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64 Cards in this Set
- Front
- Back
- 3rd side (hint)
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non-selective adrenergic agonist
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- epinepherine
- phenylpropanolamine |
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some alpha and beta adrenergic agonist
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- dopamine - alpha 1, beta 1, dopamine receptor
- dobutamine - alpha 1, beta 1, beta 2 (beta 1 is primary effect) |
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alpha-1 selective adrenergic agonist
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- phenylephrine
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beta selective adrenergic agonist
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- isoproteronol
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beta-2 selective adrenergic agonist
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- albuterol
- clenbuterol (do not use in food animal - ever) |
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general alpha/beta effector organ responses
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- heart excitation
- inhibit GI - decrease secretions - relaxation of GI/gallbladder - inhibit mucus glands - urine retention - epi release > NE release |
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general alpha effector organ responses
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- contract GI sphincters
- contract urinary sphincter - contract splenic capsule - contract piloerector muscles - ejaculation - decrease pancreatic acinar secretions |
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alpha 1 effector organ responses
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- vasoconstriction
- mydriasis - scant viscous saliva - contraction of uterus |
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alpha 2 effector organ responses
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- vasodilation of blood vessels to endothelium
- decrease kidney renin release - decrease pancreatic islet cell secretions - decrease NE release - platelet aggregation |
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beta 1 effector organ responses
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- increase HR/contractility
- relax GI smooth muscle - relax urinary fundus - increase renin release - lipolysis |
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beta 2 effector organ responses
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- vasodilation to smooth muscle, brain, kidney, heart
- bronchodilation - relax splenic capsule - glycogenolysis - gluconeogenesis - increased NE release |
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adrenergic agonists
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- epinephrine
- phenylpropanolamine - dopamine - dobutamine - phenylephrine - isoproteronol - albuterol - clenbuterol |
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adrenergic antagonists
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- carvedilol
- phenoxybenzamine - propanolol - timolol - atenolol |
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some alpha and beta adrenergic antagonists
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- carvedilol - alpha 1, beta 1 and beta 2 (counteracts dobutamine)
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alpha selective adrenergic antagonist
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- phenoxybenzamine
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beta selective adrenergic antagonist
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- propanolol
- timolol |
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beta 1 selective adrenergic antagonist
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- atenolol
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cholinergic agonist mechanism
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- direct - bind to receptor and illicit an action
- indirect - interact with acetylcholinesterase to increase concentrations of acetylcholine = less specific so result in inceased side effects |
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cholinergic direct acting drugs
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- muscarinic only
- bethanecol - pilocarpine |
- muscarinic and nicotinic
- carbachol |
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cholinergic indirect acting drugs
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- all muscarinic and nicotinic
- physostigmine - neostigmine - edrophonium - pyridostigmine - organophosphates - irreversible! atropine is antidote |
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muscarinic effector organ responses
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- gereral inhibition of heart
- vasodilation - excitation of GI tract - bronchoconstriction - miosis - urination (contract detrussor mm., relax sphincter) - contract uterus - erection - increase pancreatic secretions - SLUDD |
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nicotinic effector organ response
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- ganglionic transmission
- muscle fasiculations - tremors leading to muscle paralysis |
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cholinergic antagonist mechanism
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- competitively prevent action of acetylcholine at muscarinic receptors
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cholinergic antagonist drugs
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- muscarinic antagonists
-atropine (increase HR, decrease secretions/GI motility, bronchodilation, decrease bladder contractions) - glycopyrrolate (decrease secretions/GI motility without cardiovascular effects) |
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local anesthetics mechanism
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- interact with sodium channels to decrease permeabiliity of excited cell membranes to sodium ions = blocks sodium channles to stop nerve conduction
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local anesthetics metabolism
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- amides = first step is biotransfermation by the liver
- aminoesters = hydolysis of ester link by plasma esterases |
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local anesthetics toxicity
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- neurotoxicity = dose related
- muscle twitching - convulsions - CNS depression and death |
- cardiotoxicity
- hypotension - dysrhythmias |
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local anesthetics drugs
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- amides
- lidocaine - mepivicaine - only parentally admin local anesthetic FDA approved in horses - bupivacaine |
- aminoesters
- benzocaine - proparacaine - approved for use in animals |
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neuromuscular blockers mechanism
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- competitive (non-depolarizing) - bind to or interlock with Ach receptors, preventing transmitter fxn of Ach
- no depolarizing activity - no end plate potential = no muscle contraction because sodium doesn't enter cell |
- depolarizing - binds to receptor and allows influx of sodium causing depolarization of end plate
- does not allow subsynaptic membrane to completely repolarize - remains bound to receptor and renders motor end plate non-responsive - length of action depends on amount of plasma cholinersterases because is metabolized by them = muscle contraction then paralysis |
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neuromuscular blockers elimination
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- liver metabolism and renal clearance
- vecuronium - pancuronium - kindey and liver disease will increase duration of these drugs |
- hydrolysis by plasma cholinesterases
- atracurium (spontaneous degradation) - succinylcholine |
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neuromuscular blocker drugs
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- competitive (non-depolarizing)
- atracurium - vecuronium - pancuronium |
- depolarizing
- succinylcholine |
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effect of cholinesterase inhibitor
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- non-depolarizing
- reverse (becasue competitive) - increases Ach |
- depolarizing
- enhanced (blocks metabolism of drug) |
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reversal agent
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- non-depolarizing
- cholinesterase inhibitor (neostigmine) |
- depolarizing
- none |
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initial agent
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- non-depolarizing
- absent |
- depolarizing
- present |
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analgesic
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- non-depolarizing
- no |
- depolarizing
- no |
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opioids mechanism
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- mu and kappa receptor agonists and antagonists
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opioids actions at receptors
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- analgesia = all
- increase appetite = all - decrease GI motility = mu/kappa - sedation = mu/kappa - miosis/mydriasis = mu/kappa - immunomodulaiton = mu/kappa - euphoria = mu - antidiuresis = mu - decrease urine voiding reflex = mu - decrease uterine contractions = mu - respiratory depression = mu - nausea/vomiting/decrease biliary secretions = mu - diuresis (decrease ADH release) = kappa |
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opioids uses
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- decrease diarrhea
- antitussive (cough suppressor) - analgesia - sedation - calming/euphoria - immobilization/chemical restraint - inhibit GI motility - increase locomotor activity |
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opioids common adverse effects
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- respiratory depression
- nausea - vomiting - dysphoria - CNS excitation - dependence - decreased urination - hypotension |
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opioid agonists
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- mu agonsits
- morphine - hydromorphine - codeine - rarely used in vet medicine; less potent - fentaanyl - buprenorphine - partial (kappa antagonist) -tramadol (also muscarinic antagonist; alpha-2 agonist; 5-HT agonist) |
- kappa agonist
- butorphanol - also partial mu agonist - nalbuphine - also partial antagonist of mu |
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opioid antagonists
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- naloxone - all receptors (partial mu)
- natrexone - partial at all receptors |
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anticonvulsant uses and mechanisms
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- uses
- stop/prevent seizures, epilepsy and status epilepticus |
- mechanisms
- increase inhibitory NT (GABA) - decrease excitatory NT (less common) - alter electrolyte conductance |
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anticonvulsant GABA agonist
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- increase flow of chloride into cell
- phenobarbital - diazepam - clonazepam - more potent and less toxic than diazepam - clorazepate - pentobarbital - treats status epilepticus; euthanasia |
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anticonvulsant historical drugs
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- primidone
- phenytoin |
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NMDA receptor antagonist
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- felbamate - old, rarely used
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anticonvulsant MOA unclear
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- gabapentin - sedation, ataxia
- levetiracetem - zonisamide (blocks Na, Ca channels) - sedation, ataxia, vomiting - potassium bromide (interferes with Cl transport) |
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Phenobarbital
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MOA - GABA agonist
Use - chronic management and STATUS EPILEPTICUS |
Adverse effects - sedation, polyphagia, PU/PD, behavior changes, elevate liver enzymes*, hepatotoxicity, decrease T4 levels
*metabolizes other drugs faster |
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Diazepam
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MOA - GABA agonis
Use - STATUS EPILEPTICUS |
Adverse effects - sedation, tachyphylaxis, dependence, hepatic necrosis in cats
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Levitiracetam
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MOA - unknown
Use - chronic management |
Adverse effects - none at recommended dosing
not metabolized in liver, so good for patients with liver disease |
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Potassium Bromide
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MOA - unknown
Use - chronic management |
Adverse effect - sedation, polyphagia, behavior changes, bromide toxicosis, joint stiffness, ataxia, PU/PD, altered chloride on chem profile
must be compounded and given at loading dose renal elimination so can be used in liver disease patients |
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behavior modifying drugs
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Benzodiazepines (BZDs)
Asapriones Tricyclic antidepressants (TCA) SSRIs MAOIs |
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Diazepam
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- benzodiazepine
- MOA - GABA agonist (binds GABA receptor, increasing GABA binding affinity, increases Cl- into cell) - Use - anxiolytic - decrease anxiety; used in storms |
- NT - increases GABA
- adverse effects - low toxicity; idiosyncratic hepatic necrosis in cats; also tolerance can develop with chronic use |
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clorazepate
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- benzodiazepine
- MOA - GABA agonist (binds GABA receptor, increasing GABA binding affinity, increases Cl- into cell) - Use - anxiolytic - decrease anxiety; used in storms |
- NT - increases GABA
- adverse effects - low toxicity; idiosyncratic hepatic necrosis in cats; also tolerance can develop with chronic use |
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buspirone
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- azapirones
- MOA - full agonist at PRESYNAPTIC and partial at postsynaptic 5HT-1A agonist - uses - used in cats to reduce urine spraying; used with other drugs to treat complex behavior cases |
- NT - decreases serotonin synthesis (increase at postsynaptic)
- adverse effects - GI signs |
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amitriptyline
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- TCA
- MOA - SNRI = blocks serotonin and NE uptake - uses - separation anxiety in dogs, excessive grooming, spraying, anxiety in cats, reduce feather plucking in birds |
- NT - increases serotonin and NE
- adverse effects - also alpha-1 antagonist, antihistaminic, anticholinergic - side effects result from these; decreased secretions, dry mouth, sedation, constipation |
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clomipramine
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- TCA
- MOA - SNRI = blocks serotonin and NE uptake - uses - anxiolytic, urine spraying in cats |
- NT - increases serotonin and NE
- adverse effects - also alpha-1 antagonist, antihistaminic, anticholinergic - side effects result from these |
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fluoxetine
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- SSRIs
- MOA - inhibits serotonin reuptake - uses - anxiolytic, urine spraying in cats |
- NT - increases serotonin
- adverse effects - sedation, anorexia, irritability, agitation |
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paroxtine
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- SSRIs
- MOA - inhibits serotonin reuptake - uses - anxiolytic, canine aggression |
- NT - increases serotonin
- adverse effects - sedation, dry mouth, GI signs, irritability |
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selegiline
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- MAOIs
- MOA - beta antagonist - decreases dopamine metabolism - uses - cognitive dysfunction syndrome, pituitary dependant HAC |
- NT - increases dopamine
- adverse effects - hyperactivity |
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benzodiazepines mechanism
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- GABA-agonist: bind to/activate benzodiazepine receptor on GABA-a; increases opening of chloride ion channels which leads to hyperpolarization of postsynaptic neuron, decreasing neuronal transmission
- GABA-antagonist: competitively antagonize action of benzodiasepines on BZ receptor site on GABA-a, prevents hyperpolarization of postsynaptic neuron, increasing transmission |
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benzodiazepines uses
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- GABA-agonist used as muscle relaxants in conjunction with anesthesia; decreases seizures; decreases anxiety; sedation
- diazepam is least potent; lorazepam is most potent - diazepam is used to treat status epilepticus because it acts much quicker than lorazepam (even though it is less potent) - diazepam is a level 4 controlled drug - flumazenil - reversal of other benzodiazepines (agonists) |
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benzodiazepines adverse effects
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- agonists: transient period of agitation, vocalization, excitation, muscle fasiculations, ataxia; then sedation, ataxia, muscle relaxation, increased appetite, disinhibition of behavior
- diazepam - hepatic toxicosis in cats; has additional side effects due to propylene glycol - hemolysis of RBCs, pain when injected, cardio depression - flumazenil: abstinence syndromes-tremors, hot foot walking, twitches, tonic-clonic seizures, death |
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benzodiazepines contraindictions
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-agonists: hypersensitivity to benzodiazepines, hepatic dysfunction, narrow angle glaucoma, must taper off drug
- flumaenil: chronic dosing with BZs, suspected OD of TCAs - seizures, arrythmia, death; or if getting BZs for life-threatening condition |
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benzodiazepine drugs
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*GABA-agonists:
- diazepam - midazolam - undergo glucoronidation but can still use in cats - alternate pathways don't produce toxic metabolites - lorazepam *GABA-antagonists: - flumazenil |
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