Strong stimulant that counteracts the CNS-depressant effects of the opiate.
Diuretic that increases renal excretion of the opiate.
Drug that stimulates respiratory centers in the brain.
Competitive antagonist of opioid receptors.
Noncompetitive antagonist of opioid receptors.
Length of time a drug should be administered to achieve optimal effects
Time of day when a drug should be administered or optimal effects
Range of concentrations over which a drug is maximally effective for all patients
Range of concentrations over which a drug is safe and efficacious for most patients
Age range of patients that is optimal for a given drug
Full agonist with additive effects to adenosine at high concentrations
Partial agonist with additive effects to adenosine at high concentrations
Partial agonist with inhibitory effects to adenosine at high concentrations
Inert compound with no additive or inhibitory effects to adenosine at high concentrations
Competitive antagonist with inhibitory effects on receptor activation
Effect a new drug has on the body after its first administration.
Time it takes for a drug to be detected in the urine or feces after oral administration.
Ability of the intestines and liver to reduce the bioavailability of a drug.
Time it takes for a drug to reach therapeutic concentrations in the target tissue.
Initial effect a drug has on target tissues.
Noncellular barrier that prevents drugs from entering the CNS unless transported by specific carriers.
Cellular barrier that includes brain capillary endothelial cells that limits drug entry into the brain.
Virtual or conceptual barrier that can explain the behavior of some drug effects on the CNS.
Physical barrier that prevents blood from entering the brain.
Device that is used to prevent blood-borne drugs from entering the brain
Phase 1 metabolism always occurs prior to phase 2 metabolism.
Phase 1 metabolism occurs in the intestine where orally administered drugs can first be metabolized, whereas phase 2 metabolism occurs in the blood.
Phase 1 metabolism occurs in the liver soon after a drug is absorbed, whereas phase 2 metabolism occurs after a drug is excreted into the urine.
Phase 1 metabolic enzymes activate prodrugs, whereas phase 2 metabolic enzymes inactivate drugs.
Phase 1 metabolic reactions functionalize drugs, whereas phase 2 metabolic reactions conjugate drugs.
Route of administration.
Volume of distribution.
The pH of the urine should be increased.
The pH of the urine should be decreased.
The pH of the urine should be left unchanged.
CYP liver enzymes should be induced to increase metabolism of the drug.
The patient should drink more water to increase urine output.
Urinary excretion would be accelerated by administration of NH4Cl, an acidifying agent
Urinary excretion would be accelerated by giving NaHCO3, an alkalinizing agent
Less of the drug would be ionized at blood pH than at stomach pH
Absorption of the drug would be slower from the stomach than from the small intestine
Hemodialysis is the only effective therapy
Special carrier transport
There is only 1 metabolic path for drug elimination
The half-life is the same regardless of the plasma concentration
The drug is largely metabolized in the liver after oral administration and has low bioavailability
The rate of elimination is proportional to the rate of administration at all times
The drug is distributed to only 1 compartment outside the vascular system.
Phase 1 involves the study of a small number of normal volunteers by highly trained clinical pharmacologists
Phase 2 involves the use of the new drug in a large number of patients (1000–5000) who have the disease to be treated under conditions of proposed use (eg, outpatients)
Chronic animal toxicity studies must be complete and reported in the IND
Phase 4 involves the detailed study of toxic effects that have been discovered in phase 3
Phase 2 requires the use of a positive control (a known effective drug) and a placebo.
Animal tests cannot be used to predict the types of clinical toxicities that may occur because there is no correlation with human toxicity
Human studies in normal individuals will be done before the drug is used in individuals with hypertension
The degree of risk must be assessed in at least 3 species of animals, including 1 primate species
The animal therapeutic index must be known before trial of the agents in humans
Drugs that test positive for teratogenicity, mutagenicity, or carcinogenicity can be tested in humans
Food supplements and herbal (botanical) remedies are subject to the same FDA regulation as ordinary drugs
All new drugs must be studied in at least 1 primate species before NDA submission
Orphan drugs are drugs that are no longer produced by the original manufacturer
Phase 4 (surveillance) is the most rigidly regulated phase of clinical drug trials
Thiazide A is more efficacious than thiazide B
Thiazide A is about 100 times more potent than thiazide B
Toxicity of thiazide A is less than that of thiazide B
Thiazide A has a wider therapeutic window than thiazide B
Thiazide A has a longer half-life than thiazide B
Drug A is most effective
Drug B is least potent
Drug C is most potent
Drug B is more potent than drug C and more effective than drug A
Drug A is more potent than drug B and more effective than drug C
A chemical antagonist
An irreversible antagonist
A partial agonist
A physiologic antagonist
A spare receptor agonist
α adrenergic receptors.
β adrenergic receptors.
α1 adrenergic receptors.
β2 adrenergic receptors.