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42 Cards in this Set
- Front
- Back
Prototypical opioid?
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Morphine
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Uses other than analgesia for opioids?
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1) Cough suppressant
2) Component of anesthesia 3) Decreases GI motility 4) Adjunct to pulmonary edema 5) Drug abuse |
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3 Major type of opiod receptors?
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1) Mu
2) Kappa 3) Delta |
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Mu opioid
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1) Strongest analgesic
2) Most and most severe sideE 3) Resp. depression, constipation, increased risk |
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Side effects of Mu opioids
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Resp. depression, Constipation, Highest risk of dependence
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Kappa opiod
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Analgesia, sedation, psychotropic
Less likely to have as severe SE as Mu |
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Delta opiod
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Analgesic, SideE are least severe.
No risk for resp. depression, no psychotropic effects |
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Describe a Mixed opioid
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Opioid is agonist to 1 or more receptor and antagonist to others.
i.e, Agonist = kappa; antagonist = Mu |
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Opiod mechanism?
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Binds to opioid G-coupled protein receptor
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Opioids affect on presynpatic transmission of pain?
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G-proteins inhibit the release of Ca++ and cAMP release this causes less neurotransmitter release
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Opioid's effect on postsynaptic neuron?
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The G-proteins create an outflux of K+ which causes hyperpolarization making it more difficult of a synapse to occur.
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A way that opiods can alter descending pathways?
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Via disinhibition. The G-protein coupled receptors disinhibit descending pain control pathways.
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Mild-to-moderate agonist (i.e. codeine)
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Works for all receptors but has a lower affinity -> lower efficacy
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Which opioid receptors lead to possible CV problems?
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All
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Define tolerance
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Requires a greater dose for the same functional effect
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Opioid withdrawal symptoms?
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Flu-like symptoms, irritability, insomnia, tachycardia, uncontrollable yawning, muscle aches
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Methadone
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Strong opioid agonist used to taper for addicts
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Buprenex
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Buprenophine. A mixed agonist-antagonist - partial Mu agonist and Kappa antagonist.
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Prototypical NSAID?
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Aspirin
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Uses/Effects of NSAIDS?
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1) Decreased inflammation
2) Analgesic 3) Decreased fever (antipyretic) 4) Anticoagulant |
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Mechanism of NSAIDS?
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Anti-inflammatory/analgesic d/t inhibition of eicosanoid synthesis
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3 Eicosanoids?
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Porstaglandins, Thrombaxanes, Leuokotrienes
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Prostaglandin
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Endogenous lipidlike compound that is pro-inflammatory
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Thrombaxane
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Vasoconstriction & Platelet aggregation
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Leukotrienes
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Pro-inflammatory (esp. in air way)
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Function (PGs &TXs)
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Cause inflammation, pain, fever, menstral problems, clots.
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Brief description of how PGs and TXs are formed?
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Arachadonic acids (phospholipase) -> COX (cycloxagenase) -> Variety of PGs and TXs
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Which pathway formed from arachadonic acid creates leukotrienes?
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The LOX pathway (lipoxygenase)
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Which two eicosanoids are inhibited with NSAIDS?
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PGs and TXs
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Which COX is normally produced in our bodies?
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COX-1
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Why do NSAIDS cause GI disturbances?
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b/c NSAIDS often inhibit COX-1s and COX-1s help supply the protective lining to our GI tract
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Two conditions that ASA may cause Renal and/or liver problems?
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1) Pre-existing disease
2) decreased body water |
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signs/symptoms of ASA OD?
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HAs, decreased hearing, confusion, GI distress, possible metabolic acidosis & dehydration
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What can induce Reye syndrome?
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Adversion to ASA in children. The children can be intolerant (supersensitive) to the drug. Usually onsets after flu or chicken pox.
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Adverse effects of celebrex?
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1) MI
2) Stroke |
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Why are COX-2 inhibitors potentially very harmful?
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Because the cause a shift that favors increased platelet aggregation which increases the pt's risk of clotting.
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Popular analgesic OTC that is not an NSAIDS?
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Acetaminophen (Tylenol/Excedrin)
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Anti-inflammatory effects of acetaminophen?
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There are none
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Risk of high doses of acetaminophen?
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Liver toxicity
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Mechanism of acetaminophen?
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Inhibits COX, probably inhibits PGs may preferentially inhibit CNS PGs (COX-3?)
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What is odd about the pharmacokinetics of ASA?
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1) Most is bound to plasma proteins
2) Unbound drug is hydrolyzed in the blood and not the liver |
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Which chemical in the breakdown of acetaminophen is responsible for liver toxicity?
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NAPQI (must be conjugated for detoxification and excretion).
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