Midterm 2 Drugs Flashcards
Phenelzine
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)
Selegiline
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)
Tranylcypromine
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)
Amitriptyline
Tricyclic Antidepressants (TCAs): Block the reuptake of NE and 5-HT (serotonin) by inhibiting the transporter protein
Clomipramine
Tricyclic Antidepressants (TCAs): Block the reuptake of NE and 5-HT (serotonin) by inhibiting the transporter protein
Desipramine
Tricyclic Antidepressants (TCAs): Block the reuptake of NE and 5-HT (serotonin) by inhibiting the transporter protein
Doxepin
Tricyclic Antidepressants (TCAs): Block the reuptake of NE and 5-HT (serotonin) by inhibiting the transporter protein
Imipramine
Tricyclic Antidepressants (TCAs): Block the reuptake of NE and 5-HT (serotonin) by inhibiting the transporter protein
Nortriptyline
Tricyclic Antidepressants (TCAs): Block the reuptake of NE and 5-HT (serotonin) by inhibiting the transporter protein
Protriptyline
Tricyclic Antidepressants (TCAs): Block the reuptake of NE and 5-HT (serotonin) by inhibiting the transporter protein
Citalopram
Selective Serotonin Reuptake Inhibitors (SSRIs): Block the reuptake of 5-HT (serotonin) = highly selective
Escitalopram
Selective Serotonin Reuptake Inhibitors (SSRIs): Block the reuptake of 5-HT (serotonin) = highly selective
Fluoxetine
Selective Serotonin Reuptake Inhibitors (SSRIs): Block the reuptake of 5-HT (serotonin) = highly selective
Paroxetine
Selective Serotonin Reuptake Inhibitors (SSRIs): Block the reuptake of 5-HT (serotonin) = highly selective
Sertraline
Selective Serotonin Reuptake Inhibitors (SSRIs): Block the reuptake of 5-HT (serotonin) = highly selective
Duloxetine
Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs): Block the reuptake of NE and 5-HT (serotonin) (and more effective if pain is experienced along with depression)
Venlafaxine
Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs): Block the reuptake of NE and 5-HT (serotonin) (and more effective if pain is experienced along with depression)
Bupropion
Atypical Antidepressants: Weak dopamine and NE reuptake inhibitor (also help decrease craving and withdrawal symptoms for nicotine)
Mirtazapine
Atypical Antidepressants: Enhances serotonin and NE neurotransmission (block presynaptic alpha-2 receptors) and potent antihistamine activity (sedative)
Nefazodone
Atypical Antidepressants: Weak inhibitor of serotonin reuptake and potent antihistamine activity (sedative)
Trazodone
Atypical Antidepressants: Weak inhibitor of serotonin reuptake and potent antihistamine activity (sedative)
Alprazolam
Benzodiazepines (Intermediate): Bind to benzodiazepine receptor that increase the affinity of GABA for its receptor and also decrease the release of GABA
Chlordiazepoxide
Benzodiazepines (Long): Bind to benzodiazepine receptor that increase the affinity of GABA for its receptor and also decrease the release of GABA
Clorazepam
Benzodiazepines (Long): Bind to benzodiazepine receptor that increase the affinity of GABA for its receptor and also decrease the release of GABA
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
