Pharmacology Toughest Exam Quiz assesses advanced knowledge in pharmacology, focusing on drug interactions, effects, and medical responses. It's ideal for students and professionals aiming to deepen their understanding of pharmacological principles and their application in clinical settings.
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.
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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
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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
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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.
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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
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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.
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Bioavailability.
Route of administration.
Volume of distribution.
Clearance.
Elimination t1/2
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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.
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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
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Aqueous diffusion
Endocytosis
First-pass effect
Lipid diffusion
Special carrier transport
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About 1%
About 10%
About 50%
About 90%
About 99%
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.
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Distribution
Excretion
First-pass effect
First-order elimination
Zero-order elimination
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0.5h
1h
3h
4h
7h
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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.
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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
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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
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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
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A chemical antagonist
An irreversible antagonist
A partial agonist
A physiologic antagonist
A spare receptor agonist
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Chemical antagonist
Noncompetitive antagonist
Partial agonist
Pharmacologic antagonist
Physiologic antagonist
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Norepinephrine
Serotonin
Glutamate
Acetylcholine
Epinephrine
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Muscarinic receptors.
α adrenergic receptors.
Nicotinic receptors.
β adrenergic receptors.
Glutamate receptors.
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Serotonin receptors.
α1 adrenergic receptors.
β2 adrenergic receptors.
Nicotinic receptors.
Acetylcholinesterase.
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Acetylcholine.
Norepinephrine.
Serotonin.
Aspartate.
Epinephrine.
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Bacteria causing the brain infection are not sensitive to the antibiotic.
Blood brain barrier excludes the antibiotic if it is administered systemically.
Antibiotic binds to brain cells and is not available to the bacteria.
Antibiotic is activated by the cerebrospinal fluid.
Bacteria are mostly located in the cerebrospinal fluid.
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Increased sedation.
Hyperexcitability.
A depressed mood.
Nausea.
Blurred vision
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α1 Adrenergic
β1 Adrenergic
β2 Adrenergic
M2 muscarinic
Nicotinic
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Sweating
Dry eyes
Dry skin
Confusion
Tachycardia
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Stimulating the release of ACh.
Stimulating the release of norepinephrine.
Blocking the release of ACh.
Blocking the release of norepinephrine.
Blocking muscarinic receptors.
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Butyrylcholinesterase.
Acetylcholinesterase.
Na+, K+-A Pase.
Tyrosine hydroxylase.
Monoamine oxidase.
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Physostigmine
Bethanechol
Pralidoxime
Morphine
Gentamicin
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Stimulating the release of ACh.
Blocking the reuptake of norepinephrine.
Inhibiting monamine oxidase.
Blocking the release of ACh.
Inhibiting AChE.
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Blocking ACh at nicotinic receptors of neuromuscular endplate.
Blocking ACh at nicotinic receptors in the adrenal medulla.
Increasing Na+ and K+ permeability of the postsynaptic neuromuscular membrane.
Blocking the transmission of the action potential along the nerve axon.
Blocking the release of ACh from neuromuscular presynaptic vesicles.
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Blockade of transmission at autonomic ganglia and neuromuscular junctions.
Blockade of muscarinic receptors.
Stimulation of adrenergic receptors.
Blockade of adrenergic receptors.
Stimulation of muscarinic receptors.
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Her lips to turn black.
Her heart to beat faster.
Numbness in her fingers and toes.
Transient blindness.
Transient diminished hearing
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The act that her spray container is empty.
Degradation of the oxymetazoline.
A manufacturing defect in the nasal spray container.
A loss of innervation to her nasal mucosa.
Rebound hyperemia of her nasal mucosa
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A nonselective α adrenergic antagonist such as phenoxybenzamine.
A selective α2 adrenergic receptor agonist such as clonidine.
A selective β2 adrenergic receptor agonist such as terbutaline.
A nonselective β adrenergic receptor antagonist such as propranolol.
A selective α1 adrenergic receptor antagonist such as terazosin.
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β adrenergic receptors are more sensitive to IV than oral propranolol.
The IV dose avoids the “first pass” metabolism of oral propranolol.
Treatment of hypertension requires a higher dose of propranolol than does treatment of a cardiac arrhythmia.
The density of β2 receptors in the heart is greater than the density of β2 receptors on blood vessels.
Oral propranolol is excreted by the kidney at a faster rate than IV propranolol.
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Stimulates 5-HT receptors.
Enhances the release of 5-HT from presynaptic nerve endings.
Inhibits the presynaptic uptake of 5-HT.
Blocks MAO which degrades 5-HT.
Enhances the synthesis of 5-HT.
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Bronchoconstriction from α-blocking agents
Acute heart failure exacerbation from β blockers
Impaired blood sugar response with α blockers
Increased intraocular pressure with β blockers
Sleep disturbances from α-blocking drug
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Increased GI absorption of clozapine.
Decreased renal excretion of clozapine.
A decrease in his blood-brain barrier function.
Decreased metabolism of clozapine.
A pharmacy mistake.
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24 hours.
12 hours.
3 days.
1 week.
3 to 4 weeks.
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α1-adrenergic receptor antagonism.
β-adrenergic receptor antagonism.
5-HT receptor stimulation.
D2 receptor antagonism.
Blockade of norepinephrine uptake into presynaptic terminals.
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An unusual taste.
Increased libido.
Weight gain.
Her urine turned green.
Hirsutism.
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Sertraline may take 2 weeks or more to become effective
It is preferable that she take the drug in the morning
Muscle cramps and twitches can occur
She should notify you if she anticipates using other prescription drugs
All of the above
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Bulimia
Chronic pain of neuropathic origin
Generalized anxiety disorder
Obsessive-compulsive disorder
Premenstrual dysphoric disorder
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Acidify the urine
Acidify the blood
Alkalinize the blood
Alkalinize the urine
Use a drug to stimulate hepatic CYP 2C19
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