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| ester enzyme (breaks down esters at a slower rate than the normal esterase) --caused by idiosyncracy |
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| causes muscle contractions (can be broken down by cholinesterase) |
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| cytochrome in liver the metabolizes drugs including amides |
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| vasoconstrictor dependent on alpha receptors |
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| vasoconstrictor dependent on alpha receptors |
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| vasoconstrictor dependent on alpha receptors |
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| vasoconstrictor independent of alpha receptors |
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| preservative used with local anesthetics that causes hypersensitivity cases |
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| prilocaine, lidocaine, benzocaine (3 local anesthetics that have metabolites to cause...) |
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| only inhalation agent that is a weak anesthetic GAS |
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| volatile liquids used as inhalation agents for general anesthesia |
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| only effective drug that "uncouples" activation of nicotinic receptors releasing calcium ions --> used in hyperthermic patients (adverse idiosyncric effect of general anesthesia) acting on the RYANADINE receptor |
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| representative IV agent that enhances inhibitory GABA neurotransmission (general anesthesia) |
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| thiopental drug (enhances inhibitory GABA) |
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| thiopental drug (enhances inhibitory GABA) |
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| thiopental drug (enhances inhibitory GABA) |
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| thiopental drug (enhances inhibitory GABA) |
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| IV agent that inhibits excitatory NMDA neurotransmission (structurally related to phencyclidine) - used to be an IV anesthetic but causes hallucination in patients over 16 years old |
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| neuroleptanalgesia.Synergistic effect. Effects include psychic indifference to pain, potential for cardiovascular or respiratory depression |
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| agonist at opioid receptor (g protein-coupled opioid receptors resulting in changes of enzymatic activity --> inhibition of adenylyl cyclase, reduction of neurotransmitter release), decrease sodium, calcium influx, increase potassium efflux |
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| antagonist of the opioid receptor ligands. Used for patients who have had too much morphine. |
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| the naloxone will block opioid effects and it will act as a cough suppressant |
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| antitussive non-analgesis analog of levorphanol |
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| morphine antidote (like naloxone but lasts several hours) |
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| opium alkaloids, most notably the phenanthrenes |
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| morphine (standard narcotic analgesic), codeine (mainly antitussive and weak analgesic) |
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| semisynthetic opiate drugs- all phenanthrenes |
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| hydromorphone, oxymorphone, hydrocodone, oxycodone, diacetylmorphine or heroin |
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| Diacetylmorphine or heroin |
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Phenylheptylamines: Methadone, Levomethadyl
Phenylpiperidine: meperidine, fentanyl, alfentanil,sufentanil,carfentanil |
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| 8,0000 x morphine potency |
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| brain and spinal cord neurotransmitter; also released from adrenalal medulla as a hormone. mainly at mu and delta opioid receptors |
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| neurotransmitter; also released from adrenal medulla as a hormone. mainly at mu and delta opioid receptors |
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| brain and spinal cord neurotransmitter; also released from adrenal medulla as a hormone. mainly at mu and epsilon opioid receptors |
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| brain and spinal cord neurotransmitter, almost exclusively at kappa opioid receptors. Only one has predominant action on kappa receptors |
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| endomorphin-1 and endomorphin-1 (only 4 AA long) |
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| endomorphin-1 and endomorphin-2 |
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| brain neurotransmitter; almost exclusively at mu opioid receptors |
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| for morphine and most clinical narcotic analgesics; thought to produce the strongest analgesic |
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| for mixed agonist-antagonists |
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| under development, but analgesic properties generally equal to morphine |
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| buprenorphine (suboxone with naloxone) |
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| mu antagonist, kappa agonist |
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| mu antagonist, kappa agonist |
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| mu antagonist, kappa agonist |
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| ergot-derived prophylactic agent (blockade of cerebral vascular 5HT2a and/or 5HT2c receptors to prevent initial 5HT-induced vasoconstriction and prevent onset of migraine attack |
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| Ergotamine, ergotamine plus caffeine |
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| nonspecific vascular smooth muscle stimulation to reverse reactive vasodilation |
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| Sumatriptan, rizatripan, eletriptan |
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| stimulation of 5HT1b and/or 5HT1d receptors --> vasoconstriction |
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| neurochemicals in the ascending reticular activating system |
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| norepinephrine, dopamine, acetylcholine, histamine, serotonin, GABA |
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| activated barbiturate receptors |
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| lowers the threshold for the GABA receptor to be turned on. prolong the duration that the chloride gate is opened for chloride ion influx |
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| activated benzodiazepine receptors |
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| sensitizes the GABA receptor. causes the chloride gate to open more frequently for chloride ion influx. |
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| ultrashort-acting (thio) barbiturates-- physical redistribution to fat and skeletal muscle |
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| secobarbital, pentobarbital, amobarbital |
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| short to intermediate acting (oxy) barbiturates-- 100% hepatic metabolism) |
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| long-acting (oxy) barbiturate-- 2/3 metabolized, 1/3 excreted unchanged |
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| Uses of ultrashort-acting barbiturates |
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| intravenous general anesthetics |
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| uses of short to intermediate acting barbiturates |
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| uses of long-acting barbiturates |
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| barbiturates, alcohol, and carbamenzapine decreases the effects of these drugs |
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| warfarin, chloramphenical, morphine, and oral contraceptives |
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| benzodiazepine used for hypnosis, short acting, no hang-over or sleepniness the next day |
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| benzodiazepine used for hypnosis, short acting, no hang-over or sleepniness the next day |
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| benzodiazepine used for hypnosis, short acting, no hang-over or sleepniness the next day |
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| benzodiazepine used for hypnosis, short acting, no hang-over or sleepniness the next day |
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| reverses benzodiazepine intoxication, affinity but no efficacy |
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| agonist at melatonin MT1 and MT2 receptors in the suprachiasmatic nucleus, only non-scheduled prescription drug in the US to be used to treat insomnia |
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| facilitates inhibotry GABAa neurotransmission (spasmolytic drugs) |
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| facilitates inhibotry GABAa neurotransmission (spasmolytic drugs) |
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| facilitates inhibotry GABAa neurotransmission (spasmolytic drugs) |
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| facilitates inhibotry GABAa neurotransmission (spasmolytic drugs) |
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| stimulate inhibotry GABAb receptors |
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| facilitate inhibitory alpha2 adrenergic neurotransmission |
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| peripherally acting muscle relaxant (also used for malignant hyperthermia) |
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| acetaldehyde dehydrogenase inhibitor (used in aversion therapy for alcoholics) |
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| Other drugs with disulfiram like action: |
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| griseofulvin, metronidazole, sulfonylureas |
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| thiamine (Vitamine B1) deficiency causes 2 types of alcoholic dementia: |
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| Wernicke's encephalopathy (neurological disturbance) and Korsakoff's psychosis (mental disturbance) |
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| reduces excitation of neurons that mediate alcohol withdrawal |
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| blocks opioid receptors in reward circuit (treatment of alcoholism) |
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| restores balances between glutamate and GABA by either blocking NMDA receptors or activating GABA receptors (treatment of alcoholism |
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| primary excitatory transmitter |
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| primary inhibitory transmitter |
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| treatment of tonic-clonic or psychomotor epilepsies. interferes with electrical activity in epilepsy |
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| treatment of psychomotor epilepsy |
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| prodrug for phenobarbital. treatment of psychomotor and tonic-clonic epilepsies |
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| treament of absence and myoclonic epilepsies (clonazepam); emergency treatment of status epilepticus (diazepam) |
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| hepatic metabolism decreased by: |
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| valproic acid, propranolol |
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| hepatic metabolism of oxidized benzodiazepines decreased by: |
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| estrogen-dominant oral contraceptics |
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| hepatic metabolism of glucuronidation of conjugated benzodiazepines increased by: |
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| treatment of psychomotor and tonic-clonic epilepsies; treatment of trigeminal and facial neuralgias |
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| treatment of psychomotor, tonic-clonic, absence and myoclonic epilepsies |
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| ethosuximide, trimethadione |
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| treatment of petit mal epilepsy |
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| centrally acting GABA agonists (anticonvulsant) |
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| positive modulator of GABAa receptors; possibly blocker of NMDA receptors (anticonvulsant |
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| inhibitor of GABA reuptake into neurons and glial cells (anticonvulsant) |
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| sodium channel blocker but may also block voltage-activated calcium channels (anticonvulsant) |
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| inhibit spread of electrical activity by unknown mechanism |
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