Final Exam Review Flashcards

1
Q

A 32-year-old woman with bipolar disorder has been maintained on 900 mg/day of lithium. She was
doing well for a long time and had even been able to lose the weight she had initially gained with lithium. She broke up with her boyfriend 5 months ago and has been feeling depressed ever since. You augment her with 300 mg/day of quetiapine, but after several weeks she complains of weight gain and wants to change medications. Blockade of which two receptors was most likely responsible for this weight gain induced by quetiapine?
-Dopamine 2 and alpha 1 adrenergic
-Muscarinic 1 and serotonin 6
-Serotonin 2C and histamine 1
-Serotonin 2A and muscarinic 3

A

Blockade of serotonin 2C receptors and histamine 1 receptors has been linked to weight gain.

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2
Q

A patient with bipolar depression has been treated for 6 months with lamotrigine plus an atypical
antipsychotic with partial response. The decision is made to stop the atypical antipsychotic; however, during down-titration, the patient develops withdrawal dyskinesias. No treatment for the dyskinesias is initiated, and after 2 weeks they still remain. Which of the following is true?
-An anticholinergic medication, such as Benztropine, should be started.
-If the withdrawal dyskinesias still remain after 2 weeks, they are likely to be permanent.
-The antipsychotic should be restarted.
-The patient’s withdrawal dyskinesias may take several weeks to months to resolve.

A

Withdrawal dyskinesias are often reversible with time and usually resolve within a few weeks; however, they can take several months to resolve, depending on their seriousness. Thus, although the patient’s withdrawal dyskinesias still remain after 2 weeks, this does not indicate that they are likely to be permanent.

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3
Q

According to DSM-5 criteria, which of the following are characteristics of Schizophrenia? Select all that
apply.
-Disorganized Speech
-Hallucinations
-Compulsive Behaviors
-Delusions

A

Characteristic symptoms of Schizophrenia include Delusions, Hallucinations, Disorganized Speech, Grossly disorganized or catatonic behavior, and/or Negative symptoms.

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4
Q

Based on thorough evaluation of a patient and his history, his care provider intends to begin treatment with a typical antipsychotic but has not selected a particular agent yet. Which of the following is most true about typical antipsychotics?
-They differ in therapeutic profile but are similar in side effect profile
-They are very similar in therapeutic profile but differ in side effect profile
-They differ in both therapeutic and side effect profile
-They are very similar in both therapeutic and side effect profile

A

They are very similar in therapeutic profile but differ in side effect profile.
Although individual effects may vary from patient to patient, in general conventional antipsychotics share
the same primary mechanism of action and do not differ much in their therapeutic profiles. There are,
however, differences in secondary properties, such as degree of muscarinic, histaminergic, and/or alpha adrenergic receptor antagonism, which can lead to different side effect profiles.

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5
Q

A 34-year-old man is initiated on an atypical antipsychotic for the treatment of schizophrenia. The
majority of atypical antipsychotics:
-Have higher affinity for serotonin 2A receptors than for dopamine 2 receptors
-Don’t have affinity for dopamine 2 receptors or serotonin 2A receptors
-Have higher affinity for dopamine 2 receptors than for serotonin 2A receptors
-Have higher affinity for GABA receptors

A

Have higher affinity for serotonin 2A receptors than for dopamine 2 receptors.
Serotonin neurons originate in the raphe nucleus of the brainstem and project throughout the brain,
including to the cortex. They synapse there with glutamatergic pyramidal neurons, which project to the substantia nigra in the brainstem. The substantia nigra is the origin of dopaminergic neurons that project to the striatum. All serotonin 2A receptors are postsynaptic. When they are located on cortical pyramidal neurons, they are excitatory. Thus, when serotonin is released in the cortex and binds to serotonin 2A receptors on glutamatergic pyramidal neurons, this stimulates them to release glutamate in the brainstem, which in turn stimulates gamma-aminobutyric acid (GABA) release. GABA binds to dopaminergic neurons projecting from the substantia nigra to the striatum, inhibiting dopamine release.

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6
Q

Atypical antipsychotics, the “pines”

A

The “pines” – clozapine, olanzapine,
quetiapine, asenapine, and zotepine – all bind much more potently to the 5HT2A receptor than they do to the D2 receptor.

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7
Q

Atypical antipsychotics, the “dones” and “rone”

A

The “dones” and “rone” – risperidone, paliperidone, ziprasidone, iloperidone, lurasidone, and lumateperone – also bind more potently to the serotonin 2A receptor than to the dopamine 2 receptor or show similar potency at both receptors.

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8
Q

Atypical antipsychotics, aripiprazole and caripazine

A

Aripiprazole and cariprazine bind
more potently to the dopamine 2 receptor than to the serotonin 2A receptor; however, they are also
partial agonists at dopamine 2 receptors

pneumonic: Ari and the Car Dare for D2, leaving 5HT2A behind!

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9
Q

Atypical antipsychotics, brexipiprazole

A

Brexpiprazole (also a dopamine 2 partial agonist) has comparable binding affinity to the dopamine 2 and serotonin 2A receptors.

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10
Q

A 34-year-old male recently began experiencing breast secretions while receiving perphenazine. After
switching to quetiapine, the secretions ceased. Which of the following is the most likely pharmacological explanation for the resolution of this side effect?
-Dopamine 2 antagonism
-Serotonin 2C antagonism
-Histamine 1 antagonism
-Serotonin 2A antagonism

A

Dopamine 2 antagonism. Prolactin secretion is directly regulated by dopamine acting on D2 receptors in the hypothalamus and pituitary gland.
Perphenazine, as a potent D2 antagonist, increases prolactin levels, leading to breast secretions.
Quetiapine, with its weaker D2 antagonism, allows prolactin levels to normalize, resolving the side effect.

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11
Q

A 22-year-old male diagnosed with paranoid schizophrenia has been taking haloperidol for the past 6
months. During this visit, the PMHNP acknowledges involuntary repetitive muscle movements and
excessive eye-blinking that were not documented at his last visit. An appropriate next course of action
would be to:
-Measure serum creatinine
-Administer AIMS questionnaire and compare to baseline value
-Measure serum ALT/AST
-Administer PHQ-9 questionnaire and compare to baseline value

A

This patient is showing new Extrapyramidal symptoms and possible drug-induced acute dystonia. An AIMS (Abnormal Involuntary Movement Scale) Questionnaire should be administered and compared to
the patient’s baseline questionnaire. A possible change in medication or addition of an anticholinergic agent may be necessary.

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12
Q

A 44-year-old woman with schizophrenia has developed tardive dyskinesia after taking haloperidol 15 mg/day for 2 years. Which of the following would be the most appropriate pharmacological mechanism to manage her tardive dyskinesia?
-Antagonism of beta-adrenergic receptors
-Inhibition of vesicular monoamine transporter 2
-Antagonism of muscarinic acetylcholine receptors
-Antagonism at serotonin 2A receptors

A

Inhibition of vesicular monoamine transporter 2.
The best evidenced (including approved) medications to treat tardive dyskinesia are selective inhibitors of vesicular monoamine transporter 2 (VMAT2), which packages monoamines, including dopamine, into synaptic vesicles of presynaptic neurons in the central nervous system.

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13
Q

A 28-year-old man was recently diagnosed with schizophrenia. He has a body mass index of 30, fasting triglycerides of 220 mg/dL, and fasting glucose of 114 mg/dL. Which of the following is least likely to worsen his metabolic profile?
-Ziprasidone
-Quetiapine
-Risperidone
-Olanzapine

A

Ziprasidone in general seems to be weight neutral and has been shown to lower triglyceride levels. It is
therefore a recommended choice for individuals for whom metabolic issues are a primary concern. Other
newer antipsychotics that may be less likely to cause weight gain or metabolic side effects include
aripiprazole (although data suggest that weight gain may occur more in children and adolescents),
lurasidone, and lumateperone.

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14
Q

Carol is a 47-year-old patient with schizophrenia. She was taking a conventional antipsychotic but
decided to stop taking it when she developed parkinsonian symptoms. Secondary to stopping her conventional antipsychotic, Carol’s auditory hallucinations and paranoia returned, and she was rehospitalized. You recommend that she be started on an atypical antipsychotic. Which of the following has the lowest risk of drug-induced parkinsonism associated with it?
-Asenapine
-Iloperidone
-Olanzapine
-Paliperidone

A

iloperidone has a relatively
lower risk of drug-induced parkinsonism. Other agents with a relatively lower risk of drug-induced
parkinsonism include clozapine, lumateperone, and quetiapine

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15
Q

A 10-year-old girl is referred for evaluation of behavioral difficulties. Her teachers report that she is easily distracted and fails to complete any class work, and often stares off into space or tries to chat with her neighbor. Her mother reports that mornings are the most difficult because of her general disorganization and forgetfulness. Otherwise, she is socially engaged and enjoys many activities. Which of the following is the most likely diagnosis?
-Attention deficit disorder
-Conduct disorder
-Disruptive behavior
-Oppositional defiant disorder

A

Attention deficit disorder inattentive type: She is very distractible and forgetful in school as well as at
home with impaired ability to function. There are no displays of aggression, destruction of property,
deceitfulness, theft, or serious violations of rules that are associated with conduct disorders and
oppositional defiant disorder. Disruptive behavior disorder is reserved for conduct disorders not meeting
full DSM-5 diagnostic criteria.

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16
Q

According to DSM-5 criteria, what is the maximum age threshold for symptom onset when making a
diagnosis of ADHD?
-12
-7
-5
-15

A
  1. In the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, the maximum age
    threshold for symptom onset for diagnosing ADHD changed from 7 to 12. Other revisions included the
    fact that, although symptoms must have been present prior to age 12, there does not have to have been
    impairment prior to age 12 when diagnosing someone who is older. The symptom count threshold also
    changed for adults (defined as age 17 and older), with five (instead of six) symptoms required in the
    inattention and/or hyperactive/impulsive categories.
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17
Q

A 15-year-old with inattentive-type ADHD has a hard time staying focused on the task at hand, has
trouble organizing her work, and relies heavily on her mother to follow through with her homework.
Problem solving is one of the hardest tasks for her. Her difficulty with sustained attention could be
related to deficient activation in the:
-Orbital frontal cortex
-Prefrontal motor cortex
-Supplementary motor cortex
-Dorsolateral prefrontal cortex

A

DLPFC. Sustained attention is hypothetically modulated by the cortico-striatal-thalamic-cortical loop involving
the dorsolateral prefrontal cortex (DLPFC). Inefficient activation of the DLPFC can lead to problems
following through or finishing tasks, disorganization, and trouble sustaining mental effort; the patient
exhibits all these symptoms. The dorsal anterior cingulate cortex is important in regulating selective
attention, and is associated with behaviors such as losing things, being distracted, and making careless
mistakes. This area is certainly also inefficient in this patient.

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18
Q

Irina is a 35-year-old patient with untreated ADHD who reports abusing alcohol to manage severe anxiety. Irina’s symptoms may represent a case where the firing of __________ and __________ neurons innervating her prefrontal cortex is dysregulated and causing excessive arousal.
-Dopamine; serotonin
-Dopamine; glutamate
-Norepinephrine; glutamate
-Norepinephrine; dopamine

A

When norepinephrine (NE) and dopamine (DA) neurotransmission in the prefrontal cortex are optimally
tuned, modest stimulation of postsynaptic alpha 2A receptors and dopamine 1 receptors allows for
efficient cognitive functioning. If NE or DA neurotransmission is excessive, as in situations of stress or
comorbid conditions such as anxiety or substance abuse, this can lead to overstimulation of postsynaptic
receptors and consequently to cognitive dysfunction as well as other symptoms.

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19
Q

Aggregate data suggest that, compared to stimulants, nonstimulants have:
-Approximately the same effect sizes
-Larger effect sizes
-No effect on ADHD symptoms
-Smaller effect sizes

A

Smaller effect sizes. Multiple meta-analyses assessing the effects of stimulant medications have shown that, as a class,
nonstimulants have smaller effect sizes than stimulants. Due to differences in study design, these meta
analyses do not address potential differences in efficacy among specific medications.

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20
Q

Isaac is an 8-year-old patient with ADHD. Among male children with ADHD, which of the following is the
most commonly seen comorbidity?
-Learning Disability
-Depression
-Oppositional defiant disorder
-Anxiety

A

ODD. Argumentative, disobedient, and aggressive behaviors are often seen in patients suffering from ADHD
and oppositional symptoms. The presence of comorbid disruptive behavior disorders such as
oppositional defiant disorder, or conduct disorder, within children with ADHD has been well established.
About five in ten children with ADHD have a behavior or conduct problem and this is seen at a higher
rate in boys than in girls in studies.

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21
Q

Which of the following is considered a first-line treatment for ADHD in children and adolescents?
-Cognitive-behavioral therapy (CBT)
-Prescription stimulant medication
-Nutritional supplements
-Mindfulness meditation

A

Prescription stimulant medication, such as methylphenidate or amphetamine-based medications, is often
considered a first-line treatment for ADHD in children and adolescents due to their proven effectiveness
in managing symptoms.

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22
Q

What is the primary goal of medication treatment for ADHD?
-Eliminating all symptoms of ADHD
-Inducing sleep and relaxation
-Reducing impulsivity and hyperactivity
-Enhancing intelligence and cognitive abilities

A

The primary goal of medication treatment for ADHD is to reduce impulsivity and hyperactivity and
improve the individual’s ability to focus and concentrate, rather than eliminating all ADHD symptoms.

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23
Q

Which of the following is an evidence-based non-pharmacological treatment option for ADHD in both
children and adults?
- Herbal supplements like ginkgo biloba
-Behavioral therapy and psychoeducation
-Daily caffeine consumption
-Dietary restriction of carbohydrates

A

Behavioral therapy and psychoeducation are evidence-based non-pharmacological treatment options for
ADHD in both children and adults. They can help individuals develop coping strategies and improve their
executive functioning skills.

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24
Q

What is a potential side effect of stimulant medication commonly used to treat ADHD?
-Slower heart rate
-Enhanced emotional regulation
-Improved sleep quality
-Increased appetite

A

Increased appetite

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25
Q

The PMHNP is consulted to see a 70-year-old female who was admitted to the skilled nursing facility 3 days ago from the hospital, where she was treated for urinary tract infection, pneumonia, and dehydration. The staff reports that the patient is restless and agitated, awake most of the night, intermittently sleeping during the day, and has poor PO intake. What should the PPMHNP do first?
-Prescribe quetiapine 12.5 mg PO at bedtime and every 6 hours as needed for agitation
-Call family members for collateral information on her baseline functioning
-Transfer the patient to the ED
-Physical exam and diagnostic tests (complete blood count, basic metabolic profile, and urinalysis)

A

Physical exam and diagnostic tests are used to rule out delirium given the patient’s history, age, and
clinical presentation. Prescribing medication can worsen delirium and mask symptoms of an underlying
cause. Transferring the patient to the ED may worsen or trigger delirium. Obtaining collateral information
is helpful in helping to establish a baseline pattern of function, but the acute problem of delirium must be
addressed and ruled out first

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26
Q

A 53-year-old man presents to the emergency department with complaint of sore throat progressively worsening for 3 days with intermittent fever. In triage he tells the RN that he has taken ibuprofen 400 mg 4 hours ago for the pain, and currently his vital signs are blood pressure 120/80, heart rate 88, respiratory rate 12, SPO2 96% on room air. While waiting for the results of the rapid strep test the patient becomes agitated, restless, confused, and increasingly difficult to redirect. He is transferred to the psychiatric emergency department because it is a locked unit. Which of the following is the most likely
diagnosis?
-Mixed delirium
-Mood disorder
-Presenile dementia
-Personality disorder

A

Mixed delirium is characterized by a cyclical manifestation of psychomotor retardation and agitation with a disturbance in consciousness; risk factors include infectious process, fever, and relocation. Dementia
is a slowly progressive process that impairs cognition with the preservation of level of consciousness.
Personality disorder is characterized by a historical pattern of rigid maladaptive coping mechanisms that
cause distress. Mood disorder is a diagnosis of exclusion in which there are an insufficient number of
symptoms to meet full criteria for major depressive disorder, bipolar disorder, or generalized anxiety
disorder.

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27
Q

A 55-year-old woman reports to the PMHNP that since she accepted early retirement last year she finds
that her memory has gotten worse and she has trouble sleeping at night. She denies any medical
problems. What should the PMHNP do first?
-Prescribe mirtazapine 15 mg PO at bedtime to help her sleep
-Encourage her to volunteer with something she feels passionate about
-Perform a Mini-Mental State Exam and Confusion Assessment Methods Instrument
-Refer her to her primary care provider for a physical exam

A

MMSE.A formalized assessment such as the Mini-Mental State Exam and Confusion Assessment Methods
Instrument provides a reproducible means of establishing baseline function and distinguishing delirium
from reversible cognitive impairment. Mirtazapine is indicated for major depressive disorder and anxiety
but both are a diagnosis of exclusion and are lower priority than delirium. Encouraging volunteer activity
may be a good way to develop psychological activation in a patient with a mood disorder, but there is no
evidence to support this diagnosis. Referring the patient to her primary care provider for a physical exam
does negates the PMHNP’s responsibility to evaluate for neurocognitive disorders.

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28
Q

A 66-year-old woman employed as a federal appeals lawyer is being seen by the PMHNP accompanied
by her son, who has been concerned about progressive memory problems. Which of the following would
be most helpful in distinguishing between common forgetfulness and cognitive impairment?
-Montreal Cognitive Assessment (MoCA)
-Brain MRI with and without contrast
-Family history
-Hamilton Depression Scale (HAM-D)

A

MoCA. The Montreal Cognitive Assessment is a psychometrically validated screening tool for mild cognitive
impairment including visuospatial abilities, short-term recall, trail making, attention, concentration,
language, and orientation. A brain MRI is helpful in identifying structural changes that may account for
behavior if the affected brain region correlates with the impairment. Family history is important for
stratifying risk factors and genetic predisposition but does not confirm a current diagnosis. The Hamilton
Depression Scale is used to screen for major depressive disorder which can affect cognition, but the
chief complaint was related to cognition.

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29
Q

The primary treatment for delirium is:
-Mood stabilizing medications
-Anticipatory guidance and psychoeducation
-Antipsychotic medications
-Identifying and treating the underlying cause

A

Identifying and treating the underlying cause is the primary treatment for delirium. Adding medications
to a patient with delirium with an unknown underlying cause may worsen or compound the delirium as
polypharmacy is another causative factor. Anticipatory guidance and psychoeducation is appropriate
when tailored to a specific condition

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30
Q

Delirium characterized by apathy, psychomotor retardation, and inattentiveness is known as:
-Mania
-Mixed delirium
-Hyperactive delirium
-Hypoactive delirium

A

Hypoactive delirium is characterized by psychomotor retardation and apathy. Hyperactive delirium is
characterized by psychomotor agitation, restlessness, and hypervigilance. Mixed delirium is
characterized by cycling through psychomotor agitation and retardation ranging from apathy to hypervigilance. Mania is characterized by grandiosity, reduced need for sleep, more talkative than usual,
flight of ideas and racing thoughts, distractibility, and psychomotor agitation with an increase in goal
directed, pleasure-seeking behaviors.

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31
Q

A middle-aged man brings his 72-year-old mother in for an appointment because he is concerned that
his mother may have Alzheimer’s disease. The mother does not feel that anything is wrong, but her son
states that she seems somewhat depressed and forgetful lately. Data have shown that: (Select all that
apply)
-Depression may increase the risk of developing Alzheimer’s disease
-There is no link between Depression and Alzheimer’s disease
-Depression is often comorbid with Alzheimer’s disease
-Depression may be a prodromal symptom of Alzheimer’s disease

A

1st, 3rd, and 4th choice. Mood symptoms can occur as part of Alzheimer’s disease and in fact are typically the first notable
symptom (often manifested as apathy rather than sadness). In addition, depression is a common
comorbid illness in patients with Alzheimer’s disease. Depression has been hypothesized to be a
possible risk factor for Alzheimer’s disease. Depression has been hypothesized to be a possible
prodromal symptom of Alzheimer’s disease, with some evidence suggesting that it may exacerbate the
progression of Alzheimer’s pathology

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32
Q

Marie, a 70-year-old mid-stage Alzheimer’s patient, has been on donepezil, 10 mg/day for approximately
8 months to aid in stabilizing her cognitive functioning. Her daughter has noticed a loss of effectiveness
over the past month, and they present today to determine a new course of action. You decide to
augment Marie’s donepezil with 5 mg/day of memantine. Which of the following properties of memantine
may be useful in treating Alzheimer’s disease?
- N-methyl-D-aspartate (NMDA) antagonism
-D2 Antagonism
-Sigma antagonism
-Serotonin 3 (5HT3) antagonism

A

NMDA. Memantine is an NMDA antagonist that binds to the magnesium site. It works as an uncompetitive open
channel NMDA receptor antagonist (i.e., low–moderate affinity, voltage dependence, fast
blocking/unblocking kinetics). Memantine is quickly reversible if phasic bursts of glutamate occur but is
able to block tonic glutamate release from having negative downstream effects. This hypothetically stops
the excessive glutamate from interfering with the resting glutamate neuron’s physiological activity, thus
improving memory

33
Q

A 79-year-old man presents to your office with his wife. She lists significant medical history, such as
chronic renal failure, mild cirrhosis, arrhythmia, and a recent diagnosis of moderately severe Alzheimer’s
disease by their family physician. Which of the following medications for Alzheimer’s disease has a “do
not use” warning for patients with renal and hepatic impairment?
-Rivastigmine
-Donepezil
-Memantine
-Galantamine

A

Galantamine has a “do not use” warning in patients with renal and hepatic impairment, as well as a
caution warning when used in cardiac impaired patients. Furthermore, galantamine, a cholinesterase
inhibitor, is often prescribed as one of the first-line treatments for early-stage Alzheimer’s, rather than
moderately severe cases.

34
Q

Mitchell is a 90-year-old patient with Lewy body dementia. His daughter, who is his full-time caregiver,
reports that her father has started to exhibit worsening of agitation, wandering, and confusion in the early
evening – also known as sundowning. Which of the following treatments has actually been shown to
worsen sundowning behavior?
-Benzodiazepines
-Bright light therapy
-Melatonin
-Cholinesterase inhibitors

A

The use of benzodiazepines and other hypnotics has been linked with a paradoxical increase in
behavioral issues, such as sundowning, in patients with dementia. Furthermore, benzodiazepines are
particularly not recommended in elderly patients with dementia as they may greatly increase the risk of
falls, fractures, and death as well as worsening cognitive impairment.

35
Q

One of the most common electrolyte abnormalities associated with the use of psychotropic medication
is:
-Hyponatremia
-Hypernatremia
-Hypercalcemia
-Hyperkalemia

A

Hyponatremia is the most common electrolyte abnormality associated with psychotropic medication; the
condition is called drug-induced syndrome of inappropriate 93antidiuretic hormone secretion.

36
Q

Hyperkalemia

A

related to renal insufficiency, which can be acute or chronic

37
Q

Hypercalcemia

A

associated with neoplastic disorders and abnormal bone metabolism and resorption

38
Q

Hypernatremia

A

related to a water deficit

39
Q

A patient has been taking valproic acid for mood stabilization from a manic episode but is still not
sleeping through the night. His last drug level was 50 mcg/mL. The PMHNP notices the patient seems
disoriented to time and is flapping his wrists. What should the PMHNP do next?
-Augment with an atypical antipsychotic
-Increase the dose of valproic acid
-Give the patient lactulose 20 g PO
-Draw an ammonia level

A

Draw an ammonia level. Patients can develop encephalopathy due to hyperammonemia when taking valproic acid. It is essential
to check the ammonia level before treating the patient. Increasing the dose of medication would worsen the situation, and adding another agent does not address the underlying problem.

40
Q

A patient who has been taking paroxetine for 3 years wants to come off due to sexual side effects. He had gradually tried to wean the dose on his own but noticed feelings of dizziness, fatigue, headaches, anxiety, and electric-like shocks in his head. These findings are most consistent with SSRI discontinuation. What would be a reasonable action for the PMHNP to take?
-Have the patient resume the paroxetine and prescribe the patient a PD5-inhibitor
-Prescribe the patient fluoxetine for 1 week
-Start the patient on an antipsychotic for his somatic delusions
-Reassure the patient that the symptoms will go away eventually

A

Prescribing the patient fluoxetine (a long half-life selective serotonin reuptake inhibitors [SSRI]) will reduce the discontinuation syndrome symptoms. Resuming the medication and prescribing a second agent for sexual dysfunction does not solve the present problem.
There is no evidence that the patient is having a somatic delusion as discontinuation syndrome is well documented in the literature associated with paroxetine.

41
Q

A 60-year-old man has been treated for depression for the last 2 years with a medication he cannot
remember. He reports that he has had increasing urinary hesitancy, xerostomia, and intermittent
lightheadedness. Which of the following medications is this patient most likely prescribed?
-Lithium
-Fluoxetine
-Doxepin
-Lamictal

A

Doxepin is a tricyclic antidepressant known for its anticholinergic properties including dry mouth, orthostasis, urinary hesitancy, and retention leading to dysuria. Fluoxetine is a selective serotonin
reuptake inhibitor mostly associated with GI upset and sexual dysfunction. Lithium is most often associated with nephrogenic diabetes insipidus, and symptoms include polyuria, polydipsia, altered mental status, and tremor. Lamictal is an antiepileptic drug commonly used for mood stabilization associated with GI upset and, during periods of titration, Stevens-Johnson syndrome.

42
Q

In addition to baseline monitoring, which laboratory parameter should be assessed regularly during Depakote therapy to monitor for potential hematologic side effects?
-Serum creatinine
-Serum amylase
-Complete blood count (CBC)
-Serum albumin

A

Complete blood count (CBC). Regular monitoring of the CBC is essential to assess for any hematologic side effects associated with Depakote, such as thrombocytopenia and leukopenia.

43
Q

What is the recommended baseline blood serum monitoring requirement(s) for patients starting Depakote (divalproex sodium) therapy? (Select all that apply)
-Thyroid function tests (TFTs)
-No baseline monitoring is required
-Complete blood count (CBC)
-Liver function tests (LFTs)

A

Complete blood count (CBC) & Liver function tests (LFTs)
Baseline monitoring for Depakote should include a CBC to assess for any potential hematologic issues, as it can cause blood dyscrasias. It should also include Liver Function Tests (LFTs) to monitor for liver
damage (transaminitis)

44
Q

Which laboratory parameter should be regularly monitored during lithium therapy to assess kidney function?
-Liver function tests (LFTs)
-Thyroid function tests (TFTs)
-Serum glucose levels
-Serum creatinine levels

A

Regular monitoring of serum creatinine is important to assess kidney function because lithium can affect the kidneys, potentially leading to renal impairment.

45
Q

Which of the following is a characteristic clinical feature of Stevens-Johnson Syndrome (SJS)?
-Isolated conjunctivitis
-Painless oral ulcers
-Mild itching and erythema on the palms and soles
-Generalized blistering of the skin and mucous membranes

A

Generalized blistering of the skin and mucous membranes. SJS is characterized by widespread blistering of the skin and mucous membranes, which is a key clinical feature that distinguishes it from
other skin conditions.

46
Q

What is the most common cause of Stevens-Johnson Syndrome (SJS) and its severe form, Toxic Epidermal Necrolysis (TEN)?
-Fungal infection
-Autoimmune disorders
-Bacterial infection
-Medications, especially sulfonamides and antiepileptic drugs

A

Medications, especially sulfonamides and antiepileptic drugs. Medications, particularly certain classes like sulfonamides and antiepileptic drugs, are the most common triggers for SJS and TEN.

47
Q

Which of the following is a serious potential complication of Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) that may necessitate specialized care?
-Isolated itching and discomfort
-Ocular involvement, leading to corneal scarring and blindness
-Mild mucous membrane involvement
-Superficial skin peeling

A

Ocular involvement is a serious complication of SJS and TEN that may require specialized care to prevent corneal scarring and vision impairment.

48
Q

Presenting symptoms with stimulant use

A

agitation, restlessness, irritability, grandiosity, elatedness, euphoria, aggression, and mood lability
(methamphetamine, amphetamines, cocaine)

49
Q

Presenting symptoms with depressant use

A

dysphoria, impaired attention/memory, disinhibition, psychomotor retardation, paranoia
(alcohol/benzodiazepine/opiates)

50
Q

Tolerance

A

condition in which repeated administration of a dosage causes a decreased effect despite increasingly larger doses

51
Q

Addiction

A

Persistent and increased use of a substance or behavior that when discontinued causes distress and an urge to resume use despite related adverse consequences (psychological dependence)

52
Q

Dependence

A

repeated use of a substance for physical needs, leading to increased tolerance, and when discontinued results in physical withdrawal symptoms

53
Q

Withdrawal Syndrome dx

A

2 or more of the following are present:
-Palpitations
-Sweating
-Sleep disturbance
-Nausea/vomiting/diarrhea
-Hallucinations
-Agitation/restlessness/fidgety/irritable mood/depressed mood
-Anxiety or nervousness
-Seizures
-Shaking
-Fever/chills/cold sweats/piloerection (goosebumps)
-Headache
-Yawning
-Muscle aches

54
Q

Medication for opioid withdrawal

A

Buprenorphine (reduces symptoms)
Detox guided by Clinical Opioid Withdrawal scale (COWS)

55
Q

Medication for benzodiazepine and alcohol withdrawal

A

“LOT” drugs: Lorazepam, Oxazepam, Temazepam <safer in liver disease pts
Other supportive measures = IV, nutrition
Detox guided by CIWA-Ar scale

56
Q

Disulfiram (Antebuse)

A

For alcohol addiction treatment. Only use once pt alcohol free for 12 hours. Avoid any alcohol containing products (mouthwash, vinegar, cough medicine) for up to 14 days after last dose of Antebuse. When using monitor pt liver enzymes and evaluate for elevated mood in pt with bipolar disorder.

57
Q

Antidepressants in pregnancy

A

CAN be used = SSRIs, Sertraline (Zoloft), Escitalopram (Lexapro)

58
Q

Valproic acid (Depakote) in pregnancy

A

Mood stabilizer. Sedating and cause neural tube defects/fetal toxicity. Also is excreted in breast milk

59
Q

Lithium (Lithobid) in pregnancy

A

Mood stabilizer. Toxic to thyroid and can cause damage over time. Contraindicated in first trimester of pregnancy (Ebstein’s anomaly; defect heart tricuspid valve).
Excreted in breast milk.

60
Q

Lamotrigine in pregnancy

A

Mood stabilizer. CAN be used in pregnancy with caution if benefits outweigh risk.
Excreted in breastmilk ->Monitor infant for poor sucking, drowsiness, and apnea

61
Q

Fibromyalgia medications

A

SNRIs (Duloxetine, Milnacipran, Venlafaxine, Desvenlafaxine), Alpha 2 delta ligands (Gabapentin and Pregabalin), AD2 and SNRI combo
OPIATES NOT EFFECTIVE

62
Q

Neuropathy medications

A

Alpha 2 delta ligands (Gabapentin and Pregabalin); Duloxetine (cymbalta) dosed at bedtime; antidepressants

63
Q

Pediatric ADHD Tx

A
  1. Behavioral therapy for children 5 years and younger
  2. Dextroamphetamine & amphetamine salts for 3 years and older
  3. Methylphenidate for 6 years and older
64
Q

How to manage side effects of ADHD stimulants

A

Common Side Effects: Insomnia, reduced appetite, weight loss, irritability, and potential for increased anxiety. Cardiovascular side effects such as increased heart rate and blood pressure.

Take the medication with food to minimize stomach upset, adjust the dosage with your doctor if needed, avoid caffeine, take the medication earlier in the day to avoid sleep disruption, eat small frequent meals to combat appetite loss, and use long-acting

65
Q

ADHD: DA and NE

A

Excessive noradrenergic neurotransmission can lead to impaired working memory due to stimulation of α1 (and β1) receptors. Excessive dopaminergic neurotransmission can lead to overstimulation of D1 receptors in the prefrontal cortex

66
Q

Amphetamines mechanism of action

A

Competitive inhibitor and pseudosubstrate for NETs and DATs, binding at the same site that the monoamines bind to the transporters, thus inhibiting NE and DA reuptake

67
Q

Diagnosing ADHD

A

-Symptoms must be present before the age of 12, cannot diagnose before age 3.
-Impairment present in at least 2 different settings
-Evidence of functional interference: Socially, Academically, or in Extracurricular activities
-Subtypes = Inattentive, Hyperactive/Impulsive, and Combined

68
Q

ADHD Tx

A
  1. Assess/manage substance abuse problems
  2. Treat mood and anxiety
  3. Evaluate for other common ADHD comorbidities
  4. Stimulants or non-stimulants
69
Q

DLPFC is linked to ___________ symptoms

A

sustained attention and problem solving

70
Q

dACC is linked to ___________ symptoms

A

selective attention

71
Q

Prefrontal motor cortex is linked to ___________ symptoms

A

hyperactive

72
Q

Orbitofrontal cortex is linked to _________________symptoms

A

impulsive

73
Q

ADHD “causes”

A

-Genetic (75%)
-Delayed maturation of prefrontal cortex circuitry
-Ineffective “tonic” NE and DA neurotransmission/hypoactivity of dopamine and norepinephrine pathways in brain regions such as the prefrontal cortex (PFC)

74
Q

Donepezil (Aricept)

A

reversible long-acting inhibitor of acetylcholinesterase; without inhibition of BuChE; inhibits AChE at pre- and postsynaptic neurons and other CNS areas → boosts availability of ACh at remaining sites normally innervated by cholinergic neurons; also inhibits AChE in periphery → GI side effects
GI side effects usually transient
Most widely prescribed

75
Q

Galantamine (Razadyne)

A

dual mechanism of action AChE inhibition + positive allosteric modulation (PAM) of nicotinic and cholinergic receptors; no evidence this second action = clinical advantages

76
Q

Memantine (Namenda)

A

non-competitive, low affinity, NMDA receptor antagonist, binds to Mg site when channel is open → blocks downstream effects of excessive tonic Glu release by plugging up NMDA ion channel → improve memory and prevents neuronal death

77
Q

Brexpiprazole (Rexulti) for dementia

A

treats agitation in dementia

78
Q

Dextromethorphan-Bupropion (Auvelity)

A

treats agitation in dementia

79
Q

SSRIs in dementia

A

Sertraline, citalopram, escitalopram, fluoxetine
treats depression
some side effects: increased falls, osteoporosis, worsen PD symptoms