Monoamine oxidase inhibitors work by:
Inhibiting Dopamine production in the hypothalamus and limbic system
Inhibiting the 5-HT2 receptors on the postsynaptic membrane
Inhibiting the reuptake of 5-HT and Norepinephrine into the presynaptic neuron
Inhibiting the enzyme responsible for terminating the actions of dopamine, norepinephrine and serotonin
The Correct Answer is D
Monoamine oxidase inhibitors (MAOIs) are a class of antidepressants used primarily in treatment-resistant depression and some anxiety disorders. They work by increasing levels of key monoamine neurotransmitters in the brain, including serotonin, norepinephrine, and dopamine. This is achieved through inhibition of the enzyme responsible for breaking down these neurotransmitters. Understanding this mechanism is essential because it also explains their significant food and drug interaction risks.
Rationale:
A. Monoamine oxidase inhibitors do not work by inhibiting dopamine production in the hypothalamus or limbic system. Instead, they act after neurotransmitters are released, affecting their breakdown rather than their synthesis. Dopamine production itself is not directly suppressed by this medication class.
B. Inhibition of 5-HT2 receptors on the postsynaptic membrane is the mechanism of atypical antipsychotics, not MAOIs. Monoamine oxidase inhibitors do not exert their primary effect through receptor blockade but through preventing enzymatic degradation of monoamines. This option describes a different pharmacologic class entirely.
C. Inhibition of serotonin (5-HT) and norepinephrine reuptake into the presynaptic neuron is the mechanism of action of selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs). MAOIs do not block reuptake transporters; instead, they prevent breakdown of neurotransmitters within the neuron and synaptic cleft.
D. Monoamine oxidase inhibitors work by inhibiting the monoamine oxidase enzyme responsible for breaking down dopamine, norepinephrine, and serotonin in the brain. This leads to increased availability and prolonged action of these neurotransmitters in the synaptic cleft. This mechanism explains both their antidepressant effects and their high risk for serious drug and food interactions.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is B
Explanation
Carbamazepine (Tegretol) is an anticonvulsant used for seizure disorders, trigeminal neuralgia, and mood stabilization. It has a narrow therapeutic index and is associated with potentially serious hematologic adverse effects due to bone marrow suppression. Because of these risks, ongoing laboratory monitoring is required to ensure patient safety during long-term therapy. Nursing and provider follow-up focus heavily on blood dyscrasias and drug toxicity surveillance.
Rationale:
A. Annual eye examinations for cataracts are not a standard monitoring requirement for Carbamazepine (Tegretol). While some anticonvulsants may have rare ocular side effects, cataract formation is not a recognized routine long-term complication of carbamazepine. Therefore, routine ophthalmologic screening is not part of standard monitoring guidelines.
B. Complete blood count every three to four months is essential because Carbamazepine (Tegretol) can cause serious hematologic effects such as leukopenia, agranulocytosis, and aplastic anemia. Regular CBC monitoring helps detect early signs of bone marrow suppression, allowing timely intervention before severe complications develop. This is a key safety measure in long-term therapy.
C. Routine troponin testing is not indicated for patients taking Carbamazepine (Tegretol) because it is not associated with direct myocardial injury. Troponin is used to assess acute cardiac ischemia, which is unrelated to carbamazepine’s pharmacologic profile. Cardiac monitoring is not part of standard long-term surveillance for this medication.
D. Monthly pregnancy testing is not routinely required for all women of childbearing age on Carbamazepine (Tegretol). Although carbamazepine is teratogenic and requires counseling on contraception and pregnancy risks, standardized frequent pregnancy testing is not universally mandated. Monitoring focuses more on ensuring effective contraception and preconception counseling rather than monthly testing.
Correct Answer is B
Explanation
Migraine prophylaxis is indicated in patients who experience frequent attacks, significant functional impairment, or poor quality of life despite effective abortive therapy. Preventive medications aim to reduce the frequency, severity, and duration of migraine episodes. In patients with comorbid conditions such as asthma, medication selection must avoid agents that may worsen respiratory function. Individualized therapy is essential to balance efficacy with safety.
Rationale:
A. Referral for ergotamine-based infusions is not appropriate for long-term migraine prevention. Ergotamine therapies are primarily used for acute or refractory migraine attacks, not routine prophylaxis. Additionally, infusion therapy is reserved for severe, treatment-resistant cases and would not be first-line for a stable outpatient with controlled abortive response using triptans.
B. Amitriptyline (Elavil) is an appropriate choice for migraine prevention in this patient. It is effective in reducing migraine frequency by modulating serotonin and norepinephrine pathways involved in pain transmission. It is also safe in patients with asthma, unlike beta-blockers, making it a suitable prophylactic option for MN’s clinical profile.
C. Propranolol (Inderal) is commonly used for migraine prophylaxis but should be avoided in patients with asthma. As a non-selective beta-blocker, it can cause bronchoconstriction by blocking beta-2 receptors in the lungs, potentially worsening asthma symptoms. Therefore, it is contraindicated in this patient despite its effectiveness for migraines.
D. Phenytoin (Dilantin) is not indicated for migraine prophylaxis. It is primarily used for seizure disorders and has no established role in preventing migraines. Its adverse effect profile, including gingival hyperplasia and neurologic toxicity, makes it inappropriate for this clinical scenario.
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