Drug Quiz 1 MOA Flashcards

1
Q

Acetaminophen

A

Inhibits brain prostaglandin synthesis, leading to analgesic and antipyretic activity

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2
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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3
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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4
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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5
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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6
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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7
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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8
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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9
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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10
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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11
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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12
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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13
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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14
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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15
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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16
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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17
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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18
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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19
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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20
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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21
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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22
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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23
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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24
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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25
Phentermine
Sympathomimetic amine that stimulates the CNS and elevates blood pressure - the MOA in treating obesity is unknown
26
Alprazolam
Facilitate the activity of the inhibitory neurotransmitter GABA & other inhibitory transmitters by binding to specific benzodiazepine receptors
27
Temazepam
Facilitate the activity of the inhibitory neurotransmitter GABA & other inhibitory transmitters by binding to specific benzodiazepine receptors
28
Clonazepam
increases inhibitory actions of GABA
29
Diazepam
Facilitate the activity of the inhibitory neurotransmitter GABA & other inhibitory transmitters by binding to specific benzodiazepine receptors
30
Lorazepam
Facilitate the activity of the inhibitory neurotransmitter GABA & other inhibitory transmitters by binding to specific benzodiazepine receptors
31
Buspirone
MOA is primarily unknown - the drug has a high affinity for serotonin receptors and a moderate affinity for dopamine type-2 receptors
32
Carbamazepine
prolongs inactivation of NA+ channels
33
Gabapentin
Blockade of Ca2+ channels, decreased release of glutamate
34
Lamotrigine
prolongs inactivating of Na+ channels
35
Oxcarbazepine
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)
36
Phenobarbital
increases inhibitory actions of GABA
37
Phenytoin
prolongs inactivating of Na+ channels
38
Pregabalin
Blockade of Ca2+ channels, decreased release of glutamate
39
Topiramate
prolongs inactivating of Na+ channels
40
Valproate sodium
prolongs inactivating of Na+ channels
41
Bupropion
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
42
Mirtazapine
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
43
Trazodone
Multiple MOAs - including blocking the presynaptic reuptake of serotonin and NE, thereby increasing concentrations of these CNS neurotransmitters in the synapse
44
Duloxetine
Work in depression by blocking the neuronal reuptake of serotonin and NE
45
Venlafaxine
Work in depression by blocking the neuronal reuptake of serotonin and NE
46
Citalopram
SSRIs block presynaptic reuptake of serotonin, thereby increasing the concentration of this CNS neurotransmitter in the synapse
47
Escitalopram oxalate
SSRIs block presynaptic reuptake of serotonin, thereby increasing the concentration of this CNS neurotransmitter in the synapse
48
Fluoxetine
SSRIs block presynaptic reuptake of serotonin, thereby increasing the concentration of this CNS neurotransmitter in the synapse
49
Paroxetine
SSRIs block presynaptic reuptake of serotonin, thereby increasing the concentration of this CNS neurotransmitter in the synapse
50
Sertraline
SSRIs block presynaptic reuptake of serotonin, thereby increasing the concentration of this CNS neurotransmitter in the synapse
51
Amitriptyline
TCAs block presynaptic reuptake of serotonin and NE, thereby increasing concentrations of these CNS neurotransmitters in the synapse
52
Doxepin
TCAs block presynaptic reuptake of serotonin and NE, thereby increasing concentrations of these CNS neurotransmitters in the synapse
53
Nortriptyline
TCAs block presynaptic reuptake of serotonin and NE, thereby increasing concentrations of these CNS neurotransmitters in the synapse
54
Lithium carbonate
Produces multiple effects on CNS neurotransmitters via altered cation transport across cell membranes, which influences the reuptake of serotonin and/or NE
55
Aripiprazole
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
56
Olanzapine
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
57
Quetiapine
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
58
Risperidone
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
59
Ziprasidone
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
60
Haloperidol
Block postsynaptic mesolimbic dopaminergic D1 and D2 receptors, improving positive symptoms associated with schizophrenia and other psychotic states
61
Donepezil
Increase CNS acetylcholine concentrations, which can be deficient in pts with Alzheimers disease, through the reversible inhibition of hydrolysis by acetylcholinesterase
62
Rivastigmine
Increase CNS acetylcholine concentrations, which can be deficient in pts with Alzheimers disease, through the reversible inhibition of hydrolysis by acetylcholinesterase
63
Carbidopa/levodopa
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
64
Ropinirole
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
65
Memantine
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
66
Zolpidem
Although not benzos, they also facilitate the activity of the inhibitory neurotransmitter GABA
67
Eszopiclone
Although not benzos, they also facilitate the activity of the inhibitory neurotransmitter GABA
68
Baclofen
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
69
Carisoprodol
Metabolized to meprobamate, which has anxiolytics and sedative effects
70
Cyclobenzaprine
Structurally related to TCAs & acts primarily at the brainstem within the CNS
71
Amphetamine/dextroamphetamine
Mediate CNS stimulation through either the release of NE and dopamine (amphetamine/dextroamphetamine) or blocking the reuptake of NE and dopamine (Methyphenidate)
72
Methylphenidate
Mediate CNS stimulation through either the release of NE and dopamine (amphetamine/dextroamphetamine) or blocking the reuptake of NE and dopamine (Methyphenidate)
73
Lisdexamfetamine
Mediate CNS stimulation through either the release of NE and dopamine (amphetamine/dextroamphetamine) or blocking the reuptake of NE and dopamine (Methyphenidate)
74
Guanfacine
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