Midterm Exam: NR546/ NR 546 (Latest Update 2024/ 2025) Psychopharmacology for the Psychiatric-Mental Health Nurse Practitioner Review| Complete Guide with Questions and Verified Answers| 100% Correct- Chamberlain
Midterm Exam: NR546/ NR 546 (Latest
Update 2024/ 2025) Psychopharmacology for
the Psychiatric-Mental Health Nurse
Practitioner Review| Complete Guide with
Questions and Verified Answers| 100%
Correct- Chamberlain
Q: when could the client’s cognitive status create an ethical issue
Answer:
if the client is unable to self determine care or is a danger to self or others
Q: informed consent
Answer:
client has the right to receive enough information to make decisions about treatment
-must be informed about potential risks associated with meds
-clients have the right to refuse treatment and cannot be forcibly medicated in non emergencies
-clients can be forcibly medicated if they are a danger to themselves or others and less restrictive
methods have failed
Q: compliance
Answer:
a client may be court ordered to receive treatment against their will if they are a danger to
themself or others
Q: examples of special situations for compliance
Answer:
-schizophrenia
-sex offenders
-guardians can provide consent if client is lacks the cognitive function to do so
-PMHNP be knowledgable about state laws and abide
Q: example of off label prescribing
Answer:
SSRIs are used to treat anxiety and OCD but are not FDA approved for this. Can raise legal
concerns, remain up to date with recs
Q: epigenetics
Answer:
the study of how your behaviors and environment can cause changes that affect the way your
genes work
Q: in mental health, activation of a gene is often caused by
Answer:
a stressful event
Q: when is there an increased risk for psychiatric disease?
Answer:
when a stressful event is combined with genetic risk (can also be due to normal genes that
should not be active)
Q: are epigenetic changes reversible?
Answer:
yes! they don’t change the DNA se- quence, they change the way the body reads the DNA
sequence
Q: transcription factors
Answer:
proteins that bind to promotor sequences of DNA to turn gene expression on and off
Q: epigenetic changes can be influenced by
Answer:
infections, cancer, nutrition during pregnancy
Q: how is genetic testing useful
Answer:
can provide more information on how clients might respond to certain psychotropic medications
by providing info on how a client metabolizes a drug based on the CYP450 system
Q: incidence of mental health
Answer:
30% of the world is suffering from neurologic or psychiatric disorder
20% of children and adolescents are affected
Q: client factors that may affect adherence
Answer:
s/e, fear of addiction, misunder- standing of expected outcomes
Q: clinician factors that might contribute to adherence
Answer:
lack of shared decision making with client, providing inadequate education about meds, lack of
follow up
Q: structiral factors that may contribute to adherence
Answer:
medication access, costs, and stigma associated with mental illness
Q: CYP450 phase 1 metabolism
Answer:
drug is ingested orally
-oxidation (most common)
-reduction
-hydrolysis
Q: 3 possible outcomes of phase 1 metabolism
Answer:
1.drug becomes completely inactive
2.drug becomes partially inactive by one+ metabolites remain active
3.original drug is not pharmacologically active, but one metabolite remains active
Q: what is the relationship between CYP450 and the gut wall, liver, blood- stream
Answer:
CYP450 enzymes in the gut wall or liver convert drug substrate into bio- transformed product in
the bloodstream. After passing through the gut wall and
liver, the drug will exist partially as unchanged drug and partially as biotransformed product in
the bloodstream
Q: where do genetics play into CYP450 system
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what does grey matter consist of? cerebellum, cerebrum, brainstem, butterfly shaped portion of the central spinal cord
What is grey matter associated with? learning (changes linked to alzheimer’s, schizphrenia, MDD)
what is white matter? “nerve fibers that connect neurons from different regions into functional circuit “”transit system”””
what is white matter associated with? sensory and motor function, cognition (changes in white matter associated with autism and vascular dementia)
frontal lobe intelligence, abstract thinking, ability to organize, personality, behavior, emotion control
injury to frontal lobe personality changes, difficulty controlling emotion
prefrontal cortex executive function
thalamus motor command processing
amygdala anxiety/fear, perception of odors
hippocampus memory (long term), anxiety
wernicke’s area speech comprehension
broca’s area Speech production
basal ganglia voluntary motor movements, cognition, emotion
limbic system emotion and learning
parietal lobe somatic senses
temporal lobe CONTAINS limbic system, amygdala, hippocampus (disorders: ADHD, dementia)
occipital lobe visual processing (seizures here cause hallucinations such as lines of color)
when could the client’s cognitive status create an ethical issue if the client is unable to self determine care or is a danger to self or others
informed consent
compliance a client may be court ordered to receive treatment against their will if they are a danger to themself or others
examples of special situations for compliance -schizophrenia-sex offenders-guardians can provide consent if client is lacks the cognitive function to do so -PMHNP be knowledgable about state laws and abide
example of off label prescribing SSRIs are used to treat anxiety and OCD but are not FDA approved for this. Can raise legal concerns, remain up to date with recs
epigenetics the study of how your behaviors and environment can cause changes that affect the way your genes work
in mental health, activation of a gene is often caused by a stressful event
when is there an increased risk for psychiatric disease?
are epigenetic changes reversible? yes! they don’t change the DNA sequence, they change the way the body reads the DNA sequence
transcription factors proteins that bind to promotor sequences of DNA to turn gene expression on and off
epigenetic changes can be influenced by infections, cancer, nutrition during pregnancy
how is genetic testing useful can provide more information on how clients might respond to certain psychotropic medications by providing info on how a client metabolizes a drug based on the CYP450 system
incidence of mental health 30% of the world is suffering from neurologic or psychiatric disorder 20% of children and adolescents are affected
client factors that may affect adherence s/e, fear of addiction, misunderstanding of expected outcomes
clinician factors that might contribute to adherence lack of shared decision making with client, providing inadequate education about meds, lack of follow up
structiral factors that may contribute to adherence medication access, costs, and stigma associated with mental illness
CYP450 phase 1 metabolism drug is ingested orally -oxidation (most common) -reduction-hydrolysis
3 possible outcomes of phase 1 metabolism 1. drug becomes completely inactive 2. drug becomes partially inactive by one+ metabolites remain active 3. original drug is not pharmacologically active, but one metabolite remains active
what is the relationship between CYP450 and the gut wall, liver, bloodstream CYP450 enzymes in the gut wall or liver convert drug substrate into biotransformed product in the bloodstream. After passing through the gut wall and liver, the drug will exist partially as unchanged drug and partially as biotransformed product in the bloodstream
where do genetics play into CYP450 system Not all people have the same genetic form of CYP450 enzymes, variations in the genes encoding for the different CYP450 enzymes can alter the activity of these enzymes. This results in alterations of drug levels at standard doses
poor metabolizer
vortioxetine considerations cut dose in half for poor metabolizers. especially at risk for tox
extensive metabolizer people who have normal rates of drug metabolization -most drug doses are set at values for extensive metabolizers
rapid metabolizers
how does inhibitor effect medication efficacy decrease medication metabolism – makes med stay in the body longer, may need to decrease dose
how does inducer effect medication efficacy
CYP450 inhibitors
CYP450 inducers
carbamazepine – inducer or inhibitor? what happens when you combine it with other medications? inducer -can make other medications less effective
carbamazepine dose adjustments often requires dose increase over time, the drug induces its own metabolism – lowering the plasma levels over the first several weeks to months of treatment
agonist allows second messenger to act at its greatest potential
antagonists “blocks an agonist that may be overstimulating the neurotransmitters -considered “”silent””-cause bad s/e”
partial agonist considered stabilizers and help maintain balance
inverse agonists stabilizes g protein in a totally inactive form to cause a reduction in signal transduction
communication between neurons is _ chemical
neurotransmission chemicals or neurotransmitters are released from their transport vesicles to bind with receptor sites to perform their duties, which are either excitatory or inhibitory
excitatory NT increase the likelihood that the neuron will fire an action potential
inhibitory NT decrease the likelihood that a neuron will fire an action
how is a neurotransmitter removed either returned and store for future use (reuptake), or is inactivated and dissolved by enzymes
4 categories of NT 1. cholinergics (acetylcholine)2. monoamine (norepinephrine, dopamine, serotonin, histamine)3. amino acids (gamma-amino-butyric acid (GABA) and glutamate)4. neuropeptides
how do psychotropic medication relate to NT either enhancing or decreasing the NT ability to bind to receptors
what does calcium do leads to release of NT into synapse
sodium channels propagation of an action potential is mediated by voltage sensitive sodium channels
GABA “*chief inhibitory NT- aka “”chill pill””-targeted by benzos”
Norepinephrine (NE) responsible for fight or flight -helps with focus and productivity
dopamine (DA) -affects balance and coordination -excitatory -low dopamine found in parkinsons -increased dopamine found in schizophrenia and psychosis -dopamine has its own pathways *
acetylcholine (ACH) affectes arousal, motivations, learning, REM sleep
serotonin (5HT) “””happy hormone””regulates mood”
glutamate (GLU) *main excitatory NTaffects almost every neuron in the brain
signal transduction cascades the process through which cells communicate-controlled by signaling cascades such as g-linked protein system
g-linked protein systems pass messages from first receptor to second messenger -g linked and ion channel cascades are triggered by NTs
voltage sensitive sodium channels propagation of action potential. influx of sodium through channel at axon terminal leads to opening of calcium channel. influx of calcium leads to docking of synaptic vesicles and secretion of NT into synapse
psychotropic drug metabolism may be impacted by age, smoking, caffiene, other meds, food
why do some drugs take time to take effect signal transduction cascades can produce downstream (delayed) and/or long lasting effects
5 dopamine pathways 1. nigrostriatal 2. mesolimbic3. mesocortical4. tuberoinfundibular 5. thalamic
nigrostriatal
mesolimbic
mesocortical
Tuberoinfundibular
hyperprolactinemia serum prolactin level rises due to blockade of dopamine in hypothalamus. may be asymptomatic or -irregular menses -male gynecomastia -nipple discharge -osteoporosis – secual dysfunction and infertility (both genders)
thalamic -multiple sites function not well known
first generation antipsychotic (FGA) (typical antipsychotic)
FGA examples -haldol (high potency, for acute/severe agitation or aggression)-thioridazine (high potency)-fluphenazine (high potency)-thiothixene (medium potency)-mesoridazine ( low potency )-chlorpromazine (low potency, 2nd line due to QTc))
low potency meds require higher doses to achieve efficacy -have more anticholinergic, antihistamine, and alpha-1 properties, which can result in more sedation
dosing antipsychotics there is no evidence that higher doses are more effective -adjust dose after 2 weeks -establish efficacy and effective meds before switching to a long acting injectable (LAI)-the LAI will be same dose as oral
adverse effects of FGA -neurolepsis (cognition and behavior issues P=psychomotor nigrostriatal pathway, E=emotional quieting mesocortical, A=affective indifference mesocortical)-cardiac (QT prolongation, torsades, sudden cardiac death)-blood dyscrasias (neutropenia, leukopenia, agranulocytosis)-esophageal dysmotiltity, aspirartion -fall risk-imbalance of ach = anitcholinergic side effects (can’t see can’t pee can’t shit can’t spit)-block of histamine = drowsy -block of alpha 1 adrenergic receptors = orthostatic hypotension, dizzy, drowsy
second generation antipsychotics (SGA) (atypical antipsychotics)
-pines (about) -bind more potently to 5HT than DA-sedation is common (highest risk amongst SGAs, if pt cant sleep – give these at bedtime)-lowest risk of EPS-high risk of weight gain and metabolic effects
-pines (drugs) -olanzapine (zyprexa) best tolerated antipsychotic -quetiapine (seroquel)-asenapine (saphris) MOSt appropriate for overweight pts, sublingual and td -clozapine (clozaril) do not use in acute presentation of schizophrenia
clozapine special considerations -only use when others have failed -after 2 sequential trials-hold if pts absolute neutrophil count is less than 1500 (frequent CBCs q week x6 mo, q other week x6 mo, monthly)-one of the only antipsychotics that does not cause dystonia -gold standard, but last thing to try due to serious side effects (agranulocytosis, seizures, myocarditis)
“SGA “”many dones and a rone”” (about)” -either bind more potently to 5HT tha DA or equally -less sedating -less risk of metabolic s/e and weight gain -higher risk of EPS and hyperprolactinemia
many dones and a rone (drugs) -risperidone (risperidol) highest risk of galactorrhea and hyperprolactinemia -paliperdone (invega)-ziprasidone (geodon) monitor for a rash = DRESS, IM to pts with acute agitation -iloperidone (fanapt) for pts with cholesterol issues – lurasidone (latuda) take with at least 350 calories for absorption
2 pips and a rip (about) -pips bind more potently to DA than 5HT-rip binds equally -lowest metabolic s/e-low risk of weight gain -potential for EPS
2 pips and a rip (drugs) -aripiprazole (abilify) lowest risk of weight gain *black box = increased risk of suicide in children -brexipiprazole (rexulti)-cariprazine (vraylar)
prescribing antipsychotics -begin with monotherapy -multiple antipsychotics can increase risk of QT prolongation -combos only considered after monotherapy has not worked -when switching, try to switch to different drug within the same class to avoid withdrawal-cross titration over several days to weeks is required to prevemt side effects such as agitation, activation, insomnia
Neuroleptic Malignant Syndrome *a medical emergency -diaphoresis, anxiety, tachypnea, muscle stiffness, AMS, tachycardia, hyperthermia _treatment = hydration, benzos, muscle relxants, reversible when caught early
olanzapine special considerations use caution when suspected alcohol withdrawal, stimulant intoxication, anticholinergic intoxication -high and repeated doses of amphetamines and cocaine can mimic positive symptoms of paranoid schizophrenia
which 2 medications are decreased risk of death by suicide clozapine and olanzapine
Haloperidol -starting dose 1-15mg once a day or divided doses -increase prn up to 100mg/day
olanzapine -schizophrenia age 13 and older -best tolerated antipsychotic -5-10mg once/day -increase by 5 mg a day each week max 20 mg/day-high metabolic risk-highest weight gain risk
quetiapine -schizophrenia ages 13 and older -moderate metabolic risk -low eps risk -starting dose 50 mg BID-risk of orthostatic hypotension, weight gain, prolonged QT
asenapine -schizophrenia age 10 and up-sublingual or TD patch -low metabolic risk
clozapine -treatment resistant schizophrenia and chronic suicidal behavior in schizophrenia or schizoaffective disorder -NOT indicated for acute presentation of schizophrenia -absolute neutrophil count must be below 1500-high metabolic risk-highest weight gain risk-block box = severe neutropenia-contraindicated in liver disease and hepatic failure -not first choice
risperidone -schizophrenia ages 13 and up-highest risk for hyperprolactinemia-blood, QT prolongation, cardiovascular events, CVA
paliperidone -schizophrenia ages 12 and up-moderate metabolic risk
ziprasidone -schizophrenia ages 10 and up-IM dosing in acute agitation -low metabolic risk-lowest risk for weight gain -contraindicated in clients with QT, recent MI, HF-DRESS
iloperidone -schizophrenia -moderate weight gain risk-low risk for hyperlipidemia
lurasidone -schizophrenia age 13 and up-should be taken with food -low metabolic risk
aripiprazole -schizophrenia ages 13 and up -10-15 mg/day max 30 mg/day -low metabolic risk-low risk for weight gain -low risk orthostatic hypotension
brexpiprazole -considered procognitive -schizophrenia
first line of treatment for hallucinations antipsychotics (olanzapine)
EPS group of symptoms related to motor control and coordination -dystonia, akathisia, parkinsonism, bradykinesia, tremors, tardive dyskinesia -caused by dopamine excess-basal ganglia -may effect med compliance and can be an emergency
tardive dyskinesia hyperkinetic movement disorder characterized by abnormal facial and tongue movements, quick, jerky limb movements, can occur from long term blockade of D2 receptors in the nigrostriatal pathway -failure to dc typical antipsychotics can result in permanent condition -FGAs (especially high potency)
dystonia involuntary contractions of muscles, can cause pain
akathisia inner restlessness leading to repetitive motion
parkinsonism combination of abnormal movements like those seen in parkinsons disease, tremor, slow movement, impaired speech, muscle stiffness
priority data used to determine treatment plan for mental health disorders patient symptoms!
benzo benefits “-occasional, intermittent use for surge of symptoms and sudden relief is needed -“”top up”” an SSRI or SNRI for pts only experiencing partial relief”
benzo risks -do not use in pts with substance abuse, particularly alcohol -use in caution with patients with PTSD-high risk for abuse -OD can lead to resp depression and coma -withdrawal can be severe (psychosis, hallucinations, delirium, seizures)
which benzo is safe in lactation lorazepam
which benzo should not be prescribed in pregnancy flurazepam, estazolam
recomended length of treatment for benzos short term2-4 weeks
how to wean benzos taper to prevent withdrawal symptoms, rebound anxiety, seizures -before tapering, assess underlying conditions and discuss alternate therapies -withdrawal symptoms occur faster in shorter acting agents (2-3days) than with longer acting (5-10 days)-reduce daily dose by 10-20% every 1-2 weeks
diversion prevention -pt only uses 1 pharmacy -BZO prescribed by only 1 provider -check state PMP-no early refills -followup requires symptom assessment, PMP program, UDS, care plan with informed consent, appropriate documentation
hypothalamus fight or flight response by activating sympathetic nervous system
fear amygdala interprets sights and sounds associated with stress or fear and sends a distress signal to hypothalamus -hypothalamus initiates fight or flight response (SNS)-adrenal glands send adrenaline to prepare body -adrenaline subsides and hypothalamus activates pituitary for cortisol -serotonin, GABA, glutamate, dopamine, norepinephrine
worry -cortico striato thalamo cortical (CSTC) circuit -feedback loops from prefrontal cortex -GABA
treatment for GAD 1.SSRI2.SNRI3.buspirone4. drug therapy at least 1 year -SSRI/SNRI first line, take several weeks for efficacy -adding anxiolytic or BZO at beginning may give relief until efficacy is reached with antidepressant -combo of psychotherapy and med management is best -SSRI or SNRI used for anxiety, use half the dose you would for depression -onset 2-4 weeks -do not stop abruptly because it can result in rebound anxiety
to take away SNS symptoms of anxiety alpha 2 delta ligands, beta blockers, histamine receptor antagonist
PTSD -paroxetine-sertraline -most PTSD pts do not take montherapy -alpha 1 agonist at night to prevent nightmares -exposure therapy is most effective
1st line treatment for OCD fluoxetine
pregancy considerations -risk of withdrawal symptoms in newborn-EPS evident during delivery -SGAs more dangerous than FGAs due to increased risk of gestational metabolic considerations -avoid clozapine, ziprasidone, olanzapine, rsiperidone, and quetiapine especially in 3rd tri
why is paroxetine contraindicated in pregancy risk of atrioseptal defects
can you take hydroxyzine in 1st tri no
BZOs and pregnancy -BZOs cross the placents so there is an increase risk of neonatal complications -intrauterine growth restriction -oversedation at birth -potential learning disabilities – autism, ADHD-neonatal withdrawal
black box warning arirpiprazole increase of suicide in children
black box warning quetiapine increase risk of suicide in adolescents/young adults during intial 1-2 months
first line of treatment for children and adolescents psychotherapy -SSRIs for severe symptoms or psychotherapy ineffective -increased risk of suicide in clients less than 30 years using SSRIs-gabapentin not approved for anxiety in children, only seizures
avoid which meds in elderly barbiturates, BZOs, antihistamine, alpha 2 delta ligands -Beers criteria avoid haloperidol, ziprasidone, olanzapine
antipsychotcs and breast feeding all antipsychotics expected to be in breast milk, dc drug or bottle feed -no gabapentin, BZOs, antihistamines, alpha 2 ligands
monitor clients on antidepressants for what SI
SSRI
escitalopram dose 10-20mg/day
fluoxetine dose 20-80 mg/day
sertraline dose 50-200 mg/day
paroxetine dose 10-60 mg/day
citalopram dose 20-40 mg/day
adverse effects of SSRI
SNRI
venlafaxine dosing 37.5 mg once a day for extended release, 25-30 mg divided into 2-3 doses for IR-if tolerated increase no faster than 75 mg every 4 days -max 375mg/day
s/e of SNRI SHAT-same adverse reactions of SSRI-htn-adrenergic effects (awake, anxious, agitated)-tachycardia avoid in pts with liver issues and htn increase anxiety because they target NE
buspirone -short term anxiety treatment -bind to 5HT, DA, and increase NE metabolism in brain -dose: 15 mg BID-increase 5 mg/day every 2-3 days max 60 mg/day -use as adjunct, not monotherapy
buspirone s/e and pearls severe renal impairment, severe hepatic impairment, MAOIs are avoided here, decrease sexual s/e when used with SSRIas effective as BZO but non sedative, non habit forming, no abuse potential, no withdrawal effects 2-3x/day due to short half life
alpha 2 delta ligands -off label for GAD-bind with glutamate ca channel blockers to inhibit release of several NT-precautions: SI, substance abuse, HF, renal impairment, -do not use in myopathy or with BZOswork quickly
alpha 2 delta ligands drugs and doses pregabalin: 150-600 mg/day 2-3 doses gabapentin 900-1800 mg/day divided in 3 doses
beta blockers used to treat somatic anxiety effects such as tachycardia, and physical tension -blocks effects of NE and Epi -atenolol, propranolol (40-400 mg/day)-caution in HF, bradycardia, 1st degree HB, DM, hyperthyroidism -may be prescribed during traumatic event to help permanent fear response
histamine receptor agonists -anxiety and skeletal muscle tension associated with psychoneurosis, anxiety from alcohol withdrawal, anxiety related to cardiac impairment -targets histamine -hydroxyzine 50-100mg 4x/day -monitor hepatic status, k+, QT-unsure if anxiety releif is due to sedation or anxiolytic
alprazolam starting dose anxiety:.75-1.5 mg/day divided in 3 doses -increase every 3-4 days max 4mg/day panic:1.5 mg/day divided into 3 doses-increase 1 mg every 3-5=4 days max 10 mg/day
lorazepam dose 2-6 mg/day
clonazepam dose 0.5-2 mg/day in divided doses or at bedtime
diazepam 2-40mg/day in divided doses
adverse effects of BZO dose related -oversedation, memory impairment, depression, tolerance, dependence, paradoxical effects
which medication is most associated with unwanted activation or panic attacks SNRIs because they target NE