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Systemic Pharmacology II > Drugs to Know 2 > Flashcards

Drugs to Know 2 Flashcards

1
Q

Phenelzine

A

Monoamine Oxidase Inhibitor (MAOI)

inhibits metabolism of NE, 5HT, and dopamine; increased effectiveness of synaptic transmission by increasing the amount of neurotransmitter released per action potential

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2
Q

Selegiline

A

Monoamine Oxidase Inhibitor (MAOI)

Depression: inhibits metabolism of NE, 5HT, and dopamine; increased effectiveness of synaptic transmission by increasing the amount of neurotransmitter released per action potential

Anti-Parkinson: inhibition of MAO to increase DA storage in vesicles; MAOI for dopaminergic neurons but is essentially inactive against MAO in noradrenergic neurons (except in very high doses)

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3
Q

Tranylcypromine

A

Monoamine Oxidase Inhibitor (MAOI)

inhibits metabolism of NE, 5HT, and dopamine; increased effectiveness of synaptic transmission by increasing the amount of neurotransmitter released per action potential

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4
Q

Amitriptyline

A

Tricyclic Antidepressants (TCA)

blocks reuptake of NE and 5HT

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5
Q

Desipramine

A

Tricyclic Antidepressants (TCA)

blocks reuptake of NE and 5HT

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6
Q

Imipramine

A

Tricyclic Antidepressants (TCA)

blocks reuptake of NE and 5HT

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7
Q

Nortriptyline

A

Tricyclic Antidepressants (TCA)

blocks reuptake of NE and 5HT

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8
Q

Citalopram

A

Selective Serotonin Reuptake Inhibitor (SSRI)

blocks reuptake of 5HT (highly selective); leads to increased concentration in the synaptic gap

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9
Q

Escitalopram

A

Selective Serotonin Reuptake Inhibitor (SSRI)

blocks reuptake of 5HT (highly selective); leads to increased concentration in the synaptic gap

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10
Q

Fluoxetine

A

Selective Serotonin Reuptake Inhibitor (SSRI)

blocks reuptake of 5HT (highly selective); leads to increased concentration in the synaptic gap

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11
Q

Paroxetine

A

Selective Serotonin Reuptake Inhibitor (SSRI)

blocks reuptake of 5HT (highly selective); leads to increased concentration in the synaptic gap

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12
Q

Sertraline

A

Selective Serotonin Reuptake Inhibitor (SSRI)

blocks reuptake of 5HT (highly selective); leads to increased concentration in the synaptic gap

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13
Q

Duloxetine

A

Serotonin/Norepinephrine Reuptake Inhibitor (SNRI)

blocks reuptake of NE and 5HT

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14
Q

Venlafaxine

A

Serotonin/Norepinephrine Reuptake Inhibitor (SNRI)

blocks reuptake of NE and 5HT

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15
Q

Bupropion

A

Atypical Antidepressant

weak dopamine and NE reuptake inhibitor

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16
Q

Mirtazapine

A

Atypical Antidepressant

enhances serotonin and NE neurotransmission (blocks presynaptic alpha-2 receptors); potent antihistamine activity (sedative)

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17
Q

Nefazodone

A

Atypical Antidepressant

weak inhibitor of serotonin reuptake; potent antihistamine activity (sedative)

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18
Q

Trazodone

A

Atypical Antidepressant

weak inhibitor of serotonin reuptake; potent antihistamine activity (sedative)

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19
Q

Alprazolam

A

Benzodiazepine

binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effect of GABA; also decreases the release of GABA

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20
Q

Chlordiazepoxide

A

Benzodiazepine

binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effect of GABA; also decreases the release of GABA

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21
Q

Clorazepate

A

Benzodiazepine

binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effect of GABA; also decreases the release of GABA

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22
Q

Clonazepam

A

Benzodiazepine

binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effect of GABA; also decreases the release of GABA

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23
Q

Diazepam

A

Benzodiazepine

binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effect of GABA; also decreases the release of GABA

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24
Q

Estazolam

A

Benzodiazepine

binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effect of GABA; also decreases the release of GABA

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25
Q

Flurazepam

A

Benzodiazepine

binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effect of GABA; also decreases the release of GABA

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26
Q

Lorazepam

A

Benzodiazepine

binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effect of GABA; also decreases the release of GABA

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27
Q

Midazolam

A

Benzodiazepine

binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effect of GABA; also decreases the release of GABA

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28
Q

Oxazepam

A

Benzodiazepine

binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effect of GABA; also decreases the release of GABA

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29
Q

Temazepam

A

Benzodiazepine

binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effect of GABA; also decreases the release of GABA

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30
Q

Triazolam

A

Benzodiazepine

binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effect of GABA; also decreases the release of GABA

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31
Q

Flumazenil

A

Benzodiazepine Antagonist

antagonist at benzodiazepine binding site; rapidly reduces cellular effects of benzodiazepines

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32
Q

Busprione

A

serotonin receptor agonist used to treat anxiety

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33
Q

Pentobarbital

A

Barbiturate

binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effect of GABA

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34
Q

Phenobarbital

A

Barbiturate

binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effect of GABA

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35
Q

Secobarbital

A

Barbiturate

binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effect of GABA

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36
Q

Eszopiclone

A

Benzo-Like

high affinity for the benzodiazepine binding site of GABA receptors; mimic effects of BZDs

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37
Q

Zaleplon

A

Benzo-Like

high affinity for the benzodiazepine binding site of GABA receptors; mimic effects of BZDs

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38
Q

Zolpidem

A

Benzo-Like

high affinity for the benzodiazepine binding site of GABA receptors; mimic effects of BZDs

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39
Q

Reamelteon

A

melatonin receptor agonist

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40
Q

Acamprosate

A

Treatment of Alcohol Dependence

poorly understood MOA

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41
Q

Disulfiram

A

Treatment of Alcohol Dependence

inhibits aldehyde dehydrogenase; blocks important oxidation step; causes acetaldehyde accumulation in the blood (causes flushing, tachycardia, hyperventilation, nausea); patients avoid alcohol in order to avoid above effects

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42
Q

Naltrexone

A

Treatment of Alcohol Dependence

long-acting opiate antagonist; used along with psychotherapy support

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43
Q

Chlorpromazine

A

First Generation Antipsychotic

dopamine antagonist; decreases effectiveness of DA to produce action potential by blocking post-synaptic dopamine receptors

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44
Q

Fluphenazine

A

First Generation Antipsychotic

dopamine antagonist; decreases effectiveness of DA to produce action potential by blocking post-synaptic dopamine receptors

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45
Q

Haloperidol

A

First Generation Antipsychotic

dopamine antagonist; decreases effectiveness of DA to produce action potential by blocking post-synaptic dopamine receptors

46
Q

Thioridazine

A

First Generation Antipsychotic

dopamine antagonist; decreases effectiveness of DA to produce action potential by blocking post-synaptic dopamine receptors

47
Q

Thiothixene

A

First Generation Antipsychotic

dopamine antagonist; decreases effectiveness of DA to produce action potential by blocking post-synaptic dopamine receptors

48
Q

Aripiprazole

A

Second Generation Antipsychotic

dopamine and 5HT receptor antagonists; have activity at more dopamine receptors than First Generation Antipsychotics

49
Q

Clozapine

A

Second Generation Antipsychotic

dopamine and 5HT receptor antagonists; have activity at more dopamine receptors than First Generation Antipsychotics

50
Q

Lurasidone

A

Second Generation Antipsychotic

dopamine and 5HT receptor antagonists; have activity at more dopamine receptors than First Generation Antipsychotics

51
Q

Olanzapine

A

Second Generation Antipsychotic

dopamine and 5HT receptor antagonists; have activity at more dopamine receptors than First Generation Antipsychotics

52
Q

Quetiapine

A

Second Generation Antipsychotic

dopamine and 5HT receptor antagonists; have activity at more dopamine receptors than First Generation Antipsychotics

53
Q

Risperidone

A

Second Generation Antipsychotic

dopamine and 5HT receptor antagonists; have activity at more dopamine receptors than First Generation Antipsychotics

54
Q

Ziprasidone

A

Second Generation Antipsychotic

dopamine and 5HT receptor antagonists; have activity at more dopamine receptors than First Generation Antipsychotics

55
Q

Carbamazepine

A

Drugs Used to Treat Mania and Bipolar Disorder

anti-epileptic

56
Q

Lithium

A

Drugs Used to Treat Mania and Bipolar Disorder

MOA not understood; appears to inhibit two signal transduction pathways; effects on synthesis and release of NE, 5HT, and DA; effects on cellular actions of above neurotransmitters

57
Q

Valproic Acid

A

Drugs Used to Treat Mania and Bipolar Disorder

anti-epileptic

58
Q

Levodopa/Carbidopa

A

Anti-Parkinson Drugs

boost DA synthesis- increases content of DA vesicles, increases amount of DA released, increased activation of postsynaptic receptors

59
Q

Amantadine

A

Anti-Parkinson Drug

MOA in Parkinson’s is unknown; also an antiviral (inhibits viral uncoating; possibly more than usual DA-containing vesicles in the axon terminal are induced to release contents into the synapse; affects all dopaminergic neurons in the brain

60
Q

Apomorphine

A

Anti-Parkinson Drug- Dopamine Agonist

induces DA release; enhances release without directly affecting synthesis or metabolism of DA

61
Q

Pramipexole

A

Anti-Parkinson Drug- Dopamine Agonist

induces DA release; enhances release without directly affecting synthesis or metabolism of DA

62
Q

Ropinirole

A

Anti-Parkinson Drug- Dopamine Agonist

induces DA release; enhances release without directly affecting synthesis or metabolism of DA

63
Q

Rotigotine

A

Anti-Parkinson Drug- Dopamine Agonist

induces DA release; enhances release without directly affecting synthesis or metabolism of DA

64
Q

Resagiline

A

Anti-Parkinson Drug- MAOI

inhibition of MAO to increase DA storage in vesicles; MAOI for dopaminergic neurons but is essentially inactive against MAO in noradrenergic neurons (except in very high doses)

65
Q

Entacapone

A

Anti-Parkinson Drug- COMT Inhibitor

catechol-O-methyltransferase appears to interfere with levodopa uptake; entacapone inhibits this enzyme which increases the bioavailability of levodopa

66
Q

Benztropine

A

Anti-Parkinson Drug- Antimuscarinic Agent

reduces cholinergic influence; assumes imbalance can be corrected by reducing cholinergic influence; blocks cholinergic receptors

67
Q

Biperiden

A

Anti-Parkinson Drug- Antimuscarinic Agent

reduces cholinergic influence; assumes imbalance can be corrected by reducing cholinergic influence

68
Q

Trihexphenidyl

A

Anti-Parkinson Drug- Antimuscarinic Agent

reduces cholinergic influence; assumes imbalance can be corrected by reducing cholinergic influence; blocks cholinergic receptors

69
Q

Donepezil

A

Treatment of Alzheimer’s- Cholinesterase Inhibitor

Binds reversibly to acetylcholinesterase; inhibits activity of the enzyme; leads to an increase in acetylcholine in the synapse; maximizes the remaining pool of ACh by inhibiting breakdown

70
Q

Galantamine

A

Treatment of Alzheimer’s- Cholinesterase Inhibitor

Binds reversibly to acetylcholinesterase; inhibits activity of the enzyme; leads to an increase in acetylcholine in the synapse; maximizes the remaining pool of ACh by inhibiting breakdown

71
Q

Rivastigmine

A

Treatment of Alzheimer’s- Cholinesterase Inhibitor

Binds reversibly to acetylcholinesterase; inhibits activity of the enzyme; leads to an increase in acetylcholine in the synapse; maximizes the remaining pool of ACh by inhibiting breakdown

72
Q

Memantine

A

Treatment of Alzheimer’s- NMDA Receptor Antagonist

binds to glutamine receptors on the post-synaptic neuron; prevents binding of glutamine; theory is that blockage of NMDA receptors reduces cytotoxic effects on neurons caused by Ca influx across the plasma membranes

73
Q

Caffeine

A

Drugs of Abuse: Psychomotor Stimulants
Methylxanthine

several proposed mechanisms; most important: blockade of adenosine receptors in CNS; adenosine inhibits dopamine release; caffeine indirectly enhances dopamine transmission

74
Q

Theophylline

A

Drugs of Abuse: Psychomotor Stimulants
Methylxanthine

several proposed mechanisms; most important: blockade of adenosine receptors in CNS; adenosine inhibits dopamine release; caffeine indirectly enhances dopamine transmission

75
Q

Nicotine

A

Drugs of Abuse: Psychomotor Stimulants
Parasympathetic Agonist

low doses: causes ganglionic stimulation;
high doses: causes ganglionic blockade;
affects nicotinic receptors in the PNS ganglia as well as dopamine neurons in the CNS- enhances DA transmission and impairs regulatory systems

76
Q

Varenicline

A

Drugs of Abuse: Psychomotor Stimulants
Parasympathetic Agonist

partial agonist at neuronal nicotinic acetylcholine receptors in CNS; produces less of an effect than nicotine

77
Q

Cocaine

A

Drugs of Abuse: Psychomotor Stimulants

blocks reuptake of monoamines; NE, 5-HT, DA (especially); prolongs the effects of these neurotransmitters; increased DA in pleasure system of brain causes intense euphoria; chronic use actually depletes DA (triggers craving)

78
Q

Amphetamine

A

Drugs of Abuse: Amphetamines

is a substrate for the enzyme responsible for reuptake of NE and DA; is NOT metabolized by MAO and is instead stored in neurotransmitter storage vesicles (leaves NE and DA out of storage vesicles); causes release of intracellular stores of neurotransmitter via a reversal of the reuptake enzyme; also inhibits MAO to a certain extent

79
Q

Armodafinil

A

Drugs of Abuse: Amphetamines

similar to amphetamine; specific for dopamine transporter; prevents reuptake of dopamine

80
Q

Dexmethylphenidate

A

Drugs of Abuse: Amphetamines

is a substrate for the enzyme responsible for reuptake of NE and DA; is NOT metabolized by MAO and is instead stored in neurotransmitter storage vesicles (leaves NE and DA out of storage vesicles); causes release of intracellular stores of neurotransmitter via a reversal of the reuptake enzyme; also inhibits MAO to a certain extent

81
Q

Dextroamphetamine

A

Drugs of Abuse: Amphetamines

is a substrate for the enzyme responsible for reuptake of NE and DA; is NOT metabolized by MAO and is instead stored in neurotransmitter storage vesicles (leaves NE and DA out of storage vesicles); causes release of intracellular stores of neurotransmitter via a reversal of the reuptake enzyme; also inhibits MAO to a certain extent

82
Q

Lisdexamfetamine

A

Drugs of Abuse: Amphetamines

is a substrate for the enzyme responsible for reuptake of NE and DA; is NOT metabolized by MAO and is instead stored in neurotransmitter storage vesicles (leaves NE and DA out of storage vesicles); causes release of intracellular stores of neurotransmitter via a reversal of the reuptake enzyme; also inhibits MAO to a certain extent

83
Q

Methamphetamine

A

Drugs of Abuse: Amphetamines

is a substrate for the enzyme responsible for reuptake of NE and DA; is NOT metabolized by MAO and is instead stored in neurotransmitter storage vesicles (leaves NE and DA out of storage vesicles); causes release of intracellular stores of neurotransmitter via a reversal of the reuptake enzyme; also inhibits MAO to a certain extent

84
Q

Methylphenidate

A

Drugs of Abuse: Amphetamines

exact mechanism is unknown; very similar to amphetamine-
is a substrate for the enzyme responsible for reuptake of NE and DA; is NOT metabolized by MAO and is instead stored in neurotransmitter storage vesicles (leaves NE and DA out of storage vesicles); causes release of intracellular stores of neurotransmitter via a reversal of the reuptake enzyme; also inhibits MAO to a certain extent

85
Q

Modafinil

A

Drugs of Abuse: Amphetamines

similar to amphetamine; specific for dopamine transporter; prevents reuptake of dopamine

86
Q

Dronabinol

A

Drugs of Abuse: Hallucinogens

cannabinoid used to treat nausea

87
Q

Lysergic Acid Diethylamide (LSD)

A

Drugs of Abuse: Hallucinogens

shows 5-HT agonist activity and activation of sympathetic nervous system; also shown to stimulate DA receptors

88
Q

Phencyclidine (PCP)

A

Drugs of Abuse: Hallucinogens

inhibits reuptake of DA, 5-HT, and NE; main action is to block NMDA glutamate receptor; prevents passage of Ca

89
Q

Tetrahydrocannabinol (THC)

A

Drugs of Abuse: Hallucinogens

THC receptors found on inhibitory presynaptic nerve terminals

90
Q

Fentanyl

A

Opioid Agonist

opiate receptor activation

91
Q

Heroin

A

Opioid Agonist

opiate receptor activation

92
Q

Hydromorphone

A

Opioid Agonist

opiate receptor activation

93
Q

Levorphanol

A

Opioid Agonist

opiate receptor activation

94
Q

Loperamide

A

Opioid Agonist

opiate receptor activation; selectively targets GI opiate receptors

95
Q

Meperidine

A

Opioid Agonist

opiate receptor activation

96
Q

Methadone

A

Opioid Agonist

opiate receptor activation

97
Q

Morphine

A

Opioid Agonist

opiate receptor activation

98
Q

Oxycodone

A

Opioid Agonist

opiate receptor activation

99
Q

Oxymorphone

A

Opioid Agonist

opiate receptor activation

100
Q

Codeine

A

Partial Opioid Agonists (weak)

opiate receptor activation

101
Q

Hydrocodone

A

Partial Opioid Agonists (weak)

opiate receptor activation

102
Q

Tramadol

A

Mixed Mechanism Opioid

binds to opioid receptor weakly and inhibits reuptake of NE and serotonin

103
Q

Naloxone

A

Opioid Antagonist

104
Q

Naltrexone

A

Opioid Antagonist

105
Q

Buprenorphine

A

Mixed Opioid Agonist-Antagonists

show agonist activity in drug naive patients;
show antagonist activity in patients with opioid dependence

106
Q

Nalbuphine

A

Mixed Opioid Agonist-Antagonists

show agonist activity in drug naive patients;
show antagonist activity in patients with opioid dependence

107
Q

Lortab

A

Opioid Combination

108
Q

Percocet

A

Opioid Combination

109
Q

Percodan

A

Opioid Combination

110
Q

Tylenol #2/#3/#4

A

Opioid Combination

Systemic Pharmacology II (4 decks)

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