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38 Cards in this Set

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