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60 Cards in this Set

  • Front
  • Back
fluoxetine
SSRI

prevents the reuptake of serotonin from synaptic cleft
paroxetine
SSRI

prevents the reuptake of serotonin from synaptic cleft
sertraline
SSRI

prevents the reuptake of serotonin from synaptic cleft
fluvoxamine
SSRI

prevents the reuptake of serotonin from synaptic cleft
escitalopram
SSRI

prevents the reuptake of serotonin from synaptic cleft
citalopram
SSRI

prevents the reuptake of serotonin from synaptic cleft
desipramine
Tricyclic Antidepressants

block reuptake of NE and serotonin from synaptic cleft. Also inhibit muscarinic, histamine and alpha adrenergic receptors leading to a slew of side effects.
nortriptyline
Tricyclic Antidepressants

block reuptake of NE and serotonin from synaptic cleft. Also inhibit muscarinic, histamine and alpha adrenergic receptors leading to a slew of side effects.
imipramine
Tricyclic Antidepressants

block reuptake of NE and serotonin from synaptic cleft. Also inhibit muscarinic, histamine and alpha adrenergic receptors leading to a slew of side effects.
amitryiptyline
Tricyclic Antidepressants

block reuptake of NE and serotonin from synaptic cleft. Also inhibit muscarinic, histamine and alpha adrenergic receptors leading to a slew of side effects.
doxepin
Tricyclic Antidepressants

block reuptake of NE and serotonin from synaptic cleft. Also inhibit muscarinic, histamine and alpha adrenergic receptors leading to a slew of side effects.
trazodone
Tricyclic Antidepressants

block reuptake of NE and serotonin from synaptic cleft. Also inhibit muscarinic, histamine and alpha adrenergic receptors leading to a slew of side effects.
bupropion
Tricyclic Antidepressants

block reuptake of NE and serotonin from synaptic cleft. Also inhibit muscarinic, histamine and alpha adrenergic receptors leading to a slew of side effects.
venlafaxine
Heterocylcic Antidepressant

Blocks the reuptake of neorepinephrine and serotonin from synaptic cleft (like TCA's!)
trancylcypromine
MAO inhibitors

when monoamine oxidase is inhibited, levels of serotonin, dpomanine and NE increase in the presynaptic neuron since MAO is a presynaptic enzyme responsible for metabolizing NE and serotonine and dpamine. The excess causes theneurotransmitters to leak out of the neuron into presynaptic space and activate serotonin and NE receptors.
phenelzine
MAO inhibitors

when monoamine oxidase is inhibited, levels of serotonin, dpomanine and NE increase in the presynaptic neuron since MAO is a presynaptic enzyme responsible for metabolizing NE and serotonine and dpamine. The excess causes theneurotransmitters to leak out of the neuron into presynaptic space and activate serotonin and NE receptors.
isocarboxazid
MAO inhibitors

when monoamine oxidase is inhibited, levels of serotonin, dpomanine and NE increase in the presynaptic neuron since MAO is a presynaptic enzyme responsible for metabolizing NE and serotonine and dpamine. The excess causes theneurotransmitters to leak out of the neuron into presynaptic space and activate serotonin and NE receptors.
haloperidol
typical antipsychotic agents

blocks postsynaptic dopamine D2 receptors in the limbic system of the brain, decreasing the respons of the postsynaptic neuron to dopamine excitation.
fluphenazine
typical antipsychotic agents

blocks postsynaptic dopamine D2 receptors in the limbic system of the brain, decreasing the respons of the postsynaptic neuron to dopamine excitation.
chlorpromazine
typical antipsychotic agents

blocks postsynaptic dopamine D2 receptors in the limbic system of the brain, decreasing the respons of the postsynaptic neuron to dopamine excitation.
clozapine
atypical antipsychotic agents

block both serotonin (5HT2) and dopamine receptors in the limbic system of the brain, thus decreasing the response of hte postsynaptic neuron to dopamine and serotonin excitation.
risperidone
atypical antipsychotic agents

block both serotonin (5HT2) and dopamine receptors in the limbic system of the brain, thus decreasing the response of hte postsynaptic neuron to dopamine and serotonin excitation.
olanzapine
atypical antipsychotic agents

block both serotonin (5HT2) and dopamine receptors in the limbic system of the brain, thus decreasing the response of hte postsynaptic neuron to dopamine and serotonin excitation.
ziprasidone
atypical antipsychotic agents

block both serotonin (5HT2) and dopamine receptors in the limbic system of the brain, thus decreasing the response of hte postsynaptic neuron to dopamine and serotonin excitation.
aripriprazole
atypical antipsychotic agents

block both serotonin (5HT2) and dopamine receptors in the limbic system of the brain, thus decreasing the response of hte postsynaptic neuron to dopamine and serotonin excitation.
quetiapine
atypical antipsychotic agents

block both serotonin (5HT2) and dopamine receptors in the limbic system of the brain, thus decreasing the response of hte postsynaptic neuron to dopamine and serotonin excitation.
triazolam
benzodiazepine, short acting (only one listed)

bind to site directly adjacent to GABA receptor and enhance the activity of the receptor, resulting in increased flow of chloride ion thru the channel leading to cell membrane hyperpolarization and decreased activity of the neurons fo the limbic, thalamic and hypothalamic regions of the CNS
lorazepam
benzodiazepine, intermediate acting

bind to site directly adjacent to GABA receptor and enhance the activity of the receptor, resulting in increased flow of chloride ion thru the channel leading to cell membrane hyperpolarization and decreased activity of the neurons fo the limbic, thalamic and hypothalamic regions of the CNS
temazepam
benzodiazepine, intermediate acting

bind to site directly adjacent to GABA receptor and enhance the activity of the receptor, resulting in increased flow of chloride ion thru the channel leading to cell membrane hyperpolarization and decreased activity of the neurons fo the limbic, thalamic and hypothalamic regions of the CNS
alprazolam
benzodiazepine, intermediate acting

bind to site directly adjacent to GABA receptor and enhance the activity of the receptor, resulting in increased flow of chloride ion thru the channel leading to cell membrane hyperpolarization and decreased activity of the neurons fo the limbic, thalamic and hypothalamic regions of the CNS
chlordiazepoxide
benzodiazepine, intermediate acting

bind to site directly adjacent to GABA receptor and enhance the activity of the receptor, resulting in increased flow of chloride ion thru the channel leading to cell membrane hyperpolarization and decreased activity of the neurons fo the limbic, thalamic and hypothalamic regions of the CNS
diazepam
benzodiazepine, long acting

bind to site directly adjacent to GABA receptor and enhance the activity of the receptor, resulting in increased flow of chloride ion thru the channel leading to cell membrane hyperpolarization and decreased activity of the neurons fo the limbic, thalamic and hypothalamic regions of the CNS
clonazepam
benzodiazepine, long acting

bind to site directly adjacent to GABA receptor and enhance the activity of the receptor, resulting in increased flow of chloride ion thru the channel leading to cell membrane hyperpolarization and decreased activity of the neurons fo the limbic, thalamic and hypothalamic regions of the CNS
flurazepam
benzodiazepine, long acting

bind to site directly adjacent to GABA receptor and enhance the activity of the receptor, resulting in increased flow of chloride ion thru the channel leading to cell membrane hyperpolarization and decreased activity of the neurons fo the limbic, thalamic and hypothalamic regions of the CNS
phenobarbital
barbiturates

interfere with electrolyte transport across neurla cell membranes and indirectly potentiate GABA receptor activity in the brainthus leading to hyperpolarization adn decreased activity of CNS neurons
thiopental
barbiturates

interfere with electrolyte transport across neurla cell membranes and indirectly potentiate GABA receptor activity in the brainthus leading to hyperpolarization adn decreased activity of CNS neurons
pentobarbital
barbiturates

interfere with electrolyte transport across neurla cell membranes and indirectly potentiate GABA receptor activity in the brainthus leading to hyperpolarization adn decreased activity of CNS neurons
phenytoin
it's own "class", standalone.

decreases the flow of sodium adn calcium ions acrosss the cell membrane thus decreased depolarization of the cells of the nervous system.

used to treat simple and complex partial seizures and generalized tonic clonic seizures and status epilepticus. Also trigeminal neuralgia adn torsades de pointes.
valproic acid
it's own "class", standalone.

unclear MOA

used for generalized tonic clonic seizures, moclonic seizures, absence seizures and treatment of mania ass with bipolar disorder and in prevention of migranes
carbamazepine
it's own "class", standalone.

inhibits flow of siodium ions thru sodium channels on neural cell membranes , thus causign hyperpolarization and decreased activity of neuron

used to treat ismple and complex partial seizures and generalized tonic clonic siezures and used in trigeminal neuralgia
succinylcholine
it's own "class", standalone.


is a depolarizing neuromuscular blocker that competes with ACh to reversibly bind to nicotinic receptors at the neuromuscular junction
pancuronium
nondepolarizing neuromuscular blocker that acts to competitively bind nicotinic receptors at the neuromuscular junction.

used as an adjunct to general anesthesia induction to reduce skeletal muscle contraction for facilitation of endotracheal intubation
Gabapentin
standalone. exact MOA unknown.

Used to treat postherpetic neuralgia,
partial seizures and chronic neuropathic pain
lidocaine, procaine, cocaine
local anesthetic agents

act by blocking sodium channels on neuronal cell membranes. used during minor surgical procedures where sensation needs to be blocked in a localized area of hte body, but unconsciousness is not necessary
halothane
general inhaled anesthetic

MOA not completely understood.

Used for general anesthetic induction and maintenance for surgical procedures
isoflurane
general inhaled anesthetic

MOA not completely understood.

Used for general anesthetic induction and maintenance for surgical procedures
propofol
general intravenous anesthetic agents

MOA unknown
Used for induction and maintenance of anesthesia and conscious sedation
morphine
opiod

produce analegesia by binding to specific opioid receptors located thru nervous system (mostly in brainstem, spinal cord, peripheral nerves, amygdala, thalamus and hypothalamus). Results in hyperpolarizationadn decreased activity of neural cells.

Used for pain control (morphine, fentanyl, codeine), cough suppression (codeine, dextromethorphan), diarrhea and acute pulmonary edema (morphine reduces anxiety and cardiac preload)
codeine
opiod

produce analegesia by binding to specific opioid receptors located thru nervous system (mostly in brainstem, spinal cord, peripheral nerves, amygdala, thalamus and hypothalamus). Results in hyperpolarizationadn decreased activity of neural cells.

Used for pain control (morphine, fentanyl, codeine), cough suppression (codeine, dextromethorphan), diarrhea and acute pulmonary edema (morphine reduces anxiety and cardiac preload)
oxycodone
opiod

produce analegesia by binding to specific opioid receptors located thru nervous system (mostly in brainstem, spinal cord, peripheral nerves, amygdala, thalamus and hypothalamus). Results in hyperpolarizationadn decreased activity of neural cells.

Used for pain control (morphine, fentanyl, codeine), cough suppression (codeine, dextromethorphan), diarrhea and acute pulmonary edema (morphine reduces anxiety and cardiac preload)
hydrocodone
opiod

produce analegesia by binding to specific opioid receptors located thru nervous system (mostly in brainstem, spinal cord, peripheral nerves, amygdala, thalamus and hypothalamus). Results in hyperpolarizationadn decreased activity of neural cells.

Used for pain control (morphine, fentanyl, codeine), cough suppression (codeine, dextromethorphan), diarrhea and acute pulmonary edema (morphine reduces anxiety and cardiac preload)
hydromorphone
opiod

produce analegesia by binding to specific opioid receptors located thru nervous system (mostly in brainstem, spinal cord, peripheral nerves, amygdala, thalamus and hypothalamus). Results in hyperpolarizationadn decreased activity of neural cells.

Used for pain control (morphine, fentanyl, codeine), cough suppression (codeine, dextromethorphan), diarrhea and acute pulmonary edema (morphine reduces anxiety and cardiac preload)
heroin
opiod

produce analegesia by binding to specific opioid receptors located thru nervous system (mostly in brainstem, spinal cord, peripheral nerves, amygdala, thalamus and hypothalamus). Results in hyperpolarizationadn decreased activity of neural cells.

Used for pain control (morphine, fentanyl, codeine), cough suppression (codeine, dextromethorphan), diarrhea and acute pulmonary edema (morphine reduces anxiety and cardiac preload)
meperidine
opiod

produce analegesia by binding to specific opioid receptors located thru nervous system (mostly in brainstem, spinal cord, peripheral nerves, amygdala, thalamus and hypothalamus). Results in hyperpolarizationadn decreased activity of neural cells.

Used for pain control (morphine, fentanyl, codeine), cough suppression (codeine, dextromethorphan), diarrhea and acute pulmonary edema (morphine reduces anxiety and cardiac preload)
fentanyl
opiod

produce analegesia by binding to specific opioid receptors located thru nervous system (mostly in brainstem, spinal cord, peripheral nerves, amygdala, thalamus and hypothalamus). Results in hyperpolarizationadn decreased activity of neural cells.

Used for pain control (morphine, fentanyl, codeine), cough suppression (codeine, dextromethorphan), diarrhea and acute pulmonary edema (morphine reduces anxiety and cardiac preload)
dextromethorphan
opiod

produce analegesia by binding to specific opioid receptors located thru nervous system (mostly in brainstem, spinal cord, peripheral nerves, amygdala, thalamus and hypothalamus). Results in hyperpolarizationadn decreased activity of neural cells.

Used for pain control (morphine, fentanyl, codeine), cough suppression (codeine, dextromethorphan), diarrhea and acute pulmonary edema (morphine reduces anxiety and cardiac preload)
sumatriptan
stimulates presynaptic 5-HT1D receptors

used for migranes and cluster HAs
bupropion
smoking cessation agent and antidepressant

acts to inhibit reuptake of NE and dopamine but also acts as a nicotinic antagonist at the nicotinic ACh receptors found in the brain. By binding at nicotinic receptors in that part of the brain, they block the ability of nicotine to stimulate the mesolimbic dopamine system (antagonism), thus interfering with teh reinforcement/reward loop experienced with smoking.
varenicline
smoking cessation agent

acts as partial agonist and antagonist at the nicotinic ACh receptors found in the brain. By binding at nicotinic receptors in that part of the brain, they block the ability of nicotine to stimulate the mesolimbic dopamine system (antagonism), thus interfering with teh reinforcement/reward loop experienced with smoking.
buspirone
standalone.

Acts at 5-HT1A presynaptic receptor partial agonist.

Treatment of deneralized anxiety disorder. Can also be used in conjunction with SSRIs in treating depression