Drug Quiz 1 MOA Flashcards by Abigail Kent | Brainscape

Q

Acetaminophen

A

Inhibits brain prostaglandin synthesis, leading to analgesic and antipyretic activity

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Q

Butalbital, caffeine, acetaminophen

A

Butalbital is a barbiturate that depresses the sensory cortex and motor activity, producing sedation and drowsiness.
Caffeine increases cAMP and acts as a vasoconstrictor and CNS stimulant. Combination is commonly used to treat headaches

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Q

Buprenorphine/naloxone

A

Act as a μ-opioid receptor agonists, altering the perception and response to pain centrally and peripherally – is a μ-agonists with weak k-antagonist activity - both partial agonist of μ- and k-receptors

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Q

Fentanyl

A

One of the strongest opiate analgesics - acts as a μ-opioid receptor agonists, altering the perception and response to pain centrally and peripherally

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Q

Hydromorphone

A

One of the strongest opiate analgesics - acts as a μ-opioid receptor agonists, altering the perception and response to pain centrally and peripherally

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Q

Methadone

A

One of the strongest opiate analgesics - acts as a μ-opioid receptor agonists, altering the perception and response to pain centrally and peripherally

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Q

Morphine

A

One of the strongest opiate analgesics - acts as a μ-opioid receptor agonists, altering the perception and response to pain centrally and peripherally

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Q

Oxycodone

A

One of the strongest opiate analgesics - acts as a μ-opioid receptor agonists, altering the perception and response to pain centrally and peripherally

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Q

Tramadol

A

Inhibit the reuptake of NE, which modifies the ascending pain pathway, in addition to being μ-opioid receptor agonists

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Q

Codeine, Acetaminophen

A

The narcotic component binds to opioid μ-receptors, altering the perception and response to pain. The non-narcotic analgesic inhibits brain prostaglandin synthesis

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Q

Hydrocodone/acetaminophen

A

The narcotic component binds to opioid μ-receptors, altering the perception and response to pain. The non-narcotic analgesic inhibits brain prostaglandin synthesis

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Q

Hydrocodone/ibuprofen

A

The narcotic component binds to opioid μ-receptors, altering the perception and response to pain. The non-narcotic analgesic inhibits brain prostaglandin synthesis

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Q

Oxycodone/acetaminophen

A

The narcotic component binds to opioid μ-receptors, altering the perception and response to pain. The non-narcotic analgesic inhibits brain prostaglandin synthesis

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Q

Celecoxib

A

Inhibits prostaglandin synthesis by decreasing the activity of the enzyme COX-2, which results in decreased formation of prostaglandin precursors - lower incidence of GI ulcers than nonselective NSAIDS

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Q

Aspirin

A

Inhibit prostaglandin synthesis by decreasing the activity of COX enzymes 1 & 2, resulting in decreased formation of prostaglandin precursors associated with inflammation & pain

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Q

Diclofenac

A

Inhibit prostaglandin synthesis by decreasing the activity of COX enzymes 1 & 2, resulting in decreased formation of prostaglandin precursors associated with inflammation & pain

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Q

Ibuprofen

A

Inhibit prostaglandin synthesis by decreasing the activity of COX enzymes 1 & 2, resulting in decreased formation of prostaglandin precursors associated with inflammation & pain

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Q

Indomethacin

A

Inhibit prostaglandin synthesis by decreasing the activity of COX enzymes 1 & 2, resulting in decreased formation of prostaglandin precursors associated with inflammation & pain

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Q

Ketorolac

A

Inhibit prostaglandin synthesis by decreasing the activity of COX enzymes 1 & 2, resulting in decreased formation of prostaglandin precursors associated with inflammation & pain

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Q

Meloxicam

A

Inhibit prostaglandin synthesis by decreasing the activity of COX enzymes 1 & 2, resulting in decreased formation of prostaglandin precursors associated with inflammation & pain

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Q

Naproxen

A

Inhibit prostaglandin synthesis by decreasing the activity of COX enzymes 1 & 2, resulting in decreased formation of prostaglandin precursors associated with inflammation & pain

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Q

Eletriptan

A

5-HT1B/1D receptor agonist at extracerebral and intracranial blood vessels, liekely resulting in vasoconstriction and decreased trigeminal nerve transmission

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Q

Rizatriptan

A

5-HT1B/1D receptor agonist at extracerebral and intracranial blood vessels, liekely resulting in vasoconstriction and decreased trigeminal nerve transmission

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Q

Sumatriptan

A

5-HT1B/1D receptor agonist at extracerebral and intracranial blood vessels, liekely resulting in vasoconstriction and decreased trigeminal nerve transmission

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Q

Phentermine

A

Sympathomimetic amine that stimulates the CNS and elevates blood pressure - the MOA in treating obesity is unknown

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Q

Alprazolam

A

Facilitate the activity of the inhibitory neurotransmitter GABA & other inhibitory transmitters by binding to specific benzodiazepine receptors

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Q

Temazepam

A

Facilitate the activity of the inhibitory neurotransmitter GABA & other inhibitory transmitters by binding to specific benzodiazepine receptors

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Q

Clonazepam

A

increases inhibitory actions of GABA

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Q

Diazepam

A

Facilitate the activity of the inhibitory neurotransmitter GABA & other inhibitory transmitters by binding to specific benzodiazepine receptors

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Q

Lorazepam

A

Facilitate the activity of the inhibitory neurotransmitter GABA & other inhibitory transmitters by binding to specific benzodiazepine receptors

Q

Buspirone

A

MOA is primarily unknown - the drug has a high affinity for serotonin receptors and a moderate affinity for dopamine type-2 receptors

Q

Carbamazepine

A

prolongs inactivation of NA+ channels

Q

Gabapentin

A

Blockade of Ca2+ channels, decreased release of glutamate

Q

Lamotrigine

A

prolongs inactivating of Na+ channels

Q

Oxcarbazepine

A

Multiple MOAs used - effective seizure control usually augments CNS inhibitory processes or opposes excitatory processes. Typically control is achieved through alteration of Na, Ca, &/or K ion channels &/or neurotransmitters (GABA, excitatory glutamate)

Q

Phenobarbital

A

increases inhibitory actions of GABA

Q

Phenytoin

A

prolongs inactivating of Na+ channels

Q

Pregabalin

A

Blockade of Ca2+ channels, decreased release of glutamate

Q

Topiramate

A

prolongs inactivating of Na+ channels

Q

Valproate sodium

A

prolongs inactivating of Na+ channels

Q

Bupropion

A

Multiple MOAs - including blocking the presynaptic reuptake of serotonin and NE, thereby increasing concentrations of these CNS neurotransmitters in the synapse - Bupropion is also a weak inhibitor of dopamine reuptake

Q

Mirtazapine

A

Multiple MOAs - including blocking the presynaptic reuptake of serotonin and NE, thereby increasing concentrations of these CNS neurotransmitters in the synapse - Mirtazapine has central presynaptic alpha-2 adrenergic antagonism, which leads to increased release of serotonin & NE

Q

Trazodone

A

Multiple MOAs - including blocking the presynaptic reuptake of serotonin and NE, thereby increasing concentrations of these CNS neurotransmitters in the synapse

Q

Duloxetine

A

Work in depression by blocking the neuronal reuptake of serotonin and NE

Q

Venlafaxine

A

Work in depression by blocking the neuronal reuptake of serotonin and NE

Q

Citalopram

A

SSRIs block presynaptic reuptake of serotonin, thereby increasing the concentration of this CNS neurotransmitter in the synapse

Q

Escitalopram oxalate

A

SSRIs block presynaptic reuptake of serotonin, thereby increasing the concentration of this CNS neurotransmitter in the synapse

Q

Fluoxetine

A

SSRIs block presynaptic reuptake of serotonin, thereby increasing the concentration of this CNS neurotransmitter in the synapse

Q

Paroxetine

A

SSRIs block presynaptic reuptake of serotonin, thereby increasing the concentration of this CNS neurotransmitter in the synapse

Q

Sertraline

A

SSRIs block presynaptic reuptake of serotonin, thereby increasing the concentration of this CNS neurotransmitter in the synapse

Q

Amitriptyline

A

TCAs block presynaptic reuptake of serotonin and NE, thereby increasing concentrations of these CNS neurotransmitters in the synapse

Q

Doxepin

A

TCAs block presynaptic reuptake of serotonin and NE, thereby increasing concentrations of these CNS neurotransmitters in the synapse

Q

Nortriptyline

A

TCAs block presynaptic reuptake of serotonin and NE, thereby increasing concentrations of these CNS neurotransmitters in the synapse

Q

Lithium carbonate

A

Produces multiple effects on CNS neurotransmitters via altered cation transport across cell membranes, which influences the reuptake of serotonin and/or NE

Q

Aripiprazole

A

Have effects on multiple CNS neurotransmitter systems. Dopamine inhibition & serotonin antagonism along with unknown effects on glutamate & GABA, leading to the therapeutic effect in the Tx of schizophrenia & other psychotic states

Q

Olanzapine

A

Have effects on multiple CNS neurotransmitter systems. Dopamine inhibition & serotonin antagonism along with unknown effects on glutamate & GABA, leading to the therapeutic effect in the Tx of schizophrenia & other psychotic states

Q

Quetiapine

A

Have effects on multiple CNS neurotransmitter systems. Dopamine inhibition & serotonin antagonism along with unknown effects on glutamate & GABA, leading to the therapeutic effect in the Tx of schizophrenia & other psychotic states

Q

Risperidone

A

Have effects on multiple CNS neurotransmitter systems. Dopamine inhibition & serotonin antagonism along with unknown effects on glutamate & GABA, leading to the therapeutic effect in the Tx of schizophrenia & other psychotic states

Q

Ziprasidone

A

Have effects on multiple CNS neurotransmitter systems. Dopamine inhibition & serotonin antagonism along with unknown effects on glutamate & GABA, leading to the therapeutic effect in the Tx of schizophrenia & other psychotic states

Q

Haloperidol

A

Block postsynaptic mesolimbic dopaminergic D1 and D2 receptors, improving positive symptoms associated with schizophrenia and other psychotic states

Q

Donepezil

A

Increase CNS acetylcholine concentrations, which can be deficient in pts with Alzheimers disease, through the reversible inhibition of hydrolysis by acetylcholinesterase

Q

Rivastigmine

A

Increase CNS acetylcholine concentrations, which can be deficient in pts with Alzheimers disease, through the reversible inhibition of hydrolysis by acetylcholinesterase

Q

Carbidopa/levodopa

A

Circulates in the plasma to the blood-brain barrier (BBB), where it crosses & is converted to dopamine in the CNS; inhibits peripheral decarboxylation of levodopa, decreasing the conversion to dopamine in peripheral tissues - resulting in higher plasma levels of levodopa available at the BBB

Q

Ropinirole

A

The proposed MOA is due to stimulation of postsynaptic dopamine D2-type receptors within the caudate putamen in the brain - has a moderate in vitro affinity for opioid receptors

Q

Memantine

A

Low to moderate affinity, noncompetitive NMDA receptor agonist that binds to NMDA receptor-operated cation channels & also blocks the 5-hydroxytryptamine-3 receptor and nicotinic acetylcholine receptors at carious potencies

Q

Zolpidem

A

Although not benzos, they also facilitate the activity of the inhibitory neurotransmitter GABA

Q

Eszopiclone

A

Although not benzos, they also facilitate the activity of the inhibitory neurotransmitter GABA

Q

Baclofen

A

Exerts its effects as an agonist at presynaptic GABAB receptors, acting mainly at the spinal cord level to inhibit the transmission of both monosynaptic and polysynaptic reflexes, with resultant relief of muscle spasticity

Q

Carisoprodol

A

Metabolized to meprobamate, which has anxiolytics and sedative effects

Q

Cyclobenzaprine

A

Structurally related to TCAs & acts primarily at the brainstem within the CNS

Q

Amphetamine/dextroamphetamine

A

Mediate CNS stimulation through either the release of NE and dopamine (amphetamine/dextroamphetamine) or blocking the reuptake of NE and dopamine (Methyphenidate)

Q

Methylphenidate

A

Mediate CNS stimulation through either the release of NE and dopamine (amphetamine/dextroamphetamine) or blocking the reuptake of NE and dopamine (Methyphenidate)

Q

Lisdexamfetamine

A

Mediate CNS stimulation through either the release of NE and dopamine (amphetamine/dextroamphetamine) or blocking the reuptake of NE and dopamine (Methyphenidate)

Q

Guanfacine

A

Selective alpha-2A adrenoreceptor agonist, which reduced sympathetic nerve impulses, resulting in reduced sympathetic outflow and a subsequent decrease in vasomotor tone and heart rate & also binds postsynaptic alpha-2A adrenoreceptors in the prefrontal cortex and has been theorized to improve delay-related firing of prefrontal cortex neurons –> as a result, underlying working memory and behavioral inhibition are affected, thereby improving symptoms associated with ADHD