Pharmacology NSG124- Exam with Correct Answers
Terms in this set (683)
What drugs does to body
Pharmacodynamics
Drug can have direct and indirect action
Drug can have additive / synergistic effects
What body does to the drug
A - absorption
Pharmacokinetics
D - distribution
M - metabolism
E - excretion
ED50 Dose of drug required to produce 50% of its maximal effect
EC50 Cocentration of drug required to produce 50% of its maximal effect
LD50 Dose of drug required to produce lethal effect in 50% of the given population
Therapeutic ratio LD50/ED50
Ability of a drug to cause a defined effect
Potency
Determined by the dissociation constant
Usually the more lipid soluble the drug the more potent
Affinity How avidly a drug binds to its receptor
The extent to which a drug activates a receptor once bound
Intrinsic activity 1 for agonists
0 for antagonists
-1 for reverse agonists
Efficacy The ability of a drug to produce the maximal effect when bound to its receptor
Drug that binds to a receptor and produces a maximal effect
Full agonist
IA = 1
, Drug that binds to a receptor and produces a submaximal effect (even with high
doses)
Partial agonist IA = between 0 and 1
Acts as an antagonist if combined with full agonist
eg, buprenorphine at MOR
Drug that binds to a receptor and produces the opposite effect to an agonist
Inverse agonist IA = between -1 and 0
eg, naloxone
Drug that binds to a receptor and produces no effect
Antagonist
IA = 0
Binds at the same site as the agonist
Competitive antagonist Effect can be overcome by increasing concentration of agonist
eg, non depolarising NMB
Binds to a different site to the agonist which results in conformational change of
agonist's receptor
Non-competitive antagonist
Cannot be overcome by increasing concentration of agonist
eg, ketamine antagonises glutamate at NMDA receptors
Binds to same receptor as agonist or different site
Irreversible antagonist Cannot be overcome by increasing concentration of agonist
eg, aspirin to COX1
Alter agonist binding site by binding to a remote site altering binding characteristics
Allosteric modulators Can enhance or reduce activity of the agonist
eg, benzos at GABA A receptor
Rapid decrease in response to repeated doses over a short period of time
Tachyphylaxis Usually due to deplete neurotransmitters
eg, ephedrine
Slow decrease in response to repeated doses over a long period of time
Densensitisation
Due to change in morphology or number of receptors
Larger doses needed to have the same effect
Tolerance Due to altered sensitivity
eg, chronic opioid use
The proportion of drug that reaches systemic circulation compared to the dose
given IV
Bioavailability
Drugs administered IV hav 100% bioavailability
% = oral / IV
Whereby a drug is absorbed and metabolised prior to being reaching the systemic
circulation
The usual process is absorption by the GI tract and transported to the liver where
they undergo metabolism
eg
First pass metabolism
verapamil - 20%
morphine - 40%
codeine - 60%
aspirin - 70%
paracetamol - 80%
Terms in this set (683)
What drugs does to body
Pharmacodynamics
Drug can have direct and indirect action
Drug can have additive / synergistic effects
What body does to the drug
A - absorption
Pharmacokinetics
D - distribution
M - metabolism
E - excretion
ED50 Dose of drug required to produce 50% of its maximal effect
EC50 Cocentration of drug required to produce 50% of its maximal effect
LD50 Dose of drug required to produce lethal effect in 50% of the given population
Therapeutic ratio LD50/ED50
Ability of a drug to cause a defined effect
Potency
Determined by the dissociation constant
Usually the more lipid soluble the drug the more potent
Affinity How avidly a drug binds to its receptor
The extent to which a drug activates a receptor once bound
Intrinsic activity 1 for agonists
0 for antagonists
-1 for reverse agonists
Efficacy The ability of a drug to produce the maximal effect when bound to its receptor
Drug that binds to a receptor and produces a maximal effect
Full agonist
IA = 1
, Drug that binds to a receptor and produces a submaximal effect (even with high
doses)
Partial agonist IA = between 0 and 1
Acts as an antagonist if combined with full agonist
eg, buprenorphine at MOR
Drug that binds to a receptor and produces the opposite effect to an agonist
Inverse agonist IA = between -1 and 0
eg, naloxone
Drug that binds to a receptor and produces no effect
Antagonist
IA = 0
Binds at the same site as the agonist
Competitive antagonist Effect can be overcome by increasing concentration of agonist
eg, non depolarising NMB
Binds to a different site to the agonist which results in conformational change of
agonist's receptor
Non-competitive antagonist
Cannot be overcome by increasing concentration of agonist
eg, ketamine antagonises glutamate at NMDA receptors
Binds to same receptor as agonist or different site
Irreversible antagonist Cannot be overcome by increasing concentration of agonist
eg, aspirin to COX1
Alter agonist binding site by binding to a remote site altering binding characteristics
Allosteric modulators Can enhance or reduce activity of the agonist
eg, benzos at GABA A receptor
Rapid decrease in response to repeated doses over a short period of time
Tachyphylaxis Usually due to deplete neurotransmitters
eg, ephedrine
Slow decrease in response to repeated doses over a long period of time
Densensitisation
Due to change in morphology or number of receptors
Larger doses needed to have the same effect
Tolerance Due to altered sensitivity
eg, chronic opioid use
The proportion of drug that reaches systemic circulation compared to the dose
given IV
Bioavailability
Drugs administered IV hav 100% bioavailability
% = oral / IV
Whereby a drug is absorbed and metabolised prior to being reaching the systemic
circulation
The usual process is absorption by the GI tract and transported to the liver where
they undergo metabolism
eg
First pass metabolism
verapamil - 20%
morphine - 40%
codeine - 60%
aspirin - 70%
paracetamol - 80%
