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Pharmacology > RA > Flashcards

RA Flashcards

1
Q

When do you need to start prescribing DMARDS for RA dx?

A

within 3 months of diagnosis

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2
Q

T/F NSAIDS and and corticosteroids are considered adjunctive therapy with DMARDS

A

TRUE

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3
Q

What is first line therapy for RA?

A

DMARDS

usually methoxtrexate choosen first

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4
Q

What is MOA of methoxtrexate?

A
  • blocks cytokine production
  • blocks purine synthesis
  • stimulate release of adenosine
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5
Q

Which nutrient is deficiency when giving methotrexate

A

folic acid

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6
Q

Who should no receive methotrexate?

A 
pregnant women
chronic liver disease 
immunodeficient
leukopenia
CrCl <40
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7
Q

What toxicities are associated with methotrexate?

A

pulmonary fibrosis
hematologic thromobocytopenia
hepatic elevated liver enzymes
stomatitis

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8
Q

What labs could you monitor for methorexate?

A

CBC

ALT/AST

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9
Q

What is MOA if leflunomide?

A

blocks pyrimidine synthesis and decreases lymphocyte proliferation and modulation of inflammation

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10
Q

What is a contraindication for leflunomide?

A

liver disease
teratogenic
long half life 14-16 days

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11
Q

What toxicities are associated with leflunomide?

A

GI, hair loss, liver, bone marrow toxicity

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12
Q

Which drug can be given to lower leflunomide levels in the body?

A

Cholestyramine: binds it and can clear it

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13
Q

What is MOA of hydroxychloroquine?

A

dampens ab-antigen response at site of inflammation

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14
Q

what is the clinical use of hydroxychloroquine?

A

mild RA

combination therapy with DMARD for progressive disease

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15
Q

What are ADE with hydroxychloroquine?

A
  • myelosuppression
  • N/V/D
  • ocular: decreased night or peripheral vision
  • rash, alopecia
  • neuro: vertigo insomnia
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16
Q

T/F Hydroxychloroquine lacks heaptic and renal toxicities

A

True

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17
Q

T/F Sulfsalasizne is cleaved in the colon

A

TRUE

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18
Q

Which two active substances does sulfsalaszine produce

A

sulfapyridine and 5-aminosalicylic acid

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19
Q

Which two diseases is sulfsalazine used for?

A

Cronh’s and RA

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20
Q

What are ADE of sulfasalazine?

A

elevated liver enzymes
may turn skin yellow
con potentiate warfarins effect

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21
Q

T/F Sulfasalazine absorption is decreased if abx destroy colonic bacteria

A

TRUE

22
Q

T/F Sulfasalazine is cleaved in the colon into a pro drug

A

TRUE

23
Q

T/F Iron can limit the absorption of sulfasalazine

A

TRUE

24
Q

What drug class is used to tx high activity and presence of poor prognostic factors of RA?

A

Biologics
Anti-TNF
Non- TNF

25
Q

T/F Methotrexate is more effective than biologic monotherapy

A

TRUE

26
Q

What are some examples of initial combination therapy with methotrextae and biologics?

A

Methotrexate and etanercept
sulfasalazine and prednisone
infliximab and methotrexate

27
Q

What are pharmacotherapy options for moderate to high disease activity?

A

methotrexate and hydroxyquinilone
methotrexate and leflunomide
methotrexate and sulfasalazine

28
Q

What is triple combination therapy?

A

methotrexate and sulfasalazine, hydroxyquinilone

29
Q

What is a JAK inhibitor? What is MOA?

A

JAK is a tyrosine kinase, it suppresses the immune system by modulating or reducing the cytokine signal downstream

30
Q

what are ADE of of JAK

A
  • serious infections
  • lymphomas
  • elevated liver enzymes,
  • live vaccines should not be given
31
Q

What is the clinical use of JAK-I?

A

moderate to severe RA who have failed wiht methotrexate

32
Q

Name 2 JAK-I?

A

Tofacitinib and Baricitinib

33
Q

What are biologic agents?

A

genetically engineered molecules that block pro inflammatory cytokines

34
Q

Name drugs that are TNF-alpha?

A

Infliximab, Etanercept, Adalimumab,

35
Q

Name IL-6 blocker?

A

Tocilizumab, Sarilumab

36
Q

Which drug depletes peripheral b-cells?

A

Rituximab

37
Q

Which drug is a T-cell costimulator blocker?

A

Abatacept

38
Q

What is MOA of TNF-alpha?

A

blocks cytokine TNF-alpha

39
Q

What are contraindications for TNF-alpha?

A

CHF

40
Q

What are ADE of TNF-alpha?

A

MS like illness or exacerbates MS

increased risk of lymphoproliferative cancer

41
Q

Name 2 TNF-alpha? how do they differ with MOA?

A

entanercept: binds TNF to inactivate it,it is a fusion protein
infliximab: chimeric antibody, binds TNF

42
Q

What should be given with infliximab to prevent ab production against infliximab?

A

methotrexate

43
Q

What is MOA of Tocilizumab, Sarilumab?

A

attaches to IL-6 receptors and prevents cytokines from binding with IL-6

44
Q

What are ADE of Tocilizumab, Sarilumab?

A 
risk of infection
elevated plasma levels 
elevated liver enzymes 
risk of GI perforation
inducer of CYP450 34A
don't give live vaccination
45
Q

What is MOA of Rituximab?

A

binds b -cells and nearly completes depletion of peripheral B cells

46
Q

when do you use Rituximab?

A

when patient fails methotrexate and TNF_alpha tx

-but continue rituximab tx with methotrexate

47
Q

What are ADE of Rituximab?

A

No vaccines

48
Q

What is MOA of Abatacept?

A

binds CD80/86 on t -cells to prevent the co stimulation needed to fully activate T cells

49
Q

What are ADE of Abatacept?

A 
nasopharyngitis 
back pain
-dyspepsia 
-UTI
rash
extermity pain
50
Q

If patient with RA needs a vaccine, which form is not accepted to be given?

A

Live vaccines are not acceptable only killed ones

Pharmacology (47 decks)

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