Question 1

A nurse is administering drug X to a patient. The drug information states that the drug acts by activating receptors in the peripheral nervous system by increasing transmitter synthesis. The nurse understands that the effect of this drug is to:

A) activate axonal conduction.
B) enhance transmitter storage.
C) increase receptor activation.
D) synthesize supertransmitters.

increase receptor activation.

Accepted Answer

Drugs that increase transmitter synthesis increase receptor activation. Other drugs that alter transmitter synthesis can decrease synthesis and would cause decreased receptor activation. Drugs that affect transmitter production do not exert their effects on axonal conduction. The amount of transmitter produced does not directly affect transmitter storage. Some drugs that alter transmitter synthesis cause the synthesis of transmitter molecules that are more effective than the transmitter itself.

Question 2

A patient receives morphine and shows signs of toxicity. The prescriber orders naloxone (Narcan) to reverse the effects of the morphine. The nurse understands that the naloxone works at the same receptor sites as the morphine to:

A) block transmitter reuptake.
B) inhibit transmitter release.
C) interfere with transmitter storage.
D) prevent activation of receptors.

Accepted Answer

Morphine and its antagonist, naloxone, both act directly at the same receptors. Morphine causes activation, and naloxone prevents activation. Neither morphine nor naloxone acts to alter transmitter reuptake, release, or storage.

Question 3

A nurse learns about a drug that interferes with transmitter storage in the PNS. The transmitter affected by this drug causes an increased heart rate. What response will the nurse expect to see when this drug is administered?

A) Bradycardia
B) Positive inotropic effects
C) Prolonged receptor activation
D) Tachycardia

Bradycardia

Accepted Answer

Drugs that interfere with transmitter storage reduce receptor activation, because disruption of storage decreases the amount of transmitter available for release. Because this transmitter increases the heart rate, the result will be a decrease in the heart rate. Inotropic effects control the force of contraction, not the rate of contraction. Decreased transmitter storage would result in decreased receptor activation. Tachycardia would occur if transmitter availability were increased.

Question 4

A patient receiving botulinum toxin injections to control muscle spasticity asks how the drug works. The nurse knows that this drug affects the transmitter acetylcholine by:&#10;A) inhibiting its release.&#10;B) interfering with its storage.&#10;C) preventing its reuptake.&#10;D) promoting its synthesis.

Accepted Answer

Acetylcholine is a neurotransmitter that activates receptors that increase skeletal muscle contraction. Botulinum toxin inhibits the release of this transmitter. It does not interfere with storage, reuptake, or synthesis of acetylcholine.

Question 5

A nursing student asks about drugs that interfere with the termination of transmitter action. Which statement by the nurse is correct?&#10;A) &#34;Drugs act on this process by altering the diffusion of the transmitter away from the synaptic gap.&#34;&#10;B) &#34;Drugs can interfere with termination by either increasing or decreasing reuptake of the transmitter.&#34;&#10;C) &#34;Drugs in this category lead to decreased activation by the transmitter in the synapse.&#34;&#10;D) &#34;These drugs reduce either reuptake or degradation of the transmitter, causing an increase in receptor activation.&#34;

Accepted Answer

Drugs that interfere with termination of transmitter action do so by blocking transmitter reuptake or inhibiting transmitter degradation, resulting in increased receptor activation, because more of the transmitter remains available. Diffusion of the transmitter occurs naturally, but it is a slow process with little clinical significance. Drugs that alter this process cause a decrease in reuptake, not an increase. The effect of drugs that interfere with termination of transmitter action is increased activation.

Question 6

A patient has allergies and takes an antihistamine. The patient wants to know how the drug works. The nurse understands that antihistamines work because they are what?&#10;A) Activators&#10;B) Agonists&#10;C) Antagonists&#10;D) Antidotes

Accepted Answer

Antihistamines bind to receptors to prevent activation by histamine; this makes antihistamines antagonist drugs. Antihistamines do not activate receptors. Agonist drugs activate receptors; they are not antidotes.

Question 7

A nurse is teaching a group of nurses about neuropharmacology. The nurse asks which classes of drugs act by reducing axonal conduction. Which response by a participant is correct?&#10;A) Antihypertensives&#10;B) Antipsychotics&#10;C) Local anesthetics&#10;D) Antidepressants

Accepted Answer

Local anesthetics are the only drugs shown to work by reducing axonal conduction. Antihypertensives, antipsychotics, and antidepressants do not act by reducing axonal conduction.

Question 8

A nurse is teaching a group of nursing students about neuropharmacology. Which statement by a student about peripheral nervous system (PNS) drugs indicates a need for further teaching?&#10;A) &#34;Drugs affecting axonal conduction have a variety of uses.&#34;&#10;B) &#34;Drugs that alter synaptic transmission can be highly selective.&#34;&#10;C) &#34;Many PNS drugs act by altering synaptic transmission.&#34;&#10;D) &#34;These drugs work by influencing receptor activity.&#34;

Accepted Answer

Local anesthetics are the only drugs shown to work by altering axonal conduction. Any drug affecting axonal conduction would be nonselective, because axonal conduction of impulses is essentially the same in all neurons. In contrast, drugs that affect synaptic transmission can be highly selective, because each transmitter has different effects on receptor sites. Most PNS drugs work on synaptic transmission processes. Through their effects on transmitters, they influence receptor activity.

Deck 12: Basic Principles of Neuropharmacology