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MSK/Derm > SM 234: Rheumatoid Arthritis > Flashcards

SM 234: Rheumatoid Arthritis Flashcards

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1
Q

What is Rheumatic Arthritis?

A

A chronic inflammatory joint disease of autoimmune nature characterized by the development of autoantibodies

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2
Q

Which sex is more likley to get RA?

A

Women > Men

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3
Q

When does RA develop?

A

Women 40 - 60 years, older men; prevalence increases with age

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4
Q

In what race is RA most common?

A

Native Americans

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5
Q

What genetic loci is associated with RA?

A

An MHC II antigen - HLA DRB*01 and HLA DRB*04

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6
Q

Why do the HLA DRB*01/04 loci predispose RA?

A

They encode a shared epitope of a specific amino motif that predisposes autoimmunity

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7
Q

What is a shared epitope?

A

A specific amino acid motif found commonly in a disease state, such as HLA DRB*01/04 in Rheumatoid Arthritis

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8
Q

Are genetic loci additive in terms of risk to RA?

A

Yes, and these interactions are worsened by the environment

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9
Q

How do epigenetics effect the development of RA?

A

Epigenetics allow for the environment to effect gene expression, with different patterns in DNA methylation around the HLA region associated with RA

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10
Q

How are RA symptoms effected by pregnancy?

A

RA improves during pregnancy, suggesting a hormonal role in RA

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11
Q

What is the impact of smoking on RA?

A

Smoking directly increases risk of developing RA

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12
Q

What can be inhaled to develop RA?

A

Dust inhalation, such as silica and asbestos, can increase risk for RA

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13
Q

How do microbiota contribute to RA risk?

A

Peridontal disease increases risk of RA (P. gigivalis), and the gut microbiome changes in RA

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14
Q

Which oral microbe increases RA risk?

A

P. gigivalis

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15
Q

What is the Synovium?

A

A layer of cells lining the inside of the Synovial membrane that produces lubricants and nutrients for Cartilage

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16
Q

What are the 2 layers of healthy Synovium?

A

Intimal lining of MLS and FLS, as well as Sublining of fibroblasts, adipocytes, blood vessels and immune cells

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17
Q

What makes up the Intimal lining of the normal Synovium?

A

Macrophage like Synoviocytes and Fibroblast like Synoviocytes (MLS and FLS) - allow for free movement of cells and proteins into Synovial fluid

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18
Q

Describe the barriers to movement of cells and proteins into Synovial fluid?

A

There isn’t one - the intimal lining of Synovium is leaky and allows for free movement of cells

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19
Q

What makes up the Sublining of normal Synovium?

A

Fibroblasts, Adipocytes, Blood Vessels and Immune Cells

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20
Q

What are the main roles of Synovium?

A

Produce nutrients and lubricants for cartilage

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21
Q

How does the Synovium change in RA?

A

Intimal lining thickens with Synoviocytes producing pro-inflammatory cytokines

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22
Q

How does the cellular composition of the Syovium change in RA?

A

Adaptive immune cells infiltrate the Synovium and Activated Osteoclasts degrade bone

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23
Q

What is the Pannus?

A

An invasive, destructive front of Synovial tissue that attaches to the surface of articular cartilage in Rheumatoid Arthritis

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24
Q

Why does RA involve bone loss?

A

Osteoclasts are activated by pro-inflammatory Synovial cytokines and degrade bone

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25
Q

How does the vasculature of the Synovium change in RA?

A

Hypervascularity of the Synovium develops in RA

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26
Q

What are stages of RA?

A

Susceptibility Preclinical Early RA Established RA

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27
Q

What is the Susceptibility phase of RA?

A

No symptoms or signs of autoimmunity, but genetic and environmental risk factors for RA are present

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28
Q

What is the Preclinical phase of RA?

A

Asymptomatic autoimmunity occurs with increased levels of Cytokines, Chemokines and CRP in circulation as well as autoantibody formation, but no clinical symptoms

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29
Q

What is the Early phase of RA?

A

Immune symptoms continues to ramp up causing symptoms to first emerge, such as joint pain

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30
Q

What is the Established phase of RA?

A

A patient presents with classifiable RA

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31
Q

What process is key to developing the immune response in Rheumatic Arthritis?

A

Citrullination

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32
Q

What is Citrullination?

A

Environmental stressors such as smoking or oral infection lead to the expression of Peptidylarginine Deaminases, which convert Arginine to Citrulline on Matrix proteins - Citrullinated peptides then bind to HLA heterodimers on APC

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33
Q

How do Citrullinated peptides interact with HLA?

A

Citrullinated peptides can bind HLA heterodimers on the surface of APC, especially if they have the shared epitope which increases risk (HLA DRB*01/04). APC’s then migrate to Lymphoid tissue to present Citrullinated peptides and activate T-cells, which induce B-cells to produce autoantibodies

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34
Q

How do autoantibodies arise in Rheumatoid Arthritis?

A

Citrullinated peptides bind to HLA on APC’s, which present the peptides on MHCII and activate T-cells, which drive B-cells to produce antibodies against self-protein

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35
Q

What factors do B-cells produce are specific for Rheumatoid Arthritis?

A

Rheumatoid Factor and Anti-Citrullinated Peptide Antibody, detectable up to 10 years prior to onset of clinical disease

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36
Q

In which stage of RA does Synovitis develop?

A

Early RA

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37
Q

What is Synovitis?

A

Influx of inflammatory cells into Synovium, such as CD4, Macrophages, and APC’s as well as B/Plasma cells

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38
Q

What cells are the major source of pro-inflammatory cytokines in RA?

A

Activated Synoviocytes, producing IL-1, IL-6, and TNFalpha as well as Matrix Metalloproteaes and RANKL

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39
Q

What stage of RA invovles the onset of joint damage?

A

Establised RA, which mediates Cartilage and Bone Destruction

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40
Q

What causes Cartilage destruction in RA?

A

MMP’s produce by Fibroblast Like Synoviocytes and RANKL-mediated activation of Osteoclasts

41
Q

What do Fibroblast Like Synoviocytes produce in Early RA?

A

MMP’s and RANK-L

42
Q

What do Macrophage Like Synoviocytes produce in Early RA?

A

Inflammatory cytokines: IL-1, IL-6, TNFalpha

43
Q

How does Rheumatoid Arthritis present?

A

Onset of symmetric polyarthritis, especially small joints of hands and feet, over several weeks-months; joint swelling, decreased ROM, and worse in the morning with stiffness after rest

44
Q

What is gelling?

A

Stiffness after rest, found in Rheumatoid Arthritis

45
Q

How long does morning stiffness last in Rheumatoid Arthritis?

A

More than 1 hour

46
Q

How do non-inflammatory arthritis present?

A

OA also has an insidious onset and gelling, but with bony enlargement of joints and morning stiffness lasting < 60min

47
Q

What joints does RA involve?

A

Small joints of hand (MCP, PIP, but not the DIP)

48
Q

What joints does OA involve?

A

Small joints of hand (PIP, DIP, but not the MCP)

49
Q

How can RA and OA be differentiated at the feet?

A

RA involves all joints in the foot, while OA only effects the first MTP

50
Q

How can OA and RA be differentiated in the spine?

A

RA involves the Cervical spine only, while OA involves the entire spine, especially the Lumbar spine

51
Q

How do patients with RA present on physical exam?

A

Symmetric joint swelling and tenderness with palpapble swelling/bogginess (unlike OA where joints are harder)

52
Q

How does advanced RA effect the joints on physical exam?

A

Ulnar deviation of the MCP with limited ROM and rheumatoid modules at pressure points

53
Q

What is the Swan-neck deformity and what disease is it associated with?

A

Flexion at DIP and hyperextension at PIP; found in Rheumatoid Arthritis

54
Q

What is the Boutonniere deformity and what disease is it associated with?

A

Flexion at PIP and hyperextension at DIP; found in Rheumatoid Arthritis

55
Q

What are extra-articular mainfestations of RA in the skin?

A

Rheumatoid nodules at pressure points

56
Q

What are extra-articular mainfestations of RA in the Hematologic system?

A

Anemia, thrombocyotpenia

57
Q

What are extra-articular mainfestations of RA in the Pulmonary system?

A

Pleural thickening and pleural effusion

58
Q

What are extra-articular mainfestations of RA in the Cardiac system?

A

Pericarditis and premature Atherosclerosis

59
Q

What are extra-articular mainfestations of RA in the Opthalmic system?

A

Scleritis

60
Q

What are extra-articular mainfestations of RA in the Neurologic system?

A

Entrapment syndromes like Medial Nerve compression via Carpal tunnel or Ulnar Nerve compression at the Medial fossa of the ELbow

61
Q

What is the most common cause of mortality in RA?

A

Cardiovascular Disease + premature Atherosclerosis, because atherosclerosis is driven by inflammation

62
Q

Why are RA patients at risk for infection and cancer?

A

Immune system dysfunction and immunosuppression to treat RA predisposes mortality due to infection and cancer

63
Q

What radiographic changes accompany RA?

A

Soft tissue swelling, uniform and symmetric joint space loss, marginal erosions and symmetric deformities

64
Q

What are marginal erosions?

A

A pannus eating away at a joint in RA

65
Q

What specific bone is often eroded in RA?

A

The ulnar styloid

66
Q

What is Atlantoaxial Subluxation?

A

Atlantoaxial joint between C1 and C2 can be damaged by RA, leading to instability that can compress the spinal cord

67
Q

What autoantibodies are specific for RA?

A

Rheumatoid Factor (RF) and Anti-Citrullinated Peptide Antibodies (ACPA)

68
Q

What nonspecific antibodies can be found in RA?

A

ANA

69
Q

What is a Rheumatoid Factor?

A

An autoantibody with specificity for the Fc fragment of IgG, with high titers= worse diagnosis

70
Q

What can cause a rise in Rheumatoid Factor outside of RA?

A

HCV, chronic bacterial infection, inflammatory disease, and hypergammaglobulinemia - all without RA

71
Q

What are ACPA’s also called?

A

Anti-CCP

72
Q

Which antibodies is most specific and sensitive for RA?

A

Anti-CCP, associated with erosive disease and poor prognosis - always check ACCP and RF

73
Q

What are the goals of treatment in RA?

A

Reduce joint pain and swelling, and prevent joint damage

74
Q

What is treating to target in RA?

A

Treating with a goal of remission or low disease activity

75
Q

How is treating to target tracked in RA?

A

Objectively track the disease with validated intruments for joint damage, patient pain, physician assessment and lab measurements

76
Q

What is used for acute symptom control in RA?

A

NSAIDS for symptomatic relief only as well as corticosteroids

77
Q

What are side effects of NSAIDS?

A

GI and renal toxicity

78
Q

How do NSAIDS slow the progression of RA?

A

They don’t - symptomatic relief only

79
Q

What are long term side effects of Corticosteroids?

A

HTN, hyperglycemia, osteoperosis

80
Q

What is used for chronic treatment of RA?

A

DMARDS such as Methotrexate, Hydroxychloroquine, and biologics (TNFantagonists, Antaracept, IL-6 inhibitors)

81
Q

What is the cornerstone of RA therapy and why?

A

DMARDS because they reduce RA symptoms and slow radiographic progression/damage

82
Q

What are the non-biologic DMARDS for RA?

A

Methotrexate, Sulfasalazine, Hydroxychloroquine

83
Q

What are the biologic DMARDS for RA?

A

TNFantagonists, CTLA4 antagonists, IL-6 antagonists, CD-20 antagonists, JAK inhibitors

84
Q

What is the best DMARD for RA?

A

Methotrexate

85
Q

Describe the mechanism of action of Methotrexate?

A

Inhibits Dihydrofolate Reductase to limit DNA synthesis, lowering neutrophil activation, vascular proliferation, and cytokine production

86
Q

Describe the mechanism of action of Leflunomide?

A

Inhibits Dihydroortate Dehydrogenase to limit DNA synthesis, lowering expression of cell adhesion molecules and blocks antigen presentatino, cytokine secretion, and MMP production

87
Q

What group should not be given Leflunomide and why?

A

Leflunomide is a teratogen with a long half life due to enterohepatic circulation and should not be given to women of childbearing age

88
Q

What is Sulfasalazine and what is it’s mechanism of action?

A

A linked antibiotic (sulfapyridine) to an anti-inflammatory agent (5-aminosalicylic acid) to suppress lymphocyte and leukocyte function

89
Q

What is Hydroxychloroquine and how does it work?

A

Antimalarial that may interfere with presentation of auto-antigenic peptides

90
Q

What side effect of Hydroxychloroquine requries routine screening?

A

Retinal toxicity can develop, requiring an annual eye exam

91
Q

What is the main side effect of biologic treatments for RA?

A

Increased risk of infection and cancer

92
Q

What is the order of drugs for treating RA?

A

Initiate with a non-biologic DMARD like Methotrexate. Takes a while to work, so give low dose Prednisone or NSAIDS in the mean time and remove Prednisone asap, while maintaining DMARD at the lowest dose possible - escalate to TNF inhibitor and alter biologics if disease activity persists

93
Q

What disease is this and why?

A

Rheumatic Arthritis, since the MCP’s and the PIP’s are swollen but the DIP’s are relatively spared

94
Q

What disease is this and why?

A

Rheumatoid Arthritis - All fingers swollen at MCP and PIP but spares the DIP

95
Q

What disease is this and why?

A

Severe RA - joing deformities at MCP and PIP that relatively spares the DIP

96
Q

What deformities are this and what disease causes them?

A

Swanneck = flexed DIP + extended PIP

Boutonneire = Extended DIP + flexed PIP

97
Q

What’s happenening in this Xray and what’s causing it?

A

Marginal erosions due to the Pannus from Rheumatic Arhritis

Also see some soft tissue swelling

98
Q

What is this and why?

A

Ulnar deviation due to RA

MSK/Derm (46 decks)

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