MSN 672 Psychopathopharmacology II at Northern Kentucky University
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Free MSN 672 Psychopathopharmacology II at Northern Kentucky University Questions
Which of the following statements is true regarding first-line pharmacological treatment of agitation and aggression in a patient diagnosed with dementia?
- First-line pharmacological treatment of agitation and aggression in dementia is actually considered by many experts to be therapy with selective serotonin reuptake inhibitors (SSRIs) and serotonin–norepinephrine reuptake inhibitors (SNRIs), which can help some patients.
- First-line pharmacological treatment of agitation and aggression in dementia is actually considered by many experts to be therapy with selective second-generation antipsychotics which can help some patients.
- First-line pharmacological treatment of agitation and aggression in dementia is actually considered by many experts to be therapy with valproate which can help some patients.
- First-line pharmacological treatment of agitation and aggression in dementia is actually considered by many experts to be therapy with topiramate which can help some patients.
Explanation
SSRIs—especially citalopram and sertraline—are increasingly considered first-line pharmacologic options for agitation and aggression in dementia because they carry a far safer profile than antipsychotics. Antipsychotics, while effective, are not first-line due to their black box warning for increased mortality, risk of stroke, sedation, and extrapyramidal symptoms in elderly dementia patients. SSRIs target underlying affective symptoms such as irritability, anxiety, and depressive features that frequently drive behavioral disturbances, making them safer and often effective early options.
Correct Answer Is:
A. First-line pharmacological treatment of agitation and aggression in dementia is actually considered by many experts to be therapy with selective serotonin reuptake inhibitors (SSRIs) and serotonin–norepinephrine reuptake inhibitors (SNRIs), which can help some patients.
Sam is a 73-year-old patient with Alzheimer's disease. Sam has been on donepezil, 10 mg/day for approximately 8 months to aid in improving his cognitive functioning. Sam's wife has begun to notice a loss of effectiveness over the past months of donepezil. Sam's wife is requesting an intervention. The PMHNP decides to augment the donepezil with memantine 5 mg/day at hs. Which of the following properties of memantine listed below may be useful in treating Alzheimer's disease?
- Serotonin 3 (5HT3) antagonism
- Sigma antagonism
- N-methyl-D-aspartate (NMDA) antagonism at the PCP site
- N-methyl-D-aspartate (NMDA) antagonism at the magnesium site
Explanation
Memantine works by blocking excessive activation of NMDA receptors at the PCP (phencyclidine) binding site, which reduces glutamate-mediated excitotoxicity in the brain. In Alzheimer's disease, chronic overstimulation of NMDA receptors contributes to neuronal damage and cognitive decline. By modulating this pathway, memantine helps protect neurons and can improve or stabilize cognitive functioning, especially when used together with cholinesterase inhibitors like donepezil.
Correct Answer Is:
C. N-methyl-D-aspartate (NMDA) antagonism at the PCP site
A 44-year-old unemployed male with a 20-year debilitating history of alcoholism "heavy drinker" presents to the clinic. The patient has a history of Bipolar Disorder and is currently taking lithium. The patient has not experienced withdrawal; his longest period of sobriety recently has been one week. The patient fears that he may start drinking again due to “stress.” Which of the following medications below would be most appropriate for the PMHNP to prescribe for the treatment of alcoholism for this patient?
- Disulfiram
- Naloxone
- Acamprosate
- Naltrexone
Explanation
Acamprosate is the safest option for this patient because it does not interact with lithium, does not affect mood stability in bipolar disorder, and is indicated to help maintain abstinence in patients who have recently stopped drinking. It works by modulating glutamate and GABA balance disrupted by chronic alcohol use. Disulfiram is risky in patients with poor adherence and can worsen mood instability. Naltrexone is contraindicated in bipolar patients on lithium due to increased risk of mood destabilization and possible hepatotoxicity. Naloxone is not a treatment for alcohol use disorder.
Correct Answer Is:
C. Acamprosate
Which of the following neurotransmitters are considered part of the ascending reticular activating system in the brain that works together to regulate arousal? (Select all that apply.)
- Histamine
- Dopamine
- Orexin
- Methylation
Explanation
The ascending reticular activating system (ARAS) is responsible for regulating arousal,
wakefulness, and attention. Several neurotransmitters play a central role in this process:
A. Histamine
Histamine is produced in the tuberomammillary nucleus of the hypothalamus and promotes
alertness and wakefulness. Antihistamine medications that cross the blood-brain barrier often
cause drowsiness due to histamine inhibition.
B. Dopamine
Dopamine, released from the ventral tegmental area (VTA) and other midbrain regions, is
essential for maintaining arousal, motivation, and cognitive alertness. It supports the brain’s
reward and activation pathways that sustain wakefulness.
C. Orexin
Orexin (also known as hypocretin), produced in the lateral hypothalamus, stabilizes
wakefulness by stimulating other arousal-promoting systems. Deficiency in orexin is associated
with narcolepsy.
The PMHNP is aware that Carbamazepine (Tegretol) and Oxcarbazepine (Trileptal) can both potentially cause which side effect?
- Decrease in bicarbonate
- Hyponatremia
- Hypercholesterolemia
- Hypocalcemia
Explanation
B. Hyponatremia
Both carbamazepine and oxcarbazepine can cause SIADH (syndrome of inappropriate
antidiuretic hormone secretion), leading to dilutional hyponatremia. This is a well-documented
and clinically significant adverse effect. Symptoms can include headache, confusion, lethargy,
and in severe cases seizures. Sodium levels must be monitored regularly when patients are on
either medication.
A 35-year-old man Army veteran presents with a chief complaint of excessive crying, which he notes is often triggered by thoughts of dying prior to seeing his family again. His wife reports that he is often tense and “flies off the handle,” followed by episodes of difficulty breathing and increased heart rate. The patient’s symptom of difficulty breathing is related to activation of what part of the brain?
- Hippocampus
- Hypothalamus
- Parabrachial nucleus
- Periaqueductal gray
Explanation
The parabrachial nucleus, located in the pons, plays a key role in autonomic and respiratory
regulation. It integrates input from emotional centers such as the amygdala and hypothalamus
and translates those emotional signals into physiological responses—including changes in
breathing and heart rate. In emotionally charged states such as anxiety or panic, activation of
this area can cause the sensation of difficulty breathing and hyperventilation.
A 28-year-old male returns to the clinic and reports worsening of nightmares after taking Trazodone for one month. The PMHNP reviewed the patient’s records and notices the patient has a chronic history of PTSD and alcoholism. What is likely the most appropriate alternative treatment for this patient?
- Switch to a Benzodiazepine
- Switch to Aripiprazole
- Switch to Wellbutrin
- Switch to α1 antagonists
Explanation
α1 antagonists, such as Prazosin, are effective in treating PTSD-related nightmares and sleep disturbances. Prazosin works by blocking adrenergic activity, reducing the excessive
noradrenergic response during sleep that contributes to vivid dreams and nightmares. Unlike
benzodiazepines or antidepressants, it has minimal risk for dependency—making it particularly
appropriate for a patient with a history of alcoholism. It improves sleep quality and decreases the
frequency and severity of trauma-related nightmares.
Which of the statements are true regarding Valproic Acid? Select all that apply.
- Monitor hepatic levels: LFTs
- Valproate is metabolized primarily in the kidneys
- Valproate can induce high levels of lamotrigine and risk for Stevens-Johnson Syndrome
- Valproate is effective for acute manic phase
Explanation
A. Monitor hepatic levels: LFTs
Valproic acid carries a significant risk of hepatotoxicity. Liver function tests (LFTs) must be
checked before initiating therapy and monitored periodically. Hepatic failure can occur,
especially in the first 6 months of treatment, making this an essential precaution.
C. Valproate can induce high levels of lamotrigine and risk for Stevens-Johnson Syndrome
Valproate inhibits the metabolism of lamotrigine, causing lamotrigine serum levels to rise.
Elevated lamotrigine greatly increases the risk of Stevens–Johnson Syndrome (SJS), a
life-threatening dermatologic reaction. Dose adjustments and slow titration of lamotrigine are
required.
D. Valproate is effective for acute manic phase
Valproic acid is one of the most effective mood stabilizers for acute mania, mixed episodes, and
rapid-cycling bipolar disorder. It acts quickly and is often preferred when lithium is ineffective or
contraindicated.
------ and --------------, also known as α2δ ligands since they bind to the α2δ subunit of presynaptic N- and P/Q-type VSCCs, block the release of excitatory neurotransmitters such as glutamate that occurs when neurotransmission is excessive, as postulated in the amygdala to cause fear.
- Gabapentin and Pregabalin
- Serotonin and Norepinephrine reuptake inhibitors (SNRIs)
- Histamine and Serotonin
- Pregabalin and Histamine
Explanation
Gabapentin and Pregabalin are α2δ (alpha-2-delta) ligands that bind to the α2δ subunit of
presynaptic voltage-sensitive calcium channels (VSCCs), specifically the N-type and P/Q-type.
This binding reduces calcium influx and inhibits the excessive release of excitatory
neurotransmitters like glutamate. By dampening overactive neurotransmission in regions such as
the amygdala, these drugs help reduce symptoms of anxiety and fear, making them effective in
conditions like generalized anxiety disorder and neuropathic pain.
Opioid withdrawal syndrome is characterized by which of the following symptoms (select all that apply)
- Bradycardia
- Dysphoria
- Irritability
- Pilo-erection
Explanation
B. Dysphoria
Dysphoria is a common symptom of opioid withdrawal because the abrupt loss of opioid stimulation leads to reduced dopamine activity in the reward pathways. This produces emotional distress, sadness, anxiety, and a strong sense of unease as the body adjusts to the absence of opioids.
C. Irritability
Irritability occurs due to noradrenergic overactivity in the locus coeruleus when opioids are removed. This sudden increase in sympathetic activity makes patients feel tense, restless, and easily angered during withdrawal.
D. Pilo-erection
Pilo-erection, or “goosebumps,” results from autonomic hyperactivity during opioid withdrawal. Increased sympathetic output triggers involuntary contraction of the tiny muscles attached to hair follicles, making pilo-erection a classic physical sign of withdrawal.
Correct Answer Is:
B. Dysphoria
C. Irritability
D. Pilo-erection
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