Dementia and its treatmentThis chapter will provide a brie.docx

Dementia and its treatment
This chapter will provide a brief overview of the various causes
of dementias and their pathologies,
including the most recent diagnostic criteria and the emerging
integration of biomarkers into clinical
practice for Alzheimer’s disease. Full clinical descriptions and
formal criteria for how to diagnose the
numerous known dementias should be obtained by consulting
standard reference sources. The
discussion here will emphasize the links between various
pathological mechanisms, brain circuits,
and neurotransmitters and the various symptoms of dementia,
with an emphasis on Alzheimer’s
disease. The goal of this chapter is to acquaint the reader with
ideas about the clinical and biological
aspects of dementia and its currently approved treatments as
well as new treatments that are on the
horizon. The emphasis here is on the biological basis of
symptoms of dementia and of their relief by
psychopharmacologic agents, as well as on the mechanism of
action of drugs that treat these
symptoms. For details of doses, side effects, drug interactions,
and other issues relevant to the
prescribing of these drugs in clinical practice, the reader should
consult standard drug handbooks
(such as ).Stahl’s Essential Psychopharmacology: the
Prescriber’s Guide
Causes, pathology, and clinical features of dementia
Dementia consists of memory impairment (amnesia) plus

deficits in either language (aphasia), motor
function (apraxia), recognition (agnosia), or executive function
such as working memory and problem
solving. Personality changes can also be present,
Table 13-1 Pathological features of selected degenerative
dementias
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Table 13-2 Not all memory disturbance is Alzheimer’s disease:
clinical features of selected
degenerative dementias
sometimes even before memory impairment begins. There are
many causes of dementia (Tables
through ), and the unique pathologies associated with some of
the major dementias are13-1 13-3
listed in . Knowing the pathology does not mean that a
treatment is available, as it is oftenTable 13-1
not evident how to translate information about brain pathology
into pharmacological treatments. The
best hope currently is in the area of amyloid pathology, where
new treatments under investigation are
attempting to interfere with amyloid processing in Alzheimer’s
disease, as will be discussed later in
this chapter.
Just because a patient develops memory disturbance does not

mean it is Alzheimer’s disease (Table
). Alzheimer’s dementia is perhaps the best-known and
commonest dementia, but it is often the13-2
other symptoms associated with memory loss that help make the
diagnosis clinically ( ).Table 13-2
Just to complicate things, many patients have mixed types of
dementia, particularly Alzheimer’s
dementia plus dementia with Lewy bodies, or Alzheimer’s
dementia plus vascular dementia (Figure
). Such cases13-1
distribution.
Figure 13-1. . There are several types of dementia, of which
Alzheimer’s disease is the mostMixed dementia
common. They are distinguished by their underlying
pathologies. It is possible to have more than one dementia,
and in fact many patients have both Alzheimer’s disease and
either dementia with Lewy bodies or vascular
dementia.
are complicated to diagnose clinically, and definitive diagnosis
sometimes must await autopsy. Most
dementias are really pathological diagnoses, not clinical
diagnoses.
Table 13-3 Nondegenerative dementias

distribution.
A wide variety of dementias are considered nondegenerative,
and these are listed in .Table 13-3
Many of these are treatable upon discovering the underlying
cause, but others are not. Extensive
clinical evaluation and laboratory testing must rule out these
causes prior to concluding that a case of
dementia is due to Alzheimer’s disease.
Alzheimer’s disease: -amyloid plaques and neurofibrillary
tangles
Without the introduction of disease-modifying treatments,
Alzheimer’s disease is poised for an
exponential increase throughout the world, with projections that
it will quadruple over the next 40
years to affect 1 in every 85 people on earth: over 100 million
people by 2050. Fortunately, new
treatments are being designed to interfere with various known
pathological processes, particularly
the formation of amyloid plaques, in an attempt to halt or slow
disease progression in Alzheimer’s
disease before neurons are irretrievably lost. To understand the
current diagnostic criteria for
Alzheimer’s disease, how and why biomarkers are being
integrated into the diagnosis of this
disorder, and the rationale behind the hot pursuit of new
therapeutics, it is necessary to understand
how the two hallmarks of this disorder, amyloid plaques and

neurofibrillary tangles, are thought to be
formed in the brain in Alzheimer’s disease.
The amyloid cascade hypothesis
The leading contemporary theory for the biological basis of
Alzheimer’s disease centers around the
formation of toxic amyloid plaques from peptides due to the
abnormal processing of amyloid
precursor protein (APP) into toxic forms of Abeta (A) peptides (
through ). Why doFigures 13-2 13-9
we make A in the first place? Although this is not fully
understood, nontoxic A peptides have
antioxidant properties, can chelate metal ions, regulate
cholesterol transport, and may be involved in
blood vessel repair, as a sealant at sites of injury or leakage,
possibly protecting from acute brain
distribution.
injury. Hypothetically, Alzheimer’s disease is a disorder in
which toxic A peptides are formed, leading
to deposition of amyloid plaque in the brain, with the ultimate
destruction of neurons diffusely
throughout the brain, somewhat analogous to how the abnormal
deposition of cholesterol in blood
vessels causes atherosclerosis.
Thus, Alzheimer’s disease may be essentially a problem of too
much formation of A amyloid-forming

peptides, or too little removal of them. One idea is that neurons
in some patients destined to have
Alzheimer’s disease have abnormalities either in genes that
code for a protein called amyloid
precursor protein (APP), or in the enzymes that cut this
precursor into smaller peptides, or in the
mechanisms of removal of these peptides from the brain and
from the body. APP is a
Figure 13-2. . The way in which amyloidProcessing of amyloid
precursor protein into soluble peptides
precursor protein (APP) is processed may help determine
whether an individual develops Alzheimer’s disease or
not. A nontoxic pathway for APP processing is shown here. APP
is a transmembrane protein with the C-terminal
inside the neuron and the N-terminal outside the neuron. The
enzyme -secretase cuts APP close to where it
comes out of the membrane to form two peptides: -APP, which
is soluble, and an 83-amino-acid peptide that
remains in the membrane. A second enzyme, -secretase, cuts the
embedded peptide into two smaller peptides,
p7 and p3, which are not "amyloidogenic" and thus are not
toxic.
transmembrane protein with the C-terminal inside the neuron
and the N-terminal outside the neuron.
One pathway for APP processing does not produce toxic
peptides and involves the enzyme
-secretase ( ). Alpha-secretase cuts APP close to the area where
the protein comes out ofFigure 13-2
the membrane, forming two peptides: a soluble fragment known
as -APP and a smaller
83-amino-acid peptide that remains embedded in the membrane
until it is further cleaved by a
second enzyme acting within the neuronal membrane, called -
secretase ( ). That enzymeFigure 13-2

produces two smaller peptides, p7 and p3, which are apparently
not "amyloidogenic" and therefore
not toxic ( ).Figure 13-2
distribution.
Another pathway for APP processing can produce toxic peptides
that form amyloid plaques (i.e.,
"amyloidogenic" peptides). In this case a different enzyme, -
secretase, cuts APP a little bit further
away from the area where APP comes out of the membrane,
forming two peptides: a soluble
fragment known as -APP and a smaller 91-amino-acid peptide
that remains embedded in the
membrane until it is further cleaved by -secretase within the
membrane ( ). This releasesFigure 13-3
A peptides of 40, 42 or 43 amino acids that are
"amyloidogenic," especially A42 ( ).Figure 13-3
In Alzheimer’s disease, genetic abnormalities may produce an
altered APP that, when processed by
this second pathway involving -secretase, produces smaller
peptides that are especially toxic.
Individuals who do not get Alzheimer’s disease may produce
peptides that are not very toxic, or may
have highly efficient removal mechanisms that prevent neuronal
toxicity from developing. The
amyloid cascade hypothesis of Alzheimer’s disease therefore
begins with an APP that is
hypothetically genetically abnormal, or genetically or

environmentally abnormal in the way it is
processed, so that when it is cut into smaller peptide fragments
too many toxic peptides are made,
accumulate, and form neuron-destroying amyloid plaques, i.e.,
amyloidosis, and neurofibrillary
tangles. Hypothetically, this process triggers a lethal chemical
cascade that ultimately results in
Alzheimer’s disease ( through ).Figures 13-3 13-8
Figure 13-3. . The way in which amyloid precursorProcessing of
amyloid precursor protein into A peptides
protein (APP) is processed may help determine whether an
individual develops Alzheimer’s disease or not. A
toxic pathway for APP processing is shown here. APP is a
transmembrane protein with the C-terminal inside the
neuron and the N-terminal outside the neuron. The enzyme -
secretase cuts APP at a spot outside the
membrane to form two peptides: -APP, which is soluble, and a
91-amino-acid peptide that remains in the
membrane. Gamma-secretase then cuts the embedded peptide;
this releases A peptides of 40, 42, or 43 amino
acids. These toxic (amyloidogenic) peptides form amyloid
plaques.
Specifically, abnormal genes or other influences cause the
formation of an altered APP, or altered
distribution.
processing into too many toxic A42 peptides ( ). Next, the A42

peptides form oligomers (aFigure 13-4
collection of a few copies of A42 assembled together: ). These
oligomers can interfereFigure 13-5
with synaptic functioning and neurotransmitter actions such as
those of acetylcholine, but they are
not necessarily lethal to the neurons at first. Eventually, A42
oligomers form amyloid plaques, which
are even larger clumps of A42 peptides stuck together with a
number of other molecules (Figure 13-6
). A number of nasty biochemical events then occur, including
inflammatory responses, activation of
microglia and astrocytes, and release of toxic chemicals
including cytokines and free radicals (Figure
). These chemical events then hypothetically trigger the
formation of neurofibrillary tangles within13-6
neurons by altering the activities of various kinases and
phosphatases, causing
hyperphosphorylation of tau proteins, and converting neuronal
Figure 13-4. . One theory for theAmyloid cascade hypothesis,
part 1: increased production of A42
pathophysiology of Alzheimer’s disease is that there are genetic
abnormalities in amyloid precursor protein
(APP), so that when it is processed by the pathway involving -
secretase, it produces smaller, toxic peptides
(especially A42, as shown here).
distribution.

Figure 13-5. Amyloid cascade hypothesis, part 2: A42 oligomers
form and interfere with synaptic
. A42 peptides assemble together to form oligomers, which
interfere with synaptic functioning andfunction
neurotransmitter actions but are not necessarily lethal to
neurons.
Figure 13-6. .Amyloid cascade hypothesis, part 3: formation of
amyloid plaques causing inflammation
A42 oligomers clump together along with other molecules to
form amyloid plaques. These plaques can cause
inflammatory responses, activation of microglia and astrocytes,
and release of toxic chemicals such as cytokines
and free radicals.
distribution.
microtubules into tangles ( ). Finally, widespread synaptic
dysfunction from A42 oligomers,Figure 13-7
neuronal dysfunction and death from formation of amyloid
plaques outside of neurons and
neurofibrillary tangles within neurons leads to diffuse neuronal
death ( ) and regionalFigure 13-8
expansion of neuronal destruction in the cortex, causing the
relentless progression of Alzheimer’s
symptoms of amnesia, aphasia, agnosia, apraxia, and executive
dysfunction. Some investigators
believe that Alzheimer’s disease may spread from neuron to
neuron, with pathological

phosphorylated tau transported down axons, released at
synapses and then taken up by neighboring
cells. Pathological tau possibly then latches onto normal tau in
the connected neurons, triggering the
formation of new pathological mis-folded tau, from one affected
neuron to the next.
Figure 13-7. . AmyloidAmyloid cascade hypothesis, part 4:
amyloid plaque induces formation of tangles
plaques and the chemical events they cause activate kinases,
cause phosphorylation of tau proteins, and
convert microtubules into tangles within neurons.
Support for the amyloid cascade hypothesis comes from genetic
studies of those relatively rare
inherited autosomal dominant forms of Alzheimer’s disease.
Sporadic (i.e., noninherited) cases
account for the vast majority of Alzheimer’s disease cases, but
inherited cases can provide clues for
what is wrong in the usual sporadic cases of Alzheimer’s
disease. Rare familial cases of Alzheimer’s
disease have an early onset (i.e., before age 65) and have been
linked to mutations in at least three
different chromosomes: 21, 14, and 1. The mutation on
chromosome 21 codes for a defect in APP,
leading to increased deposition of -amyloid. Recall that Down’s
syndrome is also a disorder of this
same chromosome (i.e., trisomy 21), and virtually all such
persons develop Alzheimer’s disease if
they live past age 50. A different mutation on chromosome 14
codes for an altered form of a protein
called presenilin 1, a component of the -secretase enzyme
complex. A third mutation, on
chromosome 1, codes for an altered form of presenilin 2, a
component of a different form of
-secretase. It is not yet clear what if anything these three

mutations in the rare familial cases tell us
about the pathophysiology of the usual sporadic, nonfamilial,
and late-onset cases of Alzheimer’s
disease. However, they all point to abnormal processing of APP
into amyloidogenic -amyloid
peptides as a cause for the dementia, consistent with the
amyloid cascade hypothesis. Theoretically,
different abnormalities in amyloid processing may occur in
sporadic Alzheimer’s disease from those
identified in inherited cases, and there may even be multiple
abnormalities that could be responsible
for sporadic Alzheimer’s disease as a final common pathway,
but the evidence nevertheless
implicates something in the amyloid cascade that goes wrong in
Alzheimer’s disease. If so, this
implies that preventing the formation of amyloidogenic peptides
could prevent Alzheimer’s disease.
ApoE and risk of Alzheimer’s disease
A corollary to the amyloid cascade hypothesis is the possibility
that something may be wrong with a
protein that binds to amyloid peptides in order to remove them (
). This protein is calledFigure 13-9
distribution.
apolipoprotein E (ApoE). In the case of "good" ApoE, it binds
to -amyloid peptides and removes
them, hypothetically preventing the formation of Alzheimer’s

disease and dementia ( ). InFigure 13-9A
the case of "bad" ApoE, a genetic abnormality in the formation
of ApoE causes it to be ineffective in
how it binds to -amyloid peptides. This causes amyloid plaques
to be formed and deposited around
neurons, which goes on to damage neurons and cause
Alzheimer’s disease ( ).Figure 13-9B
Genes coding for ApoE are associated with different risks for
Alzheimer’s disease. There are three
alleles (or variants) of this gene coding for this apolipoprotein
called E2, E3, and E4, and everyone
has two alleles. The E4 variant on chromosome 19 ("bad" ApoE)
is linked to many cases of
late-onset Alzheimer’s disease, the usual form of this
Figure 13-8. . The effects of amyloidAmyloid cascade
hypothesis, part 5: neuronal dysfunction and loss
plaques and the build-up of neurofibrillary tangles can
ultimately lead to neuronal dysfunction and death.
illness. ApoE is associated with cholesterol transport and
involved with other neuronal functions
including repair, growth, and maintenance of myelin sheaths
and cell membranes. Having one or two
copies of E4 increases the risk of getting Alzheimer’s disease.
In fact, some studies show that you
have a 50-90% chance of developing Alzheimer’s disease by age
85 if you are an E4 homozygote
(i.e., you have two copies of E4); a 45% chance if you are a
heterozygote for E4, versus the risk in
the general population at 20%. Alzheimer’s patients with the E4
gene also have more amyloid
deposits and progress more rapidly to dementia than those
without the E4 gene. The E2 variant may
actually be somewhat protective.

distribution.
Alzheimer’s Disease
76-year-old Iranian Male
BACKGROUND
Mr. Akkad is a 76 year old Iranian male who is brought to your
office by his eldest son for “strange behavior.” Mr. Akkad was
seen by his family physician who ruled out any organic basis for
Mr. Akkad’s behavior. All laboratory and diagnostic imaging
tests (including CT-scan of the head) were normal.
According to his son, he has been demonstrating some strange
thoughts and behaviors for the past two years, but things seem
to be getting worse. Per the client’s son, the family noticed that
Mr. Akkad’s personality began to change a few years ago. He
began to lose interest in religious activities with the family and
became more “critical” of everyone. They also noticed that
things he used to take seriously had become a source of
“amusement” and “ridicule.”
Over the course of the past two years, the family has noticed
that Mr. Akkad has been forgetting things. His son also reports
that sometimes he has difficult “finding the right words” in a
conversation and then will shift to an entirely different line of
conversation.
SUBJECTIVE
During the clinical interview, Mr. Akkad is pleasant,
cooperative and seems to enjoy speaking with you. You notice
some confabulation during various aspects of memory testing,

so the PMHNP performs a Mini-Mental State Exam. Mr. Akkad
scores 18 out of 30 with primary deficits in orientation,
registration, attention & calculation, and recall. The score
suggests moderate dementia.
MENTAL STATUS EXAM
Mr. Akkad is 76 year old Iranian male who is cooperative with
today’s clinical interview. His eye contact is poor. Speech is
clear, coherent, but tangential at times. He makes no unusual
motor movements and demonstrates no tic. Self-reported mood
is euthymic. Affect however is restricted. He denies visual or
auditory hallucinations. No delusional or paranoid thought
processes noted. He is alert and oriented to person, partially
oriented to place, but is disoriented to time and event [he
reports that he thought he was coming to lunch but “wound up
here”- referring to your office, at which point he begins to
laugh]. Insight and judgment are impaired. Impulse control is
also impaired as evidenced by Mr. Akkad’s standing up during
the clinical interview and walking towards the door. When the
PMHNP asked where he was going, he stated that he did not
know. Mr. Akkad denies suicidal or homicidal ideation.
Diagnosis: Major neurocognitive disorder due to Alzheimer’s
disease (presumptive)
RESOURCES
§ Folstein, M. F., Folstein, S. E., & McHugh, P. R. (2002).
Mini-Mental State Examination (MMSE). Lutz, FL:
Psychological Assessment Resources.
Decision Point One
Select what the PMHNP should do:
Begin Exelon (rivastigmine) 1.5 mg orally BID with an increase
to 3 mg orally BID in 2 weeks
: Begin Aricept (donepezil) 5 mg orally at BEDTIME

Begin Razadyne (galantamine) 4 mg orally BIDAlzheimer’s
Disease
Decision Point One
Begin Exelon (rivastigmine) 1.5 mg orally BID with an increase
to 3 mg orally BID in 2 weeks
RESULTS OF DECISION POINT ONE
· Client returns to clinic in four weeks
· The client is accompanied by his son who reports that his
father is “no better” from this medication. He reports that his
father is still disinterested in attending religious
services/activities, and continues to exhibit disinhibited
behaviors
· You continue to note confabulation and decide to administer
the MMSE again. Mr. Akkad again scores 18 out of 30 with
primary deficits in orientation, registration, attention &
calculation, and recall
· Decision Point Two· Select what the PMHNP should do next:
·
· Increase Exelon to 4.5 mg orally BID
·
· Increase Exelon to 6 mg orally BID
·
· Discontinue Exelon and begin Namenda (memantine) 10 mg
orally BID
Decision Point One

: Begin Aricept (donepezil) 5 mg orally at BEDTIME
father is “no better” from this medication
· He reports that his father is still disinterested in attending
religious services/activities, and continues to exhibit
disinhibited behaviors
·
· Increase Aricept to 10 mg orally at BEDTIME
·
· Discontinue Aricept and begin Razadyne (galantamine)
extended release 24 mg orally daily
·
· Discontinue Aricept and begin Namenda (memantine)
extended release, 28 mg orally daily
Decision Point One
Begin Razadyne (galantamine) 4 mg orally BID
father is “no better” from this medication

· He reports that his father is still disinterested in attending
religious services/activities, and continues to exhibit
disinhibited behaviors
·
· Increase Razadyne to 24 mg extended release daily
·
· Discontinue Razadyne and begin Aricept (donepezil) 10 mg
orally daily
·
· Discontinue Razadyne and begin Exelon (rivastigmine) 1.5 mg
orally BID
·
Assessing and Treating Adult Clients with Mood Disorders
A mood disorder describes a psychological disorder which is
characterized as a fluctuation of one’s mood, such as a major
depressive or bipolar disorder. An estimated 20 million
individuals in the United States have depression which
comprises of symptoms such as a loss of pleasure in activities,
sadness, weight changes, feelings of hopelessness, fatigue as
well as suicidal ideation; all of which can significantly impact
daily functioning (Mental Health.gov, 2017). According to Park
and Zarate (2019) onset of depression in adulthood continues to
flourish where an estimated 30 percent of adults have a lifetime
risk of experiencing a major depressive episode with a median
age of 32.5. The author further indicates screening for
depression, a thorough evaluation, and monitoring is necessary
to ensure safety and wellbeing (Park & Zarate, 2019).
Pharmacotherapy, along with psychotherapy are first-line

therapies for effective outcomes (Park & Zarate, 2019). The
purpose of this paper is to review a case study, choose the
appropriate selection utilizing research, and discuss ethical
considerations.
Case Study
A 32-year-old Hispanic American client presents to the initial
appointment with depression. Health history, along with
medical workup, appears to be unremarkable except for the
slight back and shoulder pain due to his occupation. The clinical
interview reveals past feelings of being an “outsider” and has
few friends (Laureate Education, 2016). There is a decline in
daily activities, a weight increase of 15 pounds over two
months, along with diminished sleep and the inability to fully
concentrate (Laureate Education, 2016). The results of the
depression screening administered by the psychiatric mental
health nurse practitioner (PMHNP), indicates severe depression
with a score of 51 (Montgomery & Asberg, 1979).
Decision Point One
The selections include Zoloft 25 mg orally daily, Effexor 37.5
XR mg orally daily, or Phenelzine 15 mg orally TID. As a
healthcare professional treating a client, Zoloft (sertraline) 25
mg is the first choice at decision point one. Selective serotonin
reuptake inhibitors (SSRIs) impede the reabsorption of this
neurotransmitter; thus, increasing the serotonin levels of the
nerve cells in the brain to allow for improvement in mood
(Stahl, 2013). SSRIs have been utilized as first-line therapy to
treat major depressive disorder due to efficacy, fewer side
effects, cost-effectiveness as well as a wider availability
(Masuda et al., 2017). The therapeutic dosing range is typically
50 mg-200 mg (Stahl, 2017). However, beginning at 25 mg and
gradually titrating the dose, depending on tolerability, is an
appropriate health care decision (National Alliance on Mental
Illness, 2018b). Therefore, a low dose of Zoloft appears to be
the best option in caring for this client.
Effexor (venlafaxine) is classified as a selective serotonin-
norepinephrine reuptake inhibitor (SNRI) which impedes the

reabsorption of the neurotransmitters serotonin and
norepinephrine changing the chemistry in the brain to regulate
mood (Stahl, 2013). Bhat and Kennedy (2017) describe
antidepressant discontinuation syndrome (ADS) as a
“medication-induced movement disorder” along with various
adverse reactions such as intense sadness and anxiety; periods
of an “electric shock” sensation; sights of flashing lights; and
dizziness upon movement (Bhat & Kennedy, 2017, p. E7).
These symptoms are often experienced a few days after sudden
discontinuation of an antidepressant with a shorter-life (3-7
hours) such as venlafaxine or paroxetine (Bhat & Kennedy,
2017; Stahl, 2017). Moreover, Stahl (2017) indicates
venlafaxine is one of the drugs with more severe withdrawal
symptoms in comparison to other antidepressants. It may take
some clients several months to taper off of this medicine;
therefore, Effexor is not the optimal selection at this time.
Phenelzine is classified as an irreversible monoamine oxidase
inhibitor (MAOI) which impedes the monoamine oxidase from
deconstructing serotonin, dopamine, as well as norepinephrine.
Thus, boosting the levels of neurotransmitters in the brain to
regulate mood (Stahl, 2017). Park and Zarate (2019) purport
the use of monoamine oxidase inhibitors have a higher risk
profile; therefore, are not typically utilized unless a newer
antidepressant is considered ineffective. Bhat and Kennedy
(2017) indicate there is a need for a long taper with MAOIs.
Further, this medication may lose effectiveness after long-term
use, and it is considered to have habit-forming qualities for
some individuals (Stahl, 2017). The initial dose for phenelzine
is taken three times a day which research suggests medication
adherence is often tricky when the administration is more than
once a day (Goette & Hammwöhner, 2016). Stahl (2017)
describes certain risk factors comprising of frequent weight
gain, interference of certain food products containing tyramine,
drug interactions (serotonin syndrome), as well as a
hypertensive crisis. When utilizing this medication for
treatment-resistant depression, the advance practitioner is aware

of the detrimental adverse reactions which may occur.
Therefore, phenelzine is not the safest option for this client.
The overarching goal for this male client is to reduce the
symptoms related to his major depressive disorder and to
eventually achieve remission without relapse where he can
maintain normalcy in his life. After four weeks, his depressive
symptoms decrease by 25 percent which is progress; however,
he has a new onset of erectile dysfunction (Laureate Education,
2016). Sexual dysfunction is a notable side effect of sertraline
(Stahl, 2017). Therefore, the clinician will reevaluate the plan
of care given this new information. The outcomes were to be
expected as the client was started on a low dose of sertraline,
and treatment is typically 50 mg to 200 mg. A continuation in
progress may require more time, approximately six to eight
weeks in total (Stahl, 2017).
Decision Point Two
The present selections include decrease dose to 12.5 daily
orally, continue same dose and counsel client, or augment with
Wellbutrin 150 IR in the morning. The preference for decision
point two is Wellbutrin (bupropion) 150 IR, which is considered
a norepinephrine dopamine reuptake inhibitor (SDRI). An
SDRI elevates the neurotransmitters dopamine, noradrenaline,
and norepinephrine in the brain to achieve an improvement in
depressive symptoms (Stahl, 2017). The purpose of utilizing
this agent is three-fold: (1) To boost mood (2) To treat the new
onset of sexual dysfunction (3) To aid in weight-loss.
According to the National Alliance on Mental Illness [NAMI]
(2018a), Wellbutrin is a medication administered for major
depressive disorder often in conjunction with an SSRI (NAMI,
2018a).
Further, Wellbutrin may be prescribed with an SSRI to reverse
the effects of SSRI-induced sexual dysfunction (Stahl, 2017).
Dunner (2014) purports combining antidepressants are safe and
may enhance efficacy; however, the combination of medications
may also be utilized as an approach to reduce the effects of
antidepressant pharmacotherapy. Dunner (2014) concurs that

bupropion is frequently used with an SSRI or SNRI to alleviate
sexual dysfunction. Stahl (2017), findings indicate the most
common side effects of bupropion consist of constipation, dry
mouth, agitation, anxiety, improved cognitive functioning, as
well as weight loss. The client in this scenario has gained 15
pounds over two months; thus, this medication may aid in his
desire to lose weight (Laureate Education, 2016). Further, this
agent typically is not sedating as it does not have
anticholinergic or antihistamine properties yet have a mild
stimulating effect (Guzman, n.d).
Decreasing the Zoloft dose from 25 mg daily to 12.5 mg would
not prove feasible as the client has reached a 25 percent
reduction in symptomology. The treatment for adults is 50 mg-
200 mg, taking an approximate six to eight weeks to see the
results in some individuals (Stahl, 2017). If the provider is
tapering the medication as part of the client's plan of care,
reducing the dose to 12.5 mg would prove beneficial. Research
finds that when taking an antidepressant, the neurons adapt to
the current level of neurotransmitters; therefore, if
discontinuing an SSRI too quickly some of the symptoms may
return (Harvard Health Publishing, 2018). Under some
circumstances, discontinuation signs may appear, such as sleep
changes, mood fluctuations, unsteady gait, numbness, or
paranoia (Harvard Health Publishing, 2018). However, the
client is experiencing slow and steady progress on his current
dose of Zoloft, so no adjustments are warranted.
At this point, positive results have been verbalized with the
current dose of Zoloft 25 mg daily, with the exception of the
onset of erectile dysfunction, which is a priority at this time.
One study finds that comorbid depression and anxiety disorders
are commonly seen in adult males with sexual dysfunction
(Rajkumar & Kumaran, 2015). An estimated 12.5 percent of
participants experienced a depressive disorder before the
diagnosis of sexual dysfunction. The author’s findings suggest a
significant increase in suicidal behaviors with this comorbidity.
Moreover, the study indicates, some men experienced a sexual

disorder while taking prescribed medication such as an
antidepressant (Rajkumar & Kumaran, 2015). According to Li
et al. (2018), cognitive-behavioral therapy (CBT) is a beneficial
tool utilized with clients experiencing mood disorders. The
implementation of CBT may increase the response and
remission rates of depression. However, the option of
continuing the same dose and engaging in counseling services is
not the priority at this time. It is essential to address this side
effect to enhance his current pharmacotherapy and prevent an
increase in depressive symptoms.
The continued goal of therapy is to achieve “full” remission of
this individual’s major depressive disorder and to enhance his
wellbeing. After four weeks, the client returns to the clinic
with a significant reduction in depressive symptoms along with
the dissipation of erectile dysfunction. However, he reports
feelings of “jitteriness” and on occasion “nervousness”
(Laureate Education, 2016). This course of treatment has
proven successful thus far, and the outcomes are to be expected
due to the medication trials.
Decision Point Three
The present selections are to discontinue Zoloft and continue
Wellbutrin, change Wellbutrin to XL 150 mg in the morning, or
add Ativan 0.5 mg orally TID/PRN for anxiety. The selection
for decision point three is to change the Wellbutrin from IR to
XL 150 mg in the morning. The first formulation is immediate-
release (IR) and the recommended dosing is divided beginning
at 75 mg twice daily increasing to 100 mg twice daily, then 100
mg three times a day with the maximum of 450 mg (Stahl,
2017). The second formulation is extended-release (XL),
where the administration for the initial dose is once daily taken
in the morning; the maximum is 450 mg in a single dose (Stahl,
2017). The peak level of bupropion XL is approximately five
hours; therefore, the side effects reported may subside as the
absorption rate is slower than the IR dose (U.S. Food and Drug
Administration, 2011a). The immediate-release peak level is
approximately two hours which may account for the client’s

notable feelings of being jittery and at times nervous (U.S. Food
and Drug Administration, 2011b). Furthermore, clients are
switched to extended-release to improve tolerance and treatment
adherence to once-daily treatment (Guzman, n.d). As a mental
health provider, caring for this client, changing the formulation
is the best decision at this point as well as to continue to
monitor side effects.
As mentioned above, Zoloft, an SSRI, can be utilized as a first-
line agent for major depressive disorder (Masuda et al., 2017).
Using Wellbutrin as an adjunct to the regimen has continued to
reduce his symptoms of depression and has alleviated one of his
primary concerns which is sexual dysfunction. Therefore,
discontinuing Zoloft and maintaining the use of Wellbutrin is
not an appropriate option at this time.
Ativan (lorazepam) is a benzodiazepine with anxiolytic, anti-
anxiety, and sedative properties. It provides short-term relief of
anxiety symptoms or insomnia (U.S. National Library of
Medicine [NLM], n.d.). Lorazepam works by enhancing the
effect of the inhibitory neurotransmitter GABA, which inhibits
the nerve signals, in doing so, reducing the “nervous excitation”
(NLM, n.d., para. 1). In some instances, a low dose, 0.5 mg,
may be administered short-term to reduce side effects from
another medication. Stahl (2017), indicates many side effects
will not improve with an augmenting drug. Common side effects
consist of confusion, weakness, sedation, nervousness, and
fatigue (Stahl, 2017). Further, Ativan has an increased risk for
abuse potential as it is known to have habit-forming properties
(Stahl, 2017). As a result, administering Ativan would not be in
the best interest of the client.
The ultimate goal is to achieve remission of his mood disorder.
The medication regimen has proven effective; thus, considering
this to be a successful plan of care. Taking both the sertraline
and bupropion can exhibit side effects of jitteriness; however,
changing to the extended-release may aid in the dissipation of
these feelings. The addition of Ativan to relieve side effects,
that are perhaps temporary, is against better judgment without

first making an effort to change or modify the medication
regimen (Laureate Education, 2016).
Summary with Ethical Considerations
Mood disorders affect millions of individuals in the United
States on an annual basis. The prevalence of mental illness
continues to flourish, impacting one’s quality of life. Initiating
treatment, under the guidance of a healthcare professional, is of
the utmost importance. Further, an individualized plan of care
comprising of education, therapy, medication, and support is
crucial for overall health and wellbeing.
The client is a Hispanic American male employed as a laborer
in a warehouse (Laureate Education, 2016). It is essential to
assess his financial means before prescribing medications.
Although one cannot assume the client has financial hardships,
having this knowledge will guide in the process of treatment. If
the client is without insurance and has to pay out-of-pocket,
medication adherence may not be sustainable. Therefore, as a
psychiatric nurse practitioner, providing a cost-effective means
whether, through generic prescriptions, discount pharmacies, or
prescribing a larger quantity may be a necessary option (Barker
& Guzman, 2015). Further, the partnership among clients and
practitioners is essential; to establish trust and respect as well
as understanding cultural preferences while avoiding
stereotypes is vital.

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