Psych 202: Psychopharmacology Flashcards
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Routes of administration (general description of each, as well as specific route of administration for drugs discussed in class and the text)
Smoking - bioavailable
Injection - bioavailable
Ingestion - biotransformation
Pharmacokinetics
Collective name for all the factors that affect the relationship between a drug and it’s target receptors, such as affinity and efficacy.
Bioavailable
Referring to a substance, usually a drug, that is present in the body in a form that is able to interact with physiological mechanisms
Biotransformation
The process in which enzymes convert a drug into a metabolite that is itself active, possibly in ways that are substantially different from the actions of the original substance
Factors affecting drug effectiveness
Genetics, tolerance, sensitization
Affinity
Binding affinity
The propensity of molecules of a drug (or other ligand) to bind to receptors
Efficacy
Intrinsic activity
The extent to which a drug activates a response when it binds to a receptor
Dose-response curve
A formal plot if a drug’s effects (y-axis) versus the dose given (x-axis)
Tolerance
A condition in which, with repeated exposure to a drug, an individual becomes less responsive to a constant dose
Sensitization
A process in which the body shows enhanced response to a given drug after repeated doses
Withdrawal
Uncomfortable symptoms that arise when a person stops taking a drug he or she used frequently, especially at high doses
Exogenous
Arising from outside the body
Endogenous
Produced inside the body
Agonists
A molecule, usually a drug, that binds a receptor molecule and initiates a response like that of another molecule, usually a neurotransmitter
Antagonists
A molecule, usually a drug, that interferes with or prevents the action of a neurotransmitter
Sites of action
.
Drug effects on production of neurotransmitter
In the soma or cell body precursors to neurotransmitter are synthiesized
Agonists act as precursors, increasing the production/amount of neurotransmitter made
Antagonists inactivate enzymes needed to neurotransmitter synthesis, decreasing the production/amount of neurotransmitter made
Drug effects on storage of NT
Antagonists inactivate transporter molecules and prevent the storage of neurotransmitter so that no neurotransmitter will be released into the synapse
Drug effects on release of NT
Agonists increase Ca++ coming into the axon terminal so that more vesicles fuse and rupture into the synapse
Antagonists block Ca++ channels so Ca++ can’t get into the axon terminal and neurotransmitter will not be released
Drug effects on receptors
Direct agonists bind to the binding site of the endogenous neurotransmitter
Indirect agonists bind to a different binding site on the receptor and open ion channels to produce post synaptic potential
Direct antagonists bind to and block the binding sites for the endogenous neurotransmitter
Indirect antagonists bind to a different binding site on the receptor and prevent ion channels from opening
Drug effects on autoreceptors
Agonists block the autoreceptor to increase the amount on neurotransmitter released
Antagonists activate the autoreceptor to decrease the amount of neurotransmitter released
Drug effects on termination of synaptic transmission
Agonists inactive transporter molecules that do reputable or deactivate enzymes responsible for breakdown
Antagonists act as enzymes to break down neurotransmitter and increase efficiency of breakdown and transporters molecules
Amines
A neurotransmitter based on modifications of a single amino acid nucleus
Acetylcholine, serotonin, dopamine
Acetylcholine (characteristics, origination, systems, receptors, drug effects at various sites of action)
Moron neurons (ventral horn) - released at neuromuscular junctions - controls muscle contractions Pons - projects to cortex and thalamus - controls cortical arousal and REM sleep Basal forebrain - projects to the hippocampus, amygdala, cortex - facilitates learning and memory
Acts on nicotinic and muscarinic receptors