week 5- pharmacodynamics Flashcards
pharmacodynamics
study of the physiologic and biochemical effects that drugs have on the body and how those effects are produced
why is pharmacodynamics important for nurses?
- allows us to properly educate patients, evaluate effectiveness and administer PRN meds
- provides foundation for challenging a prescription
dose-response curve
phase 1: no measurable response
phase 2: inc in dose/inc in response
phase 3: plateau where an inc in dose leads to no change in effect
maximal efficacy
the largest effect that a drug can produce, indicated by the height of the dose-response curve
potency
the amount of drug needed to elicit a response, indicated by the relative position of the dose-response curve along the x axis
receptors
- functional macromolecules inside or on the surface of a cell where a ligand can bind
- any part of the cell can be a macromolecule that acts as a receptor
ligand
any chemical that binds to a receptor
drugs
chemicals that produce an effect by interacting with other chemicals in the body
drug-receptor complexes
drugs can only mimic or block the action of a specific receptor
types of receptors
cell-membrane embedded enzymes, ligand-gated ion channels, G protein-coupled receptor systems, transcription factors
cell membrane embedded enzymes
- span the cell membrane
- enzymes located inside the cell
- ligand binds to cell surface, activating the enzyme
- response within seconds
ligand-gated ion channels
- span the cell membrane
- used for regulating the flow of ions across the membrane
- ion flow is dependent on concentration gradient
- response within milliseconds
g-protein coupled receptors
- three components; receptor, G protein and effector
- ligand binding leads to activation of receptor, which then activates G protein, which then activates the effector
- rapid response
transcription factors
- receptor is located within the cell
- ligand binds to a receptor on the DNA (within nucleus)
- response is the transcription of mRNA
- response takes hours to days
receptor selectivity
- lock and key model
- only specific ligands can bind, leading to selective responses
example of side effects from non-selective receptors- epinephrine and alpha 1
- when binding to alpha 1, epinephrine should lead to inc HR
- however, the receptor is non-selective
- binding also controls pupil dilation, increased BP and slowed gastric motility
single occupancy theory
- states the the intensity of the response to a drug is proportional to the number of receptors occupied by that drug and a maximal response will occur when all available receptors have been occupied
- can’t explain potency or maximal efficacy
modified occupancy theory
- explains certain observations that the simple occupancy theory cannot
- the simple occupancy theory assumes that all drugs acting at a receptor are identical with respect to the ability to bind to the receptor and the ability to influence receptor function once binding has taken place
- drugs have two properties; affinity and intrinsic activity
affinity
strength of the attraction between a drug and its receptor, this is reflected in a drug’s potency (high affinity = very potent)
intrinsic activity
the ability of the drug to activate the receptor after binding, this is reflected in a drug’s maximal efficacy (high intrinsic activity = high efficacy)
drug categories
agonists, partial agonists, competitive antagonists, non-competitive antagonists
agonist
mimics an endogenous ligand, has both high affinity and intrinsic activity
ie. insulin
partial agonist
only has moderate intrinsic activity, maximum effect is half that of an agonist
antagonist
- no intrinsic activity, blocks agonist from binding
- high affinity
- outcome is dependent on amount of agonist present
ie. narcan
non-competitive antagonist
bind irreversibly to receptors, so they cannot be overcome by adding more agonist (reduces maximal response of an agonist)
competitive antagonist
reversibly binds receptors, can be overcome by adding more agonist (competes with agonist)
drug-receptor sensitivity
- cells can become desensitized when receptors are continually exposed to an agonist (dec # of receptors/dec response)
- cells can becomes hypersensitized when receptors are continually exposed to an antagonist (inc # of receptors)
ED50
- dose required to produce an effect in 50% of the population
- often given as the initial dose when starting a medication
LD50
dose required to produce toxic effects in 50% of the population
therapeutic index
measures the safety of a drug, larger TI=safer
TI = LD50/ED50
bioavailability
- amount of active drug that reaches systemic circulation from the administration site
- important to know for drugs with narrow TI
pharmacogenomics
- study of how genetics impact a person’s response to medications, metabolism is the most common genetic difference
- slow metabolism can lead to accumulation and toxicity, fast metabolism can lead to sub-therapeutic effect
other genetic variations
- altering drug receptors
- gender differences
ie. viagra inhibits PDE5, causing vasodilation in lungs and penis (reduces pulmonary HT)
