ch 1-4 mine Flashcards
pharmacology
scientific study of the actions of drugs on a living organism
neuropharmacology
study of drug induced changes in NS cells
psychopharmacology
study of drug induced changes in mood, behaviour, and thinking
drug action
molecular changes produced by drug at target receptor site
drug effect
physiological/ psychological alterations caused by drug action
therapeutic effects
desired changes
specific drug effects
based on physical/ biochemical interxns of drug at target site
non-specific drug effects
based on unique individual characteristics
placebo
belief in fake drug causing real improvement
nocebo
belief in fake drug causing real pain (expectation-induced anxiety)
pharmacokinetic
factors contributing to bioavailability (admin, absorption, distribution, binding, inactivation, excretion)
bioavailability
concentration of drug in the blood that is free to bind to specific target sites
enteral
admin through GI tract (rectal or oral)
parenteral
admin elsewhere
oral admin
- drug must be resistant to stomach acid
- mostly absorbed after stomach (in small intestine)
absorption
mvmt from admin site to blood circulation
first-pass metabolism
liver metabolizes some of drug before it circulates (may reduce bioavailability)
rectal admin
- bioavailability is difficult to predict
- drug may avoid FPM
intravenous injection
- most rapid and accurate
- drug reaches brain almost instantly
intramuscular injection
- slower than IV
- more even absorption over time
intraperitoneal
- used in lab animals
- through abdominal wall into peritoneal cavity
- rapid effects
- variable bioavail.
subcutaneous
- just below skin
- slow and steady absorption
inhalation
- rapid absorption
- preferred when oral is too slow, and GI tract would destroy drug
topical
- admin through a mucous membrane such as oral cavity, nasal, or vagina
sublingual
- under the tongue
- rapid absorption
- avoids FPM
intranasal
- local effects
- avoids FPM
transdermal
- controlled and sustained delivery
- avoids FPM
- limited drugs can penetrate skin
epidural
spinal anaesthetic injected right into CSF
gene therapy
application of DNA through viral vectors
lipid-soluble drugs
mvmt across phospholipid bilayer of a cell (always from high to low concentration)
ionized drugs
extent of ionization depends on
1. relative acidity/alkalinity of solution
2. intrinsic property of molecule
ionization of weak acids
ionize easily in alkaline (basic) env’t
ionization of weak bases
ionize easily in acidic env’t
electrical charge and lipid solubility
less charge = more soluble
distribution
body parts where blood flow is the greatest will have highest concentration of drug
how are blood capillaries helpful in distribution
numerous pores allow for drugs to move from blood to body tissues regardless of lipid solubility (unless bound by protein)
blood brain barrier
- CSF remains stable (unlike blood plasma)
- many things entering organs do not diffuse into CSF/brain tissue
- selectively permeable
- many ionized drugs dont pass BBB
how are brain capillaries different from typical capillaries
brain capillaries have astrocytes surrounding the endothelial cell
astrocytes (astroglia)
star shaped glial cells w numerous extensions
- modulate env’t
- metabolically assist neurons
- phagocytosis for cellular debris
placental barrier
- easily lipid soluble
- less easily water soluble
acute toxicity
baby’s exposure to disproportionately high drug blood levels from mom
drug depot
aka silent receptors
- binding at inactive sites where no effect is inititated
- any drugs bound to depots cannot reach active sites nor can they be metabolized by liver
drug binding
is reversible (only bound until blood level drops causing gradual unbinding)
depot binding
has major effects on magnitude and duration of effects
- reduces concentration, delays effects
bioavailability
concentration of a drug present in the blood that is free to bind to target sites
bioactivation
metabolic process turning an inactive drug into an active drug
biotransformation
drug is eliminated through metabolism
first- order kinetics
exponential elimination of drugs from the bloodstream
steady state plasma level
desired blood concentration achieved when absorption/distribution = metabolism/excretion
how do half life and effects relate
quicker the half life, quicker the effects
zero-order kinetics
drug is cleared at constant rate regardless of concentration
role of liver in excretion
metabolizes drugs and chemically alters them before excretion
enzyme induction
- increase in liver enzymes
- speeds up biotransformation
- increased metabolic rate for all other dugs
(happens w repeated use)
enzyme inhibition
- inhibit action of enzymes
- decreases metabolism (intense, prolonged effects)
drug competition
- inhibition caused by competition for one enzyme
- bioavailability for one or both increases (can’t be metabolized)
therapeutic drug monitoring
blood samples taken after drug admin. to determine plasma levels of drug
receptors
large proteins located on cell surface or within cells that are responsive to biologically active agents
ligand
molecule that binds to a receptor w some selectivity
receptor agonists
bind to particular receptor to initiate a cellular response
affinity
ability of a molecule to bind to a receptor which then determines potency
efficacy
ability of an agonist to active its receptor
receptor antagonists
- no cellular action
- prevent an active ligand from binding by blocking receptor
partial agonists
drugs that bind to receptor but have low efficacy, producing weaker biological effects
inverse agonists
substances that activate the receptor but produces the opposite effect of an agonist
up regulation
receptor amount increases
down regulation
receptor amount decreases
dose response curves
describes extent of drug effect
potency
absolute amount of drug necessary to produce a specific effect
therapeutic index
TD50/ED50 margin of safety
competitive antagonists
compete w agonists to bind to receptors but fail to initiate an effect (reduces effect of agonists)
non-competitive antagonists
reduce agonist effectiveness in other way than competing for receptor
physiological antagonism
2 drugs acting in diff. ways but interxn reduces each others effectiveness
potentiation
combination of 2+ drugs producing a greater effect than sum of individual effects
tolerance
response diminishes w same dose after use
sensitization
response increases w same dose of drug
cross tolerance
tolerance to one drug creating tolerance for similar drugs
acute tolerance
happens after one use
metabolic tolerance
drug increases their own rate of metabolism
pharmacodynamic tolerance
most dramatic, changes in nerve cell function to compensate for drug presence (withdrawal)
behavioral tolerance
occurs in same env’t as drug admin
- classical/ operant conditiong
sensory neurons
sensitive to env’tal stimuli, signals interneurons
interneurons
within brain and spinal cord
motor neurons
direct biobehavioral responses
soma
cell body containing nucleus
dendrites
tree-like projections that receive info from other cells
axon
conducts electrical signal from cell body to terminal buttons
cytoplasm
intracellular fluid
convergence
dendrites receive and integrate info from numerous cells
divergence
dendrites transmit their info to others
axon collaterals
branches of axons
myelin sheath
fatty, insulating coating made of glial cells
nodes of ranvier
breaks in myelin sheath to increase conducting of AP
terminal buttons
enlargements at the end of axon, contain synaptic vesicles of NTs
transcription
mRNA makes a copy of active gene in nucleus and transports it to ribosomes to decode it and make a protein
DNA methylation
env’tally induced epigenetic covalent attachment or methyl groups to a gene to decrease its expression