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Summer pharm 3 > Rheumatoid arthritis > Flashcards

Rheumatoid arthritis Flashcards

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1
Q

What is the MC systemic inflammatory disease

A

RA

characterized by symmetric joint involvement

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2
Q

What extraarticular sites are involved in RA

A 
Rheumatoid nodules 
vasculitis 
eye inflammation 
neuro dysfunction 
cardiopulmonary disease 
LAD
splenomegaly
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3
Q

What is the pathogenesis of the inflammatory response in RA

A
  • Antigen presenting cells present antigens to T cells
  • T cells stimulate B cells to make antibodies and osteoclasts, which destroy and remove bone
  • Immune response stimulates macrophages, which promote inflammation by stimulating T cells and osteoclasts
  • Macrophages also stim. fibroblasts (degrade bone matrix, produce inflammatory cytokines)
  • Activated T cells and macrophages release factors that increase blood flow&destroy tissue= cellular invasion of synovial joint
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4
Q

What are assessment tools used to measure RA activity and remission

A

Clinical Disease Activity Index: Remission <2.8; Dz >2.8-10

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5
Q

What are the goals of RA treatment

A

achieve remission or low disease activity (treat to target)

Reduce inflammation using drugs known to alter disease progression

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6
Q

What deformities are associated with RA

A

Ulnar deviation
Swan neck deformity
Active synovitis
Nodules

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7
Q

What is the overall treatment plan for rheumatoid arthritis

A

Drug therapy should be part of comprehensive management; PT, exercise, and rest, assistive devices, +/- orthopedic services

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8
Q

When should you start disease modifying anti-rheumatic drugs

A

within 3 months of RA diagnosis

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9
Q

What is considered adjunct treatment early in RA Tx

A

NSAIDs and Corticosteroids

can also use them as needed if Sx are not controlled with DMARDs

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10
Q

What are your options when DMARDs fails

A

combination therapy w/ 2+ DMARDs
DMARD + biologic agent
-in either case, pt needs closer monitoring for toxicity and therapeutic benefit for duration of Tx

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11
Q

Early, aggressive Tx of RA may prevent

A

irreversible joint damage and disability

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12
Q

How do you decide which patients get which Tx

A

Less active disease and good prognostic indicator: Tx with oral monotherapy
High activity dz or poor prognostic factors: combo therapy and biologics

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13
Q

Controlling inflammation w/ therapeutic interventions improves

A

symptoms

also slows disease course

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14
Q

What are the non-biologic DMARDs

A 
Methotrexate 
Leflunomide 
Hydroxychloroquin 
Sulfasalazine 
Minocycline 
Tofacitinib
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15
Q

Less frequently used agents 2/2 reduced efficacy or greater toxicity include

A 
Azathioprine
D-penicilamine 
Gold 
Cyclosporine
Cyclophosphamide
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16
Q

Biologic DMARDs include

A

Anti-TNF: etanercept, infliximab, adalimumab, certolizumab, golimumab
Non-TNF: Abatacept, Tocilizumab, Rituximab, Anakinra

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17
Q

What type of drugs are the non-TNF drugs

A

Abatacept: costimulation modulator
Tocilizumab: IL-6 receptor antagonist
Rituximab: peripheral B cell depletion
Anakinra: IL-1 receptor antagonist

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18
Q

Long term data suggests superior outcomes of RA patients on this drug

A

Methotrexate, that is why it’s first line

Leflunomide has similar long-term efficacy as methotrexate

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19
Q

Examples of combination therapy are

A

Methotrexate, Sulfasalazine + Prednisone
Infliximab + Methotrexate
If moderate to high dz: Methotrexate + Hydroxychloroquine, Leflunomide, or Sulfasalazine

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20
Q

Recommended triple therapy is

A

Methotrexate + Sulfasalazine + Hydroxychloroquin

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21
Q

ACR endorses the use of anti-TNF biologics (enteracept, infliximab, etc.) in patients with

A

early disease of high activity and poor prognostic factors, regardless of whether they have used DMARDs

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22
Q

Algorithm for RA treatment is essentially

A

Start with MTX (DMARD) +/- prednisone
If it’s bad, do a combo DMARD, or anti-TNF, non-TNF, or Tofacitinib +/- MTX
If a single anti-TNF fails, do non-TNF or anti-TNF +/- MTX
If non-TNF fails, do another non-TNF +/- MTX

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23
Q

What is the MOA of methotrexate

Study These Flashcards
A

inhibits cytokine production, purine biosynthesis
May stimulate release of adenosine (anti-inflammatory properties)
Folic acid antagonist (give 1-5mg xwk to counteract deficiency)

24
Q

Methotrexate is contraindicated in

Study These Flashcards
A 
pregnancy 
chronic liver disease 
immunodeficiency
Pleural or peritoneal effusions 
leukopenia
thrombocytopenia
CrCl <40
25
Toxicities of methotrexate include
``` N/V/D thrombocytopenia pulmonary fibrosis, pneumonitis elevated liver enzymes Stomatitis (first Sx) ```
26
What is the MOA of Leflunomide
inhibit pyrimidine synthesis= decreased lymphocyte proliferation Modulate inflammation
27
Leflunomide is contraindicated in
liver disease | pregnancy (teratogenic)
28
Toxicities of Leflunomide include
GI, hair loss, liver, bone marrow toxicity
29
What is the MOA of hydroxychloroquine
Lessens antigen-antibody reaction at inflammatory sites Good for mild RA or as an adjunct w/ DMARD in more severe disease NOT myelosuppressive!
30
Toxicities of Hydroxychloroquin are
``` hepatic and renal toxicities Decreased night or peripheral vision rash, alopecia HA, vertigo N/V/D ```
31
What is the MOA of Sulfasalazine
Prodrug; cleaved to Sulfapyridine and 5-aminosalicylic acid in colon Rapid absorption in GI, onset in 2 months -Decreased absorption with antibiotics (destroy colonic bacteria) and Iron supplements -Potentiated warfarin's effects
32
ADE of Sulfasalazine are
``` N/V/D Rash, urticaria leukopenia alopecia stomatitis *elevated liver enzymes *turns skin yellow-orange (normal) ```
33
What is the MOA of Minocycline
inhibit metalloproteinases that damage articular cartilage Good for low disease activity w/o poor prognosis (mildly reduces swollen joints and ESR) NO effect on erosion progression
34
What s Tofacitinib
inhibit JAK (tyrosine kinase) which suppresses the immune system by reducing cytokine response Good for moderate to severe RA who can't take MTX *Do NOT give live vaccines!*
35
ADE of Tofacitinib are
serious infections lymphomas latent TB elevated lipids and liver enzymes
36
What are ADE of other disease modifying RA drugs
``` Gold salts: myelosuppression Azatioprine: leukopenia, hepatotoxicity D-penicillamine: myelosuppression Cyclosporine: nephrotoxicity Cyclophosphamide: gastritis ```
37
what is the overall MOA of biologic agents
genetically engineered protein molecules that block the proinflammatory cytokines TNF: infliximab, enteracept, adalimumab, golimumab, certolizumab IL-1: anakinra IL-6: Tocilizumab deplete B cells: Rituximab prevent t cell costimulation needed for activation by binding CD80/86: Abatacept
38
What is the MOA of anti-TNF drugs
Block proinflammatory cytokines of TNF-a | do NOT use in CHF!
39
ADE od anti-TNF drugs are
MS like illness or MS exacerbation | Increased risk of lymphoproliferative cancer
40
What is Etanercept
a fusion protein that binds TNF and makes it biologically inactive Prevents TNF from interacting with receptors that lead to cell activation
41
What is Infliximab
Chimeric antibody combining mouse and human IgG1 Binds to TNF and prevents interaction with receptors on inflammatory cells Given WITH methotrexate to prevent formation of antibody response to the foreign protein (mouse)
42
What are the other anti-TNF biologics
Adalimumab: human IgG1 Ab to TNF Golimumab: human Ab to TNF-a Certolizumab: humanized antibody specific for human TNF-a
43
Golimumab can be used for
RA Psoriatic arthritis ankylosing spondylitis
44
What in Anakinra
IL-1 receptor antagonist
45
What is Tocilizumab
Attaches to IL-6 receptor and prevents cytokine from interacting with receptors Monotherapy or with MTX or another DMARD *Do NOT give live vaccines during Tx*
46
ADE of Tocilizumab are
``` risk of infx elevated plasma lipids and liver enzymes risk of GI perforation CYP450 3A4 inducer (warfarin) TB ```
47
What is Rituximab
Binds B cells and nearly completely depletes them Good for pts who failed MTX of anti-TNF drugs (but continue MTX in combo with Rituximab) *Do NOT give live vaccines during Tx*
48
What can be given with Rituximab to reduce the reaction
methylprednisone APAP antihistamines
49
What is Abatacept
a costimulation modulator for mod-severe RA that 1+ DMARDs don't work in Binds CD80/86 in APC, inhibit interaction between APC and T cells, and prevents T cell activation= no inflammation *Do NOT give live vaccines during Tx or 3 months after*
50
ADE of Abatacept are
``` **HTN HA nasopharyngitis dizziness cough back pain UTI rash ```
51
Abatacept results in
reductions in cytokines, T cell proliferation, and other consequences of T cell activation
52
What can be used for symptomatic relief of RA
NSAIDs or Corticosteroids Relatively rapid improvement in Sx compared to DMARDs (weeks to months) but, they do NOT impact disease progression; they are simply symptomatic Tx Also corticosteroids have a lot of long term ADE
53
What can be used for symptomatic relief of RA
NSAIDs or Corticosteroids Relatively rapid improvement in Sx compared to DMARDs (weeks to months) but, they do NOT impact disease progression; they are simply symptomatic Tx Also corticosteroids have a lot of long term ADE
54
What is the MOA of corticosteroids
interfere with antigen presentation to T cells Inhibit prostaglandin and LT synthesis inhibit neutrophil and monocyte superoxide radical generation Impair cell migration and redistribute monocytes, PMN, and lymphocytes= blunt inflammatory/auto-immune responses
55
Corticosteroids are good for
bridging therapy pain bursts or flares
56
How do you admin corticosteroids
Injection into joint q3 months (no more than 2-3x yr at the same joint)
57
ADE of corticosteroids are
``` HPA suppression Cushings Osteoporosis Glaucoma, cataracts gastritis HTN Glucose intolerance skin atrophy increased infx ```

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