2. Introduction.
• Psychotropic Medication-Medication that
affects psychic function, behavior, or
experience.
• Not intended to cure the mental illness.
• They relieve physical and behavioral
symptoms but do not resolve emotional
problems.
• Often used as an adjunct to individual or
group psychotherapy.
2
3. 3
ROLE OF THE NURSE
• Nurses must understand ethical and legal
implications related to administration of
psychotropic medications e.g. right to refuse
treatment.
• Assessment- thorough baseline assessment
before patient is put on pharmacotherapy.
• Medication administration and evaluation for
side effects, adverse reactions, and
therapeutic effects of the drug.
4. 4
• Client education on why the drug has been
prescribed, when to be taken, what to expect
on side effects and adverse reactions and
when to report to the physician.
• In advanced Practice Level, Psychiatric-mental
health nurses also have prescriptive authority.
6. 6
1. Antianxiety Agents
• Also called anxiolytics and minor tranquilizers.
Examples
• Benzodiazepines e.g. Alprazolam,
Chlordiazepoxide. Clonazepam, Clorazepate,
Diazepam, Lorazepam.
• Antihistamines e.g. Hydrxyzine.
• Carbamate derivative e.g. meprobamate.
• Azaspirodecanediones e.g. Buspirone.
7. 7
Action
• Depress subcortical levels of the CNS,
particularly the limbic system and reticular
formation. They may potentiate the effects of
the powerful Inhibitory neurotransmitter
GABA in the brain, thereby producing a
calmative effect.
• All levels of CNS depression can be affected,
from mild sedation to hypnosis to coma.
• Buspirone an exception.
9. 9
Contraindications/Precautions
• Contraindicated in individuals with:
hypersensitivity to antianxiety agents,
pregnancy and lactation, narrow angle
glaucoma, shock and coma.
• Caution taken in administering these drugs to
elderly or debilitated clients, clients with
hepatic or renal dysfunction, history of drug
abuse or addiction and with those who are
depressed or suicidal.
10. Interactions.
• Increased effects when taken concomitantly
with alcohol, barbiturates, narcotics,
antipsychotics, antidepressants,
antihistamines, neuromuscular blocking
agents, cimetidine, or disulfiram.
• Decreased effects with cigarette smoking and
caffeine consumption
10
11. 11
Side Effects/ Interventions.
• Drowsiness, confusion, lethargy (most common side
effects)
-Instruct the client not to drive or operate dangerous
machinery while taking the medication.
• Tolerance; physical and psychological dependence.
-Instruct the client on long-term therapy not to quit
taking the drug abruptly.
• Ability to potentiate the effects of other CNS depressants.
-Instruct the client not to drink alcohol or take other
medications that depress the CNS while taking this
medication.
12. 12
• Possibility of aggravating symptoms in depressed
persons.
-Assess the client’s mood daily.
-Take necessary precautions for potential suicide
• Orthostatic hypotension.
-Monitor lying and standing blood pressure and
pulse at every nursing shift.
-Instruct the client to arise slowly from a lying or
sitting position.
13. 13
• Paradoxical excitement.
-Withhold drug and notify the physician.
• Dry mouth.
-Have the client take frequent sips of water, suck
on ice chips or hard candy, or chew sugarless gum.
• Nausea and vomiting.
-Have the client take the drug with food or milk.
14. • Blood dyscrasias.
-Symptoms of sore throat, fever, malaise, easy
bruising, or unusual bleeding should be
reported to the physician immediately.
• Delayed onset(buspirone only).
-Explain to client that there is a lag time of 10-
14 days between onset of therapy and subsiding
of anxiety symptoms and they should continue
taking the medication.
14
15. Diagnosis.
• Risk for injury related to seizures; panic
anxiety; abrupt withdrawal after long-term
use; effects of intoxication or overdose.
• Risk for activity intolerance related to side
effects of sedation and lethargy.
• Risk for acute confusion related to action of
the medication on the CNS.
15
16. 16
Sedative-Hypnotics
Sedatives
• Drugs that have an inhibitory effect on the
CNS to the degree that they reduce:
– Nervousness
– Excitability
– Irritability without causing sleep
17. 17
• Hypnotic drug produces drowsiness and
facilitates the onset and maintenance of a
state of sleep that resembles natural sleep.
19. 19
Action
• Sedative-hypnotics cause generalized CNS
depression. They may produce tolerance with
chronic use and have the potential for
psychological or physical dependence.
• Benzodiazepines bind to BZ receptors in the
thalamus, limbic structures, and the cerebral
cortex facilitating inhibitory effects of GABA
through increased chloride ion conductance.
20. 20
• Barbiturates depress neuronal activity in the
midbrain reticular formation, facilitating and
prolonging the inhibitory effects of GABA and
glycine.
• Increase the duration of GABA-mediated chloride
ion channel opening. May also block the
excitatory transmitter glutamic acid, and, at high
concentration, sodium channels.
• Notorious enzyme inducers
– Stimulate liver enzymes that cause the metabolism
or breakdown of many drugs
21. 21
Indications
• Short-term management of various anxiety
states.
• to treat insomnia.
• Anticonvulsants (mephobarbital, pentobarbital,
and phenobarbital)
• preoperative sedatives (pentobarbital,
secobarbital)
• anxiety associated with drug withdrawal (chloral
hydrate).
22. 22
Contraindications/ Precautions
• Hypersensitivity.
• Pregnancy.
• Lactation.
• Severe hepatic, cardiac, respiratory, or renal
disease.
• Caution should be used in administering these
drugs to clients with cardiac, hepatic, renal, or
respiratory insufficiency, suicidal clients or clients
who may have been addicted to drugs previously.
23. 23
Side Effects: Benzodiazepines
Mild and infrequent
• Headache
• Drowsiness
• Dizziness
• Vertigo
• Lethargy
• Fall hazard for elderly persons
• “Hangover” effect/daytime sleepiness
25. 25
Side effects
Barbiturates
Body System Effects
CNS Drowsiness, lethargy,
vertigo, mental depression,
coma
Respiratory Respiratory depression,
apnea, bronchospasms,
cough
26. 26
Body System Effects
GI Nausea, vomiting, diarrhea
constipation
Other Agranulocytosis,
vasodilation, hypotension,
Stevens-Johnson syndrome.
27. 27
Barbiturates:
Toxicity and Overdose
• Overdose frequently leads to respiratory depression,
and subsequently, respiratory arrest
• Overdose produces CNS depression (sleep to coma
and death)
• Can be therapeutic
– Anesthesia induction
– Uncontrollable seizures: “phenobarbital coma”
28. 28
Treatment of overdose
Symptomatic and supportive.
-Maintain adequate airway.
-Assisted ventilation/oxygen
therapy.
-Fluids.
-Activated charcoal.
29. 29
• Before beginning therapy, obtain a thorough history
regarding allergies, use of other medications, health
history, and medical history
• Obtain baseline vital signs and I&O, including supine
and erect BPs
• Assess for potential disorders or conditions that may
be contraindications and for potential drug
interactions
Nursing Implications
30. 30
Nursing Implications (cont’d)
• Give hypnotics 30 to 60 minutes before
bedtime for maximum effectiveness in
inducing sleep (depends on drug’s onset)
• Most benzodiazepines cause REM rebound
and a tired feeling the next day; use with
caution in the elderly
• Instruct patients to avoid alcohol and other
CNS depressants.
31. 31
Nursing Implications (cont’d)
• Check with prescriber before taking any other
medications, including over-the-counter
medications.
• Rebound insomnia may occur for a few nights
after a 3- to 4-week regimen has been
discontinued .
32. 32
Nursing Implications (cont’d)
• Safety is important
– Keep side rails up or use bed alarms
– Do not permit smoking
– Assist patient with ambulation (especially the elderly)
– Keep call light within reach
• Monitor for adverse effects.
33. 33
Nursing Implications (cont’d)
• Monitor for therapeutic effects
– Increased ability to sleep at night
– Fewer awakenings
– Shorter sleep-induction time
– Few adverse effects, such as “hangover” effects
– Improved sense of well-being because of improved sleep
34. Diagnosis
• Risk for injury related to abrupt withdrawal
from long-term use or decreased mental
alertness caused by residual sedation.
• Insomnia related to situational crises, physical
condition, or severe level of anxiety.
• Risk for activity intolerance related to side
effects of lethargy, drowsiness, and dizziness.
• Risk for acute confusion related to action of
the medication on the central nervous system
34
36. Introduction
• Are drugs indicated for the treatment of
psychosis,schizophrenia and mania
• They are useful for sedation and tranquilisation
classification of antipsychotics
Can be classified as typical and atypical(newer
antipsychotics)
Atypical antipsychotics have increased efficacy for
positive and negative symptoms of schizophrenia.
They have decreased tendency to cause extra
pyramidal side effects
37. Introduction
• The antipsychotic drugs (neuroleptics)
– Drugs used in treatment of schizophrenia treatment
and other psychoses and agitated states.
• Older drugs have high affinity for dopamine D2
receptors,
– whereas newer antipsychotic drugs have greater
affinity for serotonin 5-HT 2 receptors.
• Neuroleptics do not cure schizophrenia and other
psychoses, but rather ameliorate the associated
symptoms, including
– thought disorder,
– emotional withdrawal,
– and hallucinations or delusions,
• Note: many patients require prolonged therapy
(years) and thus resulting to severe toxicity in some
cases
42. ATYPICAL ANTIPSYCHOTICS
• 1.Dibenzodiazepine example clozapine-used for
patients who have not responded to or who
cannot tolerate other neuroleptics.
• 2.Thieno benzodiazepine example olanzapine-
dosage 5-20mg/day.drowsiness,dry
mouth,akathisia,isomnia
• 3.Benzo thiazepine example quetiapine-dosage
highly reduced in elderly. .SEdyspepsia,abdominal
pain,dry mouth,orthostatic hypotension
• 4.Benzixasoles example Risperidone-fatigue and
sedation and elevation of prolactin
43. • 5.Imidazolidinone example sertindole
• 6.Substitute Benzamides example Amisulpride
• 6.Quinolinones example Aripiprazole
• N/B:A newer atypical antipsychotic is
ziprasidone(zeldox) ,with also potential
antidepressant and anxiolytic effects. dosage
40-80 mg bid. dizziness, nausea and postural
hypotension and prolactin elevation
44. Pharmacokinetics:
• Antipsychotics are lipid soluble, hence
– well absorbed when given orally, and also readily
entering the central nervous system (CNS) and most
other body tissues.
• Many are bound extensively to plasma proteins.
• They require metabolism by liver enzymes before
elimination and have long plasma half-lives that
permit once-daily dosing.
• In some cases, other drugs that inhibit cytochrome
P450 enzymes can prolong the half-lives of
antipsychotic agents.
• Parenteral forms of many agents (e.g,
fluphenazine, haloperidol) are available for both
rapid initiation of therapy and depot treatment.
Antipsychotic drugs
45. • Mechanisms of action:
– The dopamine hypothesis of schizophrenia:
• proposes that the disorder is caused by a relative excess
of functional activity of the neurotransmitter dopamine
in specific neuronal tracts in the brain
• However, the hypothesis is not fully satisfactory, given
that;
– antipsychotic drugs are only partly effective in most patients
– many effective drugs have a much higher affinity for other
receptors, including serotonin receptors, than for D2 receptors
– The mechanism of action thus differs by the
category/generation of antipsychotic drugs:
• Typical/classic antipsychotic drugs: Have higher
antagonistic affinity for dopamine d2 receptors
• Newer antipsychotic drugs: Have higher antagonistic
affinity for 5HT2 (serotonin) receptors
– With the exception of haloperidol, all antipsychotic
drugs block H1 receptors to some degree- this
feature useful in their use as antiemetics
Antipsychotic drugs
46. • Clinical applications:
– Psychiatric indications:
• Schizophrenia
• Bipolar disorder (manic phase)
– Nonpsychiatric uses:
• Phenothiazines cause blockade of H1-
receptor, thus providing the basis for
their use as:
– Antiemetic
– Sedatives
– Antipruritics
Antipsychotic drugs
47. • Toxicities:
– 1) Reversible Neurologic Effects
• These are dose-dependent extrapyramidal
effects including a Parkinson-like
syndrome with bradykinesia, rigidity, and
tremor
• The toxicity can be reversed by reduction
in dose;
– Also antagonized by co administration with
muscarinic blocking agents
• Extrapyramidal effects occur more
frequently with older drugs (e.g
haloperidol) than newer drugs (e.g
olanzapine)
Antipsychotic drugs
48. – 2) Tardive Dyskinesias
• Involuntary movements of the muscles of the tongue
,mouth,fingers,toes,and other body parts; usually
irreversible
• Tardive dyskinesias tend to develop after several years of
antipsychotic drug therapy
– but have appeared as early as 6 mo
• All neuroleptics except clozapine produce tardive dyskinesia.
• When the tardive dyskinesia symptoms are noted the
offending drug is usually discontinued and patients who
require continued neuroleptic therapy switched to clozapine
Antipsychotic drugs
49. – 3) Autonomic Effects
• Result from blockade of peripheral muscarinic
receptors and adrenoceptors
– They are more difficult to manage in elderly patients
• muscarinic receptor blockade results to atropine-like
effects: dry mouth, constipation, urinary retention, and
visual problems
• Alpha receptor blockade is associated with postural
hypotension (fainting)
– Failure to ejaculate is common in men treated with the
phenothiazines
Antipsychotic drugs
50. – 4) Endocrine and Metabolic Effects
• Effects related to dopamine blockade in the pituitary:
hyperprolactinemia, gynecomastia, the amenorrhea-
galactorrhea syndrome, and infertility
– dopamine is the normal inhibitory regulator of prolactin
secretion
• Diabetogenic actions (significant weight gain and
hyperglycemia) associated with newer/atypical agents
especially clozapine and olanzapine
Antipsychotic drugs
51. – 5) Neuroleptic Malignant Syndrome
• a malignant hyperthermic syndrome that develops in
patients who are particularly sensitive to the
extrapyramidal effects of antipsychotic drugs
• symptoms include:
– muscle rigidity,
– impairment of sweating,
– hyperpyrexia,
– and autonomic instability, which may be life threatening.
• Drug treatment;
– prompt use of diazepam, dopamine agonists.
Antipsychotic drugs
52. – 6) Sedation
• This is more marked with phenothiazines (especially
chlorpromazine) than with other antipsychotics;
• Fluphenazine and haloperidol are the least sedating of
the older drugs;
– aripiprazole appears to be the least sedating of the newer
agents.
Antipsychotic drugs
53. • Overdose toxicity:
– Hypotension: managed with fluid replacement
– Seizures:
• Most neuroleptics lower the convulsive threshold and
may cause seizures, which are usually managed with
diazepam or phenytoin
Antipsychotic drugs
54. 2.Mood stabilizers
• These agents are primarily indicated in the treatment of bipolar
disorder,typically the manic phase,schizoaffective disorder,and
cyclothymia
• The standard in this class is lithium
• Others include the following:anticonvulsants
,lamotrigine,gabapentin,topiramate
1.Lithium
The us food and drug administration banned the use of lithium
following reports of fatalities from its toxicities
Pharmacokinetics:
has a narrow therapeutic index.
Readily absorbed in GIT
Serum levels peak in 60-90 min for most standard preparations
and about 4 hours for the controlled release
55. • It does not cross the blood-brain barrier rapidly,hence
acute overdose is not usually a big problem but long term
intoxication takes time to resolve.
clinical indications:
• Bipolar disoders:used for both long term and prophylaxis
• Major depressive disorder-its used as an adjuvant
treatment in patients who have fdailed to respond to
antidepressants alone and in those patients with marked
cyclicity of mood.
• Schizoaffective disoders-lithium more likely to benefit those
patients whose disorder clinically resemble bipolar mood
disorder more than schizophrenia
57. Lithium- how to use it
• Before starting :Get baseline creatinine, TSH and
CBC. In women check a pregnancy test- during
the first trimester is associated with Ebstein’s
anomaly 1/1000 (20X greater risk than the
general population)
• Monitoring: Steady state achieved after 5 days-
check 12 hours after last dose. Once stable check
q 3 months and TSH and creatinine q 6 months.
• Goal: blood level between 0.6-1.2
• Educate patient to avoid dehydration and to
maintain relatively stable salt intake
• Do not stop lithium abruptly .
58. Adverse effect
• These affects all body systems including
CNS-
i. tremors most noticeable on overstretched
hands and which may be improved by
propranolol
ii. cognitive disturbances including
dysphoria,impaired memory,lack of
spontainety and slow reaction time
59. Renal
• Polyuria and polydipsia,which result from
antagonism of antidiuretic hormone by
lithium
• Minimal change of glomerulonephritis
,interstitial nephritis impaired renal functions
may also occur
Thyroid
• Hypothyroidism and non-toxic goiter
60. skin
• Dose dependent cutaneous lesion e.g acneiform,follicular
and maculopapular eruption etc
• Weight gain
Cardiac effects
• T-wave flattening ,arrhythmias and even arrest .All these
result from potassium imbalance
Toxicity
• Signs of toxicity include : ataxia, dysarthria ,and tremors
which may progresss to seizure delirious states,marked
dysarthria,convulsions and even coma and finally death
which may result from cardiopulmonary complications
61. 2.Valproic Acid/Depakote
Valproic acid is an anticonvulsant indicated for bipolar
disoders
• Its thought to be regulator of calcium and sodium channel
function leadng to enhanced GABA activity and reduced
Glutamate activity in the brain.
Indications of valproic acid
• Mania
• Rapidly cycling bipolar
• Bipolar disorder
• Depression
• Alcohol withdrawal
• Nonacute aggressive behavior.
62. Valproic acid
• Before med is started: baseline liver function
tests (lfts), pregnancy test and CBC
• Start folic acid supplement in women
• Monitoring: Steady state achieved after 4-5
days -check 12 hours after last dose and
repeat CBC and lfts
• Goal: target level is between 50-125
63. Valproic acid side effects
• Thrombocytopenia and platelet dysfunction
• Nausea, vomiting, weight gain
• Transaminitis
• Sedation, tremor
• Increased risk of neural tube defect 1-2% vs
0.14-0.2% in general population secondary to
reduction in folic acid
• Hair loss
64. Carbamazepine/tegretol
• Used in patients who do not respond to
lithium..
• Thought to act in the similar manner to
sodium valproate.
• Another basis for antimanic effect is the
kindling concept in which the
eletrophysiological process where repeated
subthreshold stimulations of a neuron
eventually generate an action potential
65. • Before med is started: baseline liver function
tests, CBC and an EKG
• Monitoring: Steady state achieved after 5 days
-check 12 hours after last dose and repeat CBC
and lfts
• Goal: Target levels 4-12mcg/ml
• Need to check level and adjust dosing after
around a month because induces own
metabolism.
66. Carbamazepine side effects
• Rash- most common SE seen
• Nausea, vomiting, diarrhea, transaminitis
• Sedation, dizziness, ataxia, confusion
• AV conduction delays
• Aplastic anemia and agranulocytosis (<0.002%)
• Water retention due to vasopressin-like effect
which can result in hyponatremia
• Drug-drug interactions!
67. Drug interactions
• Drugs that increase carbamazepine levels and/or toxicity:
acetazolamide, cimetidine (both can cause rapid toxic
reactions), clozapine (may act synergistically to suppress BM),
diltiazem, INH, fluvoxamine, occasionally fluoxetine,
erythromycin, clarithromycin, fluconazole, itraconazole,
ketoconazole, metronidazole, propoxyphene, verapamil,
diltiazem.
• Drugs that decrease carbamazepine levels: neuroleptics,
barbiturates, phenytoin, TCA’s
• Carbamazepine is a heteroinducer, increasing its own
metabolism and that of many other drugs, including estrogen
and progesterone (contraceptives), warfarin, methadone,
many psychotropics including antidepressants, antipsychotics,
BZD’s, in addition to cyclosporine (and other
immunosuppressants), theophylline, etc.
68. Lamotrigine ( Lamictal)
• Indications similar to other anticonvulsants
• Also used for neuropathic/chronic pain
• Before med is started: baseline liver
function tests
• Initiation/titration: start with 25 mg daily X
2 weeks then increase to 50mg X 2 weeks
then increase to 100mg- faster titration has
a higher incidence of serious rash
• If the patient stops the med for 5 days or
more have to start at 25mg again!
69. Lamotrigine: Side effects
• Nausea/vomiting
• Sedation, dizziness, ataxia and confusion
• The most severe are toxic epidermal necrolysis and
Stevens Johnson's Syndrome. The character/severity
of the rash is not a good predictor of severity of
reaction. Therefore, if ANY rash develops,
discontinue use immediately.
• Blood dyscrasias have been seen in rare cases.
• Drugs that increase lamotrigine levels: VPA (doubles
concentration, so use slower dose titration),
sertraline.
70. Case 3
• 33 year woman hospitalized with her first
episode of mania. She has no previous history
of a depressive episode. She has no drug or
ETOH history and has no medical issues. What
medication would you like to start?
71. • Given her first presentation was a manic
episode statistically she will do better on
lithium.
• Make sure to check a pregnancy test, serum
creatinine and TSH prior to initiation of
treatment.
• Discuss with her what she will use for birth
control and document this discussion.
72. • You start her at 300mg BID (average starting
dose) and when she comes to see you in one
week she is complaining about stomach
irritation and some diarrhea. What do you
think is going on and what should you do?
73. • GI irritation including diarrhea is common
particularly early in treatment. Encourage pt
to drink adequate fluid, leave at current dose
and see if side effects resolve.
74. Case 4
• 27 year male is admitted secondary to a manic
episode. In reviewing his history you find he
has 5 to 6 manic or depressive episodes a
year. He has also struggled on and off with
ETOH abuse. What medication would you like
to start?
75. • Depakote would be a good choice because pt
is a rapid cycler (4 or more depressive or
manic episodes/year) and because of
comorbid ETOH abuse.
• You start 250mg BID and titrate to 500mg BID.
His depakote level is 70. You check his lfts and
compared to baseline they have increased as
follows:
76. • ALT 48 115
• AST 62140
• ALK PHOS 3280
• What happened and what do you want to
do??
77. • It is not unusual for patients on
anticonvulsants to experience an increase in
lfts and as long as they do not more than
triple no change in therapy is indicated.
• Continue to monitor over time
79. Good to know…
Most of the anti depressions elevate mood and improve
activity by enhancing central synaptic neurotransmission..
Start of side effects will be pronounced during the first
week. Anti depressant effect of the drug will be obvious
after 2 -3 weeks only-drug molecule crosses the blood brain
barrier after 8-10 days in plasma circulation.
At least 6 to 9 months of the therapy is needed in order to
prevent the relapse of depression and termination of
treatment should be gradual.
80. Indications
• treatment of dysthymic disorder;
• major depression with melancholia or psychotic
symptoms;
• depression associated with organic disease
alcoholism, schizophrenia, or mental retardation;
• depressive phase of bipolar disorder
• depression accompanied by anxiety.
83. Adverse drug reactions
o alpha block: hypotension
o Muscarinic block: atropine like effects
o Sedation,
o Weight gain
o Overdose: arrhythmias, seizures
84. 2.Selective serotonin reuptake
inhibitors
Drugs: Citalopram, fluoxetine, paroxetine,
sertraline,
Mechanism of action
• Block 5-HT transporters
Clinical applications
Major depression, anxiety disorders,
OCD, PMDD,
PTSD, bulimia, etc
Adverse drug reactions
• Sexual dysfunction
85. 3.Monoamine oxidase inhibitors
Drugs: Isocarboxazid ,Phenelzine, Selegiline
Mechanism of action
Inhibit MAO-A and MAO-B
Clinical applications
Major depression unresponsive to other drugs
Adverse effects
Hypotension
insomnia
86. 4. Serotonin-norepinephrine reuptake
inhibitors (SNRIs)
Drugs: Venlafaxin, Desvenlafaxine, Duloxetine
Mechanism of action
Drugs that block NE and 5-HT transporters
Clinical application
Major depression,
chronic pain,
fibromyalgia,
menopausal symptoms
97. 3. Miscellaneous
• Atomoxetine inhibits the reuptake of
norepinephrine,
• bupropion blocks the neuronal uptake of
serotonin, norepinephrine, and dopamine.
• The exact mechanism by
which these drugs produce the therapeutic
effect in ADHD is unknown.
98. Tolerance and Withdrawal
• Tolerance can be marked, and an abstinence
syndrome, characterized by increased
appetite, sleepiness, exhaustion, and mental
depression, can occur on withdrawal.
Antidepressant drugs may be indicated.
98
Notes de l'éditeur
Athetosis Involuntary slow writhing movements, especially severe in the hands; "mobile spasm"
Chorea Irregular, unpredictable, involuntary muscle jerks that impair voluntary activity