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73 Cards in this Set

  • Front
  • Back
MOA of NSAIDs
Inhibit prostaglandin synthesis by inhibiting cyclooxygenase
Four main actions of NSAIDs
Antiinflammatory
Analgesia
Antipyretic
Antiplatelet
Agent used for closure of patent ductus arteriosus
Indomethacin
Aspirin is contraindicated in children with viral infection
Potential development of Reye's Syndrome
SE of Salicyclates
Tinnitus
GI Bleeding


hypersens from ↑LTs
↑bleeding
Metabolic Acidosis
UNCOUPLERS
NSAID also available as an opthalmic preparation
Diclofenac
Ketoralac
NSAID available orally, IM, and opthalmically
Ketoralac
NSAID that is used for acute condition, such as pre-op anesthesia and has limited duration (<5 days) of use due to nephrotoxicity
Ketoralac
Newer NSAID that selectively inhibits COX-2
Celecoxib
COX2 inhibitors may have reduced risk of
Gastric Ulcers
GI Bleeds
COX2 inhibitors should be used cautiously in patients with
preexisting cardiac or renal disease
Acetaminophen only has
Antipyretic and analgesic activity
SE of Acetaminophen
Hepatotoxicity
Antidote for acetaminophen toxicity
N-acetylcysteine
DMARDs are slow acting drugs for
Rheumatic Disease
Initial DMARD of choice for patients with RA
Methotrexate
Drug often used in combination with TNF-α inhibitors in RA
Methotrexate
Causes BMS
Methotrexate
SE of Penicillamine
Aplastic anemia and renal toxicity
Inferferes with activity of T lymphocytes
Hydroxychloroquine
Anti-malarial drug used in RA
Hydroxychloroquine
SE of Hydroxychloroquine
Retinal destruction and dermatitis
MOA of Leflunomide (newer DMARD)
Inhibiting dihydroorotate dehydrogenase which leads to decreased pyrimidine synthesis, decreased T cell proliferation and decreased antibody production by B cells
Proteins that prevent action of TNFα
Adalimumab
*Infliximab
*Etanercept
Anti-RA drug also used in Ulcerative Colitis
Sulfasalazine
Anti-RA agent also used in Chron's Disease
Infliximab
NSAID used in Gout
Indomethacin
NSAID contraindicated in Gout
Aspirin
MOA of Colchicine (used in Acute Gout)
selective inhibitor of microtubule assembly (M phase)
SE of Colchicine
Kidney and Liver toxicity
Diarrhea
Agent used to treat Chronic Gout by increasing Uric Acid secretion and excretion
Probenecid
Sulfinpyrazone
Allopurinol treats Chronic Gout by decreasing uric acid production by inhibiting
Xanthine Oxidase
Agent used to treat Chronic Gout by increasing Uric Acid secretion and excretion
Probenecid
Sulfinpyrazone
Allopurinol treats Chronic Gout by decreasing uric acid production by inhibiting
Xanthine Oxidase
What reaction do NSAIDs inhibit?
Conversion of Arachidonic Acid to PGs/TxA2/Prostacyclin
NSAID with greatest antiinflammatory effect
Indomethacin
NSAID used for analgesic effects during surgergy
Ketorolac
Only NSAID which can be administered parenterally
Ketorolac
Primary location of COX2 expression
Inflammatory cells, CNS
What is the reasoning behind aspirins strong antiplatelet effects
irreversible inhibition leads to longer inhibition of platelets

with half-life of ~10 days, reasoning why aspirin is discontinued 10 days before surgergy
Effects of aspirin at low dose (<300)
Antiplatelet
Effects of Aspirin at intermediate dose (>300-2400)
Antipyretic
Analgesic
Effects of Aspirin at high dose
Anti-inflammatory
DOC closure of PDA
Indomethacin
DOC maintaining PDA
Alprostadil (Prostacyclin/PGI2 analog)
PGI2(Prostacyclin) antidote to NSAID ulcer
Misoprostol
Elimination of aspirin at low dose
2-5 hours, first order kinetics
Elimination of aspirin at high dose
15 hours, zero order kinetics
Acidosis/Alkalosis progression of Aspirin in toxicity
First causes Respiratory Alkalosis then leads to metabolic acidosis
Contraindication to Celecoxib (COX2)

Why?
thrombosis (MI, stroke risks)

greater inhibition of prostacyclin formation than on thromboxane
Only OTC ANALGESIC commonly available in the US
Acetaminophen
Acetaminophen effects are similar to what aspirin dose
Intermediate

antipyretic and analgesic
Antidote to Acetaminophen toxicity
N-acetylcysteine
Onset of action of DMARDs
6 weeks to 6 months
#1 RA drug
Methotrexate
MOA infliximab
binds to TNF, inhibiting its action

given by injection
MOA Etanercept
TNF receptor analog, TNF binding to etanercept decreases binding to TNF receptors of body

given by injection
MOA Anakinra
IL-1 receptor anatagonist
MOA Hydroxychloroquine
interference of T lymphocyte activity
function of LTB4
chemotaxis of neutrophils and macrophages

involved in acute inflammation
function of LTC/D/E4
SRSA (slow reacting substance of anaphylaxis)

alteration of permeability
bronchoconstriction
increased secretion
=asthma
Where is Uric Acid normally reabsorbed
In proximal tubules by a general weak acid reabsorption channel
MOA of probenecid and sulfinpyrazone
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
Why is aspirin contraindicated in Gout
as a weak acid competatively competes with uric acid for secretion, can lead to ↑serum concentration
Drugs used in ACUTE Gout
Colchicine (toxicity is severe diarrhea)
Indomethacin
Drugs used in Chronic Gout
Probenecid
Sulfinpyrazone
Allopurinol
Febuxostat
MOA Allopurinol
Suicide inhibitor of Xanthine Oxidase
Allopurinol potentially causes increased serum levels of what anticancer drugs
6-MP
Azathioprine
cause of Reye's Syndrome in child with viral infection
Aspirin
Chronic toxicity of aspirin
Acute Renal Failure
Interstitial Nephritis
Upper GI bleeds
Clinical benefit of COX2 selectives (Celecoxib)
Decreased risk of GI bleeds
Mechanism of Acetaminophen toxicity?
Depletion of Phase II reactants (Glutathione) leading to formation of toxic tissue adducts
Anti-TNF ABs
Infliximab
Adalimumab