that there is hardly any synovium in it

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28
Q

why can RA result in cervical cord compression?

A

the atlanto-axial joint can be affected, which can lead to subluxation and eventually cervical cord compression

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29
Q
A
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30
Q

extra articular manifesations of RA

A

rheumatoid nodules on extensor surfaces of sites of frefquent mechanical irritation

preural effusions, interstitial fibrosis and pulmonary nodules

keratoconjunctivitis sicca, episcleritis, uveitis and nodulr scleritis

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31
Q

RA investigations

A

rheumatoid factor, anti-CCP antibody

CRP, ESR and PV are usually raised

xrays often show no abnormality

peri-articular osteopenia and soft tissue swelling

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32
Q

RA treatment

A

DMARDs (methotrexate, sulphasalazine, hydroxychlorquine, leflunomide)

simple analgesia

NSAIDs

steroids

anti-TNFa injections

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33
Q

disease activity in RA is measured using

A

DAS28

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34
Q

DAS 28 2.7-3.2

A

low disease activity

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35
Q

DAS 28 3.3-5.1

A

moderate disease activity

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36
Q

DAS 28 >5.1

A

high disease activity

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37
Q

DAS 28 <2.6

A

remission

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38
Q

patients must have a score of ____ to be eligible for biologic therapy

A

>5.1 (high disease activity)

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39
Q

operative management of RA

A

synovectomy, joint replacement, joint excision, tendon transfers, anrthrodesis, cervical spine stabilisation

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40
Q

seronegative arthropathies include

A

ankylosing spondylitis, psoriatic arthritis, enteropathic arthritis and reactive arthritis

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41
Q

characteristics of seronegative arthropathy

A

inflammation/arthritic disease of the spine (spondyloarthropathy)

asymmetric oligoarthritis

sacroiliitis

uveitis

dactylitis

enthesopathies

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42
Q

laboratory signs of seronegative arthropathy

A

HLA-B27 positive

elevated CRP and ESR

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43
Q

who is most commonly affected by ankylosing spondylitis?

A

males aged 20-40

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44
Q

which joints are affected by AS

A

spine and sacroiliac joints

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45
Q

AS symptoms

A

spinal pain and stiffness

knee or hip arthritis

morning spinal stiffness that improves with exercise

gradual loss of spinal movement

development of ‘question mark’ spine (loss of lumbar lordosis and increased thoracic kyphosis)

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46
Q

how do you measure lumbar spine flexion?

A

Schober’s test

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47
Q

AS associated conditions

A

anterior uveitis, aortitis, pulmonary fibrosis, amyloidosis

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48
Q

xray signs of AS

A

sclerosis and fusion of SI joints

bony spurs from the vertebral bodies (syndesmophytes) producing a ‘bamboo’ spine

common for xrays to be normal at time of presentation

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49
Q

MRI features of AS

A

bone marrow oedema

entheitis of the spinal ligaments

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50
Q

laboratory signs of AS

A

90% of sufferers are HLA-B27 positive

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51
Q

AS treatment

A

physiotherapy and exercise

NSAIDs

anti-TNF inhibitors for more aggressive disease

DMARDs if peripheral joint inflammation

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52
Q

psoriatic arthritis presentation

A

asymmetrical oligoarthritis

spondylitis

dactylitis

enthesitis

nail pitting and onycholysis (splitting of nail from nail bed)

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53
Q

psoriatic arthritis treatment

A

DMARDs (methotrexate)

anti-TNFa therapy for those who don’t repsond to standard therapy

joint replacement in severely affected large joints

DIP fusion

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54
Q

enteropathic arthritis definition

A

inflammatory arthritis involving the peripheral joints and sometimes spine, in patients with IBD

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55
Q

enteropathic arthritis presentation

A

large joint asymmetrical oligoarthritis

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56
Q

treatment of enteropathic arthritis

A

finding medication to manage the underlying condition and the arthritis

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57
Q

reactive arthritis definition

A

occurs in response to an infection in another part of the body, most commonly GU infection (chlamydia, neisseria) or GI infections (salmonella, campylobacter)

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58
Q

reactive arthritis presentation

A

large joints become inflamed 1-3 weeks after the infection

(infection triggers autoimmune arthropathy)

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59
Q

Reiter’s syndrome

A

urethritis, uveitis or conjunctivits and arthritis

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60
Q

SLE mainly involves…

A

skin, joints, kidneys, blood cells, and nervous system

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61
Q

clinical criteria of SLE

A
  • acute cutaneous lupus

chronic cutaneous lupus

oral or nasa lulcers

non-scarring alopecia

arthritis

serositis

renal

neurologic

haemolyitc anaemia

leukopaenia

thrombocytopaenia

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62
Q

immunologic criteria SLE

A

ANA

anti-DNA

anti-Sm

antiphospholipid Ab

low complement

direct Coombs’ test

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63
Q

what type of hypersensitivity reaction is SLE

A

type 3 - immune complex mediated

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64
Q

SLE general symptoms

A

fever

fatigue

weight loss

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65
Q

SLE MSK symptoms

A

arthralgia

myalgia

inflammatory arthritis

increased prevalence of AVN, usually of the femoral head

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66
Q

SLE muco-cutaneous symptoms

A

malar rash

photosensitivity

discoid lupus

subacute cutaneous lupus

oral/nasal ulceration

raynaud’s phenomenon

alopecia

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67
Q

SLE renal symptoms

A

lupus nephritis

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68
Q

SLE respiratory symptoms

A

pleurisy

pleural effusion

pneumonitis

pulmonary embolism

pulmonary hypertension

intersitial lung disease

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69
Q

SLE haematological symptoms

A

leukopaenia

lymphopaenia

anaemia

thrombocytopaenia

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70
Q

SLE neuropsychiatric symptoms

A

seizures

psychosis

headache

aseptic meningitis

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71
Q

SLE cardiac symptoms

A

pericarditis

pericardial effusion

pulmonary hypertension

sterile endocarditis

accelerated ischaemic heart disease

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72
Q

SLE GI symptoms

A

less common

AI hepatitis

pancreatitis

mesenteric vasculitis

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73
Q

SLE investigations

A

FBC may show anaemia, leukopaenia and thrombocytopaenia

ANA - not specific

Anti-dsDNA - specific

Anti-Sm - specific but low sensitivity

Anti-Ro, Anti-La and Anti-RNP - not specific

C3/4 levels - low when disease active

urinalysis may show signs of glomerulonephritis

imaging for organ involvement

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74
Q

SLE management

A

skin disease and arthralgia - hydroxychloroquine, topical steroids, NSAIDs

immunosuppression with azothioprine or mycophenolate mofetil

severe disease may need IV steroids and cyclophosphamide

IV Ig and rituximab may be necessary in unresponsive cases

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75
Q

SLE monitoring

A

anti-dsDNA and complement to monitor disease activity

urinalysis for blood or protein

BP and cholesterol should be monitored

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76
Q

Sjorgen’s syndrome symptoms

A

dryness of eyes and mouth (sicca)

arthralgia

fatigue

vaginal dryness

parotid gland swelling

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77
Q

Sjorgen’s diagnosis

A

ocular dryness

positive anti-Ro

positive anti-La

lip gland biopsy

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78
Q

Sjorgen’s management

A

lubricating eye drops

saliva replacement products

regular dental care

hydroxychloroquine can help with arthralgia and faitgue

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79
Q

systemic sclerosis characteristics

A

vasomotors distrubances (raynauds)

fibrosis and subsequent atrophy of the skin and subcutaneous tissue

excessive collagen deposition causes skin and internal organ changes

80
Q

cutaneous involvement of SSc has three stages

A

1 - oedematous

2 - indurative

3 - atrophic

81
Q

major features of SSc

A

centrally located skin sclerosis that affects the arms, face and/or neck

82
Q

minor features of SSc

A

sclerodactyly

atrophy of the fingertips and bilateral lung fibrosis

83
Q

what are the CREST symptoms in SSc

A

Calcinosis

Raynauds

Esophageal dysmotility

Sclerodactyly

Telangiectasia

84
Q

organ involvement in SSc

A

pulmonary hypertension, pulmonary fibrosis and accelerated hypertension

gut involvement may lead to dysphagia, malabsorption and bacterial overgrowth of the small bowel

inflammatory arthritis and myositis

85
Q

limited SSc affects

A

face, hands, forearms and feet skin changes

late organ involvement

86
Q

diffuse SSc affects

A

skin changes to the trunk

early organ involvement

87
Q

limited SSc antibody

A

anti-centromere

88
Q

diffuse SSc antibody

A

anti-Scl-70

89
Q

SSc investigations

A

anti-centromere/anti-Scl-70 antibodies

organ screening

90
Q

SSc management

A

raynauds - calcium channel blockers

renal involvement - ACE inhibitors

GI involvement - proton pump inhibitors for reflux

interstitial lung disease - immunosuppression (cyclophospohamide)

91
Q

mixed connective tissue disease features symptoms seen in other connective tissue diseases, including

A

raynauds

arthralgia/arthritis

myositis

sclerodactyly

pulmonary hypertension

interstitial lung disease

92
Q

MCTD antibodies

A

anti-RNP antibodies

93
Q

MCTD management

A

calcium channel blockers for raynauds

immunosuppression if significant muscle or lung disease

94
Q

antiphospholipid syndrome is a disorder that manifests clinically as…

A

recurrent venous or arterial thrombosis and/or foetal loss

95
Q

presentation of anti-phospholipid syndrome

A

recurrent pulmonary emboli or thrombosis

late spontaneous foetal loss/recurrent foetal loss

migraine

livedo reticularis

96
Q

APS investigations

A

thrombocytopaenia

prolongation of APTT

lupus anticoagulant, anti-cardiolipin antibodies and anti-beta 2 glycoprotein may be positive

97
Q

APS treatment

A

anti-coagulation if episodes of thrombosis

LMWH in pregnancy if recurrent pregancy loss

98
Q

gout is caused by

A

urate crystals within a joint

99
Q

hyperuricaemia may be due to…

A

renal underexcretion or excessive intake of alcohol, red meat and seafood

100
Q

the most common site of gout is

A

the first metatarsalphalangeal joint (MTP)

101
Q

gout presentation

A

intensely painful, hot swollen joint

102
Q

how long do gout symptoms normally last

A

7-10 days

103
Q

what are gouty tophi

A

painless white accumulations of uric acid in the soft tissues

104
Q

definitive diagnosis of gout

A

synovial fluid with polarised microscopy

105
Q

what shape are uric acid crystals

A

needle shaped

106
Q

what type of birefringence do uric acid crystals display

A

negative

(change from yellow to blue when lined across the direction of polarisation)

107
Q

treatment of acute gout

A

NSAIDs

corticosteroids

opioid analgesics

colchicine if cant tolerate NSAIDs

108
Q

treatment for recurrent gout (or with joint decstruction or tophi)

when should they be started

A

allopurinol or other urate lowering therapies

should not be started until an acute attack has settled as they can potentiate a further flare

109
Q

what is pseudogout caused by

A

pyrophosphate crystals

110
Q

what is chondrocalcinosis

A

deposition if calcium pyrophosphate in catilage and other soft tissues in the absence of acute inflammation

111
Q

calcium pyrophosphate deposition disease tends to affect

A

the ankle, knee and wrist

112
Q

calcium pyrophosphate deposition disease can coexist with

A

hyperparathyroidism

hypothyroidism

renal osteodystrophy

haemochromatosis

Wilson’s disease

113
Q

treatment of pseudogout

A

NSAIDs

corticosteroids (systemic and IA)

colchicine

114
Q

pseudogout prophylaxis?

A

there is no prophylaxis for pseudogout

115
Q

characteristics of polymyalgia rheumatica

A

proximal myalgia of the hip and shoulder girdles

morning stiffness that lasts over 1 hour

symtpoms improve with movement

116
Q

polymyalgia rheumatica is associated with what type of vasculitis

A

GCA

117
Q

polymyalgia rhematica investigations

A

raised CRP and PV/ESR

118
Q

polymyalgia rheumatica response to low dose steroids

(diagnostic tool)

A

symptoms respond very dramatically

119
Q

polymyalgia rheumatica treatment (and time period)

A

prednisolone dose reduced over 18 months

(condition resolved in most individuals)

120
Q

histopathologically, GCA is marked by

A

transmural inflammation of the intima, media and adventitia of affected arteries

patchy infliltration by lymphocytes, macrophages and multinucleated giant cells

121
Q

vessel wall thickening in GCA can result in…

A

arterial luminal narrowing, resulting in subsequent distal ischaemia

122
Q

GCA presentation

A

visual disturbances, headache, jaw claudication and scalp tenderness

fatigue, malaise, fever

123
Q

new onset headache in patients over 50 years with an elevated ESR, CRP or PV?

A

consider GCA

124
Q

what type of headache is present in GCA

A

continuous

located in the temporal or occipital areas

focal tenderness on direct palpation

125
Q

jaw claudication is a result of ischaemia of the ________ artery

A

maxillary artery

126
Q

visual symptoms of GCA

A

unilateral visual blurring or vision loss

occasionally diplopia

127
Q

GCA diagnosis

A

raised inflammatory markers

temporal artery biopsy

128
Q

GCA treatment

A

corticosteroids (prednisolone 40/60 mg depending on visual symptoms)

TREATMENT SHOULD NOT BE DELAYED FOR BIOPSY

129
Q

polymyositis causes…

A

symmetrical proximal muscle weakness

130
Q

dermatomyositis causes

A

symmetrical proximal muscle weakness

skin changes

131
Q

polymyositis is caused by

A

a T-cell mediated cytotoxic process directed against unidentified muscle antigens

132
Q

myositis antibodies

A

anti-Jo-1 and anti-SRP

133
Q

polymyositis presentation

A

symmetrical proximal muscle weakness in the upper and lower extermities

insidious onset

myalgia

134
Q

a poor prognostic sign in polymyositis

A

dysphagia secondary to oropharyngeal and oesophageal involvement

135
Q

anti-Jo-1 antibody in polymyositis is associated with

A

interstitial lung disease

136
Q

polymyositis investigations

A

raised inflammatory markers

serum creatine kinase raised

ANA, anti-Jo-1 and anti-SRP

muscle biopsy (exclude other casues)

137
Q

polymyositis treatment

A

prednisolone (40 mg)

methotrexate or azathioprine

138
Q

cutaneous features of dermatomyositis

A

v-shaped rash over chest

heliotrope rash (eyelids)

purple plaques on bony prominences (Gottron papules on knuckles)

poikiloderma (atrophic, red and brown skin)

139
Q

dermatomysotis is associated with an increased risk of

A

malignancy

(breat, ovarian, lung, colon, oesophagus and bladder)

140
Q

fibromyalgia is thought to be a disorder of

A

central pain processing or a syndrome of central sensitivity

141
Q

fibromyalgia is associated with

A

RA and SLE

142
Q

fibromyalgia presentation

A

persistent (>3/12) widespread pain

fatigue

disrupted, unrefreshing sleep

cognitive difficulties

other unexplained symptoms (anxiety, depression, functional impairment of ADLs)

143
Q

fibromyalgia investigations

A

rule out other differentials

hypothyroidism

RA

SLE

PMR

144
Q

fibromyalgia treatment

A

self-management techniques

graded exercise and activty pacing

amitriptyline, gabapentin and pregabalin

145
Q

GCA affects what age group

A

older than 50

146
Q

Takayasu arteritis affects what age group

A

under 50

147
Q

which arteries does GCA normally affect

A

temporal arteries

148
Q

early features of large vessel vasculitis

A

low grade fever

malaise

night sweats

weight loss

arthralgia

fatigue

149
Q

ANCA associated vasculitis includes

A

granulomatosis with polangitis

microscopic polyangitis

renal limited vasculitis

Churg-Strauss syndrome

150
Q

GPA is commonly associated with ENT symptoms such as

A

nose bleeds

deafness

recurrent sinusitis

nasal crusting

151
Q

the most important complication of microscopic polyangitis is

A

glomerulonephritis

152
Q

investigations for ANCA positive vasculitis

A

raised ESR, PV and CRP

anaemia of chronic disease

U+E for renal involvement

ANCA

CXR (cavitiating lesions in GPA)

biospy of affected area

153
Q

management of ANCA associated vasculitis

A

IV steroids and cyclophosphamide

154
Q

which of the following is not associated with anti-phospholipid syndrome?

venous thrombosis

livedo reticularis

migraine

recurrent pregnancy loss

thrombocytosis

A

thrombocytosis

155
Q

a 69 year old woman complains of pain at the base of her thumbs

on examination, she has bony swelling of her thumb CMC joints and finger DIP joints

postivie ANA and anti-RNP antibody

xray shows loss of joint space, subchondral sclerosis, subchondral cysts and osteophytes

A

osteoarthritis

156
Q

a 32 year old man is diagnosed as having a pulmonary embolus with no clinical risk factors

anticardiolipin antibodies are raised

what is the most appropriate anticoagulation treatment?

A

life long warfarin

157
Q

a patient has pain in their lower nack and a positive ANA at a titre of 1:160

is this diagnostic of SLE?

A

no - a diagnosis of SLE needs a combination of clinical and laboratory findings

ANA of this titre is seen in 13% of the normal population

158
Q

in SLE active complement levels rise when disease is active

true/false

A

false - complement is consumed in the response to the formation of immune complexes

low levels of complement are a sign of active disease

159
Q

in SLE, patients will likely be on oral steroids long term

true/false

A

false - steroids should only be used for short periods to suppress disease activity whilst other agents are introduced

long term steroids are associated with an increased risk of CV disease, T2DM and osteoporosis

160
Q

when SLE is more active the level of anti-DNA binding antibody is likely to rise

true/false

A

true

161
Q

in a patient with SLE which of the following is the least likely to be a cause of chest pain

pneumothorax

pericarditis

pulmonary embolus

pleurisy

MI

A

pneumothorax

162
Q

which of the following is not a recognised feature of limited systemic sclerosis

calcinosis

butterfly rash

raynauds

pulmonary HTN

anti-centromere antibody

A

butterfly rash

163
Q

which best describes the management of CTDs?

physio and surgery to stabilise joints

immunosuppression to normalise antibody levels

high dose steroids on diagnosis

treat symptomatically and monitor for major complications

A

treat symptomatically and monitor for major complications

164
Q

the nail changes associated with psoriatic arthritis are

A

pitting and onycholysis

165
Q

oligoarthritis, sacroiliitis, spondylitis, dactylitis and enthesitis commonly occur in which type of arthritis

A

psoriatic arthritis

166
Q

which of the following are included in the spondyloarthopathies

ankylosing spondylitis

gout

psoriatic arthritis

reactive arthritis

rheumatoid arthritis

A

AS, psoriatic arthrtitis and reactive arthritis

167
Q

following 2 months of joint pain, a 38 year old lady is diagnosed with RA

which of the following treatments is recommended first?

azathioprine

methotrexate

anti-IL6 therapy

anti-TNF therapy

diclofenac

A

methotrexate

168
Q

which of the following is an xray finding indicative of gout

subchondral cyst formation

peri-articular erosion

chondrocalcinosis

loss of joint space

peri-articular osteopaenia

A

chondrocalcinosis

(calcium pyrophosphate in the soft tissue in the absence of inflammation)

169
Q
A
170
Q

a 24 year olf patient, just diagnosed with RA, is about to commence DMARD therapy, but wants to start a family

what treatment is most appropriate

leflunomide

sulphasalazine

methotrexate

rituximab

cyclophosphamide

A

sulphasalazine

ideally, she should delay her pregnancy until her disease has improved

171
Q

a patient has had successful treatment of acute gout but has had 4 flares this year

the most appropriate treatment to prevent further flares is

prednisolone

colchicine

allopurinol

sulphasalazine

naproxen

A

allopurinol

172
Q

which of the following is not useful in a patient who presents with symmetrical, small joint swelling

on examination there is a nodule on his elow but there are no other skin changes

systemic examination reveals features of pulmonary fibrosis

hand and feet xrays

PV and/or CRP

anti-CCP antibody

CXR

anti-dsDNA antibody

A

anti-dsDNA antibody

(useful in diagnosis of SLE but not RA)

173
Q

anti-CCP antibody is associated with RA

true/false

A

true

174
Q

bamboo spine is an early radiographic change of AS

true/false

A

false

175
Q

what are the features of Reiter’s triad?

A

reactive arthritis, urethritis and uveitis

176
Q

PMR principally affects patients over the age of 50

true/false

A

true

177
Q

which of the following is not a common xray finding in osteoarthritis

subchondral cyst formation

periarticular erosion

loss of joint space

osteophyte formation

subchondral sclerosis

A

periarticular erosion

178
Q

which of these tests is the initial investigation of choice for detecting renal involvement in vasculitis?

urea

urinalysis

renal ultrasound scan

creatinine

glomerular filtration rate (GFR)

A

urinalysis

179
Q

anti-TNF agents are more effective in combination with standard DMARDs

true/false

A

true

180
Q

biological agents are associated with a higher risk of infection than synthetic DMARDs

true/false

A

true

181
Q

all patients with inflammatory arthritis should be given biological agents

true/false

A

false

182
Q

anti-TNF agents are 1.5 times more effective than standard synthetic DMARDs

true/false

A

true

183
Q

biological agents are generally more expensive than synthetic DMARDs

true/false

A

true

184
Q

methotrexate and azathioprine can be used as remission maintaining agents in vasculitis

true/false

A

true

185
Q

patients who are going to be on long term steroids should always be assessed for bone protection

true/false

A

true

186
Q

steroids are the mainstay of treatment in the early stages of vasculitis

true/false

A

true

187
Q

cyclophosphamide is always indicated in vasculitis

true/false

A

false

188
Q

which of the following is not a recognised treatment for OA

methotrexate

topical analgesics

NSAIDs

joint replacement

physiotherapy

A

methotrexate

189
Q

in a patient with PMR, the development of a headache should make you consider…

A

GCA

190
Q

allopurinol should be tritiated until target serum urate is achieved (below 360 micromol/L)

true/false

A

true

191
Q

allopurinol should be stopped during acute gout flares

true/false

A

false

192
Q

steroids can be used to reduce inflammation in acute gout

true/false

A

true

193
Q

in patients with new onset RA, DMARDs should be commeced within 3 months of onset of symptoms

true/false

A

true

194
Q

DMARDs require regular blood monitoring to ensure safety

true/false

A

true

195
Q

DMARDs are slow acting

true/false

A

true - up to 8-12 weeks to take effect

196
Q

DMARDS can reduce the rate of progression of joint damage

true/false

A

true

197
Q

DMARDs can reduce inflammation in joints and reduce pain

true/false

A

false - patients will still need analgesia alongside the DMARD

cortext (6 decks)

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