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67 Cards in this Set
- Front
- Back
Pharmacokinetics
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– the process by which drugs can be administered
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Sites of action
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the points at which molecules of drugs interact with molecules located on or in cells of the body, thus affecting some biochemical processes of these cells
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Drug effects
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the changes we can observe in an animal’s physiological processes and behavior
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Drug
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an exogenous chemical not necessary for normal cellular functioning that significantly alters the functions of certain cells of the body when taken in relatively low doses
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Psychopharmacology
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study of the effects of drugs on the NS and on behavior
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Routes of Administration
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Injection:drug is dissolved and suspended in a liquid, and injected via hypodermic needle
Intravenous, intraperitoneal, intramuscular, subcutaneous, intracerebral, intracerebroventricular --Oral: into the mouth; swallowed --Sublingual:placing substance beneath the tongue --Intrarectal:into the rectum --Inhalation: vaporous substance into the lungs --Topical:directly onto the skin or mucous membrane |
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Best way to look at drug effectiveness
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Dose response curve
--effect of drug versus dose |
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Maximum effect
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point when increasing dose does not produce stronger effect
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Margin of safety
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the difference between dose-response curves; desirable effect and toxic effect
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most desirable drug
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= LARGE margin of safety
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Therapeutic index
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measure of a drug’s margin of safety
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lower therapeutic index =
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more care taken in prescribing the drug
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Therapeutic Index Ratio
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RATIO = desired effects dose (50%)/ toxic effects dose (50%)
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Most desirable Drugs
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High affinity for therapeutic effects
Low affinity for toxic effects |
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Affinity
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the readiness with which 2 molecules join together
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High affinity
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theraputic affects
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low affinity
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toxic effect
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Sites of Drug Action
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Agonist (AGO)
Antagonists (ANT) |
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Agonist (AGO)
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facilitates or mimics NT
---DIRECT AGO: binds to receptor site --> opens ion channel ---INDIRECT AGO: attaches to alternative site--> facilitates opening of channel |
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Antagonist (ANT)
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blocks or inhibits NT
---DIRECT ANT: binds to receptor site--> prevents ion channel from opening ---INDIRECT ANT: attaches to receptor site-->prevents opening of ion channel |
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ACh (Acetylcholrine) roles
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---Movement
---Activation of the cerebral cortex- learning and memory ---REM sleep and dreaming |
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ACh has 2 components
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1. Choline – derived from breakdown of lipids
2. Acetate – anion found in vinegar |
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Production of ACh
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1. in presence of the enzyme choline acetyltransferase (ChAT)
2. the acetate ion is transferred from Acetyl-CoA to the choline molecule, yielding a molecule of ACh and CoA |
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Too much ACh in cleft
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then it opens too many channels causing either
1. Inhibitory would be paralysis 2. excite it and get spaticity |
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Botulinim Toxin
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ANT); prevents release of ACh
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Black Widow Spider Venom
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(AGO); stimulates release of ACh
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Curare:
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(ANT) blocks ACh receptors (temporary paralysis but brain still works)
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Neostigmine:
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(AGO); AChE inhibitor (used in persons with myasthenia gravis)
Defends the enzyme from destroying Ach, |
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Location of ACh
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---Dorsolateral Pons: REM sleep
----Basal Forebrain: Cortical activation; facilitates learning ---Medial Septum: controls electrical rhythms of hippocampus and modulates it s functions (including formation of memories |
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Destruction of Acetylcholine
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ACh released from terminal button-->deactivated by acetycholinesterase (AChE)-->produces choline and acetate-->reuptake returns choline to terminal button-->choline converted back to ACh
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Monoamines 2 catergories
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1. Catecholamines
2. Indolamines |
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Catecholamines
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1. Dopamine (DA)
2. Epinephrine (minor importance in the brain compared to NE) 3. Norepinephrine (NE) |
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Indolamines
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Serotonin (5-HT)
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Dopamine (DA) Roles
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1. Movement
2. Attention 3. Learning 4. Higher cortical problem solving 5. Pleasure |
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Locations of Dopamine Neurons
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1. Nigrostriatal:
Control of movement 2. Mesolimbic: Nucleus accumbens reinforces drug use 3. Mesocortical: Excitatory effect on frontal cortex; formation of STM; planning; problem solving strategy |
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Dopamine precursors
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Tyrosine-->L-Dopa-->Dopamine
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Amphetamine:
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(AGO); blocks reuptake
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Cocaine:
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(AGO); blocks reuptake
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Ritalin:
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(AGO); blocks reuptake
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Clozapine:
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Antipsychotic
(ANT); blocks D4 receptor |
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Chlorpromazine:
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(ANT); blocks D2 receptor
Antipsychotic |
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Levels of Dopamine
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Too much=schizophrenia--so you want to take an ANT
to little= Parkinson-- want to give AGO |
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Tyosine
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essential amino acid
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Blocking Receptor effect on NT
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decreases the productivity
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Blocking the uptake
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increases the effectiveness
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Parkinson treatment
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Caused by degeneration of the nigrostriatal system
---L-Dopa Increases dopamine (Agonist) |
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Depression
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not enough dopamine
give MAO-I (because the MAO is the enzyme that kills dopamine) |
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Norepinephrine (NE) Precursor
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tyrosine --> L-DOPA -->dopamine --> norepinephrine
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Norepinephrine (NE) System
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cell bodies located in locus coeruleus (dorsal pons)
---Increase in vigilance |
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Norepinephrine (NE) Role
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increased vigilance, attention, sexual behaviors, control of appetite
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Serotonin (5-HT) Roles
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1. Regulation of mood
2. Control of eating 3. Sleep/dreaming and arousal 4. Regulation of pain 5. Regulating impulsivity |
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Serotonin (5-HT) Precursors
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Tryptophan --> 5-HTP --> Serotonin (5-HT)
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Serotonin (5-HT) location
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Cell bodies in the Raphe nuclei
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LSD:
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(AGO); stimulates 5-HT release
(presynaptic) causes more synaptic vesicles to fuse |
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MDMA (Ecstasy)
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(AGO); stimulates 5-HT release
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Fenfluramine:
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(AGO); stimulates 5-HT release and inhibits reuptake
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Fluoxetine (Prozac):
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(AGO); inhibits reuptake
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3 Most Common Amino Acids in the Brain
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1. Glutamate
2. GABA 3. Glycine |
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Glutamate
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principle excitatory NT in the CNS
---Direct excitatory and inhibitory effects on axons ---They raise or lower the threshold of excitation, thus affecting the rate at which action potentials can occur |
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GABA
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principle inhibitory NT in the brain
----Stabilizes brain activity from uncontrollable neuron firing (i.e. seizures) |
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Glycine
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inhibitory effect over muscles
---Located in spinal cord and lower brain |
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ACh Receptors
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1. Nicotinic receptors (Ionotropic)
2. Muscarinic receptors (Metabotropic) |
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Nicotinic receptors (Ionotropic)
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stimulated by nicotine
---Rapid actions – ion channels directly controlled ---Some found at axoaxonic synapses in brain where they produce presynaptic facilitation ----Curare (ANT) – drug that blocks nicotinic receptors; causes temporary paralysis but the brain still works |
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Muscarinic receptors (Metabotropic)
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stimulated by muscarine (found in poisonous mushroom)
----Slower action – ion channels indirectly controlled by second messengers ---Predominate in CNS ----Atropine – drug that blocks muscarinic receptors |
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Myasthenia gravis
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a hereditary disorder caused by an attack of a person’s immune system against acetylcholine receptors located on skeletal muscles
the person becomes weaker as the muscles become less responsive to the NT (ACh) |
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Neostigmine
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(AGO) is used in persons with myasthenia gravis
----AChE inhibitor ---The person regains some strength because the ACh that is released has a more prolonged effect on the remaining receptors ----This drug cannot cross the blood-brain barrier (no effect on AChE found in CNS) |
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Can choline attach directly to Acetate?
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NO: (it is transferred from a molecule of acetyl-CoA)
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