Rheumatology Flashcards

1
Q

What are the symptoms of rheumatoid arthritis?

A
Pain
Stiffness
Early morning stiffness >1 hour
Joint swelling
Small joints > large joints
Symmetrical
Persistent - generally accumulates over time
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2
Q

What are the signs of rheumatoid arthritis?

A
Synovitis
Swan neck deformity
boutonniere
Z-thumb
Ulnar deviation
Rheumatoid nodules
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3
Q

What are the ocular features of rheumatoid arthritis?

A

Scleritis
Episcleritis
Sicca syndrome

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4
Q

What are the cardiorespiratory features of rheumatoid arthritis?

A
Pleural effusions
Pulmonary nodules
Pulmonary fibrosis
Pericarditis
Serositis
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5
Q

What are the extra-articular features of rheumatoid arthritis?

A
Ocular features
Cardiorespiratory features
Splenomegaly
Peripheral neuropathy
Anaemia
Amyloidosis
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6
Q

What are the differential diagnoses for rheumatoid arthritis?

A

Polyarticular gout
Psoriatic arthritis
Osteoarthritis
SLE

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7
Q

What are the investigations for rheumatoid arthritis?

A
CRP/ESR
FBC
Bone/urate
Immunology
Radiograph
Ultrasound
MRI
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8
Q

What is rheumatoid factor?

A

IgM antibody
Directed against Fc portion of IgG Ab
Sensitivity around 70%
Specificity around 85%

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9
Q

What is CCP antibody?

A

Inflammation leads to cellular damage. Enzymatic process leads to the conversion of arginine residues to citrulline. Alteration of shape creates a foreign antigen from self - anti citrullinated cyclic peptide antibodies.
Sensitivity 66%
Specificity 90%

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10
Q

What are the x-ray changes in rheumatoid arthritis?

A
Peri-articular osteopenia
Soft tissue swelling
Erosion
Joint destruction
Subluxation
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11
Q

What can small joint ultrasound detect in rheumatoid arthritis?

A

Subclinical synovitis.
Allows for distinction between active disease and chronic inactive synovial thickening found in long-standing inactive disease.

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12
Q

What are the functional assessments of rheumatoid arthritis?

A

HAQ-DI - health assessment questionnaire disability index.

SF-36 - Short form 36

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13
Q

What score on the EULAR classification criteria would fulfil the classification criteria for RA?

A

6 or more

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14
Q

What is the system used for disease monitoring in rheumatoid arthritis?

A

DAS-28

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15
Q

What is the step-up approach in initiating therapy for rheumatoid arthritis?

A

Introduce and escalate single drug to max tolerated dose, if ongoing disease activity add a further drug.

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16
Q

What is the step-down approach to initiating therapy for rheumatoid arthritis?

A

Several drugs started at once and then gradually withdrawn.

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17
Q

What is the parallel approach to initiating therapy for rheumatoid arthritis?

A

Combination introduced at same time and maintained.

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18
Q

What is the initial therapy in rheumatoid arthritis?

A

NSAIDs
COX-2 inhibitors e.g. etoricoxib
Steroids e.g. oral prednisolone

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19
Q

When should DMARDs be offered in rheumatoid arthritis?

A

First line and within 3 months of symptom onset.

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20
Q

Which DMARDs can be offered in rheumatoid arthritis?

A

Methotrexate
Lefluonomide
Sulfasalazine
Hydroxychloroquine if mild or palindromic disease.

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21
Q

How often is methotrexate taken in rheumatoid arthritis?

A

Once weekly

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22
Q

What is methotrexate an antagonist of?

A

Folate

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23
Q

What are the side effects of methotrexate?

A

Usually mucosal or GI side effects.

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24
Q

What are the monitoring requirements for patients taking methotrexate?

A

FBC

LFTs

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25
Q

When is methotrexate contraindicated?

A

Pregnancy

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26
Q

what are the actions of sulfasalazine?

A

Immunomodulatory. Several actions, including against folate, T and b cells.

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27
Q

How often should sulfasalazine been taken for rheumatoid arthritis?

A

Daily pill

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28
Q

What are the side effects of sulfasalazine?

A

GI
Headache
Rash

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29
Q

Is sulfasalazine safe in pregnancy?

A

Yes - but folic acid 10mg daily, started 3 months pre-conception.

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30
Q

What is the criteria for commencing biologic therapy?

A

Must have failed on at least 2 csDMARDs, one of which must be methotrexate unless contraindicated.
Must have severe disease ie. DAS-28 >5.1 on at least 2 occasions one month apart.
Treatment to be continued only if adequate response within first six months, defined as a reduction in DAS-28 of >1.2.

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31
Q

What screening should take place before commencement of DMARDs?

A

Viral hepatitis and HIV
Varicella
CXR and IGRA (TB)
Vaccination - influenza, pneumococcal

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32
Q

What are the contraindications for starting biologics?

A
Active infection
Active or latent TB
Pregnancy
Malignancy
Diverticular disease (IL-6)
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33
Q

What should be monitored in a patient on biologics?

A

Infections
Malignancy
Bloods (FBC, LFTs)
Awareness with vaccination

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34
Q

What is an example of a novel synthetic DMARD?

A

JAK inhibitors

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35
Q

What are the side effects of JAK inhibitors?

A

Side effects - viral infection including troublesome HSV infection
DVT risk in over 50s.

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36
Q

Who is involved in the MDT of a patient with rheumatoid arthritis?

A

Occupational therapists
Physiotherapists
Nurses
Podiatry

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37
Q

What are sernogeative spondyloarthropathies?

A

A group of diseases involving the axial skeleton and express a variety of extra-skeletal signs and symptoms. They are RF negative and associated with HLA-B27.

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38
Q

Give 6 examples of diseases that are seronegative spondyloarthropathies.

A
Psoriatic arthritis
Ankylosing spondylitis
Reactive arthritis
Enteropathic arthropathy
Juvenile idiopathic arthritis
Behcet's disease
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39
Q

What are the symptoms of ankylosing spondylitis?

A
Inflammatory back pain
Early morning stiffness
Improves with exercise.
Associated with peripheral arthritis. 
Enthesitis common.
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40
Q

Who gets ankylosing spondylitis?

A

M:F 5:1

Mean age on onset 3rd decade.

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41
Q

Which imaging is used to investigate ankylosing spondylitis?

A

X-ray

MRI (most helpful)

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42
Q

How should ankylosing spondylitis be treated?

A

NSAIDs and anti-TNF.

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43
Q

What is reactive arthritis?

A

Asymmetrical inflammatory arthritis that usually occurs after a diarrhoeal illness or urethritis.

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44
Q

What are the differential diagnosis for reactive arthritis?

A
Post-viral arthritis
Reactive arthritis
SLE
Psoriatic arthritis
Polyarticuclar gout
Polyarticular OA
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45
Q

How many joints does reactive arthritis usually affect?

A

Mean = 3

Monoarticular in 10%

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46
Q

Which joints does reactive arthritis most commonly affect?

A

Knees
Ankles
Feet

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47
Q

What is the management of reactive arthritis?

A
Treat underlying infection
Culture stool if diarrhoea
Sexual health review
X-ray of affected joint may show enthesitis with periosteal reaction
Rest
NSAIDs
Intra-articular steroid
DMARDs
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48
Q

What is the prognosis of reactive arthritis?

A

Most initial attacks resolve within 6 months.
50% relapse
20% chronic relapsing course
30% establishes, often with lower limb involvement.

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49
Q

What are the investigations for a suspected spondyloarthropathy?

A
Bloods:
FBC, U&Es, LFTs
ESR/CRP
RF/Anti CCP antibodies
HLA-B27
X-rays (hands, spine, pelvis)
MRI
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50
Q

What might hand x-rays show in spondyloarthropathies?

A

DIP erosion
Lysis of terminal phalanges
Asymmetry
Pencil in cup deformity

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51
Q

What might spinal x-rays show in spondyloarthropathies?

A

Erosions
Vertebral squaring
Syndesmophytes
Fused spine (bamboo spine)

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52
Q

What might a pelvic x-ray show in spondyloarthropathies?

A

Sacroiliitis

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53
Q

What might and MRI show in spondyloarthropathies?

A

Enthesitis

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54
Q

What are the common extra-articular features of spondyloarthropathies?

A
Skin - psoriasis, pyoderma gangrenosum, erythema nodosum. 
Inflammatory bowel disease
Urethritis and cervicitis
Renal involvement - amyloidosis
Thrombophilia
Respiratory - pulmonary fibrosis
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55
Q

Which seronegative spondyloarthropathies is uveitis most common in?

A

Ankylosing spondylitis

Inflammatory bowel disease

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56
Q

What type of uveitis is most common in ankylosing spondylitis?

A

Anterior, unilateral and acute

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57
Q

Which type of uveitis is most common in psoriatic arthritis and inflammatory bowel disease?

A

Posterior, bilateral and chronic

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58
Q

Which type of cardiovascular changes are often seen associated with seronegative spondyloarthropathies?

A

Aortitis
Mitral valve insufficiency
Fibrosis of the conduction system with varying degrees of AV block.

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59
Q

Which type of respiratory involvement is often seen associated with seronegative spondyloarthropathies?

A

Bilateral apical pulmonary fibrosis (relatively rare)

Restrictive lung disease.

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60
Q

What are the disease assessment tools for ankylosing spondylitis?

A

BASDAI - Bath ankylosing spondylitis disease activity index.
BASFI - Bath ankylosing spondylitis functional index
BASMI - Bath ankylosing spondylitis metrology index.

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61
Q

Describe the BASDAI.

A
Gold standard for measuring and evaluating disease activity in ankylosing spondylitis. 
6 questions measuring and evaluating 5 major symptoms:
Fatigue
Spinal pain
Arthralgia or swelling
Areas of localised tenderness
Morning stiffness duration
Morning stiffness severity. 

Visual analogue scale from 1-10 with average of 2 stiffness scores.
Resultant score 0-50 divided by 5 to give BASDAI score.

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62
Q

Which BASDAI score would indicate suboptimal control of disease?

A

4 or greater.

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63
Q

What does the BASFI assess?

A

Function of a person with ankylosing spondylitis.

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64
Q

What is the treatment for spondyloarthropathies?

A

NSAIDs
Non-pharmacological (education, exercise, physio, self help groups)
Local steroids
DMARDs
Second line: TNF alpha blocker or IL-17 blocker
Additional therapy: analgesics, surgery.

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65
Q

What is vasculitis?

A

Inflammation of blood vessels.

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66
Q

How is vasculitis classified?

A

Primary - categorised by size of vessels:
- large, medium, small

Secondary - groups of diseases thought to be caused by underlying health conditions e.g. SLE, RA, Hep B/C, HIV

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67
Q

Give some examples of large vessel vasculitides.

A

Aortitis
Giant cell arterritis
Polymyalgia rheumatica
Takayasu arteritis

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68
Q

Give some examples of medium vessel vasculitides.

A

Kawasaki disease

Polyarteritis nodosa

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69
Q

Give some examples of small vessel vasculitides.

A

Anti-glomerular basement membrane disease.
Cryoglobulinemia
Cutaneous leukocytoclastic vasulitis
Drug induced vasculitis
Eosinophilic granulomatosis with polyangiitis

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70
Q

What is the clinical presentation of giant cell arteritis?

A
Headache: 
 - temporal headache with tenderness
 - subacute onset
 - constant
 - little relief with analgesics
Visual symptoms
Jaw claudication occurs in 50%
Polymyalgia rheumatica symptoms in up to 50%
Constitutional upset
71
Q

What are the complications of giant cell arteritis?

A

Visual loss - acute ischaemic optic neuropathy due to vasculitis and interruption of blood flow int eh posterior ciliary arteries. Sudden painless loss of vision, occasionally preceded by amaurosis fugax.
Large vessel vasculitis - vascular stenosis and aneurysms
Cerebrovascular accident - obstruction or occlusion of internal carotid artery or vertebral arteries.

72
Q

How is giant cell arteritis diagnosed?

A

Clinical presentation
Examination findings - temporal artery asymmetry, thickening, loss of pulsatility, tenderness.
Acute phase response - ESR/CRP, often elevated but not specific.
Temporal artery biopsy - gold standard.

73
Q

What would be found on a temporal artery biopsy in giant cell arteritis?

A

Interruption of internal elastic laminae with mononuclear inflammatory cell infiltrate within vessel wall. Multinucleated giatn cells are typical but their absence does not exclude a diagnosis.

74
Q

What could be found on ultrasound scan in giant cell arteritis?

A

Sign of halo, which is hypoechogenic mural thickening.

75
Q

What is the treatment for giant cell arteritis?

A

If strong clinical suspicion, treat. 1mg/kg/day prednisolone - max 60mg.
IV methylprednisolone if visual symptoms.
Aspirin 75mg daily to reduce ischaemic complications.

76
Q

How long should treatment for giant cell arteritis continue for?

A

Maintain prednisolone 60mg for 1 month.
Taper to 15mg by 12 weeks.
Aim to discontinue corticosteroids for 12-18 months.
Corticosteroid sparing therapy for patients with disease relapse on steroid sparing: methotrexate, tocilizumab.

77
Q

What is the classic presentation of Henoch Schonlein Purpura?

A

Classic purpuric rash: buttocks, thighs
Urticarial rash, confluent petchiae, ecchymoses, ulcers.
Arthralgia, arthritis

78
Q

What are the complications of Henoch Schonlein Purpua?

A

GI: pain, bleeding, diarrhoea
Renal: IgA nephropathy
Urology: orchitis
CNS: very rare

79
Q

What is the management of Henoch Schonlein purpura?

A

Exclude secondary causes (e.g. multisystem disease, recent infections, recent drugs)
Often no treatment required.
Corticosteroids for certain complications.

80
Q

What is granulomatosis with polyangiitis characterised by?

A

Granulomatous necrotising inflammatory lesions of the upper and lower respiratory tract and often a pauci-immune glomerulonephritis.

81
Q

Which immunological blood tests should be carried out when there is suspicion of vasculitis?

A

ANCA
MPO
PR3

82
Q

What does ANCA test for?

A

Autoantibodies directed against the cytoplasmic constituents of neutrophils and monocytes.

83
Q

What are common treatments for vasculitis?

A

Prednisolone plus either cyclophosphamide or rituximab.

84
Q

What are the risk factors for septic arthritis?

A
Primary joint disease
Prosthetic joints
Recent joint surgery
Leg ulceration
Intravenous drug abuse
Low socioeconomic status
Immunosuppression
85
Q

What is the pathogenesis of septic arthritis?

A

Direct inoculation
Contigious spread from adjacent bone.
Haematogenous seeding from a distant site

86
Q

What are the causative organisms of septic arthritis?

A
Staph. aureus
MRSA
Streptococci
Gram negative bacteria
Neisseria gonorrhoeae
87
Q

Which virulence factors are produced by staph. aureus?

A

Diverse extra-cellular toxins
Enzymes
Components of bacterial cell wall.

88
Q

What are the clinical features of septic arthritis?

A
Pain
Swelling
Rubor
Restricted movement in a single joint
Fever
89
Q

What are the differential diagnosis of acute monoarthritis?

A
Septic arthritis
Crystal arthritis (gout or pseudogout)
Reactive arthritis
Seronegative arthritis
Haemarthrosis
90
Q

Which laboratory investigations should be carried out to investigate septic arthritis?

A
FBC and white cell differential
ESR and CRP
U&Es, LFTs
Serum urate
ANA and RF
Reactive arthritis screen
91
Q

What should be done in the investigation of septic arthritis?

A

Joint aspiration before antibiotics - gram stain, microscopy, crystals.
Blood cultures even if apyrexial.
Urinalysis
MSSU
Sputum
Wound swab
Chest x-ray
X-ray of affected joint as baseline
Ultrasound to facilitate diagnosis and guide aspiration.
MRI if osteomyeltis is suspected or deep joint.

92
Q

What is the management of septic arthritis?

A

Aspirate to dryness

Antibiotic therapy

93
Q

Which antibiotics should be used in septic arthritis?

A

Cover staphylococci and streptococci.
Flucloxacillin + gentamicin. Clindamycin if penicillin allergy.
Usual practice to use combination therapy.
2 weeks IV and 4 weeks oral therapy.
6 weeks IV if prosthetic joint.

94
Q

When should methotrexate be withheld?

A

Any infection
Cytopenia
Overdose

95
Q

What are the common side effects of sulfasalazine?

A

Headaches
GI disturbance
Blood abnormalities

96
Q

What does sulfasalazine interact with?

A

Digoxin

97
Q

What are the features of DRESS syndrome?

A

Rash and fever
Lymphadenopathy
Hepatitis
Haematological abnormaliteis

98
Q

What are possible side effects of hydroxychloroquine?

A
Mild headache
Nausea
Hair bleaching
Increased skin pigmentation
Maculopathy
99
Q

List three TNF inhibitors.

A

Infliximab
Adalimumab
Etanercept

100
Q

What are the possible side effects of TNF inhibitors?

A

Local skin reactions
Infections
Drug-induced lupus
TNF induced demyelination

101
Q

What happens in an IL-6 blockade?

A
Flu-like illness
Hypercholesterolaemia
Abnormal LFTs
Increased incidence of herpes virus, pneumonia dn URTIs
Skin reactions
102
Q

Name 2 JAK inhibitors.

A

Baricitinib

Tofacitinib

103
Q

Name 5 different types of psoriasis.

A
Plaque psoriasis
Flexural psoriasis
Erythrodermic psoriasis
Pustular psoriasis
Guttate psoriasis
104
Q

Describe plaque psoriasis.

A

Well-circumscribed, erythematous, flat-topped plaques with adherent silvery scale on extensor srufaces, scalp, trunk, or buttocks.

105
Q

Describe flexural psoriasis.

A

Characterised by erythematous plaques with minimal scale in skin folds or flexural surfaces.

106
Q

Describe erythrodermic psoriasis.

A

Generalised erythema covering nearly the entire body surface with varying degrees of scaling.

107
Q

Describe pustular psoriasis.

A

Localised pustules involving soles and palms occurring with or without plaque-type disease.

108
Q

Describe guttate psoriasis.

A

Characterised by 1-10mm pink papules with fine scale primarily on trunk and proximal extremities.

109
Q

What happens in psoriatic nail dystrophy?

A
Discoloured nails
Onycholysis
Nail pitting
Ridging
Subungual hyperkeratosis
110
Q

What are the clinical features of psoriatic arthritis?

A

Women more often present with a symmetric polyarticular arthritis, while men tend to have more spinal involvement.
Peripheral joint disease occurs in most patients, usually as a polyarthritis (>5 joints affected).
Assymetric
Distal interphalangeal joint involvement is common.
Severity of arthritis and skin symptoms usually do not correlate.
Axial disease in about 5% of patients.

111
Q

What are the 5 clinical forms of psoriatic arthritis?

A
Oligoarticular
Asymmetric DIP form
Symmetrical polyarthritis
Psoriatic spondyloarthropathy
Arthritis mutilans
112
Q

What are the risk factors for psoriatic arthritis?

A
Genetic risk factors - first degree relatives, HLA-Cw6 or HLA-B subtypes
Recent trauma
Psoriasis
Obesity
Alcohol excess
Smoking
113
Q

What is the pathogenesis of psoriatic arthritis?

A

T cell activation and proliferation in skin. T cells amplify chronic inflammatory disease process.
CD4+ T cells more frequent in dermal papillae and joints.
CD8+ T cells more frequent in epidermis and inflamed enthesis.
Multiple cytokines released, causing further destruction.
Elevated TNF levels increase frequency of circulating osteoclast precursors, which may result in osteolysis.

114
Q

Which criteria must be met to diagnose psoriatic arthritis?

A

Caspar criteria

115
Q

Which investigations would be carried out in cases of suspected psoriatic arthritis?

A
Bloods: 
- ESR/CRP
- FBC
- Rheumatoid factor
- Synovial fluid aspirate to rule out crystals
Radiology:
- Plain x-rays
- US
- MRI
116
Q

What are the signs of psoriatic arthritis on x-ray?

A

Mild bony erosion at edge of cartilage with bone proliferation.
Asymmetric erosive changes in small joints of the hands and feet.
DIP/PIP involvement.
Erosion of distal tuft of distal phalanx
Periostitis.

117
Q

When should biologics be considered in psoriatic arthritis?

A

If patient has inadequate response to at least one DMARD.
Active enthesitis, dactylitis and insufficient response to NSAIDs.
Active axial disease.
>3 tender/swollen joints.
Two other DMARDs have not worked.

118
Q

Which tool is used to express the severity of psoriasis?

A

PASI

119
Q

What is polymyalgia rheumatica?

A

A chronic, inflammatory rheumatic disease characterised by muscle pain and stiffness, particularly affecting the neck, shoulders and hips.

120
Q

What are the clinical features of polymyalgia rheumatica?

A

Muscle pain in neck, shoulder or pelvic girdle for >2 weeks.
Neck stiffness, especially in morning.
Eleveated ESR or CRP.

121
Q

Which systemic symptoms occur in about half of patients with polymyalgia rheumatica?

A

Fatigue
Anorexia
Low-grade fever

122
Q

Which criteria would help you make a diagnosis of polymyalgia rheumatica?

A

Age over 50
Duration more than 2 weeks
Bilateral shoulder and pelvic girdle aching.
Morning stiffness lasting more than 45 minutes.
Evidence of acute phase response.

123
Q

Which investigations should be carried out in suspected polymyalgia rheumatica?

A
FBC, biochem, ESR, CRP
TFTs, CK, RF, CCP
Igs and PEP
Vit D
Chest x-ray
Echo
CT CAP
124
Q

What is the differential diagnosis of polymyalgia rheumatica?

A
Giant cell arteritis
Osteoarthritis
Rheumatoid arthritis
Polymyositis
Fibromyalgia
Active infection or malignancy
Myalgia due to statins
Hyperparathyroid
Hypothyroid
125
Q

What is paraneoplastic syndrome?

A

A group of rare disorders triggered by an abnormal tumour response to a cancerous tumour.

126
Q

What is the treatment for polymyalgia rheumatica?

A

Start prednisolong 15mg/day for 3 weeks, taper over 1-2 years.

127
Q

What are the side effects of steroid therapy?

A
Weight gain
Osteoporosis
Adrenal suppression
Cushing's syndrome
Peptic ulceration
Pancreatitis
Candidiasis
Cataracts
Increased susceptibility of infection
Hypertension
Diabetes
Depression
Psychosis
128
Q

What is Reiter’s syndrome?

A

Arthritis, conjunctivitis, urethritis

129
Q

Which joints are most likely to be affected by pseudogout?

A

Wrists
Knees
Elbows

130
Q

Which type of crystals are found in pseudogout?

A

Weaky positive, bi-refringent, rhomboid shaped crystals

131
Q

What is the treatment for pseudogout?

A
NSAIDs
Colchicine
Analgesia
Joint aspiration and injection - local anaesthetic +/- steroids
Systemic steroids
132
Q

What are the predisposing factors to gout?

A
Male>Female
Family history
Previous attack
Body size
Alcohol
Purine rich diet
Diuretics
Increased turnover (psoriasis/chemo)
Renal diseases
133
Q

Which kind of crystals are found in gout?

A

Negatively, bi-refringent, needle shape crystals

134
Q

What is the treatment for gout?

A

NSAIDs
Steroids
Colchicine

135
Q

What can be taken as prophylaxis for gout?

A

Allopurinol

136
Q

What is lupus?

A

A multi-system autoimmune disease characterised by vasculopathy, vasculitis, inflammation.

137
Q

What is the pathogenesis of lupus?

A

Autoantibodies target nuclear antigens.

138
Q

What are the signs and symptoms of lupus?

A
Malar rash
Raynaud's
Cytopenia
Nephritis
Alopecia
Sicca
Photosensitivity
Arthralgia
139
Q

What are the investigations of lupus?

A
FBC
ESR
CRP
Serum albumin
Serum creatinine
Urinalysis
Urine protein/creatinine ratio
Renal biopsy (if lupus nephritis suspected)
Plain x-rays of hands and feet
Autoantibodies
140
Q

Which autoantibodies should be measured in suspected lupus?

A
Antinuclear antibody (ANA)
Anti-double stranded DNA antibody (dsDNA)
Anti-Ro antibody
Anti-La antibody
Anti-RNP antibody
Anti-Sm antibody
Anti-phospholipid antibody
C3, C4
141
Q

Which laboratory abnormalities might be found in lupus?

A
Haemolytic anaemia
Leukopaenia
Thrombocytopenia
ANA>1:80
dsDNA positive
142
Q

How many of the ACR criteria are required for a diagnosis of lupus?

A

4 of 11 serially or simultaneously.

143
Q

What is on the ACR criteria for lupus?

A
Malar rash
Discoid rash
Photosensitivity
Oral ulcers
Arthritis
Serositis
Renal disorder
Neurologic disorder
Haematologic disorder
Immunologic disorder
ANA
144
Q

How many of the SLICC criteria are needed for a diagnosis of lupus?

A

4 criteria, at least 1 clinical and 1 immunological or lupus nephritis in presence of ANA or anti-dsDNA.

145
Q

How is SLE treated generally?

A
NSAIDs
Smoking cessation
Sunblock
Exercise
Assess comorbidities
146
Q

How is mild SLE treated?

A

NSAIDs

Hydroxychloroquine

147
Q

How is moderate SLE treated?

A
Corticosteroids
Methotrexate
Mycophenylate
Azathioprine
Cyclosporine A
148
Q

How is severe SLE treated?

A

Cyclophosphamide

IV pulsed 6 x 3 weekly

149
Q

What is Sjogren’s syndrome?

A

A chronic inflammatory disorder characterised by dysfunction of the lacrimal and salivary glands.

150
Q

What are are the classification criteria for Sjogren’s syndrome?

A

• Ocular symptoms of inadequate tear production
• Ocular signs of inadequate tear production
• Oral symptoms of decreased saliva production
• Tests indicating decreased salivary gland function
• Salivary gland histopathology
• Presence of characteristic autoantibodies (anti
ro/SSA and/or anti la/SSB)

151
Q

How can salivary and lacrimal gland function be tested?

A

Shirmer’s test

Unstimulated salivary flow test.

152
Q

What is the pathophysiology of Sjorgens syndrome?

A

Immune-mediate inflammation.
Targets exocrine glands of eyes and mouth.
Extensive lymphocytic infiltration in germ-centre type foci.
Glandular and ductal atrophy.

153
Q

Which antibodies are found in patients with sjorgen’s syndrome?

A

Anti-Ro

Anti-La

154
Q

What are the clinical symptoms of primary sjorgen’s syndrome?

A

Dry eyes - grittiness, foreign body, irritation
Dry mouth - difficulty swallowing dry food, dental caries, decreased taste sensation, change in oral flora.
Vaginal dryness

155
Q

What are the other features of sjorgen’s syndrome?

A
Arthralgia
Interstitial lung disease
GI tract problems
Interstitial nephritis
Neuropathy
156
Q

What is a long term complication of Sjorgen’s syndrome?

A

Lymphoma

157
Q

What are the risk factors for lymphoma in people with Sjorgen’s?

A

Parotid englargement
Lymphadenopathy
Cryoglobulins/positive rheumatoid factor/low C4
Palpable purpura

158
Q

What is the treatment for sjorgan’s syndrome?

A

Treat symptoms
Sprays and gels for eyes and mouth.
Hydroxychloroquine for systemic disease.
Methotrexate if significant inflammatory arthritis.
Intermittent low dose prednisolone for systemic flares.

159
Q

What is scleroderma characterised by?

A

Thickening of the skin and involvement of the visceral organs, including lungs, heart, GI tract and kidneys.

160
Q

Which antibody is associated with scleroderma?

A

ANA

161
Q

What are the classifications of scleroderma?

A

Diffuse cutaneous
Limited cutaneous
Localised

162
Q

What are the features of diffuse cutaneous scleroderma?

A

Distal and proximal skin thickening, often trunk and face.
Rapid progression of skin change.
Rapid onset after Raynaud’s phenomenon.
Early appearance of visceral involvement.
Poor prognosis.

163
Q

What are the featurs of limited cutaneous scleroderma?

A
CREST
Calcinosis
Raynaud's
Oesophaegeal involvment
Sclerodactly
Telangiectasia
164
Q

What are the clinical features of scleroderma?

A

Lungs - 2/3s of patients affected by interstitial fibrosis or pulmonary hypertension.
Cardiac - pericarditis, heart failure, arrythmias, myocardial fibrosis, myocarditis
Kidneys -

165
Q

What are the investigations in scleroderma?

A
FBC, ESR
U&Es
Urinalysis
Immunology: ANA, anti-Scl 70 antibody
anticentromere antibody
166
Q

What are the clinical features of the inflammatory myopathies?

A

Proximal muscle weakness
Muscle atrophy
Dysphagia
Dyspnoea

167
Q

What happens in polymyositis?

A

Symmetrical proximal muscle weakness

168
Q

What will be elevated in polymyositis?

A

Creatinine kinase.

169
Q

What are the investigations of myositis?

A

Elevated muscle enzymes including CK, LDH, aldolase
ESR elevated
ANA positive
MRI shows inflammatory changes and muscle oedema
Muscle biopsy - definitive diagnosis

170
Q

What are the clinical features of dermatomyositis?

A

Heliotrope rash

Gottron’s papules

171
Q

What is the treatment of inflammatory myopathies?

A

Prednisolone 1mg/kg for 4-8 weeks.
Methorexate, azathioprine, mycophenolate as steroid sparing agents.
Patients with Anti-Jo-1 antibodies require long term immunosuppresion.

172
Q

What can anti-ro and anti-la antibodies cause in pregnancy?

A

Neonatal lupus syndrome

173
Q

What are the safest DMARDs in pregnancy?

A

Sulfasalazine and antimalarials.