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MSK Cortext > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Give examples of seropositive inflammatory arthritis.

A

Rheumatoid, lupus, scleroderma, vasculitis, sjogren’s.

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2
Q

Give examples of seronegative inflammatory arthritis.

A

Ankylosing spondylitis, psoriatic arthritis, reaction arthritis, IBD arthritis (enteric arthritis).

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3
Q

What autoantibody is rheumatoid arthritis associated with?

A

Anti-CCP.

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4
Q

What autoantibodies is SLE associated with?

A

ANA, anti-double stranded DNA antibody (dsDNA), anti-Sm, anti-Ro and anti-RNP.

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5
Q

What autoantibodies is sjogrens syndrome associated with?

A

ANA, anti-Ro, anti-La.

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6
Q

What autoantibodies is systemic sclerosis associated with?

A

ANA, anti-centromere antibody (limited), anti-Scl-70 (diffuse).

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7
Q

What autoantibodies is mixed connective tissue disease associated with?

A

ANA, anti-RNP.

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8
Q

What antibody is myositis associated with?

A

Anti-Jo-1.

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9
Q

What autoantibodies is anti-phospholipid syndrome associated with?

A

Anti-cardiolipin antibody and lupus anti-coagulant.

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10
Q

What autoantibody is small vessel vasculitis (GPA, EGPA, MPA) associated with?

A

Anti-neutrophil cytoplasmic antibody (ANCA).

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11
Q

What can lead to periodic flaring of OA?

A

Associated inflammation.

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12
Q

What factors may have an influence on OA?

A

Environmental factors, hobbies, type of work, joints with abnormal alignment (developmental or pathological), previous injuries (secondary OA).

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13
Q

List some causes of secondary OA.

A

Congenital dislocation of the hip, perthes, SUFE, previous intra-articular fracture, extra-articular fracture with malunion, osteochondral/hyaline cartilage injury, crystal arthropathy, inflammatory arthritis, meniscal tears, genu varum or valgum.

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14
Q

What are the 4 typical radiographic features of an OA joint?

A

L - loss of joint space.
O - osteophytes.
S - sclerosis.
S - subchondral cysts.

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15
Q

Describe the management of OA.

A

Largely pain control, physiotherapy, weight loss + exercise, possibly surgery.

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16
Q

What are the 4 main groups of inflammatory arthropathies?

A

Seropositive, seronegative, infectious and crystal deposition disorders.

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17
Q

What are 6 features suggestive of inflammatory arthritis?

A

Joint pain with associated swelling, morning stiffness, improvement in symptoms with exercise, synovitis on examination, raised inflammatory markers (CRP and plasma viscosity), extra-articular symptoms.

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18
Q

In rheumatoid arthritis, what can lead to joint instability and subluxation?

A

Tendon ruptures and soft tissue damage.

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19
Q

What hand joints are not affected in rheumatoid arthritis?

A

Distal interphalangeal (DIP).

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20
Q

What complication of rheumatoid arthritis can cause cervical compression?

A

Antlanto-axial subluxation.

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21
Q

What inflammatory markers are usually raised in rheumatoid arthritis?

A

CRP, ESR and plasma viscosity.

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22
Q

What are the early and late features of RA on x-ray?

A

Early - peri-articular osteopenia (bone thinning) and soft tissue swelling. Late - peri-articular erosions.

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23
Q

What is the timing goal for treatment of rheumatoid arthritis?

A

Commence DMARD therapy within 3 months of symptom onset.

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24
Q

What are the 4 domains of the DAS 28 score?

A

Tender joint count, swollen joint count, CRP/ESR and visual analogue score (patients own assessment of their disease activity).

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25
Q

What are the DAS 28 cut offs for remission and high disease activity?

A

Remission - <2.6.

High disease activity - >5.1 (eligible for biologic therapy).

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26
Q

What are possible surgeries performed for RA?

A

Synovectomy, joint replacement, joint excision, tendon transfers, arthrodesis, cervical spine stabilisation.

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27
Q

What are common features of seronegative inflammatory arthropathies.

A

Spine disease (spondyloarthropathy), sacroiliitis, uveitis, dactylitis (inflammation of a digit) and enthesopathies (inflammation of a tendon connection to a bone).

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28
Q

What is the gene associated with seronegative inflammatory arthropathies?

A

HLA-B27.

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29
Q

What inflammatory markers are elevated in SIA?

A

CRP and ESR.

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30
Q

What are the signs/symptoms of ankylosing spondylitis?

A

Spinal pain and morning stiffness (marked and improves with exercise), knee or hip arthritis, over time loss of spinal movement and development of q-mark spine, loss of lumbar lordosis and increased thoracic kyphosis.

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31
Q

What is lordosis and kyphosis?

A

Lordosis - normal inward lordotic curvature of the lumbar and cervical regions of the human spine.
Kyphosis - the normal outward (convex) curvature in the thoracic and sacral regions.

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32
Q

Describe Schobers test.

A

Measure 5cm below and 10cm above PSIC, ask patient to bend forwards and remeasure distance (normally should extend beyond 20cm).

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33
Q

What are the associated conditions of ankylosing spondylitis?

A

Anterior uveitis, aortitis, pulmonary fibrosis and amyloidosis.

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34
Q

What will ankylosing spondylitis look like on x-ray?

A

Sclerosis and fusion of SI joints, bony spurs from vertebral bodies (syndesmocytes) briding the IV disc resulting in fusion (bamboo spine). X-ray commonly normal at time of presentation.

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35
Q

What features of AS can MRI detect and is it later or earlier than X-ray?

A

Bone marrow oedema and enthesitis of spinal ligaments - earlier.

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36
Q

What is the treatment for AS?

A

Physiotherapy, exercise, NSAIDs and anti-TNF inhibitors. DMARDs only used if peripheral joint inflammation. Surgery not really useful.

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37
Q

What pattern does psoriatic arthritis carry?

A

An asymmetrical oligoarthritis (may also affect hands in similar pattern to RA).

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38
Q

What are some specific features of psoriatic arthritis?

A

Nail pitting, onycholysis, sometimes DIP arthritis, 5% have aggressive arthritis mutilans.

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39
Q

What is the treatment for psoriatic arthritis?

A

Similar to RA, sometimes DIP joint fusion.

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40
Q

What is the arthritis pattern in enteropathic arthritis?

A

Large joint asymmetrical oligoarthritis (2-4 joints).

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41
Q

What is the treatment for enteropathic arthritis?

A

Finding meds to manage underlying condition and arthritis.

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42
Q

What are the most common infections for reactive arthritis to follow?

A

GU and GI infections.

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43
Q

How long after infection does reactive arthritis appear?

A

1-3 weeks.

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44
Q

What is Reiter’s syndrome?

A

Triad of symptoms: urethritis, uveitis/conjunctivitis and arthritis.

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45
Q

What are the 3 outcomes for reactive arthritis?

A

Self-limiting, chronic or frequent relapses.

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46
Q

What is treatment for reactive arthritis?

A

Treat underlying infectious cause, symptomatic relief (IA or IM steroid injections), occasionally DMARDs in chronic cases.

47
Q

Describe the proposed mechanism for development of autoantibodies in SLE.

A

A defect in apoptosis that causes increased cell death and disturbance in immune tolerace, defective clearance of apoptotic cell debris allows for persistence of antigen and immune complex production.

48
Q

In what populations is SLE prevalence high and low and what does this suggest about the disease?

A

High - black persons in UK and US. Low - black persons in Africa. Suggests environmental trigger as well as genetic predisposition.

49
Q

What age is the most common onset of SLE?

A

20s-30s.

50
Q

List all the symptoms of SLE (there’s a lot).

A

Constitutional: fever, fatigue, weight loss.
MSK: arthralgia, myalgia, inflammatory arthritis.
Muco-cutaneous: malar rash, photosensitivity, discoid lupus, subacute cutaneous lupus, oral/nasal ulceration, Raynauds, alopecia.
Renal: lupus nephritis.
Resp: pleurisy, pleural effusion, pneumonitis, PE, pulmonary hypertension, interstitial lung disease.
Haem: leukopenia, lymphopenia, anaemic (may be haemolytic), thrombocytopenia.
Neuropsychiatric: seizures, psychosis, headache, aseptic meningitis.
Cardiac: pericarditis, pericardial effusion, sterile endocarditis, accelerated ischaemic heart disease.
GI (less common): autoimmune hepatitis, pancreatitis, mesenteric vasculitis.

51
Q

What are possible investigation findings in SLE?

A

FBC: anaemia, leucopenia, thrombocytopenia.
Urinalysis: evidence of glomerulonephritis.
Imaging: evidence of organ involvment - CT chest for ILD, brain MRI for cerebral vasculitis, echo for pericardial effusion.

52
Q

What autoantibodies may be present in SLE?

A

ANA (not specific), anti-dsDNA (specific, varies with disease activity), ASM, anti-Ro/La/RNP (also seen in other conditions).

53
Q

What does the management of SLE depend on?

A

Its manifestations.

54
Q

If there is organ involvement, what is the management for SLE?

A

Immunosuppression e.g. azathioprine or mycophenolate mofetil, corticosteroids at moderate doses (ideally for short periods).

55
Q

If there is severe organ disease, what is the management for SLE?

A

IV steroids and cyclophosphamide (immunosuppressive).

56
Q

Why is lupus monitoring important and what should you monitor?

A

Anti-dsDNA and complement levels (vary with disease activity), urinalysis, evaluation and management for CV risk factors.

57
Q

What is Sjogren’s syndrome and what are its symptoms?

A

Autoimmune condition characterised by lymphocytic infiltrates in exocrine organs. Dryness of eyes and mouth (sicca symptoms), arthralgia, fatigue, vaginal dryness, parotid gland swelling.

58
Q

What are potential systemic manifestations of Sjogren’s syndrome?

A

Peripheral neuropathy, ILD, increased risk of lymphoma.

59
Q

What is the diagnosis of Sjogren’s syndrome based on?

A

Confimation of ocular dryness (Schirmer’s test), positive anti-R0/La antibodies and typical features on lip gland biopsy.

60
Q

What is the management of Sjogren’s syndrome?

A

Largely symptomatic: lubricating eyedrops, saliva replacement, regular dental care, pilocarpine (increases saliva production but causes flushing).
Immunosuppression if organ involvement.

61
Q

What are the characteristics of systemic sclerosis?

A

Vasomotor disturbances (raynauds), fibrosis and atrophy of skin and SC tissue. Excessive collagen deposition causes skin and internal organ changes.

62
Q

What is most responsible for death in patients with SSc?

A

Renal and lung changes.

63
Q

What are the 3 phases of cutaneous involvement in SSc?

A
  1. oedematous, 2. indurative, 3. atrophic.
64
Q

What are the major and minor features of SSc?

A

Major: centrally located skin sclerosis affecting arms, face and/or neck.
Minor: sclerodactyly and atrophy of fingertips and bilateral lung fibrosis.

65
Q

When is a diagnosis of SSc made?

A

When a patient has 1 major and 2 minor features.

66
Q

What facial features may be seen in SSc?

A

Pinching of skin of nose (beaking), tightening of skin around mouth, telangiectasia.

67
Q

What are the potential organ involvement complications of SSc?

A

Pulmonary hypertension, fibrosis, accelerated hypertension leading to renal crisis, dysphagia, malabsorption, bacterial overgrowth of small bowel, inflammatory arthritis and myositis.

68
Q

Describe the limited form of SSc.

A

Face, hands, forearms and feet. Oran involvement later. Anti-centromere antibody association.

69
Q

Describe the diffuse form of SSc.

A

Skin changes develop more rapidly and can involve trunk. Early significant organ involvement. Anti-Scl-70 antibody association.

70
Q

What organ screenings are performed regularly in SSc?

A

Pulmonary function testing, echo and monitoring of renal function.

71
Q

What is the management of specific issues in SSc?

A

Raynauds/digital ulcers: calcium channel blockers, iloprost, bosentan.
Renal involvement: ACE inhibitors.
GI: PPI for reflux.
ILD: immunosuppression (cyclophosphamide).

72
Q

What is mixed connective tissue disease?

A

Defined condition which features symptoms also seen in other CTDs.

73
Q

What features are seen in MCTD?

A

Raynauds, arthalgia/ritis, myositis, sclerodactyly, pulmonary hypertension, ILD.

74
Q

What antibodies is MCTD associated with?

A

Anti-RNP.

75
Q

What does screening in MCTD involve?

A

Pulmonary function tests, regular echocardiograms (for risk of pulmonary hypertension).

76
Q

What is the management of MCTD?

A

Management varies according to presentation, immunosuppression if significant muscle of lung disease.

77
Q

What is anti-phospholipid syndrome (APS)?

A

Disorder that manifests clinically as recurrent venous or arterial thrombosis and/or fetal loss.

78
Q

What are the possible presentations of APS (usually due to thrombosis)?

A

Stroke or MI in younger individuals, Libman-Sacks (sterile) endocarditis, pulmonary emboli/thrombosis, catastrophic APS (multiorgan infarctions over days/weeks), late spontaneous fetal loss (can occur anytime tho), migrane, livedo reticularis (mottled discolouration of skin).

79
Q

What antibodies and blood tests are present in APS?

A

Thrombocytopenia, prolongation of APTT.

Antibodies: anticoagulant, anti-cardiolipin antibodies and anti-beta 2 glycoprotein.

80
Q

What is the management of APS?

A

Anti-coagulation (LMWH in pregnancy as warfarin is teratogenic). If no episodes of thrombosis anti-coagulation not required.

81
Q

What is gouty tophi?

A

Painless white accumulations of uric acid which can occur in soft tissues and occasionally erupt through the skin.

82
Q

What do the gout crystals look like under polarised microscopy?

A

Needle shaped with negative birefringence.

83
Q

What is the treatment for acute gout?

A

NSAIDs (colchicine if not tolerated), corticosteroids, opioid analgesics

84
Q

What is chondrocalcinosis and what disease does this and pseudogout come under?

A

When calcium pyrophosphate deposition occurs in catilage and other soft tissues in the absence of acute inflammation. Calcium pyrophosphate deposition disease (CPPD).

85
Q

Where does CPPD affect and what other conditions is it associated with?

A

Knee, wrist and ankle. Hyperparathyroidism, hypothyroidism, renal osteodystrophy, haemochromatosis, wilson’s disease, OA (can also cause this).

86
Q

What is the treatment for acute attacks of CPPD?

A

NSAIDs, corticosteroids (systemic/intra-articular) and occasionally colchicine (no prophylactic medications).

87
Q

Who does polymyalgia rheumatica tend to affect and what is it characterised by?

A

Elderly individuals. Proximal myalgia of hip and shoulder girdles with accompanying morning stiffness (lasts more than 1 hours).

88
Q

What other disease is largely associated with PMR?

A

Giant cell arteritis (15%).

89
Q

What inflammatory markers are raised in PMR?

A

CRP, PV and ESR.

90
Q

What is the treatment for PMR?

A

Low dose steroids (15mg prednisolone) daily for 18 months.

91
Q

What is the histopathological picture for giant cell arteritis?

A

Transmural inflammation of intima, media and adventitia of affected arteries. Infiltration by lymphocytes, macrophages and multinucleated giant cells.

92
Q

What are the common signs and symptoms of GCA?

A

Visual disturbances, headache, jaw claudication and scalp tenderness.
Constitutional: fatigue, malaise and fever.

93
Q

What is the treatment of GCA?

A

Corticosteroids (prednisolong 40mg or 60mg if visual impaorment), gradually tapered off over around 2 years.

94
Q

What is polymyositis and dermatomyositis and who do they most commonly affect?

A

Idiopathic inflammatory myopathy causing symmetrical, proximal muscle weakness (dermatomyositis has cutaneous manifestations). Adults over 20 years esp 45-60.

95
Q

What autoantibodies are present in poly/dermatomyositis?

A

Unique: anti-Jo-1, anti-SRP antibodies.

96
Q

What are the signs/symptoms of myositis?

A

Symmetrical proximal muscle weakness (insidious onset), maybe myalgia, dysphagia (only 1/3rd of patients), ILD.

97
Q

What are the investigations used in myositis?

A

Inflammatory markers, serum CK levels, autoantibodies (ANA, anti-Jo-1, anti-SRP), MRI (localise extent of muscle involvement), electromyographic studies, muscle biopsy (crucial).

98
Q

What is the management of myositis?

A

Prednisolone combined with immunosuppressive drugs. Usually responds to treatment but slowly.

99
Q

What are the cutaneous features of dermatomyositis?

A

V-shaped rash over chest, Gottron’s papules (rash on knuckles), heliotrope rash (around eyes).

100
Q

What is associated with myositis and what are the most common ones?

A

Malignancy (should be screened at time of diagnosis). Breast, ovarian, lung, colon, oesophagus and bladder.

101
Q

What are the signs and symptoms of fibromyalgia?

A

Persistent (>3 months) widespread pain, fatigue (disrupted/unrefreshing sleep), cognitive diffisulties, unexplained symptoms, anxiety/depression, functional impairment of activities of daily living)

102
Q

What conditions are associated with fibromyalgia?

A

Depression, IBS, migraine.

103
Q

What is the management of fibromyalgia?

A

Mainstay is for patient to learn self-management techniques and understand the condition. Advice regarding graded exercise and activity pacing, atypical analgesia (tricyclics, gabapentin and pregabalin), CBT.

104
Q

What are the common features of small vessel vasculitis?

A

Fever and weight loss, raised non-blanching purpuric rash, arthralgia/arthritis, mononeuritis multiplex, glomerulonephritis, lung opacities on x-ray.

105
Q

What are feature of granulomatosis with polyangiitis that are not associated with EGPA?

A

Nasal cartilage collapse.

106
Q

What features of EGPA are not also associated with GPA?

A

Late onset asthma, raised peripheral blood eosinophil count, neurological symptoms such as mononeuritis multiplex.

107
Q

What is the most important complication of microscopic polyangiitis?

A

Glomerulonephritis.

108
Q

What investigations are done for ANCA-positive small vessel vasculitis?

A

Inflammatory raised (common), anaemia of common disease, U+E, ANCA, urinalysis, CXR, biopsy of affected area.

109
Q

What is the treatment of ANCA associated vasculitis?

A

IV steroids and cyclophosphamide (due to aggressive disease course).

110
Q

What is Henoch-Schonlein purpura?

A

An acute IgA-mediated disorder characterised by a generalised vasculitis.

111
Q

Who does Henoch-Schonlein purpura affect?

A

Children (commonly history of an URTI predates the symptoms by a few weeks).

112
Q

What are the common symptoms and treatment of this condition?

A

Purpuric rash over the buttocks and lower limbs, abdo pain, vomiting and joint pain. Usually self-limiting (weeks to months).

113
Q

What vasculitises have cANCA and what have pANCA?

A

cANCA - GPA

pANCA - EGPA, microscopic polyangiitis.

MSK Cortext (4 decks)

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