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21 Cards in this Set
- Front
- Back
Morphine
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Full opiod agonist given IV or SC
Metabolite M6G exhibits increased analgesic potency relative to morphine |
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Fentanyl
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Full opiod agonist given transdermally
-very lipophilic, very potent -short duration / fast acting -often used for outpatient procedures |
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Codeine
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Full opiod agonist
About 1/10 of the drug is converted to morphine in the liver (by cytochrome P450 enzymes). Works as an antitussive, antidiarrhea, and analgesic drug. Is often combined with acetaminophen or NSAIDs |
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Tramadol
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Full opiod agonist whose analgesic properties are partially due to inhibition of serotonin and norepinephrine reuptake.
Analgesia is not entirely reversed by naltrexone (antagonist). Side effects: fewer morphine-like side effects (e.g. respiratory depression, constipation), increased incidence of seizure, serious interactions w/ MAO inhibitors, increased risk of seizures w/ SSRIs |
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Nalbuphine
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Partial opiod agonist: agonist at kappa receptors and antagonist at m receptors
Caution use in patients with opiod dependency. |
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Naltrexone
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Antagonist at the mu opiod receptor
Can reverse full agonist adverse effects such as respiratory depression and can be used to diagnose physical dependence to opioids Has a shorter half-life than most full agonists, effects can dissipate after single administration |
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Methylnaltrexone
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Opiod antagonist incapable of penetrating BBB
Reduces peripheral full agonist side effects including nausea, vomiting, cardiovascular side effects (respiratory depression) **But leaves a portion of the analgesic property intact (unlike naltrexone)** |
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Aspirin
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NSAID; salicylate
MOA: covalently modifies COX 1 & 2 resulting in an irreversible inhibition of cyclooxygenase activity **More selective for cox-1** (but cox-2 mediates antipyretic, antiinflammatory and analgesic effects) Used for analgesia and antipyresis; lacks abuse potential of opiods and can treat neuropathic pain Need high concentrations of aspirin to treat inflammatory disorders like RA. |
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Ibuprofen
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NSAID
Greater peak effect and less GI side effects than aspirin Inhibition of platelet aggregation: inhibition of COX 1 in platelets does not always persist throughout the dosing interval (why aspirin is more cardioprotective) -however, is often used in place of chronic aspirin therapy in the treatment of inflammatory disorders |
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Contraindications to NSAID use
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Ulcers, asthma, gout, influenza, chicken pox, hypocoagulation states, heavy ethanol use, h/o hypersensitivity to any NSAIDS, pregnancy
**Use acetaminophen instead** |
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Ketorolac
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NSAID
-Potent analgesic, poor anti-inflammatory effects - effective in reducing postoperative pain after the surgical removal of impacted third molars (works on moderate to severe pain) -severe side effects (including acute renal failure) |
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Rofecoxib (Vioxx)
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Cox 2 selective drug
-effective against inflammation, pain, and fever - 50-60% decrease in serious GI complications - can result in renal complications (COX 2 is constitutive in the kidneys). -increased cardiovascular risks (inhibits prostacyclin synthesis so there is no natural inhibition of clot formation) |
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Acetaminophen
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NOT an NSAID: does not inhibit inflammation or platelet aggregation
MOA: inhibition of central COX; works strictly in the CNS as is broken down in the periphery by hydrogen peroxide Used as an analgesic and antipyretic (first line for mild/moderate pain). Adverse effects largely confined to overdose (hepatotoxicity). |
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Duloxetine
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Antidepressant
Inhibits the reuptake of NE and serotonin (typically most effective); used for neuropathic pain (especially fibromyalgia) |
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Gabapentin
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Antiseizure agent used for neuropathic pain
MOA: increases GABA levels to prolong the inactive state of voltage-dependent Na+ channels (regardless of stimulus intensity, the channel will not open – this is different from a closed state); this prevents repeated burst firing that occurs in a C fiber |
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Ketamine
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NMDA receptor antagonist
-inhibits central sensitization by decreasing calcium-mediated activation of kinase -can prevent phosphorylation of AMPA Rs (AMPA receptors underlie fast transmission of pain sensation) -reduce chronic and postoperative pain -use is limited due to psychotomimetic effects (hallucinogenic: produces dissociated general anesthetic state – will be hallucinating and immobilized) |
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Triazolam (short), alprazolam (intermediate), diazepam (long)
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Benzodiazepines (anxiolytic)
MOA: target the GABA A receptor and binds between the alpha and gamma subunits to increase the receptor's affinity for GABA (increase the frequency of the Cl channel opening) **There is no difference in peak effect among the different benzos - differences depend on half-life** Indications: tx for situational anxiety, insomnia, and generalized anxiety disorder **With benzodiazepine, you never decrease CNS function to the point of anesthesia or coma (has an upper limit) - partially because benzos can only bind to receptors with gamma subunit and depends on the presence of GABA to be effective |
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Flumazenil
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Benzodiazepine antagonist (reverses effects)
MOA: is a noncompetitive antagonist to benzos that can be administered to counteract benzo toxicity (antagonist doesn’t compete for the same binding site, so even if there is a lot of benzo around, flumazenil can still be v. effective in counteracting the effects) |
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Methohexital, phenobarbital, pentobarbital
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Barbituates
MOA: increases the activity of all GABA A receptors - binds at the barbituate site and increases the duration of the channel opening; at high doses, works independent of the presence of GABA **Greater peak effect with pentobarbital because it binds to both barbituate and GABA receptors - used as an anesthetic** **Phenobarbital is used as an anticonvulsant** Only used instead of benzos to induce a general anesthesia and for seizure tx. |
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Zolpidem, zaleplon
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Non-benzodiazepine hypnotics
Indications: insomnia -Exhibit affinity for the a1 containing GABA A receptors - Increases sleep time w/o altering REM sleep -more restricted effect than benzodiazepines; effects reversed by flumazenil SE: amnesia, hallucinations, delusions, euphoria (but avoid homeostatic changes that cause physical dependency = less abuse potential) |
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Buspirone
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5-HT1A partial agonist
MOA: Inhibits firing of 5-HT neurons (agonist at the autoreceptors = less release of serotonin) Indications: situational anxiety, generalized anxiety disorder **Effects take ~2 weeks to emerge** |