ATI RN
Central and Peripheral Nervous System Drugs Questions
Question 1 of 5
A 44-year-old woman was admitted to the psychiatric hospital for the sixth time since the age of 36. She was confused and threatening, saying that the voices are back. The woman had been on antipsychotic therapy for several years, but she of the patient's presenting symptoms
Correct Answer: C
Rationale: Step-by-step rationale for why choice C, Mesolimbic pathway, is correct: 1. The mesolimbic pathway is involved in the reward and pleasure system. 2. Dysfunction in this pathway can lead to psychotic symptoms like hallucinations. 3. Antipsychotic medications target this pathway to reduce psychotic symptoms. 4. The patient's symptoms of hearing voices suggest dysfunction in the mesolimbic pathway. Summary of why other choices are incorrect: A. Frontal cortex: Primarily involved in executive functions, not directly related to psychotic symptoms like hallucinations. B. Vestibular nuclei: Responsible for balance and spatial orientation, not related to psychotic symptoms. D. Striatum: Involved in motor control and procedural learning, not directly linked to hallucinations or psychotic symptoms.
Question 2 of 5
Which of the following drugs most likely caused the patient's symptoms?
Correct Answer: C
Rationale: The correct answer is C: Amitriptyline. The patient's symptoms suggest anticholinergic toxicity, which aligns with amitriptyline's side effects due to its strong anticholinergic properties. Amitriptyline can cause dry mouth, blurred vision, urinary retention, and confusion. Bupropion (A) is unlikely to cause these specific symptoms. Mirtazapine (B) is more sedating than anticholinergic. Paroxetine (D) is an SSRI and does not typically cause anticholinergic toxicity.
Question 3 of 5
Which of the following molecular actions in the enteric nervous system most likely mediated the adverse effect of the drug in the patient?
Correct Answer: A
Rationale: The correct answer is A: Blockade of M receptors. The enteric nervous system predominantly utilizes muscarinic receptors to regulate gastrointestinal motility. Blocking these receptors can lead to adverse effects such as constipation, as it disrupts normal peristalsis. Increased serotonergic activity (B) would typically enhance gastrointestinal motility. Activation of β receptors (C) would enhance smooth muscle relaxation, potentially improving motility. Increased adrenergic activity (D) could also enhance motility due to the role of adrenergic receptors in promoting smooth muscle contraction. However, the adverse effect described in the question is more likely to be caused by the blockade of M receptors, making choice A the correct answer.
Question 4 of 5
A drug has a complex molecular mechanism of action that includes a blockade of presynaptic alphareceptors. Which of the following drugs was most likely given?
Correct Answer: B
Rationale: The correct answer is B: Clonidine. Clonidine is an alpha-2 adrenergic agonist, which means it acts by stimulating presynaptic alpha-2 receptors, leading to a decrease in norepinephrine release. This matches the drug described in the question that blocks presynaptic alphareceptors. Amitriptyline (A) is a tricyclic antidepressant that primarily acts by blocking the reuptake of serotonin and norepinephrine. Bupropion (C) is an atypical antidepressant that inhibits the reuptake of dopamine and norepinephrine. Mirtazapine (D) is a noradrenergic and specific serotonergic antidepressant that enhances serotonin and norepinephrine activity through different mechanisms. Therefore, Clonidine is the most likely drug given due to its action on presynaptic alphareceptors, while the other choices have different mechanisms
Question 5 of 5
What was most likely the reason for the adverse effects reported by the patient?
Correct Answer: B
Rationale: The correct answer is B: Decreased renal elimination of lithium. Thiazides reduce lithium excretion leading to lithium accumulation and toxicity. Thiazide-induced dilutional hypernatremia (A) is unlikely as thiazides generally cause hyponatremia. Decreased hepatic metabolism of lithium (C) is not a major factor in lithium toxicity. Thiazide-induced hypokalemia (D) is a possible side effect but not the primary reason for lithium toxicity in this scenario.