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Internal Medicine: PGY-1 > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Joint pain:
Monoarticular
Polyarticular (sym)
Polyarticular (asym)

A

Monoarticular
- Septic
- Gout, CPPD
- OA
- Trauma
- Hemarthrosis

Polyarticular (sym)
- RA
- PsA
- PMR
- EA
- AS

Polyarticular (asym)
- Gonococcal
- Lyme
- ARF
- ReA
- Viral

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2
Q

Examples of seroNEGATIVE spondyloarthropathies?

A

“PEAR”:
- PsA
- EA
- AS
- ReA
- Undifferentiated

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3
Q

Examples of seroPOSITIVE spondyloarthropathies?

A
  • RA
  • SLE
  • Scleroderma
  • Sjogren
  • Inflam. myopathies (PM/DM)
  • Mixed CTD
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4
Q

Develop DDx for Joint Pain: articular vs. Non-articular

A

Articular
- Inflam: infectious, post-strep, AI, crystal
- Degenerative: primary (OA), secondary
- Neoplasm

Non-Articular
- Localized Pain: mechnical, neuropathic, vascular
- Generalized Pain: non-inflam, inflam, Psych, endocrine

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5
Q

Cardinal features of inflam. arthritis?

A
  • Morning stiffness (typically >60m)
  • Worse with rest, better with activity
  • Night pain (esp. latter half of night)
  • Swelling
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6
Q

What characterizes the following arthritides: mono, oligo, poly

A
  • Mono: 1 joint
  • Oligo: 2-4 joints
  • Poly: >=5 joints
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7
Q

Synovial Fluid Analysis: [1] Non-inflam, [2] inflam/crystals, [3] septic. Comment on fluid appearence, WBC, %PMN, crystals.

A

Non-Inflam
- Fluid: clear
- WBC: <2000
- %PMNs: 50%
- Crystals: no

Inflam
- Fluid: cloudy
- WBC: 10,000-100,000
- %PMNs: >50%
- Crystals: -birefring (gout), +birefring (CPPD)

Septic
- Fluid: cloudy/pus
- WBC: >50,000 [bacterial], 10-30K [fungal/myco]
- %PMNs: 90% [bact.]
- Crystals: +/-

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8
Q

Develop DDx approach to mono vs polyarthritis

A

Mono
- Acute: infection, crystal, trauma, new IA
- Chronic: non-inflam (OA), IA, infection (fungal, TB), AVN

Poly
- Acute: infectious (viral, IE), new IA
- Chronic: inflam, crystal, ReA, paraneoplastic

IA: inflam arthritis
Chronic (>6/52), Acute (<6/52)

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9
Q

Classic S&S for RA? (joint-wise)

A
  • Symmetrical
  • Tender, swollen joints: wrists, MCP, PIP
  • Morning stiffness
  • Joint deformity: swan-neck, boutonniere, hitchiker thumb
  • Atlantoaxial subluxation
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10
Q

RA DDx?

A
  • Other CTD
  • HCV/cryo
  • IE
  • Malignancy (B-cell most common)
  • Age
  • Normal variation
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11
Q

In RA, which test can predict more “erosive” disease if positive prior to arthritis?

A

Anti-CCP

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12
Q

RA extra-articular manifestations?

A

Constitutional
- fever, myalgia, fatigue, wt loss

Rheumatoid nodules
- skin: nontender, firm, subQ swelling
- lung: rheum pulm nodules (may have fibrosis and pneumoconiosis [Caplan syndrome])

Cardiac
- pericarditis +/- effusion, myocarditis
- CAD, accelerated atherosclerosis (MI, CVA risk)

Lung
- ILD (NSIP, UIP)
- Pleuritis, pleural effusion (rule out infection)
- Bronchiolotus obliterans

Heme
- ACD, neutropenia, splenomegaly
- Felty’s syndrome = sero+ RA, splenomeg, neutropenia

Neuro
- Carpal tunnel (one of earliest signs)
- C1-2 instability/subluxation = life-threatening

Other
- vasculitis, Raynaud’s
- amyloidosis
- scleritis
- sicca syndrome (dry eyes, mouth)
- Sweet’s syndrome

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13
Q

What are symptomatic therapies for RA that are NOT disease modifying?

A
  • Steroids (<3/12; use lowest dose for shortest time possible)
  • NSAID
  • Analgesics
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14
Q

What are the long-term, disease modifying, therapies for RA?

A

Step 1: Conventional DMARD
- Low disease activity: hydroxychloroq (PLQ)
- Mod-high: MTX mono (oral>subQ)
- Note: triple (MTX/PLQ/SFZ) no longer recommended

Step 2: biologic or small molecule DMARD
- Use when failed MTX mono
- Usually start with TNFi + con’t MTX
- Dose can be reduced if low-disease or remission >=6/12

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15
Q

What are the broad categories of therapies for RA management?

A

Conventional DMARD
- MTX, PLQ, SFZ, Leflunomide

Biologic DMARD
- TNFi: adalimumab (humira), etanercept (enbrel), infliximab (remicade), golimumab (simponi), certolizumab pegol (cimzia
- Tocilizumab (actemra)
- Abatacept (orencia)
- Rituximab

Small molecule/targeted DMARD
- Tofacitinib (xeljanz)
- Baricitinib (olumiant)
- Upadacitinib (rinvoq)
- Apremilast (otezla)

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16
Q

Broad S&S of vasculitides?

A
  • Constitutional: fever, fatigue, wt loss, anorexia
  • Arthralgia, myalgia, arthritis
  • Mononeuritis multiplex
  • Organ ischemia: mesenteric ischemia, stroke, blindnesss, peripheral neuropathy, GN
  • Skin changes: palpable purpura, livedo reticularis, necrotic lesions, infarcts of tips digits
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17
Q

Other than vasculitis, what other DDx can cause elevation of p-ANCA?

A
  • Crohn’s, UC
  • Drugs (PTU, cocaine)
  • CTD
  • Malignancies
  • Infections (HBV, HCV, HIV)
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18
Q

eGPA typically presents with which symptoms?

A
  • asthma
  • allergic rhinitis
  • peripheral eosinophilia
  • peripheral neuropathy
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19
Q

What are the elements part of the Five-Factor Score that should be used to guide therapy in eGPA?

A
  • Proteinuria [>1g/d]
  • Cr [>138.7]
  • GI tract involvment
  • Cardiomyopathy
  • CNS involvement

1 or more = severe disease

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20
Q

Which DMARD should you not start in someone who has CHF?

A

TNFi, may worsen HF - if NYHA III or IV HF

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21
Q

Which are main S/E of the following DMARDs? MTX, PLQ, Leflunomide, SSZ

A

MTX
- hepatotox, pancytopenia, PO ulcers, teratogenic
- Rx Folic acid to reduce S/E

PLQ
- retinal tox, photosensitivity

Leflunomide
- GI, hepatoxicity, myelossup, teratogenic

SSZ
- GI tox, HA, rash; CI’d if Sulfa allergy

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22
Q

Low-dose MTX toxicity - management: nausea, stomatitis, hepatotox, rash, cytopenias, pneumonitis

A

Nausea:
- increase folic acid to 5mg daily
- trial H2-b/PP
- add leucovorin post-MTX-dosS

Stomatitis:
- increase folic acid
- add leucovorin
- reduce MTX dose if not better

Hepatotox:
- mild - reduce MTX dose
- if >2 ULN - hold MTX then resume a lower dose 1-2 weeks after normalization

Rash:
- dose reduce MTX, d/c if persists

Cytopenias:
- dose reduce or d/c if severe

Pneumonitis:
- d/c MTX, do not restart

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23
Q

Low-dose MTX toxicity - management: nausea, stomatitis, hepatotox, rash, cytopenias, pneumonitis

A
  • Nausea: increase folic acid to 5mg daily, trial H2-b/PPI; add leucovorin post-MTX-dosS
  • Stomatitis: increase folic acid, add leucovorin; reduce MTX dose if not better
  • Hepatotox: mild - reduce MTX dose, if >2 ULN - hold MTX then resume a lower dose 1-2 weeks after normalization
  • Rash: dose reduce MTX, d/c if persists
  • Cytopenias: dose reduce or d/c if severe
  • Pneumonitis: d/c MTX, do not restart
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24
Q

Keypoints - Biologics: Risks, baseline testing

A

Risks
- infection (new, reactivation)
- drug induced SLE/antibodies
- local skin reactions
- malignancy (esp. non-melanomatous skin Ca)

Testing:
- HBsAg, HBsAb, HBcAb
- HCV (treat concurrently if +ve)
- TST, IGRA, and/or CXR

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25
Q

Special situations/controversial use for biologics:
- NYHA III or IV HF
- Active hepatitis
- Prior lymphoproliferative malignancy
- Prior solid organ malignancy
- Prior skin cancer
- Prior serious infection
- Flare: mx of dose/frequency

A
  • TNFi can worsen CHF
  • start hepatits tx 1st, consult GI
  • use Ritux
  • Consult Onco before starting
  • csDMARDs preferred
  • consider using csDMARDs if serious infection <12mo
  • modify frequency rather than dose first
  • DO NOT combine biologics
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26
Q

Non-live vaccines for patients on RMD? (MTX, Ritux, Pred)

A
  • MTX: hold x2/52 after influenza, all other vaccines unchanged
  • Ritux: time all vaccines when next RTX due, then delay RTX x2/52
  • Prednisone: give influenza, defer other vaccine if on >20mg until tapered
  • Others: continue unchanged
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27
Q

Seroneg SpA: clinical features

A

SI joint/axial involvement

Enthesitis, dactylitis, uveitis, conjunctivitis

Peripheral joints:
- asymmetric, large joint (AS, PsA, ReA, IBD type 1 [fewer large joints, associated w/ bowel activity])
- symmetric, small joint (PsA [DIP], IBD type 2 [many joints, independent bowel])

Skin:
- IBD: erythema nodosum, pyoderma gangrenosum
- ReA: keratoderma blennorrhagicum, circinate balanitis
- Psoriasis: psoriative skin and nail changes

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28
Q

Seroneg SpA: imaging features [peripheral, spine, SI joint]

A

Peripheral XR
- erosions, periosteal new bone formation, ankylosis

Spine XR
- syndesmophytes

SI Joint XR
- sclerosis, narrowing, erosions, ankylosis
- symmetric in AS, asym in PsA

SI Joint MRI
- BM edema

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29
Q

Seroneg SpA: Mx of axial disease

A

Non-Pharm
- PT, exercise
- Quit smoking

Pharm
- 1st-line: NSAID; strongly recommend AGAINST systemic GCs

Step up therapy to Biologics if:
- No response or intolerance to at least 2 different NSAIDs at maximal doses over 1 month, or
- Incomplete response to at least 2 NSAIDs over 2 months
- 1st-line: TNF-a inhibitors: etanercept (enbrel), infliximab (remicade), adalimumab (humira), certulizumab (cimzia), golimumab (simponi), or biosimilars;
- if primary non-response = progress to IL-17i; if secondary non-response (relapse after initial response) = change to alternae anti-TNF
- 2nd-line: IL-17i (secukinumab [cosentyx], Ixekizumab [Taltz])
- 3rd-line: JAKi (tofacitinib [Xeljanz])

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30
Q

Seroneg SpA: Mx of peripheral disease

A

Non-Pharm:
- PT, OT
- Weight loss, exercise
- Quit smoking

Pharm:
NSAIDS
- 1st-line for peripheral arthritis 2/2 AS, ReA
- IBD: use w/ caution, discusss with GI
- PsA: for sx only

GCs: avoid if possible, IA inj can be used for mono/oligoarthritis
DMARD: MTX, SSZ [Leflu, Cyclo, Apremilast in PsA]
Biologics/sm: selected based on disease

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31
Q

Seroneg SpA: associate biologic class with typical disease it treats (TNF-a, IL-17, IL-12/23, JAKi, CTLA-4)

A
  • TNF-a: AS, IBD, PsA, ReA
  • IL-17: AS, PsA
  • IL-12/23: PsA, IBD
  • IL-23: PsA
  • JAKi: AS, PsA, IBD (UC only)
  • CTLA-4: PsA
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32
Q

ReA: definition, incubation time, causative agents, joint manifestations, common associated sx (1), treatment

A

Definition: Arthritis s/p gastro or urethritis
Incubation: ~4 weeks after infection
Causative agents:
- C. trachomatis
- Yersinia
- Salmonella
- Shigella
- Campylobacter

Joint: Asym, mono/oligo; lower extremity predominant
Sx: 50-75% may have uveitis, conjunctivitis
Tx: NSAID, IA steroids
- DMARDs in recurrent/chronic disease (MTX, SSZ, rarely TNFi)
- NO role for Abx

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33
Q

SLE Classification Criteria? (as per ACR 2019)

A

ANA titre >=1:80
- If present, apply additive criteria

Additive Criteria (1 clinical + >=10 points)
- See picture below

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34
Q

DDx for ANA+

A
  • Rheum: SLE, scleroderma, MCTD, drug-induced lupus, PM/DM, RA
  • Thyroid disease, AI hepatitis, PBC, IBD, IPF
  • Infection: HCV, Parvo, TB
  • FHx of any of the above
  • Healthy (healthy titres: 1:40=20%, 1:80=10%, >1:160=5%)
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35
Q

SLE Labs?
Which can be used to monitor disease activity?

A

ANA (sensitive 95%, not specific)
Anti-dsDNA (specific 97-98%, not sensitive)
- Can be used to monitor disease activity along with C3/4 in concordant in dividuals (concordant = when flare, high antids-DNA + low C3/4)

ENA
* Anti-Sm: specific, not sensitive (30-40%)
* Anti-histone: drug0induced lupus, SLE (50-70%)
* Anti-RNP: required for MCTD, SLE (30-40%)
* Anti-Ro (SSA): risk of congenital heart block + neonatal cutaneous lupus
* Anti-La (SSB): Sjogren’s

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36
Q

Rashes: Malar vs. Rosacea

A

Malar
- Last few days-weeks
- Spares nasolabial folds
- Precipiated by sun exposure
- Look for other systemic manifestations!!!

Rosacea
- Frequent flushing (last few hours)
- Telangectasia, papules, pustules
- Aggravated by sun, spicy foods/drinks, EtOH
- Can cross nasolabial fold

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37
Q

What are the 5 types of Lupus Nephritis + general Mx?

A

Class I: minimal mesangial
- Supportive +/- immunosuppression if proteinuria >3g/d

Class II: mesangial proliferative
- Aggressive immunosuppression

Class III: focal (<50% golmeruli)
- Aggressive immunosuppression

Class IV: diffuse (>=50% glomeruli)
- Anti-proteinuric/HTN agents +/- immunosuppression if refractory

Class V: membranous
- Supportive +/- treat extrarenal manifestations

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38
Q

Overview of Lupus Nephritis Management? (Class III/IV)

A

Induction:
- Pulse steroids [IV GC 250-500mg/d x3d then Pred 0.6-1mg/kg/d] + 1 other (Cyclo, MMF)
- Cyclophosphamide: low-dose preferred (500mg q2wk x6)
Risks: infertility, infection, malig esp. GU (+++ hydration), cytopenias
- MMF: 2-3g/d x6 months (preferred if considering future fertility)
Risks: GI S/E, cytopenias, unsafe in pregnancy
- HCQ for all; ACEi for proteinuria

Maintenance:
- HCQ + MMF 1-2g/d +/- low dose Pred (target <7.5mg/d by 3 months)
- Alternative to MMF: AZA (if preg plans or intolerant), Tacro

39
Q

Class V (membranous) Lupus Nephritis typically does not progress to renal failure UNLESS? % risk of progression? Mx?

A
  • Nephrotic range proteinuria
  • 10-30%
  • Same as Class III/IV
40
Q

Management of non-renal SLE: All, mild, mod, severe manifestations?

A

All
- sun protection
- vaccines, smoking cessation, exercise
- BMI, BP, lipids, glucose
- anticoagulation/anti-platelet if aPL+

Mild (constitutional sx, mild arthritis, rash, plt 50-100)
- HCQ +/- GC (PO/IV) + topicals (GC, retinoids) for skin
- refractory: add MTX/AZA

Moderate (RA-like arthritis, cutaneous vasculitis, plt 20-50, serositis)
- HCQ +/- GC (PO/IV) +/- MTX/AZA
- refractory: belimumab, calcineurin inhibitor, MMF

Severe (organ threatening disease [nephritis, cerebritis, myelitis, penumonitis, mesenteric vasculitis], plt <20, TTP-like disease, AIHA)
- HCQ +/- GC (PO/IV) +/- MMF or Cyclo
- refractory: Cyclo, Ritux

41
Q

Anti-phospholipid criteria?

A

Criteria: clinic + laboratory criteria

Clinical:
- Vascular thrombosis: >=1 episode of arterial, venous, small vessel
OR
- Pregnancy: >=1 unexplained death of normal detus >10 GA or >=1 premature delivery of normal fetus < 34 GA bc pre/eclampsia or placental insufficiency or >=3 unexplained consecutive miscarriages <10wk

Lab: 2 positive results >12wk apart and no more than 5yr prior to S&S
- Lupus Anticoagulant (most powerful predictor of thrombosis): DOACS can cause false positive LAC; warfarin does not interfere
- Anticardiolipin-Ab (IgM, IgG): no affected by anticoagulation
- Anti-B2 Glycoprotein I: not affected by anticoagulation

42
Q

Lupus & Pregnancy - Mx considerations for the following: SLE, Ro/La+, aPL+

A

SLE
- Continue HCQ during pregnancy
- Start ASA 81 daily prior to 16 GA [reduce risk pre-eclampsia]

Ro/La+
- No hx neonatal lupus: HCQ + serial fetal echo from 16-26 GA
- Hx neonatal lupus: HCQ + serial echo weekly from 16-26 GA

aPL+
- No APS: ASA alone
- OB APS: ASA + propjhylactic heparing until 6-12wk P-P
- Thrombotic APS: ASA + therapeutic heparin during preg + P-P

43
Q

SLE Trivia:
- Drug-induced lupus: examples, serology
- Shrinking Lung Syndrome: definition, imaging findings
- Libman Sacks Endocarditis: associated with which disease, risks, tx

A

DIL
- Hydralaine, procainamide, TNFi, isoniazid
- ANA+, dsDNA-, anti-histone-Ab+

SLS
- rare complication r/t diaphragmatic muscle weakness
- lungs clear on imaging, but volume decreased (CXR, MIP/MEPs)

LSE (non-infectious)
- associated with APLAS
- thrombus on valve consists of accumulations of immune complexes, mononuclear cells, hematoxylin bodies, fibrin/plt thrombi
- can result in embolic phenomena
- steroids, anticoagulation

44
Q

DDx for bilateral parotid gland enlargment?

A
  • Sjogren’s
  • Infectious: mumps, TB, bacterial
  • Sarcoidosis, IgG4 syndrome
  • Lymphoma
  • Alcoholism, anorexia/bulimia
45
Q

Sjogren’s: S&S, Serology, Epi, Dx

A

S&S
- Xerostomia, keratoconjunctivitis
- Non-glandular: arthritis, vasculitis, demyelinating neuropathy, RTA

Serology: ANA, Anti-Ro/La, RF

Epidemiology:
- >40x increased risk of B-cell lymphoma
- Can occure with SLE, RA

Diagnosis:
- Ophtho: Schirmer’s test [<5mm in 5 min]
- Unstimulated salivary flow
- ENT: minor salivary gland biopsy = focal lymphocytis sialadenitis

46
Q

Systemic Sclerosis (scleroderma): S&S
- Diffuse
- Limited cutaneous/CREST Syndrome
- Serology: tests, which are useful for disease monitoring

A

Diffuse
- Sclerodactyly proximal to elbows/knees
- Internal organ involvement (risk of ILD, renal crisis)

Limited/CREST
- Calcinosis
- Raynaud’s
- Esophageal dysmotility
- Sclerodactyly
- Telangiectasias
- pHTN in up to 5%

Serology
- anti-centromere: CREST (60%), diffuse (15%)
- anti-Scl-70/topo I: ~40% of scleroderma patients; mostly diffuse
- neither useful for disease monitoring

47
Q

Complications of Systemic Sclerosis: name 3

A
  • Renal crisis
  • pHTN
  • Gastric antral vascular etasis (results in GIB that can be life-threatening)
48
Q

Complications of Systemic Sclerosis:
- Renal Crisis: more common in which form, risk fx, clinical signs, tx
- pHTN: more common in, monitoring
- Gastric antral vascular ectasis

A

Renal Crisis
- 10-20% diffuse systemic sclerosis
- Increased risk: pred, RNAP3-Ab, early disease
- S&S: renal failure, HTN, mild proteinuria - but can be normotensive
- Tx: Captopril (ACEi)

pHTN
- 5-19% of all systemic sclerosis; more common in limited/CREST
- Monitor: BNP, echo, PFTs annually

49
Q

Scleroderma Renal Crisis vs. TTP: S&S, Hx, Labs, Tx

A

S&S
- SRC: SOB, aLOC, HTN (not always), S&S scleroderma
- TTP: fever, HTN, purpuric rash, bleeding, neuro S&S

Typical Hx
- SRC: MAHA, AKI, proteinuria, hematuria
- TTP: MAHA, thrombocytopenia, AKI, proteinuria, hematuria

Labs
- SRC: Anti-Scl-70/TopoI, Anti-centromere
- TTP: ADAMTS13 (low)

Treatment
- SRC: captopril
- TTP: PLEX, steroids, Ritux

50
Q

Secondary causes of Raynaud’s Phenomenon?

A
  • Drugs: bb, ergotamine, bleomycin
  • Infection: HBV, HCV, Parvo B19
  • Smoking
  • Occup trauma: from handling vibrating tools, typing
  • Hyperviscocity: polycythemia, paraproteinemias (plasmacytoma, Waldenstrom), cryo, cold agglutinin disease
  • Vasculitides (eg., Buerger’s)
  • CTD: scleroderma, CREST, SLE, MCTD
  • HypoT4, Carcinoid, PCC
  • Heme malignancy
51
Q

Raynaud’s Phenomenon: Epi & S&S - primary vs. secondary

A

Primary
- F>M, onset ~20yo, often FHx
- Sym., typically not progressive
- Predictable onset (cold)
- ANA negative

Secondary
- Males, >40s
- Asym., can be progressive
- Abnormal nail folds
- Pits and ulceration of digits

52
Q

Raynaud’s Phenomenon: Labs, Treatment

A

Labs
- Only if suspicious of secondary
- CBC, Cr, U/A, LFT, CK, ESR, CRP
- ANA, ENA, RF, C3/4, Cryo
- TSH, SPEP/UPEP
- HBV, HCV
- PTT, APLA

Treatment
- Conservative
- 1st line: CCB
- Can consider topical nitrates, PDE5i

53
Q

DDx Myopathy

A

Drugs:
- statins, anti-psych, colchicine, anti-retrovirals, Li, SSRIs

Idiopathic myopathy
- PM/DM/IBM/NAM

Infectious
- Viral: HIV, EBV, CMV, inluenza
- Pyomyositis

Hypothyroid myopathy
Electrolytes disorders [hypoK/Phos]
Genetic myopathy

54
Q

DM/PM Clinical Features: [1] muscle weakness [2] cardiac [3] pulmonary [4] skin

A

Muscle Weakness
- Insidious over weeks/months
- Symmetric; proximal > distal
- Can involve: heart, diaphragm, oropharynx, esophagus

Cardiac
- myocarditis, arrhythmia, CHF

Pulmonary
- ILD (NSIP, UIP), DLCO or CT abn, pHTN

Skin
- Gottron’s
- Shawl sign
- Heliotrope rash
- Generalized erythroderma
- Periungal erythema
- Mechanic’s hand
- Scalp psoriasiform changes
- Calcinosis cutis

55
Q

Cutaneous manifestations of DM/PM?

A
  • Gottron’s papules
  • Heliotrope rash
  • Shawl sign
  • Generalized erythroderma
  • Periungal erytherma
  • Mechanic’s hand
  • Scalp psoriasisform changes
  • Calcinosis cutis
  • Nailfold capillary dilatations
56
Q

DM/PM: Investigations?

A
  • Labs: CK, AST, LDH, ESR, CRP, myositis panel, ANA, ENA; trop, ECG, +/- Echo to r/o cardiac
  • MRI muscle
  • Muscle biopsy (gold standard)
  • Muscle EMG: irritability, low amp, repetitive dc
  • SLP assessment: r/o oropharyngeal/esoph involvement
  • Spirometry w/ MIP/MEPs: r/o diaphragmatic involevment
  • Age appropriate cancer screening: consider CT c/a/p
57
Q

What is typically present at the time of Dermatomyositis diagnosis or within 1 year of diagnosis?

A

Malignancy

58
Q

Myositis panel associated with which antibodies/diseases?

A

Anti-Jo1-Ab
- Anti-synthetase syndrome
- Acute onset, constitutional sx
- Rapidly progressive ILD
- Raynaud’s phenomenon, mechanic’s hand, skin ulceration, arthritis

Anti-Mi2-Ab
- Associated with classic form of DM
- Highly responsive to treatment; favourable prognosis

Anti-NXP2 & Anti-TIF1-y-Ab
- Highly associated with malignancy

59
Q

DM/PM: Management [1st line, refractory]

A

1st line
- High dose steroids (at least 1mg/kg): usually PO; IV pulse if severe
- Steroid sparing agent: MTX or AZA [HCQ helpful for skin S&S only; MMF/Cyclo if ILD]

Refractory or Severe
- IVIG
- Rituximab

Continue routine, age-appropriate cancer screening as risk of malignancy high for at least 5 years after DM diagnosis

60
Q

IBM vs. DM/PM: weakness, CK

A

IBM
- Distal > proximal
- CK tends to be lower
- Poor treatment response

DM/PM
- Proximal > distal
- CK tends to be higher (usually)

61
Q

What is Necrotizing Autoimmune Myositis? (NAM; definition, S&S, investigations)

A

Defintion
- Inflam myopathy affecting prox. muscles
- CK +++ high
- Persistent after d/c Statin

S&S
- Weakness: severe
- Progression: weeks/months
- Skin/systemic features: rare

Investigations
- CK (+++ high), ESR/CRP (N/mildly high), TSH, HBV, HCV, HIV
- Anti-HMG CoA reducatase Antibody
- Rule out paraneoplastic syndrome

62
Q

Septic Arthritis - Most common infection in:
- native/prosthetic joints
- OM and septic arthritis in Sickle CD
- Can crystal arthritis co-exicst wit infection?

A
  • S. Aureus
  • Salmonella
  • Yes - do not be fooled!
63
Q

Gonococcal Arthritis: what are the 2 common syndromes? Tx? Which syndrome requires longer treatment?

A

Syndromes:
1. Triad: tenosynovitis, vesiculopustular skin lesions, migratory polyarthralgias w/o purulent arthritis
2. Purulent arthritis w/o skin lesions

Treatment
- Ceftriaxone
- Treat CT empirically or if concurrent
- Syndrome #2 requires longer course Abx

64
Q

Gout vs CPPD: crystals

A
  • Gout: -ve birefringence
  • CPPD: +ve birefringence
65
Q

Gout Tx: acute vs chronic

A

Acute:
- NSAIDs
- Colchicine: 1.2mg load, then 0.6mg an hour later, then 0.6mg BID until sx resolution
- GC (IA/PO): IA if monoarthritis, PO if poly (or C/I to above meds)
- Il-1 blocker (anakinra): consider only in pts with frequent flares and CI to colchicine, NSAID, GC

Chronic:
Non-Pharm:
- Exercise, wt loss
- Avoid EtOH, sugar-sweetened drinks, excessive meat/seafood

Pharm: urate-lowering meds
Definite Indications:
- >=2 attacks/yr
- Tophaceous gout
- Gouty arthropathy (eg, erosions)

Conditional indications: 1 gout attack +
- CKD stage III+
- Uric acid >535
- Urolithiasis

Tx Options:
- 1st line: Allopurinol (start 100mg/d)
- Febuxostat 80mg/d (if cannot tolerate Allo)
- Oveerlap with anti-inflam proph w/ either colchicine, NSAID, or low-dose GC for 3-6 months

66
Q

Gout - Allopurinol:
- If flare, but on chronic Allo - what to do?
- Can initiate Allo during acute flare?

A
  • Continue Allopurinol
  • Yes, can overlap with NSAIDor Colchicine or low-dose GC for 3-6 months
67
Q

Vasculitides - Name examples of the following: small, medium, large, variable

A

Small
- GPA [Wegener’s]
- eGPA [Churg-Strauss]
- MPA [microscopic polyangiitis]
- HSP [Henoch-Schonlein Purpura]
- Anti-GBM, Goodpasture
- Cryoglobulinemia Vasculitis
- Cutaneous Leukocytoclastic

Medium
- PAN
- Thromboangiitis obliterans [Buerger’s]

Large
- GCA
- Takayasu

Variable
- Behcet’s
- Cogan’s

68
Q

GCA: name cranial + extracranial S&S

A

Cranial
- HA
- Jaw claudication
- Diplopia
- Scalp tenderness
- Amarausis Fugax
- Stroke (mostly posterior)

Extra-cranial
- Limb claudication (upper/lower)
- Constitutional symptoms

69
Q

Name a few exam findingsof GCA

A
  • Beaded, prominent or tender temporal arteries
  • Absent temporal artery pulses
  • Fundoscopy: acute ischemic optic neuritis
70
Q

ACR/EUCLAR 2022 diagnostic criteria for GCA?

A

50yo, AND
Score >=6

71
Q

GCA: Management
- Visual symptoms/loss or critical cranial ischemia
- No visual sx/loss or critical cranial ischemia
- Extracranial GCA
- ASA?

A
  1. IV pulse steroids 1g x3d then Pred 1mg/kg/day + Tocilizumab (TCZ)
  2. Pred 1mg/kg/day + TCZ
  3. Pred 1mg/kg/day + TCZ or MTX
  4. ASA: only if critical/flow-limiting lesion of carotid/vertebral arteries

Overall: high-dose steroids x1 month, then taper

72
Q

PMR diagnosis criteria?

A

Required**
- **Age >50yo
- High ESR or CRP**
- **Bilateral shoulder ache +/- hip pain stiffness
- Negative RF, CCP, CK [if high, think myositis]
- U/S: shoulder/hip bursitis, tenosynovitis, synovitis
- Morning stiffness >45m

73
Q

PMR management?

A
  • Prednisone 12.5-20mg/d x2-4 weeks, then taper to 10mg/d within 1-2 months if response
  • If relapse: increase to pre-relapse dose, then decrease gradually and/or add DMARD (eg., MTX)
74
Q

PAN:
- Definition
- S&S

A

Definition
- Medium vessel vasculitis leading to tissue ischemia
- Can be local or systemic

S&S
- Constitutional, wt loss >4kg
- Skin: nodules, ulcers, livedo reticularis
- Testicular pain
- Abdo pain (post-prandial)
- Myalgias (exclu. shoulders/hip girdle)
- Inflam. arthritis
- Mono/polyneuropathy or mononeuritis multiplex
- Arteriographic abn: aneurysms or stenotic lesions in mesenteric/hepatic/renal arteries + branches
- +/- HBV infection

75
Q

PAN:
- Diagnosis
- Treatment

A

Diagnosis
- Biopsy: mixed inflam cells in vessel wall + fibrinoid necrosis; no granulomas or giant cells
- Abdo CTA/MRA: determine extent of disease
Treatment

Treatment
1. If HBV-related: GC, antivirals +/- PLEX
2. If idiopathic:
- Non-severe [mild systemic sx, uncomplicated skin, arthritis]: GC + MTX or AZA
- Severe [renal, neuro, limb/cardiac/mesenteric ischemia]: pulse steroids x3-5d then Pred 1mg/kg/day + Cyclosphosphamide [PO/IV] x3-6 motnhs

76
Q

Name a few ANCA-associated small vessel vasculitides + if p- vs c- ANCA

A

GPA (Wegener’s)
- c-ANCA (PR3) [80%]

EGPA (Churg-Strauss)
- p-ANCA (MPO) [40%]
- Px as: ashtma, allergic rhinitis, peripheral eosinophilia + neuropathy

MPA
- c-ANCA [30%], p-ANCA [65%]

77
Q

Causes of p-ANCA (MPO) elevation other than vasculitis [eg., eGPA, MPA]

A
  • IBD
  • Drug [PTU, cocaine]
  • CTD
  • Malignancies
  • Infections [HBV, HCV, HIV]
78
Q

Name ANCA-associated vasculitides symptoms

A
  • Constitutional symptoms, wt loss
  • ENT: nasal crusting, sinusitis (more common in GPA)
  • Tracheal + pulm involvement: senosis, hemoptysis
  • Renal: RPGN (pauci-immune), hematuria, proteinuria
  • Pulm-renal syndrome
  • Cutaneous vasculitis
  • Mononeuritis multiplex
79
Q

Management of GPA/MPA: [1] Induction [2] Maintenance

A

Induction: Severe Disease
- Pulse steroids x3-5d then reduce dose taper AND Rituximab
- Cyclophosphamide: if CI’d/failed Ritux
- PLEX: recommend against in pulm hemorrhage and in RPGN; recommend for concurrent anti-GBM

Induction: Non-Severe Disease
- GC + MTX

80
Q

Management of GPA/MPA: [1] Induction [2] Maintenance

A

Severe:
- GC: reduced dose taper, PLUS
- Ritux q4-6mo > MTX or AZA > MMF or Leflunomide
- PJP prophylaxis in all receiving RTX of CYC

Non-Severe:
- Remission induced with MTZ, AZA, or MMF: continue on same meds
- Remission induced with RTX, CYC: consider RTX, MTZ, AZA, LEF

GC should be guided by S&S. Non-GC agents typically used for >=18mo

81
Q

GPA/MPA [1] Relapse [2] Refractory: Management

A

Relapse
- If not on RTX for maintenance: RTX
- On RTX for maintenance: CYC

Refractory
- Switch agents if refractory to RTX or CYC
- Add IVIG to remission induction

82
Q

eGPA: Management [1] induction [2] maintenance

A

Severe Disease:
- GC IV pulse or high-dose oral [1mg/kg] PLUS
- CYC or RTX

Non-Severe (asthma, non-severe vasculitis):
- GC PLUS
- Mepolizumab > MTX or AZA > CYC or RTX

83
Q

eGPA: Management [1] induction [2] maintenance

A

Severe
- GC + MTX or AZA or MMF
- Optimal duration GC tx unknown, may require ongoing low-dose GC to control asthma/allergy symptoms

84
Q

What are the 5-Factor Score used to guide therapy in eGPA?

A
  • Proteinuria >1g/d
  • Creat >138.7
  • GI tract involvememt
  • Cardiomyopathy
  • CNS involvement

Score >=1: severe disease

85
Q

eGPA: Management - Relapse

A
  • If severe, previously induced CYC: RTX
  • If severe, previously induced RTX: CYC
  • If non-severe while on MTZ/AZA/MMF/GC mono: Add Mepolizumab
86
Q

Cryoglobulinemic Vasculitis:
- Definition
- Classification

A

Definition:
- Vasculitis caused by deposition of temperature-dependent IgG/IgM Ig/immune complexes (eg., cryoglobulins)

Classification:
- Type I: monoclonal - seen in clonal heme disease (MGUS, MM, CLL, WM); S&S r/t vascular occlusion [small vessel]
- Type II: mixed - can be 2/2 chronic infection [HBV HCV, HIV, IE], CTD, lymphoproliferative disorders; S&S r/t small [rarely medium] vasculitis

87
Q

Cryoglobulinemic Vasculitis: Clinical presentation

A

Asymptomatic: +ve cryglobulins w/o EOD

Symptomatic: +ve cryo + EOD
- Mild/mod: non-ulcerating skin lesions [purpura, acrocyanosis, livedo reticularis], non-debilatating peripheral neuropathy, arthralgias/arthritis
- Severe: cutaneous ulcers, progressive/debilatating meuropathy, GN with renal failure or nephrotic syndrome
- Life-threatening: RPGN, CNS involvement, intestinal ischemia, alveolar hemorrhage

88
Q

Cryoglobulinemic Vasculitis: Management - HCV associated vs. Non-Infectious

A

HCV
Mild/mod:
- Induction: antivirals +/- GC
- Maintenance: antivirals

Severe:
- Inducation: RTX + GC
- Maintenance: antivirals

Life-threatening:
- Inducation: PLEX + GC pulse + RTX or CYC
- Maintenance: antivirals

Non-Infectious
Mild/mod:
- Treat underlying disease [if identified]
- If no disease identified, low-dose GC or colchicine

Severe:
- Inducation: RTX or CYC + GC
- Maintenance: treat underlying disease + lowest effective immunosuppression

Life-threatening:
- Inducation: PLEX + GC pulse + RTX or CYC [if RTX failed or unavailable]
- Maintenance: treat underlying disease + lowest effective immunosuppression

89
Q

Non-pharm Management of OA:
- General
- Hip/Knee
- Hand

A

General
- Exercise
- Self efficacy/mx program
- consider CBT, thermal interventions, acupuncture

Hip/Knee
- Wt loss
- Tai Chi
- Cane
- TF knee brace [knee only]
- Balance training, Yoga, PF knee brace, radiofrequency ablation
- TENS strongly recommended AGAINST

Hand
- 1st CMC orthosis
- Other hand orthoses
- Paraffin

90
Q

Pharmacologic Management of OA [hand, hips, knee]

A

Use:
- PO NSAIDs if no CI’s
- Topical NSAIDs
- IA GC injections
- Consider Tylenol, duloxetine, chondroitin [hand OA], topical capsicin [knee/hip], tramadol

DON’T use:
- Opioids
- Glucosamine
- DMARD/Biologic
- Bisphosphonate
- Platelet rich plasma, stem cell injections, IA hyaluronic acid
- Chondroitin for knee/hip

91
Q

If prescribing Tramadol - why shoud be cautious about it?

A
  1. CYP2D6 metabolized leading to high variability between patients
  2. Caution if:
    - Other SSRI [serotonin syndrome]
    - Hypoglycemia history
    - Seizure history
92
Q

Indications + CI [absolute, relative] for IA GC injections?

A

Indications:
- Knee OA, especially if with effusion
- Crystal arthritis [CPPD, gout]
- Inflam. arthritis [eg., RA]

Contraindications:
Absolute:
- Possible septic arthritis
- Prosthetic joing
- Overlying cellulitis or suspected bacteremia
- Allergy to GC

Relative:
- Brittle diabetes
- Clotting/bleeding diasthesis or anti-thrombotic meds
- Failure to respond to previous IA GC injections

93
Q

Fibromyalgia: [1] diagnostic criteria [2] screening labs [3] Rx

A

Diagnosis:
- Widespread pain index + symptom severity scale
- Symptoms present + similar level >3 months
- No other disorder to explain symptoms
- Patients often c/o: fatigue, cognitive dysfunc., non-restorative sleep
- Tender points no longer in diagnostic criteria!

Screening Labs:
- CBC< ESR, CRP, CK, TSH = all MUST be normal

Rx:
- Non-pharm: exercise, CBT, sleep, Tai Chi
- Pharm: SNRI, TCA, gabapentin

94
Q

CV Risk Reduction - Patients with Rheumatic diseases have increased CV risk compared to general population. What are special considerations for the following:
- RA
- Gout
- SLE
- APS

A

RA
- Total cholesterol & HDL-c should be used in risk factor prediction [TG, LDL-c tend to be lower]

Gout
- Serum uric acid < 0.36 can potentially lower CV event risk/mortality
- No preference between allopurinol/febuxostat
- Avoid: diuretics, favour CCB or Losartan [uricosuric]

SLE
- BP < 130/80 considered in ALL patients with SLE
- ACEi/ARB Rx’d to those w/ lupus nephritis, urine PCR >500mg/g, or HTN
- Tx with HCQ may reduce CV event risk

APS
Low-dose ASA recommended for:
- Asymptomatic aPL carriers with high-risk profile
- SLE patient with high-risk aPL profile but no APS
- Considered for SLE patient with low-risk aPL profile

Internal Medicine: PGY-1 (17 decks)

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