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SM 234: Rheumatoid Arthritis Flashcards

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
How does the vasculature of the Synovium change in RA?
Hypervascularity of the Synovium develops in RA
26
What are stages of RA?
Susceptibility Preclinical Early RA Established RA
27
What is the Susceptibility phase of RA?
No symptoms or signs of autoimmunity, but genetic and environmental risk factors for RA are present
28
What is the Preclinical phase of RA?
Asymptomatic autoimmunity occurs with increased levels of Cytokines, Chemokines and CRP in circulation as well as autoantibody formation, but no clinical symptoms
29
What is the Early phase of RA?
Immune symptoms continues to ramp up causing symptoms to first emerge, such as joint pain
30
What is the Established phase of RA?
A patient presents with classifiable RA
31
What process is key to developing the immune response in Rheumatic Arthritis?
Citrullination
32
What is Citrullination?
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
33
How do Citrullinated peptides interact with HLA?
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
34
How do autoantibodies arise in Rheumatoid Arthritis?
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
35
What factors do B-cells produce are specific for Rheumatoid Arthritis?
Rheumatoid Factor and Anti-Citrullinated Peptide Antibody, detectable up to 10 years prior to onset of clinical disease
36
In which stage of RA does Synovitis develop?
Early RA
37
What is Synovitis?
Influx of inflammatory cells into Synovium, such as CD4, Macrophages, and APC's as well as B/Plasma cells
38
What cells are the major source of pro-inflammatory cytokines in RA?
Activated Synoviocytes, producing IL-1, IL-6, and TNFalpha as well as Matrix Metalloproteaes and RANKL
39
What stage of RA invovles the onset of joint damage?
Establised RA, which mediates Cartilage and Bone Destruction
40
What causes Cartilage destruction in RA?
MMP's produce by Fibroblast Like Synoviocytes and RANKL-mediated activation of Osteoclasts
41
What do Fibroblast Like Synoviocytes produce in Early RA?
MMP's and RANK-L
42
What do Macrophage Like Synoviocytes produce in Early RA?
Inflammatory cytokines: IL-1, IL-6, TNFalpha
43
How does Rheumatoid Arthritis present?
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
What is gelling?
Stiffness after rest, found in Rheumatoid Arthritis
45
How long does morning stiffness last in Rheumatoid Arthritis?
More than 1 hour
46
How do non-inflammatory arthritis present?
OA also has an insidious onset and gelling, but with bony enlargement of joints and morning stiffness lasting \< 60min
47
What joints does RA involve?
Small joints of hand (MCP, PIP, but not the DIP)
48
What joints does OA involve?
Small joints of hand (PIP, DIP, but not the MCP)
49
How can RA and OA be differentiated at the feet?
RA involves all joints in the foot, while OA only effects the first MTP
50
How can OA and RA be differentiated in the spine?
RA involves the Cervical spine only, while OA involves the entire spine, especially the Lumbar spine
51
How do patients with RA present on physical exam?
Symmetric joint swelling and tenderness with palpapble swelling/bogginess (unlike OA where joints are harder)
52
How does advanced RA effect the joints on physical exam?
Ulnar deviation of the MCP with limited ROM and rheumatoid modules at pressure points
53
What is the Swan-neck deformity and what disease is it associated with?
Flexion at DIP and hyperextension at PIP; found in Rheumatoid Arthritis
54
What is the Boutonniere deformity and what disease is it associated with?
Flexion at PIP and hyperextension at DIP; found in Rheumatoid Arthritis
55
What are extra-articular mainfestations of RA in the skin?
Rheumatoid nodules at pressure points
56
What are extra-articular mainfestations of RA in the Hematologic system?
Anemia, thrombocyotpenia
57
What are extra-articular mainfestations of RA in the Pulmonary system?
Pleural thickening and pleural effusion
58
What are extra-articular mainfestations of RA in the Cardiac system?
Pericarditis and premature Atherosclerosis
59
What are extra-articular mainfestations of RA in the Opthalmic system?
Scleritis
60
What are extra-articular mainfestations of RA in the Neurologic system?
Entrapment syndromes like Medial Nerve compression via Carpal tunnel or Ulnar Nerve compression at the Medial fossa of the ELbow
61
What is the most common cause of mortality in RA?
Cardiovascular Disease + premature Atherosclerosis, because atherosclerosis is driven by inflammation
62
Why are RA patients at risk for infection and cancer?
Immune system dysfunction and immunosuppression to treat RA predisposes mortality due to infection and cancer
63
What radiographic changes accompany RA?
Soft tissue swelling, uniform and symmetric joint space loss, marginal erosions and symmetric deformities
64
What are marginal erosions?
A pannus eating away at a joint in RA
65
What specific bone is often eroded in RA?
The ulnar styloid
66
What is Atlantoaxial Subluxation?
Atlantoaxial joint between C1 and C2 can be damaged by RA, leading to instability that can compress the spinal cord
67
What autoantibodies are specific for RA?
Rheumatoid Factor (RF) and Anti-Citrullinated Peptide Antibodies (ACPA)
68
What nonspecific antibodies can be found in RA?
ANA
69
What is a Rheumatoid Factor?
An autoantibody with specificity for the Fc fragment of IgG, with high titers= worse diagnosis
70
What can cause a rise in Rheumatoid Factor outside of RA?
HCV, chronic bacterial infection, inflammatory disease, and hypergammaglobulinemia - all without RA
71
What are ACPA's also called?
Anti-CCP
72
Which antibodies is most specific and sensitive for RA?
Anti-CCP, associated with erosive disease and poor prognosis - always check ACCP and RF
73
What are the goals of treatment in RA?
Reduce joint pain and swelling, and prevent joint damage
74
What is treating to target in RA?
Treating with a goal of remission or low disease activity
75
How is treating to target tracked in RA?
Objectively track the disease with validated intruments for joint damage, patient pain, physician assessment and lab measurements
76
What is used for acute symptom control in RA?
NSAIDS for symptomatic relief only as well as corticosteroids
77
What are side effects of NSAIDS?
GI and renal toxicity
78
How do NSAIDS slow the progression of RA?
They don't - symptomatic relief only
79
What are long term side effects of Corticosteroids?
HTN, hyperglycemia, osteoperosis
80
What is used for chronic treatment of RA?
DMARDS such as Methotrexate, Hydroxychloroquine, and biologics (TNFantagonists, Antaracept, IL-6 inhibitors)
81
What is the cornerstone of RA therapy and why?
DMARDS because they reduce RA symptoms and slow radiographic progression/damage
82
What are the non-biologic DMARDS for RA?
Methotrexate, Sulfasalazine, Hydroxychloroquine
83
What are the biologic DMARDS for RA?
TNFantagonists, CTLA4 antagonists, IL-6 antagonists, CD-20 antagonists, JAK inhibitors
84
What is the best DMARD for RA?
Methotrexate
85
Describe the mechanism of action of Methotrexate?
Inhibits Dihydrofolate Reductase to limit DNA synthesis, lowering neutrophil activation, vascular proliferation, and cytokine production
86
Describe the mechanism of action of Leflunomide?
Inhibits Dihydroortate Dehydrogenase to limit DNA synthesis, lowering expression of cell adhesion molecules and blocks antigen presentatino, cytokine secretion, and MMP production
87
What group should not be given Leflunomide and why?
Leflunomide is a teratogen with a long half life due to enterohepatic circulation and should not be given to women of childbearing age
88
What is Sulfasalazine and what is it's mechanism of action?
A linked antibiotic (sulfapyridine) to an anti-inflammatory agent (5-aminosalicylic acid) to suppress lymphocyte and leukocyte function
89
What is Hydroxychloroquine and how does it work?
Antimalarial that may interfere with presentation of auto-antigenic peptides
90
What side effect of Hydroxychloroquine requries routine screening?
Retinal toxicity can develop, requiring an annual eye exam
91
What is the main side effect of biologic treatments for RA?
Increased risk of infection and cancer
92
What is the order of drugs for treating RA?
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
What disease is this and why?
Rheumatic Arthritis, since the MCP's and the PIP's are swollen but the DIP's are relatively spared
94
What disease is this and why?
Rheumatoid Arthritis - All fingers swollen at MCP and PIP but spares the DIP
95
What disease is this and why?
Severe RA - joing deformities at MCP and PIP that relatively spares the DIP
96
What deformities are this and what disease causes them?
Swanneck = flexed DIP + extended PIP Boutonneire = Extended DIP + flexed PIP
97
What's happenening in this Xray and what's causing it?
Marginal erosions due to the Pannus from Rheumatic Arhritis Also see some soft tissue swelling
98
What is this and why?
Ulnar deviation due to RA

MSK/Derm (46 decks)

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