Inflammatory Arthritis Flashcards

1
Q

Type 0 synovial fluid

A

Normal
Transparent, viscous
WBC <200, mainly monos

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2
Q

Type 1 synovial fluid

A

Non-inflammatory
Yellow, translucent
Viscous
WBC <200, mainly monos

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3
Q

Type 2 synovial fluid

A

Inflammatory
Yellow, cloudy
Thin/watery
2000-100 000 WBCs, mainly polys

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4
Q

Type 3 synovial fluid

A
Septic 
Opaque, cloudy
Thin/watery or thick pus 
>100 000 WBCs, mainly polys
Often +ve culture
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5
Q

Type 4 synovial fluid

A

Hemorrhagic
Bloody, non-clotted blood
RBCs

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6
Q

Viruses/parasitic disease that commonly cause arthritis

A
Rubella 
Hep B in prodrome 
Parvovirus B19 
HIV 
Chikungunya 
Tick borne arthritis 
Lyme disease
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7
Q

RA is a/symmetric poly/oligo/monoarthritis

A

Symmetric poly arthritis

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8
Q

3 Ds to rmb in RA history

A
Diurnal variation (nights vs mornings) 
Distribution of joints involves (NO DIPS)
Duration (acute vs chronic)
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9
Q

Seropositive RA means they have…

A

Rheumatoid factor and/or anti-CCP

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10
Q

Distribution of RA

A

PIPs, MCP, wrist, elbow, shoulders, hips, knees, ankles, feet (MTPs)

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11
Q

Potential articular consequences of RA

A

Ulnar deviation
Z-deformity of thumb
Swan neck of finger
Boutonnier of pink finger

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12
Q

X-ray of RA

A

Juxta-articular osteopenia
Erosions
Concentric joint sp loss

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13
Q

Chronic back pain: # months

A

> 3 months

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14
Q

4 types of spondylarthropathy

A

Psoriatic arthritis
Enteric arthritis
Axial spondyloarthritis
Reactive arthritis

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15
Q

Dx of axial spondyloarthritis

A

Sacoilitis on imaging plus >/= 1 SpA feature

OR 2. HLA-B27 plus >/= 2 SpA features

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16
Q

SpA features

A
  • Inflammatory back pain
  • Arthritis
  • Enthesitis
  • Uvelitis
  • Dactylitis
  • Psoriasis
  • Crohn’s/colitis
  • Good response to NSAIDs
  • Fam hx for SpA
  • HLA-B27
  • Elevated CRP
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17
Q

SpA strong clinical features

A

IBD, psoriasis, uveitis, peripheral arthritis

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18
Q

SpA soft clinical features

A

Enthesitis, inflammatory back pain hx, response to NSAIDs

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19
Q

Imaging used to detect sacroilitis

A

STIR MRI (fat suppression technique that looks for bone marrow edema)

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20
Q

X-ray evidenced axial spondylitis

A

Ankylosing spondylitis

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21
Q

MRI evidenced axial spondylitis

A

Non-radiographic axial spondylarthropathy

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22
Q

HLA-B27+ and strong clinical suspicion of axial spondylitis

A

Non-radiographic axial spondylarthopathy

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23
Q

Axial spondylarthoparthy typical pt

A

M:F = 3:1
20-40y.o.
Most common in Haida natives

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24
Q

Inflammatory back pain

A

Need 4 out of 5:

  • Onset of symptoms <40y. for >3mo
  • Insidious onset
  • Improves with exercise
  • Does not improve with rest
  • Pain at night and improves upon getting up

Other variables: prolonged AM stiffness, alternating buttock pain, good NSAID response

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25
Q

HLA-B27: what is it and what is the rate of occurrence?

A

Antigen presenter to T-cells –> affects production of IL23 and IL17
7-10% of population is B27+, 98% of these ppl will NOT get ankylosing spondylitis
0.2-0.5% of population gets ankylosing spondylitis
1% of population gets axial spondylarthropathy
80% of ankylosing spondylitis pts are B27+

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26
Q

Treatment for ankylosing spondyloarthropathy

A
  • Exercise/physiotherapy
  • NSAIDs
  • Biologics: TNF inhibitors, IL17A inhibitors

No role for steroids or DMARDs*

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27
Q

Screening for axial spondylarthritis

A

Symptom onset <45y and back pain >3mo AND any one of ABCDE: AM stiffness, B27+, colitis (crohn’s/UC), derm (psoriasis), eye (uveitis)

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28
Q

CASPAR criteria for PsA

A

Inflammatory articular disease (joint, spine, entheseal) and >/= 3 on:

  1. Evidence of psoriasis (current =2, past = 1, fam hx = 1)
  2. Psoriatic nail dystrophic (pitting, onycholosis, hyperkeratosis) = 1
  3. Negative test results for RF = 1
  4. Dactylitis (current or hx = 1)
  5. Radiologic evidence of juxta-articular new bone formation = 1
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29
Q

PsA epidemiology

A

M=F
4-30% of PsC patients
3% annual risk of PsC turning to PsA

30
Q

PsA process

A

70% skin precedes joints
15% joints precede skin
15% together

31
Q

Tx for mild PsA

A

Mild PsA = <5 joints, CRP-, no erosions, no dactylics
NSAIDs or steroid injections
If no resolution >3mo, start DMARD

32
Q

Tx for moderate PsA

A

DMARD

33
Q

DMARD

A

Leflunomide
Methotrexate
Cyclosporide
Sulfasalazine

34
Q

Newer tx for PsA

A
Anti-TNF Inhibitors 
IL12/23 inhibitors 
IL17A inhibitors 
JACK inhibitors 
PDE4 inhibitors 
IL23 inhibitors
35
Q

SOAPBRAIN MD for SLE

A
Serositis
Oral ulcers 
Arthritis 
Photosensitivity, pulmonary fibrosis 
Blood cells 
Raynaud's or renal 
ANA
Immunologic (anti-Sm, anti-dsDNA, APLAS)
Neuropsych
Malar rash
Discoid rash
36
Q

Malar rash

A

Fixed erythema, flat or raised, over malaria eminence tending to spare nasolabial folds

37
Q

Discoid rash

A

Erythematous raised patches with adherent keratitis scaling and follicular plugging

FEAST:
Follicular plugging 
Erythematous 
Atrophy 
Scarring
Telangiectasia
38
Q

Renal disease of SLE

A

> 0.5g/d proteinuria
/= 3+ dipstick proteinuria
Cellular casts
Lupus nephritis: 4 classes

39
Q

Neuro disease of SLE

A

Seizures

Psychosis (without other causes)

40
Q

Hematologic disease of SLE

A

Hemolytic anemia with reticulocytosis
Leukopenia (<4000/uL on >/=2 occasions)
Lymphopenia (<1500/uL on >/=2 occasions)
Thrombocytopenia (<100 000/uL in absence of offending drugs)

41
Q

Arthritis of SLE

A
  • Nonerosive, transient, symmetrical, affecting small joints, seldom deforming, less severe than RA
  • Most common presenting feature of SLE
  • Jaccoud’s arthropathy: non-erosive, reducible deformities
42
Q

Cardiovascular disease of SLE

A

Atherosclerosis
Pericarditis
Myocarditis
Libman-Sacks endocarditis (mitral, tricuspid)

43
Q

Respiratory disease of SLE

A
Interstitial lung disease
Pneumonitis 
Pleural effusions
Pulmonary hemorrhage
Pulmonary HTN
Shrinking lung syndrome
44
Q

GI and hepatic disease of SLE

A
  • Uncommon
  • Severe abdo pain indicating mesenteric vasculitis
  • Diverticulitis
  • Pancreatitis
  • Hepatic abnormalities (usually due to tx, not SLE itself)
45
Q

Lupus nephritis class I

A

normal - minimal mesangial glomerulonephritis, no tx, doesn’t lead to renal failure

46
Q

Lupus nephritis class II

A

mesangial proliferative lupus nephritis, typically responds to tx with corticosteroids, renal failure rare

47
Q

Lupus nephritis class III

A

focal proliferative nephritis, responds to tx with high dose corticosteroids, renal failure uncommon

48
Q

Lupus nephritis class IV

A

diffuse proliferative nephritis, mainly treated with corticosteroids and immunosuppressants, renal failure OCMMON

49
Q

Lupus nephritis class V

A

Membranous nephritis characterized by extreme edema and protein loss, renal failure uncommon

50
Q

Lupus nephritis class VI

A

glomerular sclerosis

51
Q

Drug-induced lupus

A
Normal complement and no anti-DNA AB 
Anti-histone +
Symptoms resolve when stopping drug 
M:F equally affected 
Nephritis and CNS abnormalities rare 
Caused by CHIMP:
Chlorpromazine 
Hydralazine 
Isoniazid 
Minocycline 
Procainamide, propylthiouracil 
Other (anti-TNFs)
52
Q

Neonatal lupus

A
  • Mom’s autoantibodies are passively transferred to fetus: SSA,SSB
  • Can cause congenital heart block –> Tx = Dexamethasone
  • Test for SSA AB
53
Q

Lab tests for SLE

A
  • Screen with ANA
  • Confirmatory tests: anti-dsDNA, anti-smith AB
  • Anti-dsDNA = prognostic and monitoring
  • If active disease, test q1-3mo
  • If inactive disease, test q6-12mo
54
Q

SLE tx

A
NSAIDs
Prednisone 
Hydroxychloroquine 
Azathioprine (immunosuppressive) 
Mycephenolate mofetil (esp good for lupus nephritis)
Cyclosporine (immunosuppressant)
Cyclophosphamide (immunosuppressant) 
Rituximab (B-cell deplete)
Belimumab (monoclonal antibody)
Sun avoidance
55
Q

3 types of small vessel vasculitis

A
  1. Granulomatosis with polyangiitis (AKA Wegener granulomatosis)
  2. Microscopic polyangitis (MPA)
  3. Eosinophilic granulomatosis with polyangitis (Churg-Strauss syndrome)
56
Q

Granulomatosis with polyangitis autoantibodies

A

c-ANCA, PR-3

57
Q

Microscopic polyangitis autoantibodies

A

p-ANCA, MPO

58
Q

Eosinophilic granulomatosis with polyangitis

A

p-ANCA,MPO

59
Q

Antiphospholipid syndrome

A

AI hyper coagulable state caused by antiphospolipid antibodies

60
Q

Antiphospholipid syndrome autoantibodies

A

Lupus anticoagulant

Anticardiolipin antibodies: ACL, B2glycoprotein antibodies

61
Q

ENAs

A
  • AB to Smith antigen
  • AB to RNP antigen
  • AB to SS-A antigen (Ro)
  • AB to SS-B antigen (La)
  • Jo1-AB
  • Scl-70 AB
62
Q

Sjogren syndrome testing

A

Screen for SS with ANA

Confirm/prognosis with SS-A (Ro), SS-B (La)

63
Q

Polymyositis/dermatomyositis testing

A

Screen with ANA

Confirm PM with Jo-1AB

64
Q

Systemic sclerosis/CREST syndrome

A

Fibrosis of skin (scleroderma) and vascular disease

CREST:
Calcinosis
Raynaud phenomenon
Esophageal dysmotility
Scerlodactyly 
Telangiectasia
65
Q

CREST syndrome testing

A

Screen with ANA

Confirm/prognosis with anticentromere AB, Scl-70AB

66
Q

Mixed CT disease testing

A

Screen with ANA

Confirm with RNP antibody

67
Q

Tx of fibromyalgia syndrome

A

Night time meds (tricyclic antidepressants – ie. amitryptilene or nortryptilene or flexeril 10mg @ 8pm, melatonin, L tryptophan)
Analgesics (plain tylenol, NSAIDs, Tramadol, tramacet)
Others:
• Treat depression: Cymbalta, other anti-depressants
• SNRI: Duloxetine
• Nerve modulating drugs/anticonvulsants: Pregabalin (lyrica), gabapentin (Neurontin)

68
Q

Tx of acute gout attack

A

Do not tx asymptomatic hyperuricemia
NSAIDs (Indocid): High dose, then taper as symptoms improve
Corticosteroids (if renal, CV, or GI disease and/or if NSAIDs C/I or failed): IA, oral, IM, IV
Ex. Prednisone
Colchicine within first 12h (blocks formation of inflammatory markers ie. IL1)
Have to be careful with colchicine in renal insufficiency
Do NOT use allopurinol for acute attack

69
Q

Tx of chronic gout attack

A

Conservative:
• Avoid foods with high purine content
• Avoid drugs with hyperuricemic effects (ie. ethambutol, thiazide, alcohol)
Medical:
• Antihyperuricemic drugs (ie. allopurinol): Decrease uric acid production by inhibiting xanthine oxidase
o Use in pt with recurrent attacks (>/=3 attacks)
o Do not start allopurinol until acute attack over
o Start allopurinol with colchicine low dose or NSAID on board
o Do down dose allopurinol in renal insufficiency and monitor Cr
Go low, go slow, esp with tophaceous gout as you can get mobilization gout
If allergic to allopurinol, new drug feboxistat is available

70
Q

Tx of CPPD arthropathy

A

o Rest, protection
o NSAIDs
o IA or oral steroids to relieve inflammation

71
Q

Tx of giant cell arteritis

A

Start prednisone (1mg/kg/d) ASAP b/c pt can go blind overnight –> Biopsy temporal artery

72
Q

Tx of dermatomyositis

A

Tx: Corticosteroids high dose (1-2mg/kg/d) and slow taper

Can be a perineoplastic syndrome (think it is related to cancer dx) –> Should do reasonable malignancy workup