Author Question: A psychiatric nurse is teaching a patient about an antidepressant medication. The nurse tells the ... (Read 64 times)

sc00by25 · **on:** Jul 23, 2018

A psychiatric nurse is teaching a patient about an antidepressant medication. The nurse tells the patient that therapeutic effects may not occur for several weeks. The nurse understands that this is likely the result of:

a. changes in the brain as a result of prolonged drug exposure.
b. direct actions of the drug on specific synaptic functions in the brain.
c. slowed drug absorption across the blood-brain barrier.
d. tolerance to exposure to the drug over time.

Question 2

A nurse is teaching nursing students about the pharmacology of methyldopa. Which statement by a student indicates the need for further teaching?

a. Methyldopa results in alpha2 agonist activation, but it is not itself an alpha2 agonist.
b. Methyldopa is not effective until it is converted to an active compound.
c. Methyldopa reduces blood pressure by reducing cardiac output.
d. Methyldopa's principal mechanism is vasodilation, not cardiosuppression.

SVictor · **Reply #1 on:** Jul 23, 2018

Answer to Question 1

ANS: A
It is thought that beneficial responses to central nervous system (CNS) drugs are delayed because they result from adaptive changes as the CNS modifies itself in response to prolonged drug exposure, and that the responses are not the result of the direct effects of the drugs on synaptic functions. The blood-brain barrier prevents protein-bound and highly ionized drugs from crossing into the CNS, but it does not slow the effects of drugs that can cross the barrier. Tolerance is a decreased response to a drug after prolonged use.

Answer to Question 2

ANS: C
Methyldopa does not reduce the heart rate or cardiac output, so its hypotensive actions are not the result of cardiac depression. The drug is not, in itself, an alpha2 agonist. When taken up into brainstem neurons, it is converted into methylnorephinephri ne, which is an alpha2 agonist; it is not effective until converted to this active compound. Its hypotensive effects are the result of vasodilation, not cardiosuppression.