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Summer pharm 3 > Rheumatoid arthritis > Flashcards

Rheumatoid arthritis Flashcards

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

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

A 
pregnancy 
chronic liver disease 
immunodeficiency
Pleural or peritoneal effusions 
leukopenia
thrombocytopenia
CrCl <40
25
Q

Toxicities of methotrexate include

A 
N/V/D
thrombocytopenia 
pulmonary fibrosis, pneumonitis 
elevated liver enzymes 
Stomatitis (first Sx)
26
Q

What is the MOA of Leflunomide

A

inhibit pyrimidine synthesis= decreased lymphocyte proliferation
Modulate inflammation

27
Q

Leflunomide is contraindicated in

A

liver disease

pregnancy (teratogenic)

28
Q

Toxicities of Leflunomide include

A

GI, hair loss, liver, bone marrow toxicity

29
Q

What is the MOA of hydroxychloroquine

A

Lessens antigen-antibody reaction at inflammatory sites
Good for mild RA or as an adjunct w/ DMARD in more severe disease
NOT myelosuppressive!

30
Q

Toxicities of Hydroxychloroquin are

A 
hepatic and renal toxicities 
Decreased night or peripheral vision 
rash, alopecia 
HA, vertigo
N/V/D
31
Q

What is the MOA of Sulfasalazine

A

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
Q

ADE of Sulfasalazine are

A 
N/V/D
Rash, urticaria 
leukopenia 
alopecia
stomatitis 
*elevated liver enzymes 
*turns skin yellow-orange (normal)
33
Q

What is the MOA of Minocycline

A

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
Q

What s Tofacitinib

A

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
Q

ADE of Tofacitinib are

A

serious infections
lymphomas
latent TB
elevated lipids and liver enzymes

36
Q

What are ADE of other disease modifying RA drugs

A 
Gold salts: myelosuppression 
Azatioprine: leukopenia, hepatotoxicity 
D-penicillamine: myelosuppression
Cyclosporine: nephrotoxicity 
Cyclophosphamide: gastritis
37
Q

what is the overall MOA of biologic agents

A

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
Q

What is the MOA of anti-TNF drugs

A

Block proinflammatory cytokines of TNF-a

do NOT use in CHF!

39
Q

ADE od anti-TNF drugs are

A

MS like illness or MS exacerbation

Increased risk of lymphoproliferative cancer

40
Q

What is Etanercept

A

a fusion protein that binds TNF and makes it biologically inactive
Prevents TNF from interacting with receptors that lead to cell activation

41
Q

What is Infliximab

A

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
Q

What are the other anti-TNF biologics

A

Adalimumab: human IgG1 Ab to TNF
Golimumab: human Ab to TNF-a
Certolizumab: humanized antibody specific for human TNF-a

43
Q

Golimumab can be used for

A

RA
Psoriatic arthritis
ankylosing spondylitis

44
Q

What in Anakinra

A

IL-1 receptor antagonist

45
Q

What is Tocilizumab

A

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
Q

ADE of Tocilizumab are

A 
risk of infx 
elevated plasma lipids and liver enzymes 
risk of GI perforation 
CYP450 3A4 inducer (warfarin) 
TB
47
Q

What is Rituximab

A

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
Q

What can be given with Rituximab to reduce the reaction

A

methylprednisone
APAP
antihistamines

49
Q

What is Abatacept

A

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
Q

ADE of Abatacept are

A 
**HTN
HA
nasopharyngitis 
dizziness
cough 
back pain 
UTI
rash
51
Q

Abatacept results in

A

reductions in cytokines, T cell proliferation, and other consequences of T cell activation

52
Q

What can be used for symptomatic relief of RA

A

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
Q

What can be used for symptomatic relief of RA

A

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
Q

What is the MOA of corticosteroids

A

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
Q

Corticosteroids are good for

A

bridging therapy
pain
bursts or flares

56
Q

How do you admin corticosteroids

A

Injection into joint q3 months (no more than 2-3x yr at the same joint)

57
Q

ADE of corticosteroids are

A 
HPA suppression 
Cushings 
Osteoporosis 
Glaucoma, cataracts 
gastritis
HTN 
Glucose intolerance 
skin atrophy 
increased infx

Summer pharm 3 (13 decks)

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