Drugs for Rheumatic Diseases - Linger Flashcards by Matt Stanton

Q

agents that slow or stop progression of rheumatic disease, reduce pain and inflammation
-longer remission free phases and better quality of life

A

DMARDs

disease modifying antirheumatic drug

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Q

better disease outcome

A

referral to rheumatologist

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Q

non-biologic DMARDs

A

hydroxychloroquine
leflunomide
methotrexate
sulfalazine

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Q

hydroxychloroquine

A

non-biologic DMARD

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Q

leflunomide

A

non-biologic DMARD

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Q

methotrexate

A

non-biologic DMARD

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Q

sulfasalazine

A

non-biologic DMARD

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Q

rarely used DMARDs

A

azathioprine
cyclosporine
gold salts
minocycline

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Q

adalimumab

A

TNF-a blocker - biologic DMARD

mAb

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Q

certolizumab

A

TNF-a blocker - biologic DMARD

mAb

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Q

etanercept

A

TNF-a blocker - biologic DMARD

recombinant fusion protein**

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Q

golimumab

A

TNF-a blocker - biologic DMARD

mAb

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Q

infliximab

A

TNF-a blocker - biologic DMARD

mAb

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Q

anti-CD20 mAb

A

rituximab

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Q

T cell Fc-fusion

A

abatacept

domain of CTLA-4 receptor

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Q

anti-IL-6 mAb

A

tocilizumab

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Q

prevention of recurrent gout

A

allopurinol
febuxostat
pegloticase
probenecid

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Q

initial tx of rheumatoid arthritis

A

MTX or leflunomide

HCQ or sulfalazine - safer - if milder disease

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Q

NSAIDs

A

adjunct of pain relief for rheumatoid arthritis

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Q

corticosteroids

A

short term - for severe acute sx

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Q

biologic therapy for RA

A

after inadequate response to non-biologics

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Q

TNF-a inhibitors

A

no study to compare if one is more effective than another

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Q

etanercept

A

common first choice biologic

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Q

MOA methotrexate

A

inhibit dihydrofolate reductase

impaired DNA synthesis
causes cell death

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MTX dosage

high - chemo low - RA tx high has myelosuppression - not a worry with RA tx and low dose

response time MTX

4-6 weeks to several months

adverse of methotrexate

nausea, upset stomach, diarrhea, stomatitis**, alopecia, fever, rash, HA, fatigue elevation of hepatic enzymes - but cirrhosis rare - should monitor levels** -screen those at risk for hepatitis, no alcohol myelosuppression if high dose

supplement with methotrexate

folic acid or leucovorin reduce adverse effects

MOA leflunomide

prodrug converted to active A77-1726 inhibits dihydroorotate dehydrogenase - reduced ribonucleotide synthesis and G1 arrest inhibit B and T cell proliferation

response time leflunomide

6-12 weeks

adverse of leflunomide

diarrhea elevated liver enzymes

category X pregnancy

leflunomide and methotrexate

MOA hydroxychloroquine

poorly understood - T cell suppression, decreased leukocyte chemotaxis, inhibit DNA/RNA synthesis, all possible causes

response time hydroxychloroquine

3-6 months

ocular toxicity

with hydroxychloroquine need to monitor eyes**

MOA sulfasalazine

poorly understood - possibly decreased IgA and IgM rheumatoid factor production - suppression of T cell and B cell prolifeation, etc. metabolized to 5-aminosalicylic acid

response time sulfasalazine

1-3 months

prevent rejection of transplant organs

azathioprine rare used DMARD

pregnant transplant patient

cyclosporine rare used DMARD

drug induced lupus

with minocycline rare used DMARD

MOA TNF-a inhibitors

prevent binding of TNF-a to TNF receptors | -down-regulation of macrophages and T cells

biologic DMARD response time

1-2 weeks faster than non-biologics**

biologic DMARDs

monotherapy - or combo (usually with MTX)

adverse of biologic DMARD

cytopenia -monitor CBC** opportunistic infection** - bacterial sepsis and TB heart failure association

before starting biologic DMARD

screen for latent TB**

rare demyelinating disease

infliximab

NSAID MOA

inhibit COX - decreased prostaglandins

DMARD induction, transition to different DMARD, and during disease flare of RA

use NSAIDs not acetaminophen - poor anti-inflammatory

adverse NSAIDs

GI ulcers and bleeds can give ranitidine (H2 histamine antagonist)

less GI toxicity

with celecoxib - COX2 selective

third trimester pregnancy

no NSAIDs**

adverse of corticosteroids

osteoporosis, weight gain, fluid retention, cataracts, glaucoma, poor wound healing, hyperglycemia, HTN, adrenal suppression should give Ca and Vit D supplements

first line for acute gout

NSAIDs inhibit urate crystal phagocytosis

aspirin and gout

NO - because inhibit urate excretion at low doses

glucocorticoids

used in severe gout

colchicine MOA

binds tubulin and prevents polymerization - inhibit leukocyte migration and phagocytosis

decrease urate synthesis

xanthine oxidase inhibitor - allopurinol

increased renal excretion of urate

uricosuric agent - probenecid

colchicine

should not be repeated within 14 days - to avoid toxicity cumulation

allopurinol MOA

purine analog that inhibits xanthine oxidase -decreased uric acid production decreased recurrence of gout regardless of pathology

allopurinol

preferred for gout during periods between acute episodes

reduce dose of chemotherapy purines

if patient on allopurinol

febuxostat MOA

non-purine inhibitor of xanthine oxidase

probenacid MOA

organic acid - acts at anionic transport site of renal tubules to reduce reabsorption of uric acid tx of hyperuricemia with gout - when tophi present

adverse of probenacid

increased likelihood of renal stone formation