Midterm 2 Drugs Flashcards by Cindy Heng

Q

Phenelzine

A

Monoamine Oxidase Inhibitors (MAOIs): Inhibit metabolism of NE, 5-HT(serotonin), and dopamine (and increasing the effectiveness of synaptic transmission by increasing the amount of transmitter replaced per action potential)

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Q

Selegiline

A

Monoamine Oxidase Inhibitors (MAOIs): Inhibit metabolism of NE, 5-HT(serotonin), and dopamine (and increasing the effectiveness of synaptic transmission by increasing the amount of transmitter replaced per action potential)

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Q

Tranylcypromine

A

Monoamine Oxidase Inhibitors (MAOIs): Inhibit metabolism of NE, 5-HT(serotonin), and dopamine (and increasing the effectiveness of synaptic transmission by increasing the amount of transmitter replaced per action potential)

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Q

Amitriptyline

A

Tricyclic Antidepressants (TCAs): Block the reuptake of NE and 5-HT (serotonin) by inhibiting the transporter protein

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Q

Clomipramine

A

Tricyclic Antidepressants (TCAs): Block the reuptake of NE and 5-HT (serotonin) by inhibiting the transporter protein

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Q

Desipramine

A

Tricyclic Antidepressants (TCAs): Block the reuptake of NE and 5-HT (serotonin) by inhibiting the transporter protein

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Q

Doxepin

A

Tricyclic Antidepressants (TCAs): Block the reuptake of NE and 5-HT (serotonin) by inhibiting the transporter protein

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Q

Imipramine

A

Tricyclic Antidepressants (TCAs): Block the reuptake of NE and 5-HT (serotonin) by inhibiting the transporter protein

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Q

Nortriptyline

A

Tricyclic Antidepressants (TCAs): Block the reuptake of NE and 5-HT (serotonin) by inhibiting the transporter protein

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Q

Protriptyline

A

Tricyclic Antidepressants (TCAs): Block the reuptake of NE and 5-HT (serotonin) by inhibiting the transporter protein

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Q

Citalopram

A

Selective Serotonin Reuptake Inhibitors (SSRIs): Block the reuptake of 5-HT (serotonin) = highly selective

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Q

Escitalopram

A

Selective Serotonin Reuptake Inhibitors (SSRIs): Block the reuptake of 5-HT (serotonin) = highly selective

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Q

Fluoxetine

A

Selective Serotonin Reuptake Inhibitors (SSRIs): Block the reuptake of 5-HT (serotonin) = highly selective

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Q

Paroxetine

A

Selective Serotonin Reuptake Inhibitors (SSRIs): Block the reuptake of 5-HT (serotonin) = highly selective

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Q

Sertraline

A

Selective Serotonin Reuptake Inhibitors (SSRIs): Block the reuptake of 5-HT (serotonin) = highly selective

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Q

Duloxetine

A

Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs): Block the reuptake of NE and 5-HT (serotonin) (and more effective if pain is experienced along with depression)

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Q

Venlafaxine

A

Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs): Block the reuptake of NE and 5-HT (serotonin) (and more effective if pain is experienced along with depression)

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Q

Bupropion

A

Atypical Antidepressants: Weak dopamine and NE reuptake inhibitor (also help decrease craving and withdrawal symptoms for nicotine)

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Q

Mirtazapine

A

Atypical Antidepressants: Enhances serotonin and NE neurotransmission (block presynaptic alpha-2 receptors) and potent antihistamine activity (sedative)

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Q

Nefazodone

A

Atypical Antidepressants: Weak inhibitor of serotonin reuptake and potent antihistamine activity (sedative)

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Q

Trazodone

A

Atypical Antidepressants: Weak inhibitor of serotonin reuptake and potent antihistamine activity (sedative)

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Q

Alprazolam

A

Benzodiazepines (Intermediate): Bind to benzodiazepine receptor that increase the affinity of GABA for its receptor and also decrease the release of GABA

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Q

Chlordiazepoxide

A

Benzodiazepines (Long): Bind to benzodiazepine receptor that increase the affinity of GABA for its receptor and also decrease the release of GABA

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Q

Clorazepam

A

Benzodiazepines (Long): Bind to benzodiazepine receptor that increase the affinity of GABA for its receptor and also decrease the release of GABA

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Diazepam

Benzodiazepines (Long): Bind to benzodiazepine receptor that increase the affinity of GABA for its receptor and also decrease the release of GABA

Estazolam

Benzodiazepines (intermediate): Bind to benzodiazepine receptor that increase the affinity of GABA for its receptor and also decrease the release of GABA

Flurazepam

Benzodiazepines (Long): Bind to benzodiazepine receptor that increase the affinity of GABA for its receptor and also decrease the release of GABA

Lorazepam

Benzodiazepines (Immediate): Bind to benzodiazepine receptor that increase the affinity of GABA for its receptor and also decrease the release of GABA

Midazolem

Benzodiazepines: Bind to benzodiazepine receptor that increase the affinity of GABA for its receptor and also decrease the release of GABA

Oxazepam

Benzodiazepines (Short): Bind to benzodiazepine receptor that increase the affinity of GABA for its receptor and also decrease the release of GABA

Temazepam

Benzodiazepines (Intermediate): Bind to benzodiazepine receptor that increase the affinity of GABA for its receptor and also decrease the release of GABA

Triazolam

Benzodiazepines (Short): Bind to benzodiazepine receptor that increase the affinity of GABA for its receptor and also decrease the release of GABA

Flumazenil

Benzodiazepines Antagonist: Antagonist/block the benzodiazepine binding site

Buspirone

Other Anxiolytic Drug: Serotonin receptor agonist (can treat anxiety but can't induce sedation)

Pentobarbital

Barbiturates: Bind to barbiturate receptor that increase the affinity of GABA for its receptor

Phenobarbital

Barbiturates: Bind to barbiturate receptor that increase the affinity of GABA for its receptor

Secobarbital

Barbiturates: Bind to barbiturate receptor that increase the affinity of GABA for its receptor

Eszopiclone

Other Hypnotic Agents ("Benzo-like"): High affinity for the benzodiazepine binding site of GABA receptors (mimicing the effects of Benzodiazepines but with shorter durations of action)

Zaleplon

Other Hypnotic Agents ("Benzo-like"): High affinity for the benzodiazepine binding site of GABA receptors (mimicing the effects of Benzodiazepines but with shorter durations of action)

Zolpidem

Other Hypnotic Agents ("Benzo-like"): High affinity for the benzodiazepine binding site of GABA receptors (mimicing the effects of Benzodiazepines but with shorter durations of action)

Ramelteon

Melatonin Receptor Agonist

Acamprosate

Treatment of Alcohol Dependence: Poorly understood MOA

Disulfiram

Treatment of Alcohol Dependence: Inhibits aldehyde dehydrogenase (causes terrible side effects so patients would avoid alcohol to prevent side effects)

Naltrexone

Treatment of Alcohol Dependence: Long acting opiate antagonist

Chlorpromazine

First Generation Antipsychotic: D2 antagonist (effects on movement - extrapyramidal side effects)

Fluphenazine

First Generation Antipsychotic: D2 antagonist (effects on movement - extrapyramidal side effects)

Haloperidol

First Generation Antipsychotic: D2 antagonist (effects on movement - extrapyramidal side effects)

Thioridazine

First Generation Antipsychotic: D2 antagonist (effects on movement - extrapyramidal side effects)

Thiothixene

First Generation Antipsychotic: D2 antagonist (effects on movement - extrapyramidal side effects)

Aripiprazole

Second Generation Antipsychotic: Antagonist with high affinity for D2 but also D3, D4, and 5-HT receptors (does NOT have effects on movement)

Clozapine

Second Generation Antipsychotic: Antagonist with high affinity for D2 but also D3, D4, and 5-HT receptors (does NOT have effects on movement)

Quetiapine

Second Generation Antipsychotic: Antagonist with high affinity for D2 but also D3, D4, and 5-HT receptors (does NOT have effects on movement)

Risperidone

Second Generation Antipsychotic: Antagonist with high affinity for D2 but also D3, D4, and 5-HT receptors (does NOT have effects on movement)

Ziprasidone

Second Generation Antipsychotic: Antagonist with high affinity for D2 but also D3, D4, and 5-HT receptors (does NOT have effects on movement)

Carbamazepine

Drugs used to treat Mania and Bipolar Disorder

Lithium

Drug used to treat Mania: MOA not understood (but thought to inhibit two signal transduction pathways)

Valprioc acid

Drugs used to treat Mania and Bipolar Disorder

Donepezil

Cholinesterase Inhibitors: Reversible inhibits the activity of acetylcholinesterase enzyme to prevent the breakdown of ACh

Galantamine

Cholinesterase Inhibitors: Reversible inhibits the activity of acetylcholinesterase enzyme to prevent the breakdown of ACh

Rivastigmine

Cholinesterase Inhibitors: Reversible inhibits the activity of acetylcholinesterase enzyme to prevent the breakdown of ACh

Memantine

NMDA Receptor Antagonist: Bind to glutamine receptors on the post-synaptic neuron to preven the binding of glutamine. This blocks NMDA receptors and prevent calcium influx caused by glutamine binding

Caffeine

Methylxanthines: Blockage of the adenosine receptors in the CNS; since adenosine inhibits dopamine, the blockage of the receptors indirectly enhances dopamine transmission

Theophylline

Methylxanthines: Blockage of the adenosine receptors in the CNS; since adenosine inhibits dopamine, the blockage of the receptors indirectly enhances dopamine transmission

Nicotine

Parasympathetic Agonist: Binds to nicotinic receptors in both the CNS and PNS (low doses = causes ganglionic stimulation; high doses = causes ganglionic blockade)

Varenicline

Parasympathetic Agonist: Partial agonist at neuronal nicotinic acetylcholine receptors in the CNS

Cocaine

Psychomotor Stimulant: Blocks the reuptake of monoamines (NE, 5-HT, and DA (especially)); Prolongs the effects of the neurotransmitters

Amphetamine

Amphetamines: is a substrate for the enzyme responsible for reuptake of NE and DA; is not metabolized by MAO and is stored in neurotransmitter storage vesicles which displaces NE and DA, Causes release of intracellular storages of NT via reversal of reuptake enzyme

Armodafinil

Amphetamines: Similar to amphetamine but specific for the DA transporter (prevents reuptake of DA only)

Modafinil

Amphetamines: Similar to amphetamine but specific for the DA transporter (prevents reuptake of DA only)

Dextroamphetamine

Amphetamines (Dextroamphetamine + Amphetamine = Adderall)

Lisdexamfetamine

Amphetamines

Methylphenidate

Amphetamines: very similar to amphetamine but enters the brain more slowly and DA levels not increased as rapidly

Dexmethylphenidate

Amphetamines

Lysergic acid diethylamide (LSD)

Hallucinogens: 5-HT agonist activity and activation of the sympathetic nervous system

Phencyclidine

Hallucinogens: Inhibits reuptake of DA, 5-HT, and Ne; Main action is to block the NMDA glutamate receptor to prevent passage of Ca

Tetrahydrocannabinol (THC)

Hallucinogens: Binds to cannabinoid receptors that are found on inhibitory presynaptic nerve terminals; this decreases inhibibity systems (like GABA) which actually leads to stimulation

Dronabinol

Hallucinogens: A cannabinoid used to treat nausea

Levodopa

Dopamine Precursors: is a precursor of DA; taken up by DA-ergic neurons and increases the content of DA vesicles, increase the amount of DA released and increases the activation of postsynaptic receptors

Carbidopa

Dopamine Precursors: is a dopa decarboxylase inhibitor that diminishes the metabolism of levodopa in the GI tract and peripheral tissues. Is taken up by peripheral nonadrenergic neurons byt not by CAN neurons, preventing levodopa from having an effect on peripheral neurons and makes levodopa more bioavailable int he brain

Amantadine

Dopamine Agonists: MOA unknown (but thought to be more than usual DA-containing vesicles are induced to release contents

Apomorphine

Dopamine Agonists: Mimic the action of dopamine by acting as DA agonists

Pramipexole

Dopamine Agonists: Mimic the action of dopamine by acting as DA agonists

Ropinirole

Dopamine Agonists: Mimic the action of dopamine by acting as DA agonists

Rotigotine

Dopamine Agonists: Mimic the action of dopamine by acting as DA agonists

Resagiline

MOAIs: MOA-B inhibitors which prevent the breakdown of DA; Selective for MOA-B (the enzyme responsible for breaking down DA)

Selegiline

MOAIs: MOA-B inhibitors which prevent the breakdown of DA; Selective for MOA-B (the enzyme responsible for breaking down DA)

Entacapone

COMT Inhibitor: COMT is upregulated in order to break down excess dopamine; inhibition of COMT by entacapone increases the bioavailability of levodopa

Benztropine

Anti-Muscarinic Agents: Since there is an imbalence between the DA-ergic and Ach-ergic symtoms in Parkinson's Disease, these drugs reduce cholinergic influence by blocking muscarinic receptors

Biperiden

Anti-Muscarinic Agents: Since there is an imbalence between the DA-ergic and Ach-ergic symtoms in Parkinson's Disease, these drugs reduce cholinergic influence by blocking muscarinic receptors

Trihexphenidy

Anti-Muscarinic Agents: Since there is an imbalence between the DA-ergic and Ach-ergic symtoms in Parkinson's Disease, these drugs reduce cholinergic influence by blocking muscarinic receptors

Fentanyl

Full Opioid Agonists: Bind to the opioid receptor and decrease the concentration of cAMP. This results in 1) an opening of K channels which results in hyperpolarization 2) prevention of Ca influx into the cell which prevents the vesicle from binding to the membrane. These drugs work to block the propagation of signaling at the level of the spinal cord

Heroin

Full Opioid Agonists: Bind to the opioid receptor and decrease the concentration of cAMP. This results in 1) an opening of K channels which results in hyperpolarization 2) prevention of Ca influx into the cell which prevents the vesicle from binding to the membrane. These drugs work to block the propagation of signaling at the level of the spinal cord

Hydromorphone

Full Opioid Agonists: Bind to the opioid receptor and decrease the concentration of cAMP. This results in 1) an opening of K channels which results in hyperpolarization 2) prevention of Ca influx into the cell which prevents the vesicle from binding to the membrane. These drugs work to block the propagation of signaling at the level of the spinal cord

Oxymorphone

Full Opioid Agonists: Bind to the opioid receptor and decrease the concentration of cAMP. This results in 1) an opening of K channels which results in hyperpolarization 2) prevention of Ca influx into the cell which prevents the vesicle from binding to the membrane. These drugs work to block the propagation of signaling at the level of the spinal cord

Meperidine

Full Opioid Agonists: Bind to the opioid receptor and decrease the concentration of cAMP. This results in 1) an opening of K channels which results in hyperpolarization 2) prevention of Ca influx into the cell which prevents the vesicle from binding to the membrane. These drugs work to block the propagation of signaling at the level of the spinal cord

Methadone

Full Opioid Agonists: Bind to the opioid receptor and decrease the concentration of cAMP. This results in 1) an opening of K channels which results in hyperpolarization 2) prevention of Ca influx into the cell which prevents the vesicle from binding to the membrane. These drugs work to block the propagation of signaling at the level of the spinal cord

Morphine

Full Opioid Agonists: Bind to the opioid receptor and decrease the concentration of cAMP. This results in 1) an opening of K channels which results in hyperpolarization 2) prevention of Ca influx into the cell which prevents the vesicle from binding to the membrane. These drugs work to block the propagation of signaling at the level of the spinal cord

Oxycodone

Full Opioid Agonists: Bind to the opioid receptor and decrease the concentration of cAMP. This results in 1) an opening of K channels which results in hyperpolarization 2) prevention of Ca influx into the cell which prevents the vesicle from binding to the membrane. These drugs work to block the propagation of signaling at the level of the spinal cord

Hydrocodone

Full Opioid Agonists: Bind to the opioid receptor and decrease the concentration of cAMP. This results in 1) an opening of K channels which results in hyperpolarization 2) prevention of Ca influx into the cell which prevents the vesicle from binding to the membrane. These drugs work to block the propagation of signaling at the level of the spinal cord

Levorphanol

Full Opioid Agonists: Bind to the opioid receptor and decrease the concentration of cAMP. This results in 1) an opening of K channels which results in hyperpolarization 2) prevention of Ca influx into the cell which prevents the vesicle from binding to the membrane. These drugs work to block the propagation of signaling at the level of the spinal cord