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RCPSC > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Differentiate arthritis based on mono- poly- acute and chronic

A
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2
Q

List the cardinal features of inflammatory arthritis

A
  1. Morning stiffness
  2. Worst with rest, better with activity
  3. Night pain (esp second half of the night)
  4. Swelling
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3
Q

Define acute vs chornic arthritis

A

<6 weeks vs over 6 weeks

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4
Q

Give a DDx for chronic inflammatory arthritis

A
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5
Q

What are the clinical features of RA

A
  1. Tender swollen symmetric small joints
    1. MCP
    2. PIP
    3. Wrists
  2. >6 weeks or arthritis
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6
Q

What are the serologies associated with RA. How sensitive and specific are each

A
  1. RF
    1. 25% are negative
  2. Anti CCP
    1. 95% specific
    2. Can precede arthritis
    3. marker of more erosive disease
  3. Elevated ESR, CRP
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7
Q

Are serologies or X-Rays necessary for a Dx of RA

A
  1. No need for serologies or XRay
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8
Q

What other conditions can raise RF?

A
  1. Other CTD
  2. HepC/ cryoglobulinemia
  3. Endocarditis
  4. Malignancy (B-Cell neoplasms most common)
  5. Age
  6. normal variation
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9
Q

List the extra-articular manifestation of RA

A
  1. Cardiac
    1. Pericarditis +/- effusion, myocarditis
    2. CAD, accelerated atherosclerosis
  2. Lung
    1. ILD (NSIP, UIP)
    2. Pleural effusion (R/O infection)
    3. Pulmonary nodules
    4. Bronchiolitis obliterans
  3. Hematological
    1. Anemia of chronic disease
    2. Felty syndrome:
      1. Seropositive RA + splenomegaly + Neutropenia
  4. Neurologic
    1. Carpal tunnel
    2. C1-C2 instability/subluxation = life threatening
  5. Other
    1. Rheumatological nodules
    2. Vasculitis
    3. Amyloidosis
    4. Scleritis
    5. Sicca syndrome (dry eyes, dry mouth)
    6. Raynauds
    7. Sweet syndrome
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10
Q

What are the conventional DMARDS that can be used in the treatment of RA

A
  1. MTx
  2. Hydroxychloroquine
  3. Sulfasalazine
  4. Leflunomide
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11
Q

What are the biological DMARDS that can be used in the treatment of RA

A
  1. TNF inhibitors
    1. Adalimumab
    2. Etanercept
    3. Infliximab
    4. Golimumab
    5. Certolizumab pegol
  2. Tocilizumab
  3. Abatacept
  4. Rituximab
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12
Q

What are the small molecules or targetted synthetic DMARDS that can be used in the treatment of RA

A
  1. Tofacitinib
  2. Baricitinib
  3. Upadacitinib
  4. Apremilast
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13
Q

What “bridge therapies” can be used for acute treatment in RA

A
  1. Steroids (smallest possible dose)
  2. NSAIDS
  3. analgesics
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14
Q

What is the long term disease modifying therapy for RA

A
  1. Step 1: DMARD
    1. Low disease activity: Hydroxychloroquine
    2. Moderate to high disease activity: MTx
  2. Step 2: Biologic or small molecule
    1. Use once failed MTx
    2. Start with TNF and continue MTx
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15
Q

What are the side effects of MTx

A
  1. Hepatotoxicity
  2. Nausea
  3. Pancytopenia
  4. Pulmonary toxicity
    1. Hypersensitivity pneumonitis
    2. fibrosis
  5. Oral ulcers
  6. Alopecia
  7. Teratogenicity
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16
Q

What are side effects of hydroxychloroquine

A
  1. Retinal toxicity
  2. Rash
  3. Photosensitivity
  4. Myotoxicity (rare)
  5. cardiotoxicity (rare)
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17
Q

What are the side effects of leflunomide

A
  1. GI
    1. Nausea
    2. GI pain
    3. Dyspepsia
    4. diarrhea
  2. Hepatotoxicity
  3. HTN
  4. Myelosuppression
  5. Peripheral neuropathy
  6. teratogenicity
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18
Q

What are the side effects of Sulfasalazine

A
  1. GI toxicity
  2. headache
  3. rash
  4. CI in sulfa allergy
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19
Q

What should be considered when treating RA in patients with pulmonary disease?

A
  1. MTx can cause pneumonitis
  2. If parenchymal lung disease is mild, incidental, stable then MTx can be used if moderate to severe RA activity
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20
Q

What should be considered when treating RA in patients with heart failure?

A
  1. TNFi can lead to heart failure
  2. Don’t start TNFi if history of NYHA III or IV CHF
  3. If patients develop CHF on TNFi, switch to another agent
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21
Q

What should be considered when treating RA in patients with Lymphoproliferative disoorders?

A
  1. Rituximab first line in lymphoproliferative disorders where rituximab is indicated
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22
Q

What should be considered when treating RA in patients with NAFLD?

A
  1. MTX can be hepatotoxic
  2. Can still use MTX if liver enzymes, liver function normal and no advanced liver fibrosis in the case of moderate to severe RA
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23
Q

How is MTx induced nausea managed

A
  1. Increase folic acid to 5mg daily
  2. Trial of H2 blocker or PPI
  3. Add leucovorin post MTx dose
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24
Q

How is MTx induced stomatitis managed

A
  1. Increase folic acid to 5mg daily
  2. Add leucovorin
  3. If folic acid, leucovorin inefective or ulcers are severe reduce MTx dose
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25
Q

How is MTx induced hepatotoxicity managed

A
  1. Mildly elevated LFTs: reduce MTx dose
  2. LFTs>2x ULN: HOLD MTx dose then resume at a lower dose 1-2 weeks after normalization
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26
Q

How is MTx induced rash managed

A
  1. Reduce MTx dose
  2. if not resolving, stop MTx
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27
Q

How is MTx induced cytopenias managed

A

Dose reduce or discontinue MTx depending on toxicity

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28
Q

How is MTx induced pneumonitis managed

A

Discontinue MTx, do not restart

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29
Q

What risks are associated with biologics

A
  1. Infection
    1. New or reactivation
  2. Drug induced SLE/antibodies
  3. Local skin reactions
  4. Malignancy risk
    1. esp. non-melanomatous skin cancer
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30
Q

What baseline tests should be sent before starting a biologic

A
  1. Heb B, C testing
    1. If positive, treat concurrently
  2. TB testing as per algorithm
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31
Q

What are the vaccination recommendations for patients on biologics

A
  1. Yearly influenza vaccine
    1. Some evidence ot hold MTX 2 weeks before and after vaccine not in guidelines
  2. Pneumococcal
    1. PCV12 prime then PPSV23 at least 8 weeks later
  3. Tetanus
    1. As per general population
  4. Hep A and B
    1. Only in patients at high risk of exposure
  5. Herpes zoster
    1. non-live (shinrix) preferred
    2. Live attenuated gan be given to high risk patients not on biologics
      1. Give at least 4 weeks before starting biologic
  6. HPV
    1. As per general population, especially in SLE patients
  7. Vaccinate ideally when disease is quiescent
  8. avoid live attenuated vaccines
    1. Except possibly MMR and herpes zoster
  9. Immunocompetent household members should be vaccinated as per national guidelines except polio vaccine
  10. Patients on B-Cell depleting therapies should be vaccinated before starting therapy or 6 months after last dose AND 4 weeks prior to next dose
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32
Q

When is biologic use controversial

A
  1. NYHA class III or IV CHF
    1. TNFs can worsen
  2. Active hepatitis
    1. Start hepatitis treatment first and consult GI
  3. Prior lymphoproliferative malignancy
    1. Use rituximab
  4. Prior solid organ malignancy
    1. Consult oncologist prior to starting
  5. Prior skin cancer
    1. conventional DMARDS preferred
  6. Prior serious infection
    1. Consider conventional DMARDS if serious infection within 12 months
  7. In flare, modify frequency rather than dose
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33
Q

What vaccination guidance should be given to newborns of mothers on biologics during pregnancy

A
  1. Avoid live-attenuated vaccines in the first 6 months of life
    1. i.e. no rotavirus vaccine
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34
Q

How should RA be managed during pregnancy?

A
  1. Pre-pregnancy: ideal in remission
    1. Discontinue MTx at least 1-3 months prior to conception
    2. Ideally, avoid leflunomide in patients with the possibility of pregnancy
      1. In patients who get pregnant on leflunomide, measure level and treat with cholestyramine washout if detectible
    3. Taper prednisone to <20mg/day
  2. In pregnancy
    1. Often patients go into remission intrapartum
    2. Hydroxychloroquine, SSZ and biologics are safe during pregnancy, can continue
    3. Certolizumab marketed as larger molecule that does not cross the placental barrier
    4. Can use low dose glucocorticoids (pred<20mg)
    5. Avoid NSAIDS
  3. Post-partum
    1. Avoid MTx and leflunomide during breastfeeding
    2. Sulfasalazine safe during breastfeeding (theoretical risk of kernictus)
    3. Biologics are safe while breastfeeding
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35
Q

How should RA meds be managed in males pre-conception

A

Can continue MTx

Avoid cyclophosphamide and thalidomide

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36
Q

What are the clinical features of seronegative arthropathies

A
  1. SI joint, axial involvement
  2. Peripheral joints
    1. Asymmetric large joints:
      1. AS
      2. PsA
      3. Reactive
      4. IBD type 1 (fewer large joints, ass. with bowel activity)
    2. Symmetric small joints
      1. PsA
      2. IBD type 2 (Many small joints, independent of bowel)
  3. Extra-articular findings
    1. Enthesitis
    2. Dactylitis
    3. Uveitis
    4. Conjunctivits
  4. Skin
    1. Erythema nodosum
    2. Pyoderma gangrenosum (IBD)
    3. Keratoderma blennorrhagicum
    4. circinate balanitis (reactive)
    5. Psoriatic skin and nail changes (PsA)
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37
Q

What is the management of seronegative spondyloarthropathies?

A
  1. non-pharmacological
    1. Physiotherapy
    2. exercise
    3. Quit smoking
  2. Pharmacologic
    1. NSAIDS ar first line: on demand if stable, continuous if active
      1. Recommend against systemic steroids
      2. IA Glucocorticoids can be considered if isolated joint arthritis
    2. If intolerant to two different NSAIDS at max dose over 1 month or incomplete response to at least 2 NSAIDS over 2 months
    3. Consider DMARDS for peripheral disease (MTx, SSZ)
      1. No role in axial disease
    4. TNF are 1st line biologics
      1. IL-17 and JAK inhibitors second line
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38
Q

WHat is the most common cause of monoarthritis in the hip or knee?

A
  1. Septic arthritis
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39
Q

What is the most common bacterial etiology of septic arthritis?

A

S. Aureus in both native and proosthetic joints

Salmonella in sickle cell

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40
Q

What is the empiric antibiotherapy for septic joint based on the gram stain

A
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41
Q

What are the 2 common syndromes in gonococcal arthritis

A
  1. Triad of tenosynovitis, vesiculopustulat skin lesions, and migratory polyarthralgias without purulent arthritis
  2. Purulent arthritis without skin lesions
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42
Q

How common is gonococcal arthritis

A

occurs in less than 5% of gonococcal infections

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43
Q

How is gonococcal arthritis treated?

A
  1. Ceftriaxone
  2. Treat concurrently for chlamydia
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44
Q

What are the clinical manifestations of reactive arthritis

A
  1. Occurs several days to 4 weeks following gastroenteritis or urethritis
  2. Typically asymmetric, mono or oligo arthritis, lower extremity predominant
  3. CAN cause inflammatory back pain and sacroillitis
  4. Can (50-75%0 cause uveitis, conjunctivitis
  5. Can reccur and become chronic
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45
Q

What are the causative microbiological organisms in reactive arthritis

A
  1. Chlamydia trachomatis
  2. Yersinia
  3. Salmonella
  4. Shigella
  5. Campylobacter
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46
Q

How is reactive arthritis treated

A
  1. NSAIDS, intraarticular corticosteroids
  2. Consider DMARDS in recurrent/chronic disease
    1. MTX, SSZ
    2. rarely TNF

* no role for ABx

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47
Q

Differentiate the clinical pictures of acute lyme infection and chronic Lyme arthritis

A
  1. Acute infection: Arthralgias and myalgias
  2. Lyme arthritis:
    1. Late onset >6months post-infection
    2. Oligoarthritis with synovitis and swelling most commonly affecting the knees.
    3. Symptoms can fluctuate – swelling and erythema without significant pain
    4. Inflammatory synovial fluid
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48
Q

How is lyme arthritis diagnosed?

A

Lyme serology + clinical picture

If Dx needs confirmation, PCR of synovial fluid or tissue

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49
Q

How is lyme arthritis treated

A
  1. Oral ABx x 28 days (Doxy or amoxil)
  2. Treatment failure with objective severe synovitis :
    1. Exclude other Dx
    2. CTx IV x2-4 weeks
  3. Post-ABx
    1. Refer to rheum for consideration of DMARD, biologics
      1. Repeated courses of ABx not suggested
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50
Q

List risk factors for gout

A
  1. Hyperuricemia
    1. Renal insufficiency
    2. Metabolic syndrome
    3. hemolysis
    4. TLS
    5. Polycythemia
  2. Meds
    1. Thiazides
    2. low dose ASA
    3. Allopurinool
    4. pyrazinamide
  3. Diet
    1. Beer
    2. red meat
    3. seafood
  4. Demographics
    1. Male
    2. Post-menopausal femalse
    3. obseity

*estrogen has protective effects

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51
Q

What joints are most commonly affected by gout

A
  1. Monoarticular in 80% of initial attacks
  2. Predilectino to lower extermitites
  3. Most commonly 1st MTP or knee
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52
Q

Where is the most common place to find tophi

A
  1. Cool extremities, EARLOBES
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53
Q

What is found on radiography in CPPD

A

Chondrocalcinosis

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54
Q

What is found on microscopy in CPPD?

A

Intra-articular rhomboid-shaped, positively birefringent crystals

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55
Q

What diseases are associated with CPPD?

A
  1. OA
  2. Hypo T4
  3. HypoMg
  4. Hypo PO4
  5. HH (2nd, 3rd MCP and PIP joint arthritis)
  6. Hyperrpara
  7. Wilson’s (rarely)
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56
Q

Who gets calcific tendinitis/Milwaukee shoulder

A

Older females

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57
Q

What is the main clinical presentation of calcified tendinitis

A
  1. Acute onset
  2. Destructive shoulder arthropathy
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58
Q

Interpret synovial fluid analysis

A
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59
Q

How is acute gout treated?

A
  1. NSAIDS
  2. Colchicine
  3. Glucocorticoids
    1. IA if monoarthritis
    2. Oral if polyarthritis
  4. Consider anakinra (IL-1 blocker) in frequent flares with CI to other treatment options
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60
Q

If a patient is already on allopurinol, should it be held during an acute flare

A

No

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61
Q

If a patient meets criteria for allopurinol on their first gout flare, when should it be started?

A

Right away with colchicine

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62
Q

What are the definate and conditional indications for uric acid lowering therapy in gout

A
  1. Definate
    1. ≥2 attacks perr year
    2. Tophaceous gout
    3. Gouty arthropathy (ie. erosions)
  2. Conditional (1 episode PLUS:)
    1. CKD stage 3
    2. Uric acid >535
    3. Urolithiasis
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63
Q

What is the non-pharmacological management of chronic gout

A
  1. Regular exercise
  2. Weight loss
  3. ETOH avoidance
  4. Sugar-sweetened drinks avoidance
  5. Avoid heavy metals and excessive intake of meat + seafood
64
Q

What sho;d also be prescribed when starting allopurinol in gout

A

Overlap with either colchicine or NSAIDS for 3-6 months to prevent flare during up-titration of uric acid lowering therapy

65
Q

What is the first-line therapy for uric acid lowering therapy

A
  1. Allopurinol
66
Q

What are the risks associated with allopurinol

A
  1. Hypersensitivity reactions (worst in combination with thiazides)
    1. Dermatitis–SJS/TEN
    2. Fever
    3. Eosinophilia
    4. Hepatic necrosis
    5. Nephritis
    6. diarrhea
67
Q

What test can be can be sent in specific populations to stratify the risk of SJS, in what populations should it be sent?

A

Send HLA-B*5801 in Southeast asian and african canadians

68
Q

When should Febuxostat be used instead of allopurinol

A

If a patient can’t tolerate allopurinol (not first line)

69
Q

What are the side effects of febuxostat

A

Rash

Diarrhea

70
Q

What are the CI to febuxostat

A

Hx of CVD or new CVD event

71
Q

What are the classification criteria for SLE?

A
  1. Need ANA ≥1:80 to classify
  2. Cutoff for criteria
    1. Fever >38.3
    2. WBC<4
    3. PLt<100
    4. Pericarditis: ≥2 of the following:
      1. Rub
      2. typical pain
      3. ECG findings
      4. New or worsening effusion
    5. Joint involvement:
      1. Synovitis in ≥2 joints or tenderness ≥ 2 joints with >30 min am stiffness
72
Q

What other conditions can increase your ANA?

A
  1. Rheum
    1. SLE
    2. Scleroderma
    3. MCTD
    4. Drug-induced lupus
    5. Polymyositis/dermatomyositis
    6. RA
  2. Thyroid disease
  3. AI hepatitis
  4. PBC
  5. IBD
  6. IPF
  7. Infection
    1. Hep C
    2. parvo
    3. TB
  8. FHx of any of the above
73
Q

What is the most sensitive and specific test for SLE

74
Q

What are the otherr serorlogies associated with SLE

A
  1. C3, C4
  2. Anti-SM
  3. Anti-histone
  4. Anti-RRNP
  5. Anti-ro
  6. anti-la
75
Q

Which lupus labs can be used to follow disease activity?

A
  1. dsDNA
  2. Complements
76
Q

Which lupus serology is also associated with mixed CTD?

77
Q

Which lupus serology is also associated with Drug induced lupus?

A

Anti-histone

78
Q

Which lupus serology is also associated with sjogren’s

A

Anti ro, anti la

79
Q

Which lupus serology is also associated with congenital heart block and neonatal cutaneous lupus

80
Q

Other than dsDNA, what is the oother specific serology for lupus

81
Q

Differentiate a malar rash from rosacea

A
  1. Malar rash
    1. Lasts days to weeks
    2. Spares nasolabial folds
    3. Precipitated by sun exposure
    4. Look for other systemic manifestations
  2. Rosacea
    1. Frequent flushing (lasting few hours)
    2. Telangiectasias, papules, pustules
    3. Aggravated by sun, spicy foods/drinks, EtOH
    4. CAN cross nasolabial fold
82
Q

How dies class III/IV lupus nephritis present?

A
  1. Hematuria
  2. proteinuria
  3. HTN
  4. renal failure
83
Q

how is class III/IV lupus nephritis managed

A
  1. Induction
    1. IV pulse steroids or pred 1mg/kg + another agent
      1. Cyclophosphamide
      2. MMF (better in African American, hispanics)
      3. ACEi for proteinuria
  2. Maintenance
    1. MMF or azathioprine, low dose pred generally done
    2. Can use rituximab if refractory but less effective
84
Q

How should patients be managed pre-pregnancy in lupus nephritis class III/IV?

A
  1. Stop ACE
  2. Continue HCQ
  3. ASA week 12-36
  4. If severe flare, consider AZA
85
Q

How does class V lupus nephritis present

A

Nephrrotic range proteinuria

does not necessarily progress to renal failure

86
Q

How should class V lupus nephritis be managed?

A
  1. Non-nephrotic proteinuia
    1. ACE
    2. Statin
    3. diuretic
  2. Nephrotic range proteinuria
    1. All patients
      1. ACE
      2. BP controrl
      3. HCQ
    2. Consider induction with MMF + pred
    3. Maintenance MMF or AZA
    4. Cyclophosphamide if continues to worsen
    5. In real life often re-Bx to ensure it is not stage III or IV
    6. Nephro consult
87
Q

When should anticoagulation be considered in lupus nephritis?

A
  1. ACR provides no guidance
  2. EULAR:
    1. Consider if albumin <20 and + APLA
    2. Controversial and not common practice
88
Q

How should non-renal SLE be managed?

89
Q

What are the diagnostic criteria for the anti-phospholipid antibody syndrome?

90
Q

How should SLE be managed in pregnancy?

A
  1. Continue HCQ throughout
  2. Start ASA 81mg before week 16 for pre-eclampsia prevention
91
Q

How should patients with SLE and a positive anti Ro/La be monitored during pregnancy

A
  1. No Hx of neonatal lupus: HCQ + serial fetal echo from week 16-26
  2. Hx of neonatal lupus: HCQ + Weekly serial fetal echo week 16-26
92
Q

How should a patent with positive aPL be treated during pregnancy

A
  1. No APS: ASA alone
  2. OB APS: ASA + Px heparin until 6-12 weeks pp
  3. Thrombotic APS: ASA + Therapeutic heparin during pregnancy and PP
93
Q

What drugs are commonly associated with drug induced lupus

A
  1. Hydralazine
  2. Procainamide
  3. TNF inhibitors
  4. isoniazid
94
Q

What is shrinking lung syndrome?

A

Rare complication of SLE related to diaphragmatic muscle weakness

Appears as clear lungs on CXR but decreased volume

95
Q

What is Libman Sacks endocarditis

A
  • Non-infectious endocarditis associated with APLA
  • Thrombus on valve from acumulation of immune complexes, mononuclear cells, hematoxylin bodies, and fibrin and platelet thrombi
  • Can cause embolic phenomena
  • Treated w steroids and anticoagulation
96
Q

What are the clinical manifestations of Sjogren

A
  1. Xerostoma
  2. Keratocunjunctivitis
  3. Non-glandular involvement
    1. Arthritis
    2. Vasculitis
    3. Demyelinating neuropathy
    4. RTA
97
Q

Give a DDx for bilateral parotid gland enlargement

A
  1. Sjogren
  2. Infectious
    1. Mumps
    2. TB
    3. bacterial
  3. Sarcoidosis
  4. IgG4 syndrome
  5. Lymphoma
  6. Alcoholism
  7. Anorexia/bulimia
98
Q

What serologies are generally positive in Sjogrens

A
  1. ANA
  2. Anti-Ro
  3. Anti-La
  4. RF
99
Q

What malignancy does Sjogren increase your risk of

A

>40x increased risk of B-Cell lymphoma

100
Q

How is Sjogren diagnosed

A
  1. Ophtho: Schirmers test
  2. Unstimulated salivary flow
  3. ENT: Minor salivary gland Bx: focal lymphocytic sialadenitis
101
Q

What are the manifestations of Diffuse systemic sclerosis

A
  1. Sclerodactyly proximal to elbows and knees
  2. Internal organ involvement
    1. Risk of ILD, renal crisis
102
Q

What are the clinical manifestations of limited cutaneous sclerosis/ CREST syndrome

A
  1. Calcinosis
  2. Raynaud’s phenomenon
  3. Esophageal dysfunction
  4. Sclerodactyly
  5. Telangiectasias

*PHTN in up to 5%

103
Q

What are the specific serologies for scleroderma

A
  1. Limited/CREST: anticentromere
  2. Diffuse: Anti-SCL70/topo I
104
Q

List 3 complications of systemic sclerosis

A
  1. Scleroderma renal crisis
    1. 10-20% of diffuse SS
    2. Increased risk with prednisone, RNA polymerase, II autoantibodies, and early disease
    3. Acute/ progressive renal failure + HTN + mild proteinuria
    4. Can have normotensive SRC
  2. Pulmonary HTN
    1. All SS patients should be monitored with echo and PFTs
    2. More common in limited SS
  3. GAVE
    1. Can cause life threatening GI bleeding
105
Q

Differentiate the findings in TTP and SRC

106
Q

How is SRC treated

A

ACE inhibitor (captopril)

107
Q

Compare and contrast primary and secondary Raynaud’s

A
  1. Primary
    1. F>M, onset in 20s, often FMHx
    2. Symmetric, typically not progressive
    3. Predictable onset
    4. ANA negative
  2. Secondary (due to CTD, vasculitis, infection)
    1. Asymmetric, can be progressive
    2. Abnoormal nail fold
    3. Pits and ulcerations of digits
    4. Males, onset >40s
108
Q

What diseases can be implicated in secondary Raynaud’s

A
  1. SSc
  2. MCTD
  3. SLE
  4. Hypo T4
  5. Carcinoid
  6. PCC
  7. HBV
  8. HCV
  9. Parvo
  10. Heme malignancies
109
Q

What investigations should be sent if suspecting secondary raynaud’s

A
  1. CBC, Cr, UA, LFTs, CK, ESR, CRP
  2. ANA, ENA, RF, C3, C4, Cryos
  3. TSH, SPEP/UPEP
  4. HBV, HCV
  5. PTT, APLA
110
Q

How is Raynaud’s treated

A
  1. Conservative measures
  2. CCB – 1st line
  3. Can consider topical nitrates PDE5 inhibitors
111
Q

What is the DDx for myositis

A
  1. Drugs/EtOH
    1. Statins. antipsychotics, colchicine, anti-retrovirals, lithium, SSRIs
  2. Idiopathic inflammatory
    1. PM
    2. DM
    3. IBM
    4. NAM
  3. Infectious
    1. Viral (HIV, influenza, EBV, CMV)
    2. Pyomyositis
  4. Hypothyroid myopathy
  5. Lyte disturbance (severe hypoK, hypo P)
  6. Genetic myopathy
112
Q

What are the clinical features of polymyositis

A
  1. Muscle weakness
    1. Insidious over weeks/months, symmetric and proximal>distal, neck flexor
      1. Can involve heart, diaphragm, oropharynx, esophagus
  2. Cardiac findings
    1. Myocarditis, arrhythmias, CHF
  3. Pulmonary
    1. ILD
    2. DLCO or CT abnormalities, pulm HTN
113
Q

What are the clinical features of dermtomyositis

A
  1. Same as polymyositis PLUS:
  2. Skin findings
    1. Gottron’s papules
    2. Shawl sign
    3. Heliotrope rash
    4. Generalized heliotrope rash
    5. periungueal erythema
    6. Mechanic’s hands
    7. Scalp psoriasiform changes
    8. Calcinosis cutis
114
Q

What investigations should be sent in DM/PM

A
  1. Labs
    1. CK
    2. AST ALT
    3. LDH
    4. inflammatory markers
    5. Myositis specific antibodies
    6. ANA
  2. Muscle MRI
  3. Muscle Bx
    1. Gold standard for Dx
  4. EMG
  5. Trop, ECG, +/- Echo: R/O cardiac involvement
  6. SLP assmst R/O oropharyngeal/esophageal involvement
  7. Spirometry with MIP/MEP: R/O diaphragmatic involvement
  8. Age appropriate cancer screening AND consider CT CAP
    1. R/O adenoCa
115
Q

List myositis specific antibodies and what they are related with

A
  1. Antisynthetase syndrome=anti Jo1
    1. Acute onset
    2. Constitutional Sx
    3. Rapidly progressive ILD
    4. Raynaud’s phenomenon, mechanic’s hands, skin ulcerations, arthritis
  2. Anti Mi2 Ab
    1. Classic form DM
    2. Highly responsive to Tx
    3. Favorable Px
  3. Anti-NXP2 and Anti-TIF1-gamma
    1. Highly associated with malignancy. FIND THE CANCER
116
Q

How is DM/PM treated

A
  1. First line
    1. High dose steroids
      1. Typically PO, Can use IV pulse if severe
    2. Steroid sparing agents
      1. MTx or AZA
      2. HCQ helpful for skin manifestations only
      3. MMF or cyclophosphamide if ILD
  2. Refractory or severe
    1. IVIG
    2. Rituximab

*Continue age-appropriate cancer screening for at least 5 years after Dx

117
Q

What is the epidemiology of IBM

A

Older, M>F

118
Q

What are the clinical manifestations of IBM

A
  1. Lower CK than other miositidies
  2. Distal and proximal muscle weakness
  3. insidious onset
  4. Poor response to treatment
119
Q

What are the clinical findings in NAM?

A
  1. Severe myopathy
  2. CK ++ elevated
  3. Often statin induced but persistent after D/C statin
  4. No skin manifestations
120
Q

What auto-antibody is usually associated with NAM

A

Anti-HMG coA reductase ab

121
Q

What should always be ruled out as the underlying cause of NAM?

A

Paraneoplastic syndrome

122
Q

What is the chapel hill nomenclature of vasculitidies

123
Q

What are the clinical manifestations of giant cell arteritis

A
  1. Headache (Sensitive)
  2. Jaw claudication (LR +4.2)
  3. Diplopia (LR+ 3.4)
  4. Scalp tenderness
  5. Extra-cranial/systemic manifestations
    1. Limb claudication
    2. Asymetric BP
  6. P/E
    1. Beaded, prominent or tender temporal artery (LR+ 4.6, 4.3, 2.6)
    2. Look for acute ischemic optic neuritis on fundoscopy and assess visual acuity
      1. Consult ophtalmology
124
Q

What investigations can be sent to rule in/out GCA?

A
  1. ESR ( to rule out LR-0,2)
  2. Temporal artery Bx (within 14 days of starting steroids) (Sn 87%)
  3. CTA or MRA: R/O aortic arch involvement if extracranial/systemic symptoms
  4. US or MRI of temporal artery NOT CURRENTLY RECOMMENDED
125
Q

How should GCA be managed

A
  1. If visual Sx or loss or critical cranial ischemia
    1. IV pulse steroids x3 days then prednisone 1mg/kg +tocilizumab
  2. No visual loss/Sx or critical cranial ischemia
    1. Prednisone 1mg/kg + Tocilizumab
  3. Treat with HD steroids x1 month then taper
  4. No ASA unless critical or flow limiting involvement of the carotid or vertebral arteries
126
Q

What are the criteria for the diagnosis of PMR?

A
  1. Age >50
  2. Elevated ESR/CRP
  3. Low grade fever/fatigue
  4. US criteria: Shoulder/hip bursitis/tenosynovitis/synovitis
  5. Bilateral shoulder ache and/or hip pain/stiffness
  6. Morning stiffness>45 min duration
  7. Negative RF, CCP
  8. Must have normal CK, otherwise think myositis
127
Q

What is the treatment of PMR?

A

Prednisone 12.5-20 mg/d x2-4 weeks then taper to 10 within 1-2 months if response

If relapse increase to pre-relapse dose then decrease gradually or add DMARD

128
Q

What is the relationship between PMR and GCA

A
  1. 50% of GCA patients have PMR
  2. 15% of PMR patients have GCA
129
Q

What are the clinical/Diagnostic findings in PAN?

A
  1. Unexplained weight loss >4kg
  2. Livedo reticularis
  3. Testicular pain or tenderness
  4. Post-prandial abdo pain
  5. Myalgias (excluding hip girdle/shoulders)
  6. Mono or polyneuropathy
  7. HBV infection
  8. Arrteriographic abnormalities (not from non-inflamatory disease)

*usually serologically negative but can have positive ANCA, RF serologies. Go by clinical presentation to make Dx

130
Q

How is PAN treated

A
  1. If HBV related:
    1. Glucocorticoids + anti-virals +/- PLEX
  2. Idiopathic
    1. Mild disease: glucocorticids alone
    2. Moderate/severe: GC + Cyclophosphamide followed by AZA/MTx
131
Q

What are the symptoms of ANCA ass. vasculitis

A
  1. Constitutional Sx
    1. Fevers
    2. Malaise
    3. Weight loss
  2. ENT Sx
    1. Nasal crusting
    2. Sinusitis
  3. Tracheal and pulm involvement
    1. stenosis
    2. hemoptysis
  4. Renal involvement
    1. RPGN
    2. hematuria
    3. Proteinuria
  5. *Pulmonary renal syndrome
  6. Mononeuritis multiplex

GPA: Most commonly pulmonary, renal and ENT involvement

MPA: Most commonly pulmonary renal involvement

EGPA: Asthma, peripheral eosinophilia, peripheral neuropathy. Cardiac involvement 15-20% (CHF, pericardial effusion, arrhythmias)

132
Q

What ANCA is associated with GPA, MPA and EGPA

A
  1. GPA: c-ANCA (PR3)
  2. EGPA: p-ANCA (MPO)
  3. MPA: p-ANCA (MPO) 65%, c-ANCA(PR3) 30%
133
Q

List non-vasculitic causes of p-ANCA (MPO) elevation

A
  1. Chron’s/UC
  2. Drugs (PTU)
  3. CTD
  4. Malignancies
  5. Infections
    1. HepB, C
    2. HIV
134
Q

Define mild, moderate, severe and life-threatening cryoglobulinemic vasculitis

A
  1. Mild-moderate
    1. Purpura
    2. Livedo reticularis
    3. Mild non-debilitating neuropathy
    4. GN without renal failure
  2. Severe
    1. Cutaneous ulcers
    2. ischemia
    3. severe debilitating neuropathy
    4. GN with renal failure/nephrotic syndrome
    5. GI involvement
  3. Life threatening
    1. RPGN
    2. CNS involvement
    3. Intestinal ischemia
    4. Alveolar hemorrhage
135
Q

How is cryoglobulinemic vasculitis 2/2 hep C treated?

A
  1. Mild-moderate
    1. Induction: Antiviral +/- corticosteroids
    2. Maintenance: Antiviral
  2. Severe
    1. Induction: rituximab + corticosteroids
    2. Maintenance: antiviral
  3. Life treatening
    1. Induction: PLEX + pulse steroids + Ritux or cyclophosphamide
    2. Maintenance: Antivirals
136
Q

What are secondary causes of chilblains

A
  1. COVID-19
  2. SLE (most common)
  3. Behcet
  4. Monoclonal gammopathies
  5. Cryoglobulinemia
  6. CML/AML
  7. APLA
137
Q

What are chilblains

A

Superficial inflammatory cutaneous disease manifesting as erythematous to violaceous lesions on sites of cold exposure (typically fingers/toes). can be primary or secondary

138
Q

How are chilblains treated?

A
  1. Smoking cessation
  2. Cold avoidance
  3. topical steroids
  4. Oral CCB
139
Q

What is the non-pharmacological management of non-inflammatory arthritis

A
  1. FOr all
    1. Exercise
    2. self efficacy/management program
    3. Consider CBT, thermal interventions, acupuncture
  2. Knee, hip:
    1. Weight loss
    2. Tai Chi
    3. Cane
    4. Balance training

NO TENS

140
Q

What is the pharmacological management of non-inflammatory arthritis

A
  1. All
    1. Oral NSAIDS if no CI
    2. Intra articular corticosteroids
    3. Consider acetaminophen, duloxetine, tramadol
  2. Don’t use
    1. Opioids
    2. Glucosamine
    3. DMARDS biologics
    4. Platelet-rich plasma
    5. Stem cell injections
    6. Intra-articular hyaluronic acid
141
Q

What are the diagnostic criteria for Fibromyalgia

A
  1. Widespread pain index and symptom severity scale
  2. Symptoms present at a similar level for 3 months
  3. No disorder to otherwise explain the pain

*Patients will often report associated fatigue, cognitive dysfunction, non-restorative sleep

142
Q

What labs MUST be normal before posing a diagnosis of fibromyalgia

A
  1. CBC
  2. ESR, CRP
  3. CK
  4. TSH
143
Q

How is fibromyalgia treated?

A
  1. Non-pharm
    1. Exercise
    2. CBT
    3. Sleep hygiene
    4. Tai Chi
  2. Pharm
    1. SNRI(duloxetine)
    2. TCA (amiitriptyline)
    3. Gabapentin
144
Q

List side effects of cyclophosphamide

A
  1. Infertility
  2. Myelosupression
  3. Infection (PCP)
  4. Hemorrhagic cystitis
  5. Malignancy
    1. bladder
    2. skin
    3. MPD
  6. Alopecia
145
Q

List side effects of colchicine

A
  1. Diarrhea
  2. Nausea
  3. Myelo-supression
  4. Myelopathy
  5. Peripheral neuropathy
    1. More common in CKD
  6. Drug interactions (CYP3A4)
146
Q

List side effects of JAK inhibitors

A
  1. Infection
    1. Tb
    2. Increased frequency of typical infections
  2. Malignancy
    1. Non-melanoma skin Ca
    2. Lymphoma
  3. Herpes zoster
  4. DVT-PE
  5. Lower GI perf

*Black box warning: increased risk of all cause mortality, MACE, thrombosis and cancer

147
Q

List side effects of IL12/23 antagosists

A
  1. Infections
    1. TB
    2. typical infections
  2. Malignancy
  3. PRES
  4. upper respiratory infections
148
Q

List side effects of IL-17A inhibitors

A
  1. URTI
  2. Infections (oral herpes)
  3. IBD?
149
Q

What monitoring is required on Cyclophosphamide?

A
  1. Bi-weekly CBC
150
Q

Compare the hand deformities, X-ray findings and other P/E findings in OA and RA?

151
Q

What is relapsing polychondritis?

A
  1. Vasculitis causing episodic inflammation in cartilagenous structures throughout the body including eyes, ears, nose, joints and respiratory tract
    1. Ear involvement is the most common feature
152
Q

What other diseases is relapsing polychondritis associated with?

A
  1. 1/3 will present in association with other systemic vasculitides, CTD (RA, SLE) malignancy (hematologic) or other autoimmune conditions (IBD, PBC)
153
Q

How is relapsing polychondritis treated?

A
  1. Mild disease (Nasal or auricular chondritis, arthritis)
    1. NSAIDS
    2. Glucocorticoids or dapsone if NSAIDS fail
  2. Life or organ threatening disease
    1. Mild-moderate organ threatening: GLucocorticoids + MTX
    2. Life threatening or severe organ threatening: Glucocorticoids + cyclophosphamide
154
Q

What are the diagnostic criteria for adult onset still’s disease?

155
Q

How is adult onset stills disease managed?

A
  1. Mild-moderate disease (non-disabling fever, rash, arthralgia or mild arthritis, no MAS): NSAIDS
  2. Moderate-severe disease (clinically significant serositis, moderate to severe polyarthritis, persistent high fevers despite NSAIDS, internal organ involvment) or failed NSAIDS: Glucocorticoids or Anakinra
  3. If MAS present treat with MAS protocol (usually etoposide + steroid)
156
Q

Differentiate Scleritis from uveitis

RCPSC (14 decks)

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