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44 Cards in this Set

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  • Back
Describe the RA histology vs. normal synovium.
Normal synovium has 1-3 cell thcik layer.

RA synovium has:
1. Marked infiltration of inflammatory cells
2. Nodular appearance
3. Thickening of synovial tissue
Stages of RA.


Describe RA progression in terms of:
- Inflammation
- Radiographic changes
- Disability
Inflammation is steady or tapers off

Radiograph changes constantly increase

Disability constantly increase
Describe the rate of joint erosion in RA
Significantly rapid rate of progression in first year, more so than second and third year.
Radiographic abnormalities seen in what type of patients?
93% have radiographic abnormalities in less than 2 years of RA onset.
Joint erosions can be detected by MRI when?
Within 4 months of onset.
In RA, describe the tissue (steps 1,2) and cell (steps 3,4) pathogenesis of RA in four steps.
Synovium thickens

Pannus develops

Neutrophils increase in the synovial fluid

The pannus and synovial membrane contains lots of lymphocytes, macrophage, fibroblasts, and other cells of chronic inflammation.
In RA, describe the cytokine signaling pathway involved in RA.
In the synovium, T and B lymphocytes to produce lots of cytokines.

T cells produce IFN-gamma to induce macrophages.

Thus macrophages will make TNF-alpha and IL-1.

This will stimulate fibroblast, osteoclasts, and chondrocytes to cause erosion and damage tissue.
What is the principle aim of DMARD therapy for RA.
Prevent or retard joint erosion/destruction.
NSAIDs improve symptoms, but.....
it does not reduce progression of joint damage.
What is a controversial drug treatment for RA.
In RA, what do you use NSAIDs for?
Base treatment for symptomatic relief --> decrease in swelling and pain.
What is prednisone (<10 mg qd) used for?
Bridge therapy --> decrease inflammation, thus patient more functional in ADL while waiting for DMARDs to kick in.
For what and when do you use intra-articular steroids.
Useful for persistent joints, or flairs.

Not feasible for multiple joints.
Name the top four DMARDs.
1. Methotrexate (Trexall)
2. Leflunomide (Arava)
3. Sulfasalazine (Azulfidine)
4. Hydroxychloroquine (Plaquenil)
Methotrexate mechanism of action.
Inhibits purine DNA synthesis via DHFR (Dihydrofolate Reductase), thus increasing adenosine (which will down regulate inflammatory process)
Methotrexate should be used in concomitant with?
Folic acid b/c it alters folic acid related mechanisms.
Use for methotrexate.
Moderate to severe RA
Leflunomide mechanism of action.
Inhibits pyrimidine DNA synthesis via dehydrooroate dehydrogenase, thus decreasing radiographic progression.
Use for leflunomide.
Moderate to severe RA
Sulfasalazine mechanism of action.
Suppresses leukocyte and lymphocyte function, thus increasing adenosine and decreasing NFkB transcription factor.
Sulfasalazine use?
Mild to moderate RA
Hydroxychloroquine mechanism.
Interferes with antigen processing.
Hydroxychloroquine use?
Mild to early RA.
Progression of Joint damage by sharp scores in terms of:

- placebo
- methotrexate
- leflunomide
Greatest to least progression of joint damage

Placebo > Methotrexate > Leflunomide
What are three ways to inhibit cytokines.
1. Receptor blockade
2. Neutralization of cytokines.
3. Activation of anti-inflammatory pathway
What to use for Receptor blockade?
1. Monoclonal antibodies
(binds to receptor)

2. Receptor Antagonist
(binds to receptor)
What to use for Neutralization of cytokines?
1. Monoclonal antibodies
(binds to cytokines)

2. Soluble receptor
(binds to cytokines)
What to use for Activation of non-inflammatory pathway?
Anti-inflammatory cytokines
List two monoclonoal antibodies used as Anti-TNF agents.
1. Adalimumab
2. Inflixamab
List a soluble receptor used as Anti-TNF agent.
List a receptor antagonist used as an anti-IL-1 agent.
Biologic DMARDs approved for use in which disorders?
Crohn's Disease
Ankylosing Spondylosis
Psoriatic Arthritis
What does Abatacept do?
Inhibits the co-stimulatory pathway required for full activation of T-lymphocytes.
What does Abatacept bind to? What will this cause?
Binds to APC CD80/86.

Prevention of CD80/86 to interact with CD28
Rituximab is what?
Antibody directed against CD20 antigen on B-lymphocytes.
What does Rituximab do?
Depletes B-cells lineage
What are the targets for Rituximab.
Pre-B cell
Immature B cell
Mature B cell
Activated B cell
Efficacy of ADA, MTX, and combo for clinical response.
Greatest to least.

Combo > MTX > ADA
Efficacy of ADA, MTX, and combo for radiographic response.
Greatest to least.

Combo > ADA > MTX
Safety issues associated with Biologic DMARDSs.
1. Serious Infection
2. Opportunistic Infection
3. Malignancies
4. Hematologic abnormalities
5. Administration reactions
6. Demyelination
7. CHF
8. Autoantibodies (and lupus like syndromes)
9. Skin reactions
10. Hepatotoxicity.
What infections need to be watched for with Anakinra?
TB needs to be monitored for with what biological DMARD?
Infliximab and Etanercept
Rank the potential for adverse effects for the following:

- Abatacept non-biologic DMARD
- Placebo non-biologic DMARD
- Abatacept biologic DMARD
- Placebo biologic
Greatest potential to least.

Abatacept non-biologic DMARD
Placebo non-biologic DMARD
Abatacept biologic DMARD
Placebo biologic