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MSK II Exam 2 > Lanigan Rheumatoid Arthritis > Flashcards

Lanigan Rheumatoid Arthritis Flashcards

1
Q

A 34 y/o day care attendant is seen after 4 weeks of polyarthritis of the wrists and knees. RA latex is low positive, and ESR is normal. She is diagnosed with RA and started on low dose MTX. Which is true?
A – A positive anti- CCP will confirm the diagnosis.
B – X-ray or ultrasound may confirm the diagnosis.
C – Treatment should always start with NSAIDs.
D – CRP should be done before starting MTX.
E – She probably has an alternative diagnosis.

A

E- probably an alternative diagnosis (parvovirus B19?)

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2
Q

Classification criteria for RA

A

Over 6 points is definite RA.

1 large joint- 0 points
2-10 large ones- 1
1-3 small ones - 2
4-10 small ones - 3
> 10 joints with at least one small- 5

Serology:
Negative- o
low positive RF OR low positive ACPA- 2
high positive RF or ACPA- 3

Symptom duration
less than 6 weeks - 0
more- 1

Acute phase reactants
Normal CRP AND normal ESR- 0
Abnormal either one- 1

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3
Q

What if RA score is less than 6?

A

Patient might fulfill the criteria…
–> prospectively over time (cumulatively)

–> restrospectively if data on all 4 domains have been adequately recorded in the past

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4
Q

ACPA is what?

A

Anti-CCP Ab

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5
Q

Rheumatoid Arthritis

A 
Symmetric inflammatory polyarthritis.
Typical affected joints:  PIP, MCP, wrists.
Morning stiffness >60 minutes.
Affects ~1% of the population.
Female-to-male ratio 2-3:1.
Peak incidence at age 30-60.
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6
Q

Pathogenesis

A

An external trigger sets off an autoimmune rxn → synovial hypertrophy and chronic joint inflammation in genetically susceptible individuals.
Genetics – there are >20 risk alleles; strongest association is with HLA-DRB1.
Autoantibodies – RF, anti-CCP Ab.
Environmental factors – smoking, occupational exposures (silica, asbestos, carpentry).
Infection – periodontal disease with Porphyromonas gingivalis.

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7
Q

strongest risk allele

A

HLA DRB-1

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8
Q

factors in RA development

A

multiple susceptibility genes

Environment- smoking, periodontal infection

Carbamylation, citrullination

Anti-CarP
ACPA

Arthralgia
Arthritis

RA

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9
Q

Pathology of RA

A

Synovial cell hyperplasia and endothelial cell activation are seen in early RA.
CD4 T cells, mononuclear phagocytes, fibroblasts, osteoclasts, and neutrophils, and B cells (RF) play major roles. Cytokines, chemokines, and other inflammatory mediators (eg, TNF-a, interleukin IL-1, IL-6, IL-8, TGF-ß, FGF, PDGF) are all active.
Ultimately, inflammation and exuberant proliferation of the synovium (ie, pannus) leads to destruction of cartilage, bone, tendons, ligaments, and blood vessels.

Destruction of the cartilage and erosion of the underlying bone with pannus from a patient with rheumatoid arthritis.

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10
Q

A 35 y/o female presents with numbness in the right thumb and index finger over the past 6 months which she attributes to typing at work. Closer questioning reveals a 3 month history of PIP and MCP swelling and tenderness of the 2nd, 3rd, and 4th digits of the right hand, and the MCP joints of the 2nd and 3rd digits of the left hand, associated with 30-60 minutes of morning stiffness. She also reports stiffness in the first metatarsal joint of each foot. She does not smoke or drink alcohol and loves to garden in her spare time.

What are some causes of numbness in the thumb and index finger?

A 
“MEDIAN TRAP” 
Myxedema
Edema
Diabetes
Infiltration (sarcoid, leukemia, fibrosis)
Amyloid
Neoplasms

Trauma
RA
Acromegaly
Pregnancy

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11
Q

Upon examination, the patient is found to have a “doughy or spongy” feeling of her PIP and MCP joints with an exquisitely tender 2nd MCP joint of the left hand. The latter joint feels warmer than the other joints and provokes pain with motion. What should be done next?

A

Joint aspiration is done.

No organisms are seen on Gram stain, and culture comes back negative.

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12
Q

Describe the differential diagnosis of symmetric polyarthritis.

A

OA
RA

Other forms of arthritis

  • Gout
  • Spondyloarthropathies
  • Lyme arthritis
  • FMF

Infections

  • Parvo B 19
  • Hepatitis C

Collagen Vascular diseases

  • SLE
  • Polymyalgia rheumatica
  • Wegeners
  • RF

Cancers

  • Hypertrophic pulmonary osteoarthropathies – lung and - GI cancers
  • Palmar fasciitis – ovarian carcinoma
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13
Q

Skin changes in RA

A

Rheumatoid nodules = RF seropositivity!

Pts. With rheumatoid nodules are more likely to have anti-CCP, and vasculitis.

can also see nodules in the sclera and lungs

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14
Q

Acute Febrile Neutrophilic Dermatosis

A

(Sweet syndrome)

Fever
Fatigue
Skin lesions
Sore eyes
Mouth ulcers

clears up with steroids

not just seen in RA, also some cancers etc.

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15
Q

when do we see Pyoderma Gangrenosum

A

Seen in RA, Crohn’s, ulcerative colitis, and IgA myeloma.

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16
Q

Skin changes (vascular) in RA

A

Livedo reticularis -
medium vessel vasculitis

Small vessel vasculitis – circular purpura

17
Q

Pulmonary Involvement

A

Pulmonary causes are a significant contributor to excess mortality in patients with RA!
Pleuritis is common (usually asymptomatic).
Exudative pleural effusions may be seen.
Rheumatoid nodules in lungs.
- Peripheral, usually <1 cm.
Interstitial lung disease with fibrosis.
- More common in smokers, highly seropositive pts., males.

↑ Prevalence of COPD.

18
Q

PE findings with rheumatoid nodules in lung

A

Cough
Dyspnea
“Cellophane crackles” – close to the ear crackles

19
Q

Caplan syndrome

A

Although rare, rheumatoid pneumoconiosis, aka Caplan syndrome, occurs only in pts with both RA and pneumoconiosis related to mining dust (coal, asbestos, silica).
Symptoms: cough, dyspnea, wheeze, joint pain and swelling.

20
Q

Cardiac Involvement

A 
CHF contributes to ↑ mortality in RA.
↑ Risk for cardiovascular disease.
- May be due to chronic inflammation.
Pericarditis
- Most common in males with severely destructive and nodular RA.
RA-associated cardiomyopathy
Coronary vasculitis
21
Q

Cervical Spine Involvement

A

Abnormalities of the cervical spine in RA:

  1. Atlantoaxial instability / atlantoaxial subluxation.
  2. Superior migration of the odontoid.
  3. Subaxial subluxation
22
Q

Eye Involvement

A

Scleritis may be seen in RA as part of the Sicca Syndrome with keratoconjunctivitis sicca.

Scleromalacia perforans is degenerative thinning of the sclera, seen in RA.

23
Q

Felty’s syndrome

A

Make sure to do ab exam on RA pt!

SANTA

Splenomegaly
Anemia
Neutropenia, Nodules
Thrombocytopenia
Arthritis (Rhematoid)

75% of Felty’s syndrome patients have rheumatoid nodules.

24
Q

What labs and imaging would you order if you suspect RA?

A

Anti-CCP

25
Q

List the rheumatologic causes and the non-rheumatologic causes of a positive RF.

A 
Rheumatic diseases with  
positive (> 50%) RF:
     Cryoglobulinemia*
     Sjogrens
     RA
     MCTD

Non-rheumatic diseases with positive RF:
Infections – parasites, leprosy, Subacute bacterial endocarditis, virus (Hep C)
Lung diseases – silicosis, idiopathic pulmonary fibrosis
Miscellaneous – primary biliary cirrhosis

*High titer RF without rheumatic disease.

26
Q

Anti-cyclic citrullinated protein /Anti- CCP

A

Antibodies target citrulline as a modified form of arginine

The anti-CCP Ab has a specificity of > 99% for RA.
It is present in 60-70% of pts. with RA.
When CCP antibody is positive, it indicates patients at ↑ risk of joint damage.
It can become positive years before the first signs of RA.

27
Q

Newer biomarkers in RA

A

14-3-3n,

Multibiomarker Disease Activity (MBDA)

28
Q

14-3-3η

A

involved in the regulation of protein phosphorylation and mitogen-activated protein kinase pathways.** It can help to diagnose early RA when CRP is negative.**

29
Q

Multibiomarker Disease Activity (MBDA).

A

Includes IL-6, TNKr type 1, VCAM 1, EGF, VEGF-A, etc*. High MBDA > 44 is associated with rapid radiologic progression, and response to TNFi over triple therapy.
-Helps target biologicals to the pts. likely to receive the greatest benefit.

30
Q

Imaging

A

X-rays, MRI, ultrasound

31
Q

DAS28

A

To calculate the DAS28:

  • Count the number of swollen joints (out of the 28),
  • Count the number of tender joints (out of the 28),
  • Measure ESR or CRP,
  • Ask patient to make a ‘global assessment of health’ (indicated by marking a 10 cm line between very good and very bad).

Results are fed into a complex mathematical formula to produce the overall disease activity score.

A DAS28 of greater than 5.1 implies active disease, less than 3.2 low disease activity, and less than 2.6 remission.

32
Q

Treatment of RA

A
  • NSAIDs
  • Steroids
  • DMARDs (nonspecific) - disease modifying anti-rheumatic therapy
    • MTX
    • Sulfasalazine
    • Hydroxychloroquine
    • Leflunamide
    • Minocycline

Biologic DMARDs (specific)

  • TNF inhibitors
  • Abatacept – blocks T cell costimulation
  • Rituximab – depletes B cells
  • Tocilizumab - blocks IL6 receptor
  • Tofacitinib – inhibits Janus Kinase 3
33
Q

32 y/o female with 3 years of RA. AM stiffness > 30 minutes. Slight wrist swelling, with some MCP and PIP swelling (synovitis). X-rays normal.
Treatment:

A

Methotrexate (DMARD monotherapy)

34
Q

36 y/o female with 1 year of RA. AM stiffness > 90 minutes. Prominent synovitis. US shows early erosions.
Treatment:

A

combination DMARD therapy

double or triple therapy, nonbiologic DMARDs

35
Q

30 year old female with 2 years of RA. Marked synovitis. Some joint deformity. Bilateral erosions. On MTX, HCQ, Sulfasalazine.
Treatment:

A

Add or switch to a biologic DMARD

TNF inhibitor, Abatacept, Rituximab

36
Q

choices in RA treatment

A

NSAIDs and prednisone?
MTX + folic acid– reevaluate in 2-3 months
MTX, sulfasalazine, hydroxychloroquine (or MTX/lefluonamide)
TNF inhibitor ± MTX
Consider other biologics if TNF inhibitors fail

37
Q

What are the long term complications of RA?

A

MI – decreased with response to anti-TNF therapy!
Osteoporosis
NSAID bleeds and perforations
Lymphoma and GU malignancies

MSK II Exam 2 (16 decks)

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