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38 Cards in this Set
- Front
- Back
What is the significance of anesthetics with decreased solubility in blood?
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rapid induction and recovery times . Ie. N20
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What is the significance of anesthetics with increased solubility in lipids?
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increased potency = I/ MAC. Ie. Halothane
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Inhaled Anesthetics list them
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halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide
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Inhaled Anesthetics What is good about lower solubility?
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the quicker the anesthetic response, and the quicker the recovery
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Inhaled Anesthetics What are these drug's effects?
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myocardial depression, respiratory depression, nausea/emesis, increase cerebral blood flow
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What toxicity mactches the following drugs 1. Halothane 2. Methoxyflurane 3. Enflurane 4. Rare
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1. Hepatotoxcity 2. Nephrotoxicty 3. Proconvulsant 4. Malignant hyperthermia
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What do barbituates, benzodiazepines, arylcyclohexylamines and narcotic analgesics have in common?
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they are IV anesthetics
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What the pharmacokinetics and uses of thiopental?
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high lipid solubility, rapid entry into brain. Used for induction of anesthesia for short surgical procedures. Terminated by redistribution from brain. Decreased cerebral blood flow
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Give an example of a benzo and what is this class's shortcoming?
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midazolam used for endoscopy. Used with gaseous anesthetics and narcotics. May cause severe post-op respiratory depressio and amnesia
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What does Ketamine (PCP analog and an arylcyclohexylamine) do?
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dissociative anesthetic. Cardiovascular stimulant. Causes disorientation, hallucination, bad dreams. Increases cerebral blood flow.
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How are narcotic analgesics used? Examples?
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Morphone and fentanyl are used with CNS depressant during general anesthesia.
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What is the advantage of propofol
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used for rapid anesthesia induction and short procedures. Less post-op nausea than thiopental
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Local anesthetics Name some esters?
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procaine, cocaine, tetracaine,
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Local anesthetics Name some amides?
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lidocaine, bupivacaine, (amides have two I's in name!)
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Local anesthetics What is the mechanism and clinical use?
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bind receptor and block Na channels. Tertiary amine local anesthetics penetrate membrane in uncharge form, then bind charged form. Use for minor surgical procedures, spinal anesthesia.
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Local anesthetics How do you decide to use ester or amides?
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if allergic to esters, give amides
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Local anesthetics what is the toxicity
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CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, arrhythmias (cocaine)
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Local anesthetics In infected ________ tissue, anesthetics are charged and cannot penetrate membrane. Therefore, ______ anesthetics are needed.
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acidic; more
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Local anesthetics What is the order of nerve blockade for size and myelination? Which factor predominates?
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small diameter> large diameter. Myelinated fibers> unmyelinated fibers. Size factor predominates
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Local anesthetics what is the order of loss of sensation?
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pain first, then temp, then touch, then pressure
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Local anesthetics Why would you give these drugs with vasoconstrictors?
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to enhance local action
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Opiod analgesics List as many as you can.
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morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan
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Opiod analgesics Mechanism: They act as _____ for opiod receptors to modulate synaptic transmission
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agonists
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Opiod analgesics which drugs act at the mu, delta, kappa receptors?
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morphine enkephalin, dynorphin
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Opiod analgesics Clinical use?
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pain, cough supression (dex), diarrhea (loperamide), acute pulmonary edema, methadone maintenance programs
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Opiod analgesics What are the major toxicities?
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addiction, respiratory depression, constipation, miosis, additive CNS depression wth other drugs
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Opiod analgesics Tolerance does not develop to __________and ______
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miosis and constipation
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Opiod analgesics How would you treat toxicity?
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naloxone, naltrexone (opiod R antagonist)
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List three nonaspirin nonselective NSAIDS?
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ibuprofen, naproxen, indomethacin
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What is the mechanism of nonselective NSAIDs?
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reversibly inhibit COX 1 and 2. Blocks PG synthesis
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What are nonselective NSAID clinical use (3As)?
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Antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a PDA.
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What are common NSAID toxicities?
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renal damage, aplastic anemia, GI distress, ulcers
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Where is cox2 found?
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in inflammatory cells and mediates inflammation and pain
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Why is cox2 inhibition better than cox1?
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cox1 helps to maintain gastric mucosa, thus, should not have the corrosive effects of other NSAIDs on the GI lining (less incidence of ulcers and bleeding)
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Clinical Use of cox2 inhibitors?
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RA and osteoarthritis
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Acetaminophen What is its mechanism and where does it work?
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reversibly inhibits cox, mostly in CNS. Inactivated peripherally.
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Acetaminophen What are its 2 As?
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antipyretic, analgesic but NOT anti-inflammatory.
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Acetaminophen Overdose effects?
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hepatic necrosis, acetaminophen metabolites depletes glutathine and forms toxic tissue adducts in the liver
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