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33 Cards in this Set

  • Front
  • Back

what are the two tenets of the simple occupancy theory?

1. the intensity of a drug's response is proportional to the number of receptors occupied

2. the maximal response occurs when all the receptors are occupied

Which theory implies that two drugs that act at the same receptor should have the same efficacy?

simple occupancy theory

what are the three tenets of the modified occupancy theory?

1. the intensity of a drug's response is proportional to the number of receptors occupied by the drug

2. different drugs that bind to the same receptor may have different binding strengths/affinities for that receptor

3. different drugs binding to the same receptor may have difference receptor activating abilities (i.e. intrinsic activities)

define affinity

the attraction a drug has for its receptor

affinity is associated with potency/efficacy?

potency. drugs with high affinity are more potent for a certain effect than drugs with low affinity

define intrinsic activity

ability of a drug to activate the receptor

intrinsic activity is associated with potency/efficacy?

it is associated with efficacy. specifically, maximal efficacy

drugs with a high intrinsic activity have high maximal efficacy

know urself

t/f agonists, antagonists and partial agonists all produce some sort of pharmacological effect


which of these do agonists have?


intrinsic ability


what are the 3 receptors dopamine binds to at the 3 different dose levels, and what is the effect?

1. at low doses dopamine binds to the dopamine receptor. This causes renal artery vasodilation, increased renal blood flow, increased urinary output

2. at medium doses dopamine binds to the beta adrenergic receptor. this causes increased cardiac output

3. at high doses dopamine binds to the alpha adrenergic receptor. this causes increased renal vasoconstriction, increased renal blood flow, and increased urinary output

which of these two do antagonists have?


intrinsic activity

they only have affinity

t/f antagonists effect is based on the presence of the corresponding agonist

true. antagonists won't do anything unless there's an agonist there too

describe the function of beta blockers

they block the binding of epinephrine beta 1 receptors, ultimately decreasing cardiac output

describe the functions of antihistamines

block the binding of histamines to H1 histamine receptors, preventing allergic symptoms

describe functions of gastric acid reducers

block the binding of histamine to histamine H2 receptors, decreases gastric acid secretion

describe the function of opiod receptor blockers

blocks binding of opiates to opioid receptors, useful for drug overdoses

Name and describe the three types of antagonists

1. competitive antagonists - binding occurs at the same site as the agonists, and binding is reversible

2. irreversible antagonists - binding occurs at the same site as the agonists, binding is irreversible

3. allosteric antagonists - binding occurs at a different site than the agonists, binding is reversible

what will happen to the DRC of an agonist, if the amount of competitive antagonist present is lowered?

the DRC will shift to the left.

how does the max efficacy of a drug change when a competitive antagonist is added, and then the same amount of agonist is added?

it doesnt

how can the effect of a competetive antagonist be overcome?

by adding more agonist

name an example of a competitive antagonist


what will happen to the DRC of an agonist, if the amount of irreversible antagonist present is increased?

the efficacy of the drug is lowered (specifically, max efficacy)

how can the effect of a non-competetive antagonist be overcome?

it cannot. it is non-competitive.

how long do irreversible agonist effects last?

until the receptor is replaced. for this reason, these antagonists are rarely used in clinical settings

describe the function of allosteric antagonists

they bind to different sites on the receptor than the agonist. the binding of which changes the conformation of the receptor, preventing agonists from binding to them. binding is reversible, but not competitive (they are not competing for the same sites)

What are the effects of allosteric antagonists on the DRC of an agonist? how can these effects be overcome?

an increase in the amount of allosteric antagonists decreases the maximal efficacy of the agonist. these effects cannot be overcome as the AA is non-competitive.

do partial agonists lower maximal efficacy or potency of the agonist?

maximal efficacy

for most drugs, their action depends on the specific location of their receptor. where should it be, and what is the exception?

receptors should be on the cell membrane surface. the exception to this is intracellular receptors/transcription factors

describe desensitization

when a receptor has been exposed to a certain agonist for a prolonged period of time, the receptor may become destroyed, or internalized by the cell. this will lead to a decrease in the number of receptors on the cell membrane surface, causing a greater amount of drug necessary to produce the same effect

describe metabolic tolerance

increased exposure to a certain agonism may cause the induction of drug metabolizing enzymes, which will lead to greater metabolic capacity, and lower free drug concentrations. more dope is needed to get the same kick

describe tachyphylaxis

a rapid decrease in response to a drug. in the case of transdermal patches, drug free periods must be enforced so tachyphylaxis does not occur.

describe receptor upregulation/sensitization

when a receptor has been exposed to an antagonist for a prolonged period of time, the opposite of desensitization may occur. the cell will synthesize more receptor and move it to the cell membrane. in this case the cell is said to become supersensitive/hypersensitive. WHen an agonist is added, then the cell goes off bang bang.