Rheumatology Pharm Flashcards
Bind and block promoter sites of proinflammatory genes IL-1 alpha and IL-2 beta. Decreased production of tumor necrosis factor alpha
glucocorticoids
How do glucocorticoids make us more susceptible to infection?
decreases adherence of leukocytes to vascular endothelium
What cells that are part of the immune system do glucocorticoids increase the production of from the bone marrow?
neutrophils (decreases eosinohils, monocytes, lymphocytes, APCs)
What vaccines are contraindicated in a patient receiving chronic glucocorticoid therapy?
live vaccines (MMR, varicella, small pox)
What do you periodically need to monitor for in a patient receiving glucocorticoids?
BP, glucose, lipids, eye exam, bone density
Do steroids need dose adjustments in patients who have renal impairment?
nope!
What severity level of RA would a patient who has < 5 inflamed joints, no extraarticular dz, negative RF and anti-CCP antibody, and no evidence of erosions on xray?
mildly active
Initial treatment recommendations for mild RA and negative RF with good prognostic signs
hydroxycholoraquine
In terms of general drug classes, what can be used in addition to DMARDs for short term symptom management of RA?
NSAIDs or steroids until DMARDs have taken effect
What severity level of RA would a patient who has at least 5 inflamed joints, elevated ESR/CRP, positive RF and ACCP antibody, and radiographic evidence of disease be?
moderate to severly active RA
Initial treatment choice for a patient who has moderate to severely active RA
methotrexate
Treatment options for a patient who has moderate to severely active RA who is unable to tolerate methotrexate
TNF inhibitors such as Etanercept (Enbrel) or Adalimumab (Humira)
How long does it take for maximal results of RA therapy take effect?
3-6 months
What is the role of narcotic analgesics in RA?
no role unless end stage disease
Antimalarial agent that is used as a single agent with mild RA and no evidence of joint destruction and no inflammatory/autoimmune markers on labs. Usually used as add-on to methotrexate tx.
Hydroxychloroquine (Plaquenil)
Toxicity associated with Hydroxychloroquine (Plaquenil)
macular damage. Need eye exam every 6-12 months
Drug class that Hydroxychloroquine (Plaquenil) decreases the metabolism of (ie increases half-life making it more potent)
beta blockers (except atenolol and nadolol)
Drug that inhibits angiogenesis and decreases inflammatory cytokines and IgM RF production
sulfasalazine (Azulfidine)
Needed to break down sulfasalazine into sulfapyridine and 5-aminosalicylic acid
coliform bacteria
Toxicity associated with sulfasalazine
myelosuppression. Monitor with CBC every 3 months
Most commonly used drug for RA. Reduces neutrophil adhesion. Suppression of cell mediated immunity. Inhibitis IL-1, 6, and 8
methotrexate
What is methotrexate a structural analog of and needs to be supplemented when patients are on this drug?
folic acid
What are the toxicities associated with methotrexate?
myelosuppression, hepatotoxicity, and pulmonary toxicity
Name the TNF inhibitors
etanercept (enbrel), infliximab (remicade), adalimumab (humira)
bind to tumor necrosis factor-alpha making it inactive interfering with inflammatory activity by decreasing production of IL-6 and CRP
TNF inhibitors
TNF factor associated with infusion reactions
Infliximab (Remicade)
Block box warning of TNF inhibitors
latent TB infection activation
What is used in conjunction with infliximab (remicade) to decrease the development of infliximab antibodies
methotrexate
Very expensive TNF inhibitor
Etanercept (Enbrel)
Decreases progression of joint erosions and joint space narrowing. Similar to methotrexate (inhibitor of dihydrofolate reductase) that leads to decreased B and T cell proliferation
Leflunomide (Avara)
What can reduce the extensive half-life of Leflunomide (Avara) to 1 day?
activated charcoal and cholestyramine
Blocks IL-1 receptor to decrease degree of joint destruction and inflammation. No known pharmacokinetic drug interactions
Anakinra (Kineret)
What should you not use in combination with Anakinra (Kineret)?
TNF inhibitors
Chelating agent used for treatment of
Wilson’s disease, arsenic poisoning, copper, lead and mercury poisoning. Depresses T cell activity
D-Penicillamine (Depen, Cuprimine)
Inhibits enzymatic activity required for DNA synthesis
Decrease production of T and B cells. Carcinogenic
Azithroprine (Imuran)
Blocks activation of T cells and IL-2. Many drug interactions that increase it’s concentration. Renal toxicity
Cyclosporine A (Sandimmune, Neoral)
Black box warning “Only physicians experienced in immunosuppressive therapy…”
Cyclosporine A (Sandimmune, Neoral)
Has similar efficacy but greater toxicity compared to traditional DMARDs. decreases prostaglandin production
gold compounds- Auranofin (Ridaura)
Gold Sodium Thimate (Myochrysine)
Meds to avoid with SLE that may cause an exacerbation
sulf containing abx, minocyclie, oral contracepties
work for both cutaneous and MSK involvement in SLE. may prevent renal and CNS damage
Hydroxychloroquine (Plaquenil)
Used in SLE for significant organ involvement
glucocorticoids
What should be include in pharm treatement if a patient with SLE is antiphophlipid antibody positive?
Warfarin. antiphospholipid antibody causes a hypercoaguable state
First line treatment for acute gout attack
NSAIDs- naproxen or indomethacin
Second line treatment for acute gout attack
colchicine
Pharm treatment used to prevent acute gout attacks, but are NOT initiated during an acute attack
allopurinol, febuxostat, or probenecid
Medications that cause fluid retention and exacerbate CHF
NSAIDs and glucocorticoids
NSAID that at higher doses doesn’t inrease CV risks
Naproxen
NSAID that cannot be given to patients with sulfa allergies
Celecoxib (Celebrex)
What should you give a patient having an acute gout attack who is already on chronic colchicine?
give a loading dose
Medications that increase uric acid or inhibit renal excretion of uric acid
thiazide/loop diuretics, niacin, aspirin
