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Psychopharmacy Notes

Mental illness arises from a complex interplay of neurobiological, genetic, and environmental factors, with neurotransmitters playing key roles in mood regulation and cognition. Treatment often involves pharmacological approaches targeting these neurotransmitters, alongside psychotherapy for optimal outcomes. Understanding the neurobiology and genetics of mental health is crucial for effective treatment and reducing stigma associated with mental illness.

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0% found this document useful (0 votes)
18 views20 pages

Psychopharmacy Notes

Mental illness arises from a complex interplay of neurobiological, genetic, and environmental factors, with neurotransmitters playing key roles in mood regulation and cognition. Treatment often involves pharmacological approaches targeting these neurotransmitters, alongside psychotherapy for optimal outcomes. Understanding the neurobiology and genetics of mental health is crucial for effective treatment and reducing stigma associated with mental illness.

Uploaded by

mariacgomezv30
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd

Psychopharmacy

Mental Illness and Its Causes

 Mental illness is influenced by neurobiological, genetic, and environmental factors.


 The exact pathophysiology of many mental health disorders is still not fully understood.
 The brain is a complex organ that relies on neurotransmitters to function.
 Mental health treatment can involve pharmacological and non-pharmacological
interventions.

Anatomical and Chemical Functioning of the Brain

 The brain processes stimuli through neurons, which make up the majority of brain
tissue.
 Neurons handle both unconscious tasks (e.g., breathing) and complex conscious tasks
(e.g., critical thinking).
 Neurotransmission is the process of communication between neurons via
electrochemical signals.

Neurotransmitters

Neurotransmitters are chemicals that transmit messages between neurons. They can either excite
or inhibit cellular processes.

1. Dopamine
o Excitatory neurotransmitter.
o Involved in emotional responses, complex movements, and cognition.
o Regulates pleasure and reward.
o Imbalance is linked to schizophrenia and other psychotic disorders.
o Anti-psychotic medications aim to regulate dopamine transmission.
2. Serotonin
o Inhibitory neurotransmitter.
o Regulates emotions, sexual behavior, temperature, sleep, and pain
management.
o Complex system with 14+ receptor sites, contributing to disorders like
depression, anxiety, and psychosis.
o Selective serotonin reuptake inhibitors (SSRIs) block serotonin reuptake to
improve mood.
3. Norepinephrine
o Excitatory neurotransmitter.
o Responsible for learning, mood, memory, attention, and sleep.
o Low levels are linked to anxiety, depression, and memory loss.
o Trauma survivors often have elevated norepinephrine, leading to anxiety and
depressive symptoms.
4. Histamine
o Regulates alertness and wakefulness.
o Involved in gastric secretions, allergic response, and cardiac stimulation.
o Antihistamine medications used to treat mental illness can cause sedation and
weight gain.
5. Gamma Amino Butyric Acid (GABA)
o Inhibitory neurotransmitter.
o Modulates other neurotransmitters and helps reduce anxiety and improve sleep.
o Benzodiazepines enhance GABA's effect to induce calmness and treat anxiety.
6. Glutamate
o Excitatory neurotransmitter.
o Interacts with dopamine to regulate motor, affective, and cognitive functions.
o Excess glutamate can be toxic, contributing to brain damage after head injuries
or stroke.
o High levels of glutamate may be linked to psychosis.
7. Acetylcholine
o Has both inhibitory and excitatory properties.
o Regulates the sleep-wake cycle and is important for muscle function.
o Decreased levels are seen in neurodegenerative conditions like Alzheimer’s
disease.

Neurobiological Causes of Mental Illness

 The exact causes of mental illness are still not fully understood, but research has helped
identify key neurotransmitters and brain systems involved in various disorders.
 Pharmacological treatments, such as antidepressants and antipsychotics, often target
neurotransmitters to regulate mood and cognition.
 Understanding neurotransmitter function is essential in treating mental health disorders
and reducing stigma related to mental illness.

Treatment of Mental Illness

 Psychotherapeutic medications are differentiated based on the disorders they treat.


 Nurses should understand the intended effects, common side effects, and serious risks
of medications.
 Substance use treatment requires a coordinated plan for detoxification and withdrawal
management.
 Nurses play a role in following detox protocols and working with an interprofessional
team for effective care.

Key Concepts

 Neurotransmission is central to brain function and mental health.


 Neurotransmitters like dopamine, serotonin, and norepinephrine play key roles in
mood regulation, cognition, and emotional responses.
 Pharmacological treatments aim to balance neurotransmitter levels to treat various
mental illnesses.
 Nurses are crucial in managing medication effects and helping reduce stigma around
mental health treatment.

Neurobiology and Genetics in Mental Health


Understanding Mental Health

 Mental illness remains poorly understood, with etiology still largely unknown.
 Genetic factors play a significant role, with some mental health disorders being
inheritable.
 Mental health is influenced by multiple factors, including environmental stressors such
as trauma or chronic stress.

Genetics and Mental Health

 Genetic Contribution:
o Some mental health disorders are linked to genetic mutations. For example:
 Early-onset Alzheimer’s disease has a known genetic mutation.
 However, most mental disorders cannot be detected through genetic
testing alone.
 Genetic Studies:
o Family Studies: Can show a higher likelihood of mental illness in individuals
with a family history.
o Twin Studies: Used to examine mental illness in genetically identical
individuals (monozygotic twins), even when exposed to different environmental
stressors. If one twin develops a disorder, the other twin has a higher chance of
developing it as well.
o Adoptive Studies: These show that a biological child of a parent with mental
illness (e.g., addiction) is more likely to exhibit similar behaviors, even if raised
by an adoptive family.

These studies support the idea that genetics plays a role in susceptibility to mental
illness, even when environmental factors differ.

Psychiatric Pharmacogenomic Testing

 Psychiatric Pharmacogenomics: A strategy that uses genetic data to guide medication


selection in mental health care.
o Helps to predict the effectiveness of psychotropic medications based on the
patient’s genetic composition.
o Can also identify potential side effects, providing insights into how the patient
may respond to certain medications.
 Benefits:
o Improved personalized treatment by aligning medication choices with the
client’s genetic profile.
o Reduces the trial-and-error approach to psychotropic medication, enhancing the
likelihood of treatment success.
 Guidelines: The International Society of Psychiatric Genetics provides
recommendations for using genetic data to guide psychotropic prescribing practices.

Stress and Its Impact on Mental Health

 Psychoimmunology: The study of how psychosocial stress affects the body’s immune
system.
o Stress may contribute to the development or exacerbation of mental illnesses by
influencing immune responses.
o The immune system can affect neurotransmission processes in the brain.
 Inflammatory Response:
o Stress-induced inflammation can lead to mood dysregulation and is often
observed in conditions like depression.
o Individuals experiencing chronic stress or trauma may exhibit depressive
symptoms due to the immune system's impact on the brain.

The Role of Infection in Mental Health

 Viral Infections: Some studies suggest that certain viral infections may alter the genetic
makeup of the central nervous system, potentially triggering mental health disorders.
o Prenatal infection: There is evidence suggesting that infections during pregnancy
(e.g., cytomegalovirus or influenza) may increase the risk of developing
schizophrenia later in life. However, more research is needed to establish
definitive causality.

Neuroplasticity: The Brain’s Adaptive Capacity

 Definition of Neuroplasticity: The brain’s ability to reorganize itself by forming new


neuronal connections in response to stress, learning, or injury.
o This process allows the brain to adapt to new experiences or recover from
damage.
 Neuroplasticity and Mental Health:
o Neuroplasticity plays a key role in the development and progression of mental
illness. Over time, chronic mental health conditions (e.g., Major Depressive
Disorder) may involve changes in brain structure and function.
o Mental illnesses like depression often increase in severity because of
neuroplastic changes that occur over time. This makes it harder to reverse
symptoms quickly, requiring ongoing treatment.
 Treatment Implications:
o Medication for chronic anxiety or depression typically does not produce
immediate relief. It can take weeks to months for patients to notice
improvements due to the gradual process of neuroplastic adaptation.
o Nurses should educate patients that medication therapy for trauma-related or
stress-related disorders takes time, and improvements may be slow.
 Neuroplasticity in Treatment:
o Chronic conditions such as depression or trauma-related disorders require long-
term treatment to allow the brain to rewire its neuronal pathways.
o Psychotherapy combined with medication is typically most effective, as therapy
provides mental and emotional tools that complement the brain’s adaptive
process.

Medication and Mental Illness Treatment

 Role of Medication:
o Medication is a crucial treatment for many mental illnesses, particularly when
symptoms are severe or persistent.
o Unlike physiological disorders (e.g., infections or injuries), mental illnesses do
not activate the body’s immune response in the same way, which can make
treatment more complex.
 Psychotherapy and Medication:
o Combining medication with psychotherapy offers the best prognosis for those
with chronic mental health conditions.
o Medication alone may not always suffice, but it can provide relief from
symptoms, especially when therapy is not immediately available or effective.

Key Takeaways

1. Mental illness results from a complex interplay of genetic, environmental, and


biological factors.
2. Genetic research (including family, twin, and adoptive studies) supports a genetic
predisposition for many mental illnesses, though specific genetic markers are still
unclear for most disorders.
3. Pharmacogenomic testing improves the likelihood of selecting the right psychotropic
medication based on an individual's genetic profile, reducing side effects and improving
outcomes.
4. Psychosocial stress can directly impact the immune system, contributing to mental
health disorders like depression.
5. Infections, particularly during pregnancy, may play a role in schizophrenia and other
mental disorders, though research is still ongoing.
6. Neuroplasticity allows the brain to adapt and reorganize in response to experiences,
stress, or injury. This explains why treatments for mental health conditions, like
depression, take weeks or months to show improvement.
7. Combining medication with psychotherapy is often the best approach to treating
chronic mental illness. Medication offers symptom relief, while psychotherapy can help
individuals develop coping strategies and emotional resilience.

Anxiolytics (Antianxiety Medications) Notes

Introduction to Anxiolytics

 Anxiolytics are medications used to treat manifestations of anxiety, which can vary in
severity (acute vs. chronic).
 Medications are chosen based on severity and duration of anxiety symptoms.
 Anxiety-related disorders are addressed with various pharmacological treatments.

Therapeutic Use of Anxiolytics

1. Benzodiazepines

 Common Medications:
o Alprazolam
o Chlordiazepoxide
o Diazepam
o Lorazepam
 Mechanism of Action:
o Benzodiazepines bind to GABA receptors, increasing chloride ion influx into
neurons, leading to inhibitory effects.
o They increase dopamine release in the limbic system, which can lead to
physical dependence.
 Use:
o Effective for acute anxiety, central nervous system agitation, and alcohol
withdrawal.
o Depending on the severity, a short half-life (for acute anxiety) or long half-life
(for ongoing anxiety) may be chosen.

2. Buspirone
 Mechanism of Action:
o Acts as a partial serotonin receptor agonist and dopamine receptor
antagonist.
o Does not affect GABA receptors.
 Use: Primarily used for chronic anxiety.
 Time to Effect: Clinical effects take several weeks to become noticeable due to the
brain’s adaptive response.

Adverse Effects of Anxiolytics

Benzodiazepines

 CNS Depression: Common side effects include:


o Sedation
o Drowsiness
o Poor concentration
o Impaired memory
 Paradoxical Response:
o In rare cases, benzodiazepines can cause agitation, hallucinations, or seizures
instead of calming effects.
o If this occurs, discontinue use and consult the healthcare provider.
 Next-Day Sedation: Long-acting formulas can cause sedation to persist for hours after
dosing (known as next-day sedation).

Buspirone

 Common side effects include:


o Sedation
o Nausea
o Headaches
o Dizziness

Teaching Considerations for Anxiolytics

 Benzodiazepines:
o Do not mix with alcohol—this can potentiate sedative effects.
o Clients should avoid activities that require full alertness, such as driving, while
under the influence of benzodiazepines.
o Tolerance and Dependence: Over time, tolerance can develop, leading to
physical dependence.
o Tapering: After long-term use, clients should never abruptly stop
benzodiazepines. A tapering schedule is essential to avoid withdrawal
symptoms.
o Addiction Risk: Extended use can lead to addiction, due to the rewarding effect
on the limbic system (dopamine release).
 Buspirone:
o Inform clients that relief may take weeks to be noticeable due to the slow onset
of effects.

Antidepressants in Anxiety and Depression Treatment

 Therapeutic Use: Antidepressants are used to treat both anxiety and depression, as
these disorders often occur together.
o Common Disorders Treated:
 Major Depressive Disorder
 Generalized Anxiety Disorder
 Bipolar Disorder
 Post-Traumatic Stress Disorder (PTSD)
o Combination Therapy: The most effective treatment is often a combination of
psychotherapy (e.g., Cognitive Behavioral Therapy) and antidepressant
medications.

Types of Antidepressants

1. Monoamine Oxidase Inhibitors (MAOIs)

 Example: Phenelzine
 Mechanism of Action:
o Inhibit the enzyme monoamine oxidase, which breaks down neurotransmitters
(serotonin, dopamine).
o This leads to higher concentrations of these neurotransmitters in the synaptic
gap, enhancing mood regulation.
 Adverse Effects:
o Weight gain, daytime sedation, sexual dysfunction, insomnia.

2. Tricyclic Antidepressants (TCAs)

 Example: Amitriptyline
 Mechanism of Action:
o Block reuptake of serotonin and norepinephrine, increasing their availability in
the synaptic gap.
 Adverse Effects:
o Anticholinergic effects (e.g., dry mouth, constipation).
o Orthostatic hypotension (especially common in older adults).

3. Selective Serotonin Reuptake Inhibitors (SSRIs)

 Example: Fluoxetine
 Mechanism of Action:
o Selective inhibition of serotonin reuptake, increasing serotonin levels.
 Adverse Effects:
o Nausea, sexual dysfunction, agitation.
o Clients may need to be consulted about sexual side effects, as this can be a major
concern.

4. Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)

 Example: Venlafaxine
 Mechanism of Action:
o Block reuptake of both serotonin and norepinephrine.
 Adverse Effects:
o Similar to SSRIs, but also includes appetite suppression.

5. Other Antidepressants

 Examples: Trazodone, Nefazodone, Bupropion, Mirtazapine


 Use: These medications are used when SSRIs/SNRIs are ineffective or cause intolerable
side effects.
 Unique Properties:
o Bupropion: Has a higher risk of seizures; should be used cautiously.
o Mirtazapine: Often used for weight gain or insomnia in depressed clients.

6. Neurosteroid Antidepressant

 Example: Zuranolone (for postpartum depression)


 Mechanism of Action: A neurosteroid used specifically for postpartum depression.
 FDA Approval: Approved as a 14-day oral treatment, with effects starting in 3 days.

Adverse Effects of Antidepressants

 MAOIs: Weight gain, sedation, sexual dysfunction, insomnia.


 TCAs: Anticholinergic effects (dry mouth, constipation), orthostatic hypotension.
 SSRIs/SNRIs: Nausea, sexual dysfunction, agitation, and for SNRIs—appetite
suppression.
 Trazodone: Can cause sedation and priapism (rare).
 Bupropion: Risk of seizures, particularly in high doses.
 Monitoring: Clients starting antidepressants, especially SSRIs, should be monitored
closely for worsening depression, suicidal thoughts, or unusual behavior.

Teaching Considerations for Antidepressants

 Delayed Onset: Educate clients that it may take 4-6 weeks for SSRIs and 2-4 weeks for
TCAs to show full therapeutic effects.
 Sedation: If sedation occurs, clients may benefit from taking the medication at night.
 Avoiding High Tyramine Foods with MAOIs: MAOIs inhibit the breakdown of
tyramine (found in aged/fermented foods), leading to hypertensive crisis if consumed.
o Foods to avoid: Aged cheeses, smoked meats, beer, red wine, soy products (like
tofu), chocolate, avocado.
o **Avoid taking with TCAs or drugs containing ephedrine (over-the-counter cold
medications).
 Seizure Risk with Bupropion: Clients taking bupropion should be cautious of seizure
risk, particularly with higher doses.

Key Takeaways

 Benzodiazepines are effective for acute anxiety but carry a risk of dependence and
sedation.
 Buspirone is useful for chronic anxiety, but effects may take several weeks to become
noticeable.
 Antidepressants treat both anxiety and depression; however, side effects vary between
classes (MAOIs, TCAs, SSRIs, SNRIs).
 Combination treatment (medication + psychotherapy) is often the most effective.
 Education is critical, especially regarding side effects, the onset of action, and food
interactions with MAOIs.

Antipsychotics (Neuroleptics) - Detailed Notes

Overview:

 Antipsychotics are used to treat symptoms of schizophrenia and other psychotic


disorders (e.g., bipolar disorder, severe depression, and psychosis).
 There are two generations of antipsychotic medications:
o First-Generation Antipsychotics (FGA): Conventional or typical antipsychotics.
o Second-Generation Antipsychotics (SGA): Atypical or unconventional
antipsychotics.
o Third-Generation Antipsychotics (TGA): Newer medications that help stabilize
dopamine levels.
Therapeutic Use:

 First-Generation Antipsychotics (FGA):


o Mechanism: Block dopamine (D2) receptors in the brain, particularly the
mesolimbic pathway.
o Effectiveness: Effective for treating positive symptoms of schizophrenia (e.g.,
hallucinations, delusions, agitation).
o Potent Dopamine Antagonists: Highly effective but can cause significant side
effects due to their strong dopamine blockade.
o Examples:
 Haloperidol (often used in acute psychosis).
 Fluphenazine (available in long-acting depot form).
 Loxapine (for both schizophrenia and agitation).
 Chlorpromazine (used for agitation and psychotic disorders).
 Second-Generation Antipsychotics (SGA):
o Mechanism: Block dopamine receptors (less potent) and inhibit serotonin
reuptake (5HT2A receptor blockade).
o Effectiveness: More effective at treating both positive and negative symptoms
of schizophrenia (e.g., social withdrawal, lack of emotion, cognitive deficits).
o Side Effect Profile: Generally have fewer extrapyramidal side effects (EPS)
compared to FGAs but may cause metabolic effects.
o Examples:
 Risperidone: Can be given as an injectable depot form.
 Olanzapine: Can cause significant weight gain and metabolic syndrome.
 Clozapine: Used for treatment-resistant schizophrenia but requires regular
blood monitoring due to risk of agranulocytosis.
 Quetiapine, Aripiprazole, Lurasidone.
 Third-Generation Antipsychotics (TGA):
o Mechanism: These medications are dopamine system stabilizers. They regulate
dopamine activity by stimulating dopamine receptors when dopamine is low and
blocking them when dopamine is excessive.
o Indications: Treatment of psychotic disorders (schizophrenia) and mood
disorders (bipolar disorder, major depressive disorder).
o Examples:
 Aripiprazole: Partial dopamine agonist; used for schizophrenia, bipolar
disorder, and major depressive disorder.
 Brexpiprazole and Cariprazine: Similar to aripiprazole with some
differences in side effect profiles.

Common Adverse Effects:

1. Anticholinergic Effects:
o Symptoms: Dry mouth, constipation, blurred vision, urinary retention, and
orthostatic hypotension.
o Management:
 Dry mouth: Encourage sugar-free gum, candies, or water.
 Constipation: Increase fiber and fluid intake.
 Blurred vision and hypotension: Fall precautions, avoid sudden position
changes.
 Photosensitivity: Advise the use of sunscreen if exposed to direct sunlight.
2. Metabolic Side Effects (More common in SGAs):
o Weight Gain: Especially with Olanzapine and Clozapine.
o Increased Blood Sugar: Risk of developing Type 2 diabetes.
o Increased Lipid Levels: Elevated cholesterol and triglycerides.
o Increased Blood Pressure: Monitor vital signs regularly, especially in patients at
risk for hypertension.
3. Prolactin Elevation:
o Symptoms: Breast enlargement, galactorrhea (breast milk production), decreased
libido, and menstrual irregularities.
o More common with Risperidone and Haloperidol.
4. Extrapyramidal Symptoms (EPS) (Mostly with FGAs):
o Tardive Dyskinesia: Repetitive, involuntary movements, usually of the face and
tongue.
o Parkinsonism: Muscle rigidity, bradykinesia (slowness of movement), and
tremors.
o Akathisia: Restlessness and inability to sit still.
o Dystonia: Muscle spasms, often in the neck or eyes.
o Management: Dose reduction, adding anticholinergic agents (e.g.,
Benztropine) for EPS.
5. Agranulocytosis (especially with Clozapine):
o Symptoms: Fever, sore throat, or infection.
o Monitoring: Regular CBC (Complete Blood Count) to monitor white blood cell
count.

Teaching:

1. Adherence:
o Educate patients that antipsychotics help control symptoms but do not cure the
underlying disorder. Even if symptoms improve, continue medication to prevent
relapse.
o Discuss the potential side effects and encourage patients to report intolerable
ones.
2. Routine Monitoring:
o SGA: Blood glucose, lipid levels, and weight to monitor for metabolic effects.
o Clozapine: Regular monitoring of absolute neutrophil count (ANC) to check
for agranulocytosis.
3. Support Systems:
o Encourage clients to have a support person (family or friends) to assist in
medication adherence, and help recognize early signs of relapse.
Mood Stabilizers - Detailed Notes

Overview:

 Mood stabilizers help manage mood swings and prevent relapses in disorders like
bipolar disorder.
 Lithium is the most commonly used mood stabilizer, though anticonvulsants like
valproic acid and carbamazepine are also used for mood regulation.

Therapeutic Use:

 Lithium:
o Mechanism: Regulates neurotransmitter levels, particularly serotonin and
dopamine. It is believed to enhance neurotransmission in the brain, particularly in
stabilizing mood.
o Indications: Primarily used for bipolar disorder, to prevent manic and
depressive episodes.
o Monitoring: Blood levels should be checked every 1-2 weeks during initiation,
and then every 3-6 months once stabilized.
o Therapeutic Range:
 0.5-1.5 mEq/L: Therapeutic range.
 >1.5 mEq/L: Signs of toxicity (nausea, vomiting, diarrhea, tremors,
confusion).
 Renal and Thyroid Function: Regular tests as lithium is processed by
kidneys and can affect thyroid function.
 Anticonvulsants (Valproic acid, Carbamazepine):
o Mechanism: Exact mechanism is unknown, but these drugs help modulate
neurotransmitter activity, inhibit the "kindling process" (which triggers mood
episodes in bipolar disorder).
o Examples:
 Valproic acid: Used for mood stabilization, particularly during manic
episodes.
 Carbamazepine: Often used when lithium is not effective, and may be
more effective in rapid cycling bipolar disorder.

Common Adverse Effects:

1. Lithium:
o Gastrointestinal Distress: Nausea, diarrhea, and weight gain.
o Fine Hand Tremors: Common, especially at therapeutic levels.
o Increased Thirst and Urination: Can cause dehydration, increasing the risk of
toxicity.
o Kidney and Thyroid Dysfunction: Regular kidney and thyroid function tests are
important.
2. Anticonvulsants:
o Sedation: Can cause drowsiness or dizziness.
o Weight Gain (valproic acid) or Weight Loss (topiramate).
o Liver Toxicity: Valproic acid and Carbamazepine can affect liver enzymes.
o Skin Rash (Carbamazepine): May indicate severe reaction, requires immediate
cessation.
o Gingival Hyperplasia: Common with phenytoin (if used for long periods).

Teaching:

1. Lithium:
o Hydration: Drink 2-3 liters of water per day to prevent dehydration and reduce
risk of toxicity.
o Regular Bloodwork: Monitor lithium levels regularly to maintain therapeutic
range.
o Recognize Symptoms of Toxicity: Nausea, vomiting, diarrhea, and tremors.
2. Anticonvulsants:
o Monitor Diet and Weight: Valproic acid may cause weight gain, while
topiramate may cause weight loss.
o Liver Function Tests: Regular liver enzyme tests, particularly for valproic acid.
o Report Rash:

Urgent reporting of skin rashes, as they can signal a life-threatening reaction.

Sedative-Hypnotics - Detailed Notes

Overview:

 Sedative-hypnotics are primarily used to treat insomnia and other sleep-wake disorders.
They include benzodiazepines, nonbenzodiazepine hypnotics, and melatonin receptor
agonists.

Therapeutic Use:

 Nonbenzodiazepine Hypnotics:
o Examples: Zolpidem, Zaleplon, Eszopiclone.
o Mechanism: They act on GABA receptors (like benzodiazepines) but with fewer
side effects, such as memory impairment.
o Indications: Short-term treatment of insomnia.
 Melatonin Receptor Agonists:
o Example: Ramelteon.
o Mechanism: Activates melatonin receptors to regulate the sleep-wake cycle,
useful for insomnia (especially those who have trouble falling asleep).

Adverse Effects:
 Common: Headache, dizziness, nausea, and fatigue.
 Serious: Sleep-driving, sleep-walking, amnesia, hallucinations, and suicidal ideation
(especially with Zolpidem).

Teaching:

1. Avoid Alcohol and CNS Depressants: Alcohol can amplify sedative effects and
increase the risk of adverse reactions.
2. Sleep Hygiene: Encourage practicing proper sleep hygiene in conjunction with
pharmacological treatments.
3. Safety: Advise against operating vehicles or machinery while taking sedatives, as
cognitive and motor function may be impaired.

CNS Stimulants - Detailed Notes

Overview:

 CNS Stimulants are used to treat ADHD and narcolepsy.


o Common Medications: Methylphenidate, Dextroamphetamine,
Amphetamines.

Therapeutic Use:

 Mechanism: Increase dopamine and norepinephrine levels by promoting their release


and inhibiting reuptake.
 Indications: Primarily used for ADHD (improves concentration, reduces hyperactivity
and impulsivity) and narcolepsy.

Common Adverse Effects:

 Nausea, dry mouth, irritability, and heart palpitations.


 Decreased Appetite leading to weight loss, especially in children.
 Growth Suppression: Prolonged use in children may impair growth due to suppressed
appetite.

Teaching:

1. Dietary Considerations: Monitor appetite, encourage a balanced diet to prevent weight


loss.
2. Avoid Caffeine: Can increase side effects like jitteriness and insomnia.
3. Avoid Late Doses: If using sustained-release formulations, avoid taking them late in the
day to prevent sleep disturbances.
Herbal Remedies and Their Impact

Common Herbal Remedies:

1. St. John's Wort


o Used for mood regulation (commonly for depression).
o Caution: Can interact with many medications, including antidepressants (e.g.,
fluoxetine), leading to serotonin syndrome.
2. Ginseng
o Known for enhancing energy and improving cognitive function.
o Caution: Can interact with anticoagulants, increasing bleeding risks.
3. Chamomile
o Often used for anxiety and sleep disorders.
o Caution: May interact with sedatives and anticoagulants.
4. Echinacea
o Commonly used to boost immune function.
o Caution: Can interfere with immunosuppressive drugs, leading to adverse effects.

Potential Drug Interactions:

 St. John's Wort + Fluoxetine (SSRIs): Increases serotonin, which can lead to serotonin
syndrome (see below).
 Herbal Remedies + Prescription Medications: Always inform healthcare providers
about the use of herbal supplements to avoid harmful interactions with prescribed
medications.

Serotonin Syndrome

 Cause: High levels of serotonin in the central nervous system.


 Potential Triggers:
o Overdose of serotonin-increasing medications (e.g., SSRIs, SNRIs).
o Mixing multiple antidepressants or combining them with migraine/pain
medications, illicit drugs (e.g., LSD, ecstasy), or herbal remedies like St. John’s
Wort.
 Symptoms:
o Restlessness, tachycardia, muscle rigidity, sweating, fever, loss of muscle
coordination, and dilated pupils.
 Nursing Care:
o Stabilize vital signs, sedate with benzodiazepines.
o Administer serotonin antagonists like cyproheptadine.

Activation Syndrome
 Cause: Initial treatment with antidepressants, particularly SSRIs.
 Symptoms: Anxiety, irritability, agitation, impulsivity, aggression, and in some cases,
thoughts of suicide.
 Onset: Can develop within the first few days to weeks after starting medication.
 Nursing Considerations:
o Monitor for suicidal behaviors (e.g., giving away possessions, making final
arrangements).
o Seek immediate intervention if risk of suicide is suspected.

Antidepressant Discontinuation Syndrome (ADDS)

 Cause: Abrupt discontinuation of antidepressants, especially after long-term use (more


than a month).
 Symptoms:
o Flu-like symptoms (fatigue, muscle aches, dizziness).
o Electric shock-like sensations in the head.
o Anxiety, depression, and difficulty sleeping.
 Management:
o Gradual tapering off antidepressants is necessary to avoid ADDS.
o Educate patients not to stop medications abruptly.

Lithium Toxicity

Early Toxicity (Serum Levels > 1.5 mEq/L)

 Causes: Dehydration, overdose, or interaction with loop diuretics.


 Symptoms: Poor coordination, confusion, nausea, coarse tremors, vomiting, and
diarrhea.
 Nursing Intervention:
o Withhold lithium and consult healthcare provider immediately.

Advanced Toxicity (Serum Levels 2.0-2.5 mEq/L)

 Symptoms: Seizures, stupor, diluted urine, blurred vision, respiratory complications, and
tinnitus.
 Management:
o Increased kidney excretion (urea or mannitol).
o Consider gastric lavage if overdose is suspected.

Severe Toxicity (Serum Levels > 2.5 mEq/L)

 Symptoms: Coma, severe respiratory complications, and death.


 Management:
o Hemodialysis to remove excess lithium.

Agranulocytosis (Clozapine)

 Cause: Clozapine, an antipsychotic, can cause agranulocytosis, a serious reduction in


white blood cells (WBC).
 Monitoring:
o Weekly WBC counts at the start of therapy.
o If WBC < 3,500/mm3, contact healthcare provider immediately.
 Symptoms:
o Flu-like symptoms (fever, sore throat, fatigue).
o Muscle aches and fever may indicate agranulocytosis.

Neuroleptic Malignant Syndrome (NMS)

 Cause: Potent first-generation antipsychotics (FGAs), especially haloperidol. NMS


can occur with initial exposure or sudden discontinuation of antipsychotics.
 Symptoms:
o Muscle rigidity, hyperthermia, unstable vital signs (tachycardia,
increased/decreased blood pressure).
o Elevated creatine kinase levels.
 Management:
o Discontinue antipsychotics.
o Initiate cooling measures, monitor fluid and electrolytes.
o Dopaminergic agents (e.g., bromocriptine) and muscle relaxants (e.g.,
dantrolene).

Extrapyramidal Symptoms (EPS)

 Cause: Primarily due to FGAs, which block dopamine transmission in the brain.

Types of EPS:

1. Acute Dystonia:
o Muscle spasms or rigidity.
o Can include oculogyric crisis, where the eyes are locked in a fixed gaze.
2. Akathisia:
o Severe restlessness that isn't relieved by movement.
o Can lead to self-discontinuation or suicidal ideation.
3. Pseudoparkinsonism:
o Symptoms resemble Parkinson’s disease: tremors, drooling, shuffling gait,
slumped posture, and pill-rolling movements.
4. Tardive Dyskinesia:
o Permanent involuntary movements (lip smacking, tongue thrusting).
o Common with prolonged use of antipsychotics.

Detoxification Protocol

Alcohol Withdrawal

 Mechanism: Chronic alcohol use causes the brain to adapt, resulting in decreased GABA
activity and increased glutamate activity.
 Withdrawal Symptoms: Increased glutamate, leading to CNS excitation (increased
heart rate, blood pressure, nausea, vomiting, seizures).
 Treatment:
o Benzodiazepines help restore balance in the brain.

Opiate Withdrawal

 Mechanism: Prolonged use causes down-regulation of opioid receptors and


desensitization.
 Withdrawal Symptoms: Release of norepinephrine causes muscle aches, sweating, GI
discomfort, and goosebumps.
 Life-threatening Complications: Severe vomiting and diarrhea can lead to dehydration
and electrolyte imbalance.
 Treatment:
o Opiate replacements like methadone or buprenorphine are used to manage
withdrawal symptoms.

Withdrawal Protocols (Alcohol & Opiates)

1. CIWA-Ar Scale (Alcohol Withdrawal):


o Nurses rate symptoms of alcohol withdrawal, and medication (usually
benzodiazepines) is administered based on severity.
2. COWS Scale (Opiate Withdrawal):
o Nurses assess and rate severity of opioid withdrawal symptoms, then provide
medication based on the score.

 Goal: Ensure safety and comfort, prevent complications during withdrawal, and assist in
long-term recovery management.
Summary

Understanding these critical pharmacological issues—ranging from herbal remedy interactions to


severe reactions like serotonin syndrome, neuroleptic malignant syndrome, and lithium
toxicity—is essential for nursing practice in mental health care. Proper monitoring, early
detection, and tailored interventions are crucial in managing these risks effectively.

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