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Rheumatology Exam > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

rheumatoid arthritis (RA) - defined

A

*a chronic autoimmune disease marked by inflammation and destruction of multiple synovial joints
*causes symmetric, inflammatory joint destruction and deformation of the joints, usually fingers, wrists, and feet

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2
Q

rheumatoid arthritis (RA) - epidemiology

A

*1% of adults; prevalence increases with age
*female predominant (2:1)
*age on onset: 40-60s

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3
Q

rheumatoid arthritis (RA) - genetic risk factors

A

*genetic component (monozygotic twin concordance rate = 12-15%), but does not explain all of it
*shared epitope: HLA-DR4 = increased risk,, especially combined with SMOKING

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4
Q

rheumatoid arthritis (RA) - environmental risk factors

A

*SMOKING = increased risk (esp. with HLA-DR4 epitope)
*bacteria (normal flora; esp poor dental hygiene)
*viruses

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5
Q

rheumatoid arthritis (RA) - pathogenesis

A

*synovial inflammation → hypertrophy of synovial lining, forming a pannus (inflamed granulation tissue) → triggers inflammation cascade
*type III hypersensitivity reaction

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6
Q

features of inflammatory arthritis

A

*morning stiffness > 1 hour
*improves with activity
*worsens with rest

note - RA classically has inflammatory arthritis

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7
Q

features of non-inflammatory arthritis

A

*morning stiffness < 30 min
*worsens with activity
*improves with rest

note - osteoarthritis classically has non-inflammatory arthritis

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8
Q

contrast inflammatory vs. non-inflammatory arthritis

A

*morning stiffness:
-inflammatory: > 1 hour
-noninflammatory: < 30 min

*effects of activity/rest:
-inflammatory: improves with activity, worsens with rest
-noninflammatory: worsens with activity, improves with rest

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9
Q

rheumatoid arthritis (RA) - clinical presentation

A

*INLAMMATORY joint pain (morning stiffness > 1 hour, improves with activity, worsens with rest)
*SYMMETRIC involvement
*most commonly involves:
-small joints of the hands, wrists, ankles, feet
-specifically, MCPs & PIPs but spares DIPs
-spares the spine (except for cervical spine C1/C2)

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10
Q

classic joints in the hands that are affected by rheumatoid arthritis

A

*disease affects:
1. MCPs (metacarpophalangeal joints) - located where the metacarpal meets the proximal phalange
2. PIPs (proximal interphalangeal joints)

*disease SPARES the DIPs (distal interphalangeal joints)

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11
Q

rheumatoid arthritis (RA) - physical exam findings

A

*swelling, warmth, and erythema at the joints in classic patterns: boggy, synovitis
* Boutonniere deformity (PIP flexion with DIP hyperextension)
*Swan neck deformity (DIP flexion with PIP hyperextension)

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12
Q

rheumatoid arthritis (RA) - C1/C2 (atlantoaxial) subluxation

A

*misalignment between the first and second cervical vertebrae in the neck
*sx include occipital headache or neck pain, upper extremity numbness and tingling, and muscle weakness of the arms
*can occur in long-standing seropositive, erosive disease
*important to consider with intubation, etc

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13
Q

rheumatoid arthritis (RA) - extra-articular manifestations: SKIN

A
  1. rheumatoid nodules:
    -extensor surfaces of the elbows; seen on hands as well
    -need to differentiate from a tophus
    -pathology: fibrinoid central necrosis with palisading histiocytes
  2. vasculitis:
    -leukocytoclastic vasculitis, small vessel vasculitis, medium vessel vasculitis
    -pyoderma gangrenosum
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14
Q

histology findings of rheumatoid nodules

A

*fibrinoid central necrosis with palisading histiocytes

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15
Q

rheumatoid arthritis (RA) - extra-articular manifestations: HEMATOLOGIC

A
  1. anemia of chronic disease/chronic inflammation:
    -result of IL-6’s influence on hepcidin
  2. Fetty’s Syndrome (splenomegaly, neutropenia, infections, non-healing ulcers)
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16
Q

Fetty’s Syndrome in RA

A

*rheumatoid arthritis PLUS characteristic features:
1. splenomegaly
2. leukopenia (neutropenia < 2000)
3. infections & non-healing ulcers
*risk factors: positive RF, nodules, extra-articular disease
*treatment: treat the underlying RA

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17
Q

rheumatoid arthritis (RA) - ADDITIONAL extra-articular manifestations:

A

*eyes: episcleritis, scleritis, uveitis
*heart: pericarditis
*lung: PLEURAL DISEASE (low glucose)

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18
Q

rheumatoid arthritis (RA) - diagnosis

A
  1. clinical symptoms & physical exam: duration and distribution, classic inflammatory symptoms, tender and swollen joints
  2. labs: RF, anti-CCP, elevated ESR and CRP
  3. imaging: hand films, foot films, imaging modalities
19
Q

x-ray findings in RA

A

*periarticular osteopenia
*marginal erosions
*symmetric joint space narrowing
*follows same pattern as swollen/painful joints

20
Q

rheumatoid arthritis (RA) - poor prognostic indicators

A

*high titer RF, positive anti-CCP
*multiple joint involvement
*erosions on X-rays
*extra-articular manifestations
*sustained elevation of acute phase reactants
*low SES/education level
*poor functional level
*HLA-DR4 shared epitope (although we do not check this)

21
Q

rheumatoid arthritis (RA) - treatment overview

A
  1. disease-modifying anti-rheumatic drugs (DMARDs):
    -methotrexate
    -hydroxychloroquine
    -sulfasalazine
    -leflunomide
  2. biologic DMARDs:
    -TNF alpha inhibitor
    -IL6 inhibitor
    -CTLA4
    -JAK inhibitors
22
Q

methotrexate - MOA, uses

A

*MOA: folic acid analog that competitively inhibits dihydrofolate reductase → decreased dTMP → decreased DNA synthesis

*first-line therapy for RA
-takes 6 to 8 wks to start working (prednisone helps in the interim)

23
Q

glucocorticoids - MOA

A

*inhibit phospholipase A2 via inhibition of NF-KB
*prevents formation of arachidonic acid
*arachidonic acid breaks down into leukotrienes, prostaglandins, thromboxanes

24
Q

methotrexate - ADEs

A

*hepatotoxicity (cannot drink alcohol)
*oral ulcers, hair loss (folic acid helps)
*myelosuppression (folic acid helps)
*PULMONARY FIBROSIS
*teratogenic

*monitor labs every 3 months
*note - we use in smaller doses in RA than in chemo; helps decrease side effects

25
Q

hydroxychloroquine in RA

A

*brand name = Plaquenil
*antimalarial (presumed through TLR inhibition, raising pH of lysosome)
*good safety profile
* retinal toxicity with high dose, long term use
*safe in pregnancy
*benefit in 3-6 months
*monitor: yearly eye exams

26
Q

sulfasalazine in RA

A

*anti-inflammatory from aspirin-like properties (“aspirin with a sulfa group”)
*ADEs: myelosuppression, hepatotoxicity, G6PD deficiency
*safe in pregnancy
*benefit in 6-8 weeks
*monitor labs every 3 months

27
Q

biologic therapy for RA - overview

A

*works better in combination with non-biologic DMARDs (methotrexate)
*universally expensive
*infection in universally the biggest risk
*cannot combine biologic therapies together

28
Q

naming of biologic therapies: -mab

A

*monoclonal antibody

29
Q

naming of biologic therapies: -ximab

A

*chimeric monoclonal antibody
*ex: infliximab, rituximab

30
Q

naming of biologic therapies: -zumab

A

*humanized monoclonal antibody
*ex: certolizumab

31
Q

naming of biologic therapies: -mumab

A

*fully humanized monoclonal antibody
*ex: adalimumab, golimumab

32
Q

naming of biologic therapies: -cept

A

*fusion protein
*ex: etanercept, abatacept

33
Q

innate immune system - review

A

*first line defense
*recognizes conserved features (shared molecular patterns) of pathogens by germ-line encoded receptors
*stimulates adaptive immunity and influences the type of adaptive response

34
Q

adaptive immune system - review

A

*requires clonal expansion of effector cells (several days) for clearance of pathogens
*pathogen-specific recognition through recombined receptors
*“remembers” pathogens for rapid response to future infections

35
Q

TNF-alpha inhibitors - overview

A

*first-line biologic therapy for RA
*contraindications: demyelinating diseases, CHF (esp. classes 3/4)
*examples:
-infliximab
-etanercept
-adalimumab
-certolizumab pegol
-golimumab

note - must screen for TB prior to initiating tx, due to risk of reactivation

36
Q

TNF-alpha inhibitors - ADEs

A

*infections (URIs)
*TB reactivation - screen prior to initiation
*drug-induced lupus

*hold medication for infection, surgery

37
Q

association between TNF inhibitors and tuberculosis

A

*need TNF to support the granuloma in TB
*once you inhibit TNF-alpha, cannot maintain granuloma → release of walled-off granuloma → reactivation of TB

*ex TB screening test: interferon-gamma release assay (aka Quantiferon)

38
Q

association between TNF inhibitors and malignancy

A

*pts with RA are already at an increased risk for malignancy
*only significantly increased association: non-melanomatous skin cancer

39
Q

rituximab

A

*anti-CD20 (B cell target)
*used to treat: RA, cancer, vasculitis, lupus, etc
*vaccinate prior to starting therapy (need B cells to create antibody)

40
Q

abatacept

A

*fusion protein of CLTA4 (aka CD80/86; T cell target)
*inhibits the necessary secondary signal for T cell activation

41
Q

tocilizumab

A

*IL-6 inhibitor
*indications: RA, GCA (temporal arteritis), COVID
*ADEs: infection, increase in lipids, bowel perforation
*caution in pts with diverticulitis

42
Q

JAK kinase inhibitors

A

*inhibits JAK-STAT pathway
*ex: toficitinib, upadacitinib
*oral therapy
*ADEs: cytopenias, infection, elevated LFTs, bowel perforation

43
Q

treatment regimen for rheumatoid arthritis

A

*START with METHOTREXATE, with prednisone to help with sx until methotrexate kicks in
*next steps vary depending on patient preference, insurance regulations, fiscal implications
*frequent visits to monitor

Rheumatology Exam (20 decks)

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