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Rheumatology Flashcards

1
Q

List 4 seronegative spondyloarthropathies

A

Ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis
Enteropathic arthritis

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2
Q

Which seronegative spondyloarthropathies are more prevalent in males? (2)

A

Ankylosing spondylitis

Reactive arthritis

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3
Q

Which skin lesions can be seen in which seronegative spondyloarthropathies?

A

AS - rare to have skin lesions

Psoriatic arthritis - 100% psoriasis

Reactive arthritis - common - keratoderma blennorrhagica

Enteropathic arthritis - occasional - pyoderma, erythema nodosum

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4
Q

How common is the HLA-B27 marker in the seronegative spondyloarthropathies?

A

90% in AS
40% in PsA
80% in ReA
30% in EnA

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5
Q

In which seronegative spondyloarthropathies is sacroiliitis more common?

A

AS and ReA (compared to PsA and EnA)

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6
Q

What is the point of HLA-B27? (4) List disadvantages

A
  1. Not routine/diagnostic/confirmatory
  2. Cannot be used as a screening test for AS in the general population
  3. Sensitivity and specificity depends on racial/ethnic background of patient
  4. Does not help distinguish AS from other B-27 associated spondyloarthropathies
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7
Q

What postural changes can be seen in ankylosing spondylitis?

A

Decreased lumbar lordosis + increased thoracic kyphosis + increased cervical flexion = increased occiput to wall distance (>5 cm)

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8
Q

What is the most common extra-articular manifestation of ankylosing spondylitis?

A

Acute anterior uveitis - occurs relatively more commonly in HLA B-27 positive compared with those who lack the gene

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9
Q

In which seronegative spondyloarthropathies can aortic regurgitation occasionally occur?

A

AS
ReA
EnA

Rare in PsA

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10
Q

Describe the aetiology and pathophysiology of AS.

A

Relatively undetermined

Enthesitis thought to be source: inflammation –> osteopaenia –> erosion –> ossification –> osteoproliferation (syndesmophytes) which causes inflammatory low back pain

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11
Q

What is ankylosing spondylitis?

A

Chronic systemic inflammatory disorder of undetermined aetiology, usually beginning in early adulthood, primarily affecting the axial skeleton (but can peripheral arthritis and enthesitis) but can exhibit some extra-articular features (opthalmic, renal, gastro, cardiac, respiratory,neurologic)

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12
Q

What kind of pain is experienced in ankylosing spondylitis? (2)

A
  1. Inflammatory low back paine from syndesmophyte formation and/or buttock pain from sacroiliitis
  2. Inflammatory characteristic - nocturnal rest pain, early morning stiffness, relief with NSAIDs
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13
Q

Describe sacroiliitis pain. (2)

A
  1. Dull in character, difficult to localise and felt somewhere deep in the gluteal region
  2. May be unilateral or intermittent at first; however within a few months it generally becomes persistent and bilateral and the lower lumbar spine area also becomes painful
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14
Q

Describe the crystals seen in gout.

A

Monosodium urate –> needle-shaped, negatively birefringent (yellow)

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15
Q

Describe the crystals seen in pseudogout

A

calcium pyrophosphate dihydrate –> rhomboid-shaped, positively birefringent (blue)

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16
Q

Which tests can be used to measure spinal mobility in ankylosing spondylitis? (4)

A
  1. Modified Schober’s test - decreased forward flexion
  2. Lumbar side flexion: decreased
  3. Occiput-to-wall distance: increased
  4. Chest expansion: abnormal (<5 cm)
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17
Q

What investigations would you order in ankylosing spondylitis? (4)

A
  1. X-ray - appearance of radiographic abnormalities typically delayed - reactive sclerosis (Romanus lesion), squaring and erosions at the edge of the vertebral bodies to syndesmophyte formation and bony bridging i.e. ossification of outer fibres of annulus fibrosis - “bamboo spine”; interspinous ligament calcification ‘dagger spine’
  2. MRI - useful in EARLY DIAGNOSIS; good at detecting oedema or vascularised fibrous tissue, enthesitis of interspinous ligaments
  3. US - useful in detecting enthestisis
  4. Lab tests - ESR/CRP - only elevated in 50-70% of AS patients; HLA-B27 (90% of those with AS have this marker; but not all those with this marker will develop AS)
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18
Q

How is AS managed? (3)

A

Symptom management

  1. education and exercise
  2. NSAIDs
  3. TNF inhibitors - for patients with inadequate responst to NSAIDs
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19
Q

What is the first line therapy of Ankylosing Spondylitis?

A

NSAIDs

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20
Q

In which type of spondyloarthropathy should NSAIDs be used in caution?

A

Enteropathic

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21
Q

How is psoriatic arthritis managed? (3)

A
  1. Treat skin lesions (e.g. steroid cream, salicylic and/or retinoic acid, tar, UV light)
  2. NSAIDs or intra-articular steroids
  3. DMARDs, biologic therapies to minimise erosive disease
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22
Q

Which dermatological features are diagnostic of ReA?

A

Keratoderma blenorrhagicum (hyperkeratotic skin lesions of palms and soles) and balanitis circinata (small, shallow, painless ulcers of glans penis and urethral meatus)

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23
Q

How is ReA investigated? (3)

A

CLINICAL PLUS LABORATORY DIAGNOSIS

  1. Bloodwork - normocytic, normochromic anaemia and leukocytosis
  2. Sterile cultures
  3. Serology: HLA-B27
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24
Q

List 2 primary causes of hyperuricaemia.

A
  1. Mostly due to idiopathic renal underexcretion

2. Idiopathic overproduction or abnormal enzyme production/function

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25
Q

List 3 secondary causes of hyperuricaemia.

A
  1. Dietary excess
  2. Underexcretion - renal failure, drugs, systemic conditions
  3. Overproduction - increased nucleic acid turnover states (e.g. malignancy, post-chemotherapy)
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26
Q

How is gout investigated? (2)

A
  1. Joint aspirate: >90% of joint aspirates show crystals of monosodium urate (negatively birefringent, needle-shaped)
  2. X-rays may show tophi as soft tissue swelling, punched-out lesions
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27
Q

How is gout managed acutely? (3)

A
  1. High dose NSAIDs: indomethacin for up to 7 days
  2. Colchicine (SE: gastrointestinal effects)
  3. +/- intra-articular steroids where the above 2 options are contraindicated (i.e. in moderate to severe renal impairment)
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28
Q

How is chronic gout managed? (4)

A
  1. Diet- avoid foods with high purine content (e.g. visceral meats - liver and kidney, sardines, shellfish, beans, peas)
  2. Manage weight
  3. Limit alcohol intake
  4. Medical - to prevent recurrence
    - Xanthine oxidase inhibitors reduce the production of uric acid (e.g. Allopurinol)
    - uricosuric drugs increases renal uric acid excretion (e.g. Probenecid)

Allopurinol to be given only in proven recurrence (more than 2 documented attacks) - start approx. 4/52 post-attack; should be continued during acute episodes once already started

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29
Q

Describe the aetiology and pathophysiology of pseudogout.

A

Acute inflammatory arthritis due to phagocytosis of IgG-coated calcium pyrophosphate dihydrate (CPPD) crystals by neutrophils and subsequent release of inflammatory mediators within joint space

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30
Q

Describe the disease pattern of pseudogout (2)

A
  1. More frequently polyarticular - knee, polyarticular wrist, hand (MCP), foot (1st MTP), hip
  2. Slower in onset in comparison to gout
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31
Q

How is pseudogout investigated? (2)

A
  1. Joint aspiration - CPPD crystals present in 60% of patients
  2. X-ray - chondrocalcinosis (visible calcification of cartilage) in 75%: radiodensities in fibrocartilaginous structures or linear radiodensities in hyaline articular cartilage
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32
Q

How is pseudogout treated? (3)

A
  1. Joint aspiration, rest and protection
  2. NSAIDs
  3. Intra-articular or oral steroids to relieve inflammation

PROPHYLACTIC COLCHICINE PO CONTROVERSIAL

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33
Q

Which joints can be affected in rheumatoid arthritis?

A 
Wrist
MCP
PIP
Elbow
Shoulder
HIp, knee, ankle

DIP SPARED

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34
Q

Describe the characteristic pattern of symptoms seen in rheumatoid arthritis (3)

A
  1. Symmetric joint involvement and tenosynovitis - swelling and tenderness, but initially involves small joints of hands and feet (persisting for at least 6 weeks - diagnostic)
  2. Morning stiffness greater than 1 hour, improves with use and aggravated by rest
  3. Constitutional symptoms - profound fatigue; rarely myalgia or weight loss
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35
Q

List 4 hand and finger joint deformities that can be seen in rheumatoid arthritis.

A
  1. Swan neck deformity - hyperextension of PIP joint with flexion of DIP joint
  2. Boutonniere’s deformity - flexion of PIP joint with hyperextension of DIP
  3. Ulnar deviation of MCP
  4. Radial deviation of wrist joint
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36
Q

List three toe joint deformities that can be seen in rheumatoid arthritis.

A
  1. Claw toe - hyperextension of MTP and flexion of PIP and DIP joints
  2. Hammer toe - abnormal flexion of PIP
  3. Mallet toe - flexion posture of DIP
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37
Q

Describe the epidemiology of rheumatoid arthritis.

A

F>M

Can occur in all age groups, but increases in incidence with advancing age, with a peak between the fourth and sixth decades

Genetic predisposition: HLA-DR4/DR1

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38
Q

What investigations would you order in rheumatoid arthritis?

A
  1. Bloodwork
    - RF sensitive 80% but not specific
    - anti - CCP - sensitive 80%
    - HB - decreased (anaemia of chronic disease)
    - increased platelets
    - elevated ESR,CRP - not specific
  2. X-ray
    - can be normal at onset however essential for monitoring
    - soft tissue swelling -> osteopenia -> joint space narrowing -> erosions -> joint destruction
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39
Q

How is rheumatoid arthritis managed?

A
  1. Non-pharmacological: weight control, patient education and self-management programmes, thermotherapy, appropriate foot care etc.
  2. Pharmacological:
    Simple analgesics - pain relief
    NSAIDs - pain relief
    Corticosteroids - local/intra-articular or systemic
    DMARD - consider if several swollen joints, MTX gold standard
  3. Surgery indicated for structural joint damage
    - joint replacement
    - arthrodesis - wrist, thumb, ankle, C-spine
    - excision - head of radius, metatarsal heads
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40
Q

Describe the diagnostic criteria for SLE.

A

4 or more of 11 must be present serially or simultaneously

“SOAP BRAIN MD”

Serositis - pleuritis or pericarditis
Oral/nasal ulcers - usually painless
Arthritis - symmetric, involving 2 more small or large peripheral joints, non-erosive
Photosensitivity - skin rash in reaction to sunlight
Blood - haemolytic anaemia, thrombocytopaenia leukopaenia, lymphopaenia,
Renal - proteinuria, haematuria
ANA - most sensitive, but not specific
Immunologic - anti-dsDNA, anti-Sm, anti-Ro/La, antiphospholipid
Neurologic - altered mood states seizures or psychosis

Malar rash - non-scarring
Discoid rash - scarring

41
Q

What do biopsies of affected skin in SLE show?

A

Deposition of IgG at dermal-epidermal junction

42
Q

List 4 vascular manifestations of SLE.

A
  1. Raynaud’s phenomenon
  2. Livedo reticularis - mottled discolouration of skin due to narrowing of blood vessels, characteristic lacy or net-like appearance)
  3. Thrombosis
  4. Vasculitis
43
Q

List 5 opthalmic manifestations of SLE.

A
  1. Keratoconjunctivitis sicca - eye dryness caused by either decreased tear production or increased tear evaporation
  2. Non-specific conjunctivitis
  3. Retinal vasculitis - SERIOUS, can cause blindness
  4. Optic neuritis - SERIOUS, can cause blindness
  5. Cytoid bodies - cotton wool exudates on fundoscopy - infarction of nerve cell layer of retina
44
Q

Comment on the specificities and sensitivities of autoantibodies that may be present in SLE. (5)

A
  1. ANA - high sensitivity, but poor specificity
  2. anti-dsDNA - highly specific
  3. anti-Sm - highly specific, do not usually correlate with disease activity or clinical manifestations
  4. anti-Ro/La - non-specific
  5. antiphospholipid antibodies (anticardiolipin/lupus Ab) - 50% prevalence - presence indicates predisposition to clotting and thrombocytopaenia
45
Q

When is conservative pharmacological therapy considered in SLE and what is involved? (4)

A

Non-life-threatening disease - symptom suppression and reduction of number of flares

  1. NSAIDs - trial of 3-4 weeks
  2. antimalarials (hydroxychloroquine, chloroquine and quinacrine) -
  3. Low doses of systemic glucocorticoids if refractory
  4. Dermatologic - preventative - use sunscreen
    pharmacological - topical glucocorticoids

-

46
Q

What is involved in the management of life-threatening/severe SLE? (3)

A

Life-threatening SLE/severe = organ-threatening e.g. lupus nephritis

  1. High-dose oral pred or IV methylpred in severe disease - 4-6 weeks
  2. Steroid-sparing agents: AZA, MTX, mycophenolate
  3. IV cyclophosphamide
47
Q

Describe the aetiology of SLE. (4)

A

Multi-factorial aetiology

  1. Genetics - common association with HLA-B8/DR3
  2. Increased oestrogen - SLE greater incidence in women, pre-pubertal and post-menopausal women have similar incidence to men
  3. Infection - viral (non-specific stimulant of immune response)
  4. Drugs
48
Q

Which drugs can cause lupus? (4)

A

Anti-convulsants (phenytoin)

Anti-hypertensive (hydralazine)

Anti-arrhythmics (procainamide)

Isoniazid

(OCP associated with exacerbation - increased oestrogen!)

49
Q

What is the pathophysiology of osteoarthritis?

A

Deterioration of articular cartilage due to local biomechanical factors and release of proteolytic and collagenolytic enzymes - OA develops when cartilage catabolism > synthesis

50
Q

Describe the pattern of symptoms in OA. (6)

A
  1. Asymmetric
  2. Localised to affected joints (not a systemic disease)
  3. Joint pain with motion, relieved with rest
  4. Short duration of stiffness (less than 30 mins) after immobility
  5. Joint instability/buckling
  6. Joint locking due to ‘joint mourse’ (bone or cartilage fragment)
51
Q

Which joints are commonly involved in OA? (6)

A
  1. Hand - DIP,PIP, 1st CMC
  2. Hip
  3. Knee
  4. 1st MTP
  5. L-spine
  6. C-spine

Uncommon:ankle, shulder, elbow,MCP, rest of wrist

52
Q

How does hip OA usually present? (2)

A
  1. Groin pain +/- dull or sharp pain in the trochanteric area, internal rotation and abduction are lost first
  2. Pain can radiate to the anterior thigh but generally does not go below knee
53
Q

How does knee OA usually present on X-rays?

A

Initial narrowing of one compartment, medial > lateral; seen on standing X-rays

54
Q

Which joints in the lumbar spine are most commonly affected by Rh arthritis?

A

L4-L5, L5-S1

degeneration of IV discs and facet joints, with reactive bone growth contributing to neurological impingement or spondylolisthesis

55
Q

What are the 4 radiographic hallmarks of OA?

A
  1. Joint space narrowing
  2. Subchondral sclerosis
  3. Subchondral cysts
  4. Osteophytes
56
Q

Name 7 seropositive rheumatic conditions

A
  1. Rheumatoid arthritis
  2. SLE
  3. Antiphospholipid antibody syndrome (APLA)
  4. Scleroderma
  5. Polymyositis/dermatomyositis
  6. Sjogren’s syndrome
  7. Mixed connective tissue disease
57
Q

What is scleroderma?

A

A non-inflammatory disorder characterised by widespread small vessel vasculopathy and fibrosis, which occurs in the setting of immune system activation and autoimmunity

58
Q

What is CREST syndrome?

A

Syndrome that can occur in patients with limited cutaneous systemic sclerosis.

Calcinosis - calcium deposits on skin
Raynaud’s phenomenon
Esophogeal dysfunction - acid reflux
Sclerodactyly - tightening of skin on digits
Telengiectasia - superficial dilated blood vessels

59
Q

What is the epidemiology of scleroderma?

A

F > M, peaking in 5th and 6h decades

Associated with HLA-DR1

Associated with environmental exposure (silica, PVC, epoxy resins etc.)

60
Q

What are the dermatologic manifestations of scleroderma?

A

Painless non-pitting oedema –> skin tightening/thickening

Ulcerations, calcinosis, peringual erythema, pruritus, telangiectasia

61
Q

What is the characteristic facies of a scleroderma patient?

A

Mask-like facies with tight lip, beak nose, radial perioral furrows

62
Q

Name one vascular manifestation of scleroderma.

A

Raynaud’s phenomenon

63
Q

Name 4 gastrointestinal manifestations of scleroderma.

A
  1. Distal oseophageal hypomotility –> dysphagia
  2. Loss of lower oesophageal sphincter function –> GORD, ulcerations
  3. Small bowel hypomotility –> diarrhoea, bloating, cramps, malabsorption, weight loss
  4. Large bowel hypomotility –> wide mouth diverticuli pathognomonic radiographic finding on barium study
64
Q

Name 3 renal manifestations of scleroderma.

A

Mild proteinuria, creatinine elevation, hypertension

65
Q

What is the most common cause of morbidity and mortality in scleroderma?

A

Lung disease - interstitial fibrosis, pulmonary HTN, pleurisy, pleural effusions

66
Q

Name 3 musculoskeletal manifestations of scleroderma.

A
  1. Polyarthralgias
  2. ‘Resorption of distal tufts’ (acro-osteolysis) radiological finding. In general radiological findings can often suggest Ddx of rheumatoid (signs of erosion, joint space narrowing etc.)
  3. Proximal weakness secondary to disease, atrophy, low grade myopathy
67
Q

How is scleroderma managed? (2)

A
  1. Treat symptomatically according to system affected e.g. GI - PPIs for GORD, Vascular - vasodilators and/or patient education on cold avoidance for Raynaud’s, Lungs - cyclophosphamide for early interstitial disease etc.
  2. Dermatologic manifestations -
    local - UVA therapy, MTX, topicglucocorticoids
68
Q

Describe the experiences of patients with diffuse as opposed to limited cutaneous involvement in scleroderma.

A

Patients with diffuse cutaneous involvement most likely to have early and sometimes severe internal organ involvement. - central criterion = extension of skin sclerosis proximal to wrists

69
Q

How can scleroderma be categorised?

A

Localised - linear (en coup de sabre) vs morphea (patches of sclerotic skin)

vs

Systemic - diffuse vs limited cutaneous SSC

70
Q

What serological tests can be done in a patient with suspected sleroderma?(4)

A
  1. ANA (sensitive but not specific)
  2. Antitopoisomerase I antibodies
  3. Anticentromere antibodies
  4. Anti-RNA polymerase III antibodies

The last three autoantibodies are highly specific but not sensitive.

71
Q

What is the most important renal manifestation of scleroderma?

A

Scleroderma renal crisis

72
Q

What is scleroderma renal crisis and what biochemistry changes can be seen? (4)

A

New onset of significant systemic hypertension (>150/85 mmHg) and decreased renal function ( more than 30% reduction in eGFR)

Biochemistry changes include: 
Increased plasma creatinine
Hyperreninaemia
Thrombocytopenia
Microangiopathic haemolytic anaemia
73
Q

What investigations need to be ordered if one suspects scleroderma? (4)

A
  1. Bloodwork - CBC, Cr, ANA, other antibodies (anti-topoisomerase I, anti-centromere, anti- RNA polymerase III)
  2. CXR for pulmonary fibrosis
  3. Echo for pulmonary HTN
  4. Nailbed capillaroscopy - giant capillaries and microhaemorrhages
74
Q

Why does MAHA occur in scleroderma?

A

Increased coagulation - formation of fibrin mesh in vessels - RBCs physically cut by protein networks

75
Q

What is Sjogren’s syndrome?

A

Autoimmune condition characterised by dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia) caused by lymphocytic infiltration of salivary and lacrimal glands

76
Q

What is the Schirmer test?

A

A small piece of sterile filter paper, supplied in a standard kit, is placed in the lateral third of the lower eyelid. The extent of wetting in a given time is measured - wetting of less than 5 mm in five minutes is considered abnormal

77
Q

Describe the primary and secondary forms of Sjogren’s

A

Primary - not assoicated with other diseases

Secondary - associated with other conditions - RA, SLE, DM and HIV

78
Q

What systemic complications can occur in Sjogren’s? (7)

A
  1. Cutaneous
  2. Arthralgia
  3. Cardiopulmonary - pericarditis, pulmonary HTN, interstitial pneumoniis
  4. Renal - interstitial nephritis, glomerulonephritis
  5. GI - GORD
  6. Neurologic - peripheral and autonomic neuropathies
  7. Endocrine - hypothyroidisim
79
Q

What investigations can be ordered to diagnose Sjogren’s? (4)

A
  1. Bloodwork - autoantibodies (anti-Ro and/or anti-La)
  2. Salivary gland biopsy (focal lymphocytic sialoadenitis)
  3. Schirmer test - to assess tear flow
  4. Rose Bengal stain and slit lamp exam
80
Q

How is Sjogren’s managed? (3)

A
  1. Ocular - artificial tears or surgical punctal occlusion for dry eyes
  2. Oral - good dental hygiene, hydration, agents that stimulat salivary flow (e.g. pilocarpine - muscarinic agnoist), topical nystatin or clotrimazole x4-6 weeks for oral candidiasis
  3. Systemic - hydroxychloroquine, corticosteroids, immunosuppressive agents
81
Q

What is granulomatosis with polyangiitis? (aka?)

A

Granulomatous inflammation of vessels that may affect the upper airways, lungs and kidneys

Wegener’s granulomatosis

82
Q

With which autoimmune marker is granulomatosis with polyangiitis most associated with?

83
Q

How is granulomatosis with polyangiitis diagnosed? (4 Criteria)

A

If 2 or more of the following 4 criteria present:

  1. Nasal or oral involvement-inflammation, ulcers, epistaxis
  2. Abnormal findings on CXR - e.g. nodules, cavitations
  3. Urinary sediment - protein, RBC casts
  4. Biopsy of involved tissue - lungs show granulomas, kidneys show necrotising segmental GN
84
Q

How is granulomatosis with polyangiitis investigated? (4)

A
  1. Bloodwork: FBE (anaemia, increased WBC), ESR (increased), UEC (increased Cr), ANCA (c-ANCA>p-ANCA
  2. Urinalysis: proteinuria, haematuria
  3. CXR: pneumonitis, lung nodules, infiltrations, cavitary lesions
  4. Biopsy: renal, lung
85
Q

How is granulomatosis with polyangiitis managed?

A

Prednisone for 3-6 months +/- cyclophosphamide for 3-6 months followed by high dose MTX or AZA

86
Q

Which size vessels does granulomatosis with polyangiitis affect?

A

small vessel vasculitis

87
Q

Which size vessels does polyarteritis nodosa affect?

A

medium vessel

88
Q

What should be considered in a non-diabetic patient with mononeuritis complex?

A

Polyarteritis nodosa

89
Q

Which size vessels does temporal arteritis affect?

A

large vessel

90
Q

What does a biopsy of the temporal artery in termporal arteritis show?

A

Mononuclear cell infiltration or granulomatous inflammation, usually with multinucleated giant cells

91
Q

What are the clinical features of temporal arteritis? (5)

A
  1. New onset temporal headache +/- scalp tenderness
  2. Sudden, painless loss of vision and/or diplopia
  3. Tongue and jaw claudication
  4. PMR occurs in 30% of patients
  5. Aortic arch syndrome - involvement of subclavian and brachial branches of aorta result in pulseless disease
92
Q

How is temporal arteritis managed?

A

Immediately start high dose prednisolone, tapering as symptoms resolve - highly effective in treatment and in prevention of blindness and other vascular complications

93
Q

What is the danger in untreated temporal arteritis?

A

Untreated can lead to permanent blindness in 20-25% of patients

94
Q

What are the 5 diagnostic criteria for polymyalgia rheumatica?

A

All of the following are required

  1. Age over 50 at onset (typically, over 70)
  2. Pain for more than one month in at least 2 of the following 3 areas: neck, shoulders or pelvic girdle
  3. Increased ESR
  4. Rapid response to corticosteroids
  5. Must rule out other potential causes e.g. infection, RA, SLE, PAN, polymyositis, malignancy
95
Q

How is PMR managed?

A

Symptom relief - start with steroid dose and taper slowly, treat relapses aggressively

96
Q

What are Gottron’s papules?

A

pink-violaceous, flat-topped papules overlying the dorsal surface of the IP joints, seen in dermatomyositis

97
Q

List 5 dermatological features of dermatomyositis

A
  1. Gottron’s papules
  2. Heliotrope rash - purple rash over the eyelids
  3. Periungal erythema
  4. shawl sign - erythematous rash over neck, upper chest and shoulders
  5. mechanic’s hands: dark,dry, thick scale on palmar and lateral surface of digits
98
Q

Which autoimmune markers is polymyositis/dermatomyositis asscoiated?

A
  1. ANA
  2. anti-Jo-1(DM)
  3. anti-Mi-2
  4. ani-SRP
99
Q

Which malignancies is dermatomyositis associated?

A

Breast, lung, colon, ovarian

Musculoskeletal (9 decks)

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