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NU 578 Study Guide Test 2 & Unit 2 Combined 2026 | Questions & Verified Answers | Latest Update | Graded A+| University of South Alabama

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Latest Update 2026/2027 exam prep featuring the University of South Alabama NU 578 Study Guide for Test 2 & Unit 2 Combined with practice questions and verified answers. This comprehensive review is designed to help you strengthen key course concepts, reinforce high-yield topics, and prepare confidently for Test 2 and the Unit 2 assessment.

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NU 578 Study Guide Test 2 & Unit 2 Combined 2026 | Questions &
Verified Answers | Latest Update | Graded A+| University of South
Alabama

1. What medication is commonly prescribed to manage levodopa-induced
dyskinesias in patients with Parkinson's disease?

Carbidopa

Rasagiline

Amantadine

Pramipexole

2. If a patient has been on a CNS drug for an extended period, what potential
symptoms might indicate adaptive changes in their brain?

No noticeable changes in symptoms

Withdrawal symptoms or altered response to medication

Consistent effectiveness of the medication

Increased energy levels and improved mood

3. Specifically, what medications are first line preferred drugs in migraine
prophylaxis?

Propranolol

Divalproex

Topiramate

All of the above

,4. What characteristic of a 5-week-old infant's blood-brain barrier must be
considered when administering a drug that affects the central nervous
system (CNS)?

Effects of the drug on the neonate's CNS will be muted.

The blood-brain barrier will block the passage of drugs from the
blood to the CNS.

In neonates, the blood-brain barrier is poorly developed.

The blood-brain barrier is not present until 4 months of age.

5. A patient taking levodopa for Parkinson's develops dyskinesias. Which drug
works to to counteract and treat these symptoms?

tolcapone

amantadine

rotigotine

bromocriptine

6. Which medication is 1st-line for treatment of dyskinesias in PD patients?

amantadine

apomorphine

pimavanserin

clozapine

7. Describe how prolonged exposure to CNS drugs can affect neurotransmitter
systems in the brain.

CNS drugs only affect the production of neurotransmitters, not their
receptors.

, CNS drugs enhance neurotransmitter release without any changes to
receptor sensitivity.

Prolonged exposure to CNS drugs can lead to changes in
neurotransmitter receptor sensitivity and availability, affecting
overall neurotransmission.

CNS drugs have no effect on neurotransmitter systems over time.

8. If a patient with Parkinson's disease experiences worsening motor symptoms
despite medication, which of the following treatment options might be
considered based on the principles of deep brain stimulation?

Prescribing a new opioid medication.

Switching to a different class of antidepressants.

Deep brain stimulation targeting the subthalamic nucleus.

Increasing the dosage of dopamine agonists.

9. What is meant by the word Tolerance?

Decreased response occurs during the course of prolonged drug
use

The drug works even more

the drug is toxic to the host

Increased response occurs during the course of prolonged drug use

10. What are the adaptive changes that the brain undergoes with long-term
CNS drug exposure?

Neuroplasticity and receptor sensitivity alterations

Increased neurotransmitter production

Decreased blood flow to the brain

, Permanent brain damage


11. Why are dopamine agonists preferred as first-line therapy for patients with
mild or moderate PD symptoms compared to levodopa/carbidopa
combinations?

Dopamine agonists are more effective in relieving PD symptoms.

Dopamine agonists do not require enzymatic conversion to become
active.

Dopamine agonists are less likely to cause dyskinesias.

Dopamine agonists do not compete with dietary proteins for
absorption.

12. What are the two primary drug classes used to restore the balance between
dopamine and acetylcholine in Parkinson's disease?

MAO-B inhibitors and COMT inhibitors

SSRIs and SNRIs

Beta-blockers and calcium channel blockers

Dopamine agonists and anticholinergics

13. Why might there be a delay in the therapeutic effects of antidepressants
despite immediate increases in synaptic levels of monoamines?

It takes weeks for downstream effects on neural circuits and
neuroplasticity.

The body quickly develops tolerance to increased monoamines.

Most antidepressants are inactive until metabolized into active
compounds.

Neurotransmitter levels need to decrease for antidepressant effects.

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