AND ANSWERS WITH COMPLETE SOLUTIONS VERIFIED
Absorption
absorption: what happens to a drug from the time it enters the body until it enters the
circulating fluid and tissues.
critical concentration
critical concentration: the concentration a drug must reach in the tissues that respond to
the particular drug to cause the desired therapeutic effect
Distribution
distribution: movement of a drug to body tissues; the places where a drug may be
distributed depend on the drug’s solubility, perfusion of the area, cardiac output, and
binding of the drug to plasma proteins
Excretion
excretion: removal of a drug from the body; routes include the kidneys, skin, lungs, bile,
and feces.
During excretion, drug is removed through the (5 examples)
kidneys, skin, lungs, bile, and feces.
First-past effect
first-pass effect: a phenomenon in which drugs given orally are absorbed by the small
intestine, then carried directly through the portal venous system to the liver, where they
,may be largely inactivated by liver enzymes before they can enter the general
circulation.
Half-life
half-life: the time it takes for the amount of drug in the body to decrease to one half of
the peak level it achieved
Loading dose
loading dose: a dose higher than what is usually used for treatment, administered to
allow the drug to reach the critical concentration sooner
pharmacodynamics
pharmacodynamics: the study of the interactions between the chemical components of
living systems and the foreign chemicals, including drugs, that enter living
organisms; the way a drug affects a body
pharmacogenomics
pharmacogenomics: the study of genetically determined variations in the response to
drugs
pharmacokinetics
pharmacokinetics: the way a medication travels through the body, including absorption,
distribution, biotransformation, and excretion; how the body acts on a drug
receptor sites
receptor sites: specific areas on cell membranes that react with certain chemicals to
cause an effect within the cell
agonists
, drugs that interact directly with receptor sites to cause the same activity that natural
chemicals would cause at that site. These drugs are called agonists
3 examples of how agonists interact at receptor sites. . .
change cell permeability (think insulin)
prevent the breakdown of natural chemicals at receptor sites (think SSRIs)
block normal stimulation therefore preventing effect (think Curare: competitive agonist,
paralytic).
Receptor theory of drug action. A. Agonist interaction with receptor site on cell.
Agonist interaction with receptor site on cell. Molecules of drug A react with specific
receptor sites on cells of effector organs and change the cells’ activity.
Receptor theory of drug action. B. Competitive antagonism.
B. Competitive antagonism. Drug A and drug C have an affinity for the same receptor
sites and compete for these sites; drug C has a greater affinity, occupies more of the
sites, and antagonizes drug A.
Receptor theory of drug action. C. Noncompetitive antagonism.
C. Noncompetitive antagonism. Drug D reacts with a receptor site that is different from
the receptor site for drug A but still somehow prevents drug A from binding with its
receptor sites. Drugs that act by inhibiting enzymes can be pictured as acting similarly
to the receptor site antagonists. Enzyme inhibitors block the binding of molecules of
normal substrate to active sites on the enzyme.
3 Key Points of Pharmacodynamics
Pharmacodynamics is the process by which a drug works within or affects the body.