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73 Cards in this Set
- Front
- Back
MOA of NSAIDs
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Inhibit prostaglandin synthesis by inhibiting cyclooxygenase
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Four main actions of NSAIDs
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Antiinflammatory
Analgesia Antipyretic Antiplatelet |
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Agent used for closure of patent ductus arteriosus
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Indomethacin
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Aspirin is contraindicated in children with viral infection
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Potential development of Reye's Syndrome
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SE of Salicyclates
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Tinnitus
GI Bleeding hypersens from ↑LTs ↑bleeding Metabolic Acidosis UNCOUPLERS |
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NSAID also available as an opthalmic preparation
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Diclofenac
Ketoralac |
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NSAID available orally, IM, and opthalmically
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Ketoralac
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NSAID that is used for acute condition, such as pre-op anesthesia and has limited duration (<5 days) of use due to nephrotoxicity
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Ketoralac
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Newer NSAID that selectively inhibits COX-2
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Celecoxib
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COX2 inhibitors may have reduced risk of
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Gastric Ulcers
GI Bleeds |
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COX2 inhibitors should be used cautiously in patients with
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preexisting cardiac or renal disease
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Acetaminophen only has
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Antipyretic and analgesic activity
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SE of Acetaminophen
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Hepatotoxicity
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Antidote for acetaminophen toxicity
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N-acetylcysteine
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DMARDs are slow acting drugs for
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Rheumatic Disease
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Initial DMARD of choice for patients with RA
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Methotrexate
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Drug often used in combination with TNF-α inhibitors in RA
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Methotrexate
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Causes BMS
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Methotrexate
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SE of Penicillamine
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Aplastic anemia and renal toxicity
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Inferferes with activity of T lymphocytes
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Hydroxychloroquine
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Anti-malarial drug used in RA
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Hydroxychloroquine
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SE of Hydroxychloroquine
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Retinal destruction and dermatitis
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MOA of Leflunomide (newer DMARD)
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Inhibiting dihydroorotate dehydrogenase which leads to decreased pyrimidine synthesis, decreased T cell proliferation and decreased antibody production by B cells
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Proteins that prevent action of TNFα
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Adalimumab
*Infliximab *Etanercept |
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Anti-RA drug also used in Ulcerative Colitis
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Sulfasalazine
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Anti-RA agent also used in Chron's Disease
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Infliximab
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NSAID used in Gout
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Indomethacin
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NSAID contraindicated in Gout
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Aspirin
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MOA of Colchicine (used in Acute Gout)
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selective inhibitor of microtubule assembly (M phase)
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SE of Colchicine
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Kidney and Liver toxicity
Diarrhea |
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Agent used to treat Chronic Gout by increasing Uric Acid secretion and excretion
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Probenecid
Sulfinpyrazone |
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Allopurinol treats Chronic Gout by decreasing uric acid production by inhibiting
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Xanthine Oxidase
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Agent used to treat Chronic Gout by increasing Uric Acid secretion and excretion
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Probenecid
Sulfinpyrazone |
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Allopurinol treats Chronic Gout by decreasing uric acid production by inhibiting
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Xanthine Oxidase
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What reaction do NSAIDs inhibit?
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Conversion of Arachidonic Acid to PGs/TxA2/Prostacyclin
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NSAID with greatest antiinflammatory effect
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Indomethacin
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NSAID used for analgesic effects during surgergy
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Ketorolac
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Only NSAID which can be administered parenterally
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Ketorolac
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Primary location of COX2 expression
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Inflammatory cells, CNS
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What is the reasoning behind aspirins strong antiplatelet effects
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irreversible inhibition leads to longer inhibition of platelets
with half-life of ~10 days, reasoning why aspirin is discontinued 10 days before surgergy |
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Effects of aspirin at low dose (<300)
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Antiplatelet
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Effects of Aspirin at intermediate dose (>300-2400)
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Antipyretic
Analgesic |
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Effects of Aspirin at high dose
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Anti-inflammatory
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DOC closure of PDA
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Indomethacin
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DOC maintaining PDA
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Alprostadil (Prostacyclin/PGI2 analog)
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PGI2(Prostacyclin) antidote to NSAID ulcer
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Misoprostol
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Elimination of aspirin at low dose
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2-5 hours, first order kinetics
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Elimination of aspirin at high dose
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15 hours, zero order kinetics
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Acidosis/Alkalosis progression of Aspirin in toxicity
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First causes Respiratory Alkalosis then leads to metabolic acidosis
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Contraindication to Celecoxib (COX2)
Why? |
thrombosis (MI, stroke risks)
greater inhibition of prostacyclin formation than on thromboxane |
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Only OTC ANALGESIC commonly available in the US
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Acetaminophen
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Acetaminophen effects are similar to what aspirin dose
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Intermediate
antipyretic and analgesic |
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Antidote to Acetaminophen toxicity
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N-acetylcysteine
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Onset of action of DMARDs
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6 weeks to 6 months
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#1 RA drug
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Methotrexate
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MOA infliximab
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binds to TNF, inhibiting its action
given by injection |
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MOA Etanercept
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TNF receptor analog, TNF binding to etanercept decreases binding to TNF receptors of body
given by injection |
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MOA Anakinra
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IL-1 receptor anatagonist
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MOA Hydroxychloroquine
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interference of T lymphocyte activity
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function of LTB4
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chemotaxis of neutrophils and macrophages
involved in acute inflammation |
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function of LTC/D/E4
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SRSA (slow reacting substance of anaphylaxis)
alteration of permeability bronchoconstriction increased secretion =asthma |
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Where is Uric Acid normally reabsorbed
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In proximal tubules by a general weak acid reabsorption channel
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MOA of probenecid and sulfinpyrazone
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weak acids which competatively compete with uric acid for absoprtion
in early phase can cause increased in uric acid by competing for secretion cause decreased secretion of many other weak acids |
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Why is aspirin contraindicated in Gout
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as a weak acid competatively competes with uric acid for secretion, can lead to ↑serum concentration
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Drugs used in ACUTE Gout
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Colchicine (toxicity is severe diarrhea)
Indomethacin |
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Drugs used in Chronic Gout
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Probenecid
Sulfinpyrazone Allopurinol Febuxostat |
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MOA Allopurinol
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Suicide inhibitor of Xanthine Oxidase
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Allopurinol potentially causes increased serum levels of what anticancer drugs
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6-MP
Azathioprine |
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cause of Reye's Syndrome in child with viral infection
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Aspirin
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Chronic toxicity of aspirin
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Acute Renal Failure
Interstitial Nephritis Upper GI bleeds |
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Clinical benefit of COX2 selectives (Celecoxib)
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Decreased risk of GI bleeds
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Mechanism of Acetaminophen toxicity?
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Depletion of Phase II reactants (Glutathione) leading to formation of toxic tissue adducts
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Anti-TNF ABs
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Infliximab
Adalimumab |