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Flashcards in Rheumatology Pharm Deck (22)
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1
Q

Biological DMARDs

A

MOA: Tumor-necrosis factor inhibitors

Etanercept (Enbrel)

Adalimumab (Humira)

Infliximab (Remicade)

Anakinra (Kineret)

Abatacept (Orencia)

2
Q

Strong CYP3A4 inhibitor examples

A

Clarithromycin

Itraconazole

Ketoconazole

Nefazodone

HIV protease inhibitors

3
Q

Moderate CYP3A4 inhibitors

A

Diltiazem

Erythromycin

Fluconazole

Grapefruit juice

Verapamil

4
Q

P-glycoprotein inhibitors

A

Cyclosporine

Ranolazine

Amiodarone

5
Q

Glucocorticoid Effects

A

Block proinflammatory genes IL-1 alpha and IL-2 beta

Decreases TNF-alpha - direct DNA interaction

Inhibit proinflammatory mediators phospholipase A2, COX2, Nitric oxide synthetase, prostaglandins, leukotrienes, thromboxanes

Decrease leukocyte adherence to vascular endothelium - can’t exit to infection/injury site

6
Q

Glucocorticoid Inflammatory Suppression

A

Increased neutrophils = increased wbc production w/ impaired transport and decreased apoptosis

Decreased eosinophils = increased apoptosis, trapped in tissues

Decreased monocytes = decreased accumulation and vasculature migration

Decreased lymphocytes = inhibition of T and B cells -> decreased APCs (macrophage, DC)

7
Q

Mineralocorticoid activity

A

Alter sodium transport

Cause fluid retention

Fludrocortisone has high mineralocorticoid effects

Prednisone and Methylpred have less mineralocorticoid activity

8
Q

Rheumatoid Arthritis Treatment

A

NSAIDs and steroids for short-term pain

  • withdrawal once DMARDs take effect
  • NSAIDs do not, and steroids only mildly prevent joint damage

DMARDs used indefinitely unless significant toxicity occurs

-choice of DMARD depends on disease severity, prognosis factors, and patient preference

9
Q

DMARDs

A

Disease-Modifying Antirheumatic Drugs

Variable patient response

If no remission w/in 3 months, change DMARD or do combo therapy

Assess efficacy every 3-6 months

10
Q

Methotrexate (Rheumatrex)

A

1st line for RA

2-6 week efficacy, 1X/week dosing to reduce toxicity risk

MOA: stimulate adenosine release, decrease neutrophil adhesion, suppress cell-mediated immunity, antiproliferative

Folic acid analog - require 1mg/day folic supplementation

CI: pregnancy, Liver dx, ETOH abuse, GFR <30

Monitor CBC, LFTs, Albumin, Creatinine

SE: Alopecia, myelosuppression, hepatic and pulmonary toxicity

11
Q

Sulfasalazine (Azulfidine)

A

2nd line for RA

MOA: inhibit PNM cell migration, decreased lymphocyte response and angiogenesis

90% excreted in feces, only 30% absorbed and returned in bile - coliform bacteria needed to break down

CI: sulfa allergy, pregnancy (D), GU/GI obstruction, porphyria, thrombocytopenia, LFTS >2X ULN, hepatitis

SE: orange-yellow skin pigment, depression, neutropenia, thrombocytopenia

Monitor CBC monthly 3X then q3months

12
Q

Leflunomide (Avara)

A

Anti-inflammatory and antiproliferative - decreases joint erosion

MOA: complete dihydrofolate inhibitor - decreased B and T cell proliferation - inhibits pyrimidine synthesis

2 years until women are fertile after use

CI: pregnancy, liver disease, alcoholism

SE: reversible alopecia, hepatoxicity, rash, HTN, myelosuppression

Affects Warfarin, rifampin, and bile sequestrant drugs

13
Q

Hydroxychloroquine (Plaquenil)

A

Anti-malarial

Not great for RA - used only with mild RA w/o joint destruction or inflammatory/AI markers

MOA: inhibit lysosomal, IL-1, PMNs, lymphocyte

Toxicity - macular damage - get fundoscopic and VA q6-12 mo

SE: photosensitivity, skin pigment changes, rash, macular damage

Effects BB, cyclosporin, and digoxin levels

14
Q

TNF Inhibitors

A

For severe RA

Etanercept (SQ), Infliximab (IV), Adalimumab (SQ)

Decrease joint damage

CI: latent TB (BBW), high infection risk

Use of Remicade w/ MTX decreases risk of infusion reaction, use w/ other TNFI causes too much immunosuppression

SE: Injection reaction, increase risk infection

15
Q

Anakinra (Kineret)

A

Immune modulator - recombinant IL-1 receptor antagonist

Decreases joint destruction and inflammation

Decrease dose w/ GFR <30

CI: TNF inhibitor use - increased infection risk

CI: E. coli protein sensitivity, infection, TNFI

SE: reaction @ site, infection, angioedema/anaphylaxis, leukocytopenia

Monitor CBC X3 mo then q4 months for 1 year

16
Q

Non-preferred DMARDs

A

D-Penicillamine (Depen, Cuprimine) - chelating agents

Azathioprine (Imuran) - carcinogenic, inhibits DNA synthesis enzyme

Cyclosporin A - never give (BBW says so) - renal failure; blocks T cell and IL-2 activation

Gold compounds - similar to DMARD efficacy with much higher risk toxicity

17
Q

Meds that cause SLE exacerbation

A

Sulfa antibiotics (Bactrim, sulfadiazine)

Minocycline

OCP

18
Q

Causative agents for Drug-induced Lupus

A

Procainamide

Hydralazine

Griseofulvin

Do not cause exacerbations of idiopathic lupus

19
Q

SLE therapy considerations

A

Target at the organ/system involved

Antimalarials for cutaneous and MSK w/o renal/CNS damage

-used to prevent flares

Cutaneous only = topical

Musculoskeletal only = NSAIDs

Glucocorticoids w/ significant organs

Lifelong anticoagulation (Warfarin w/ INR 2-3) if positive for antiphospholipid antibodies

MTX, Rituximab if steroid resistant

20
Q

Medications that increase uric acid production or inhibit renal excretion of uric acid

A

Thiazides

Loop diuretics

Niacin

ASA

21
Q

Allopurinol (Zyloprim)

A

DOC for gout prevention

Xanthine Oxidase Inhibitor

Goal serum urate <6 - check 2-4 wks adjustment, then q3 mo confirmation, then q6-12 mo maintenance

D/C @ first sign of rash - hypersensitivity (SJS)

-ACEI, amoxicillin, diuretics aggravate hypersensitivity

Myelosuppression high risk - use cautiously w/ other causative agents

22
Q

Probenecid

A

2nd line for gout prevention

Uricosuric Acid - blocks tubular reabsorption filtered urate to increase urinary excretion

Ineffective w/ CrCl <50

CI w/ nephrolithiasis history

Prevent stones w/ increase fluid intake and urine alkalizing agent to keep pH >6 (potassium citrate)