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NYCC MSP > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

Inflammatory joint pathologies are generally characterized by an ____ response

A

osteolytic

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2
Q

Degenerative joint pathologies are generally characterized by an ____ response

A

osteoblastic

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3
Q

Inflammatory joint pathologies have potential for what type(s) of joint fusion?

A

fibrous or osseous

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4
Q

If Rheumatoid arthritis (RA) creates ankylosis, it is usually what type?

A

fibrous

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5
Q

RA generally occurs (unilateral/bilateral) and (symmetrical/asymmetrical)

A

bilateral
symmetrical

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6
Q

Inflammatory joint pathologies are not just arthropathies, they are ____ inflammatory conditions

A

systemic

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7
Q

What is the most common inflammatory arthropathy?

A

Rheumatoid Arthritis

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8
Q

In what age group does RA begin most commonly?

A

20s - 30s
(can occur at any age, biased toward younger)

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9
Q

RA generally affects ____ joints first, and moves to ____ joints

A

smaller to larger

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10
Q

Describe the involvement of the spine in RA

A
  • rarely affected early
  • ~80% of pts eventually experience c/s involvement (destruction of transverse ligament -> instability)
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11
Q

TRUE/FALSE:
A patient who complains of pain only in the distal interphalangeal joints is more likely to have RA

A

FALSE
(RA does not like DIPs in early stage)

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12
Q

TRUE/FALSE:
A patient who complains of pain only in the metacarpophalangeal joints is more likely to have RA

A

TRUE
(DJD doesn’t like MCP, RA does)

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13
Q

Most inflammatory conditions follow a pattern of ____

A

exacerbation/remission

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14
Q

What are the clinical features of vasculitis in a patient with RA?

A
  • painful rashes in hands & feet
  • vasospasm (narrow lumen)
  • ^risk of heart attack & stroke
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15
Q

What 2 factors contribute to the development of RA?

A

genetic & environmental

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16
Q

What 2 genetic factors are involved in RA?

A
  • Human Leukocytic Antigen (HLA)
  • PTPN22
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17
Q

What is the role of HLA in RA?

A

involved in location of binding site for arthitogens that initiate inflammation

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18
Q

What is the role of PTPN22 in RA?

A

deficient in RA
normally encodes protein tyrosine phosphate which inhibits T-cell activation

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19
Q

What environmental factors are involved in the development of RA?

A
  • infection
  • smoking (decreases collagen formation)
  • EBV (many different Ag’s; not proven)
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20
Q

Name the 6 steps in the pathogenesis of RA

A
  1. autoimmune response
  2. synovial hyperplasia & hypertrophy
  3. pannus proliferation
  4. cartilage & bone destruction
  5. fibrous or osseous ankylosis
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21
Q

What is involved in the autoimmune response in RA?

A
  • CD4+ T-helper cells
  • cytokines
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22
Q

What do IL-1, PGE2, and RANKL stimulate in RA?

A

osteoclasts & bone resorption

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23
Q

What does IFN-y activate in RA?

A

macrophages & resident synovial cells

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24
Q

What does IL-7 signal in RA?

A

neutrophils & monocytes

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25
Q

What do TNF and IL-1 stimulate in RA?

A

synovial cells to secrete proteases (destroy hyaline cartilage)

26
Q

What causes synovial hyperplasia & hypertrophy in RA?

A

lymphocytes & plasma cells accumulate in synovium

27
Q

Chronically inflamed synovium is called a _____

A

pannus

28
Q

Describe how pannus proliferation occurs in RA

A
  • enzymes & proteases ^ in joint
  • ^vascularity (hemorrhage + hemosiderin deposition)
  • covers articular cartilage, separating it from synovial fluid (less diffusion, starves cartilage)
  • eventually fills entire joint space (jt. stiffness & decreased ROM)
29
Q

What is the term used to describe the appearance of a pannus?

A

“frond-like” (fern-like)

30
Q

What causes rice bodies in a joint?

A

^vascularity in a pannus brings small fibrin nodules which float in jt space

31
Q

In general, what causes joint achiness in RA?

A

inflammation

32
Q

In general, what causes joint stiffness in RA?

A

pannus formation

33
Q

What causes cartilage destruction in RA?

A

proteases (chondrolytic enzymes) secreted by synovium destroy hyaline cartilage

34
Q

What causes bone destruction in RA?

A

RANKL, PGE2, IL-1 stimulate osteoclasts

35
Q

Why is joint space loss in RA uniform?

A

chemically mediated destruction of cartilage (not biomechanical)

36
Q

Inflamed synovial tissue against the bare area causes ____ radiographically

A

marginal erosion

37
Q

Bone destruction in the bone around a joint in RA causes ____ radiographically

A

periarticular (juxta) osteopenia)

38
Q

Tendon sheathes and bursa are lined with ____

A

synovium

39
Q

What causes ulnar deviation of the fingers in RA?

A

rupture of tendon pulleys allows tendons to pull to ulnar side (tendon subluxation)

40
Q

What type of ankylosis is more common in RA?

A

osseous > fibrous
(still rare)

41
Q

How does the gross appearance of joints with RA compare to that of degeneration?

A

raw bloody bone instead of eburnation
(will also accelerate degenerative change)

42
Q

What are the clinical manifestations of RA?

A
  • gradual onset, exacerbation/remission pattern
  • warm, swollen, painful jts (bilateral), crepitus
  • ^pain with motion, worst after disuse (lasts longer than degenerative)
  • tenosynovitis (creates deformities)
  • ligament subluxation
  • Haygarth’s nodes
  • Rheumatoid nodules
  • secondary jt degeneration
  • Anemia of chronic disease -> fatigue (marrow fibrosis)
  • acute necrotizing vasculitis
43
Q

What are examples of systemic manifestations of RA?

A
  • emphysema (without smoking)
  • pericarditis
  • vasculitis
  • liver/renal fibrosis
44
Q

What joints are affected by Haygarth’s nodes?

A

MCP

45
Q

What is the term for severe deformities of the digits in RA?

A

arthritis mutilans

46
Q

What is a swan neck deformity?

A

flexion of DIP jt, extension of PIP jt

47
Q

What is a Boutonniere deformity?

A

extension of DIP jt, flexion of PIP jt

48
Q

What joints are most commonly affected by RA?

A
  • wrists + MCP
  • ankles + MTP
  • PIP (does NOT prefer DIP)
  • c/s
  • elbow
  • knee
49
Q

What are common sites of Rheumatoid nodules?

A

elbow & legs
(can also occur in skin & visceral organs)

50
Q

Describe the pathogenesis of acute necrotizing vasculitis that occurs in RA

A
  • inflammation of BVs
  • vascular narrowing
  • impaired blood flow to tissues
  • ischemia and necrosis
51
Q

How does acute necrotizing vasculitis manifest in RA?

A
  • conjunctivitis
  • ulcers
52
Q

What are the relevant lab findings for RA?

A
  • ^ESR & CRP
  • positive rheumatoid factor (RF; 80%)
  • positive Anticitrullinated protein antibody (ACPA; 60%)
  • low RBC & platelets (anemia of chronic disease)
53
Q

When should labs be taken in a patient with suspected RA?

A

during period of exaccerbation

54
Q

What does rheumatoid factor represent?

A

multiple antibodies: IgM, IgG or directed against the Fc fragment of IgG

55
Q

What is Anticitrullinated protein antibody (ACPA) also known as?

A

Anti-cyclic citrullinated peptides (anti-CCP Ab)

56
Q

Which lab finding is more specific for RA?

A

ACPA
(less sensitive, more specific)

57
Q

Which lab finding is more sensitive for RA?

A

RF
(less specific, more sensitive)

58
Q

What are the radiographic characteristics of RA?

A
  • osteolytic lesions at joint margins (marginal erosions AKA “rate bite” lesions)
  • juxta/periarticular osteopenia
  • bilateral, uniform loss of joint space
  • pseudocysts
  • deformities
  • stair-step appearance in c/s (spondylolisthesis)
  • ^atlanto-dental interspace due to destruction of transverse lig.
59
Q

What are the treatment options for RA?

A
  • low impact, regular activity
  • anti-inflammatory diet
  • drug therapy (NSAIDs, corticosteroids, DMARDs)
60
Q

What drug therapy is used long-term for RA?

A

Disease modifying antirheumatic drugs (DMARDs)

61
Q

Name 5 examples of DMARDs

A
  • methotrexate
  • TNF antagonists
  • T-cell costimulatory blockers
  • B-cell depleting agents
  • IL-1 receptor antagonists
62
Q

What is a common corticosteroid used for severe RA at the time of diagnosis?

A

Prednisone

NYCC MSP (33 decks)

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