3. DEFINITION OF PSYCHOPHARMACOLOGY
•Psychopharmacology is the study of drugs used to
treat psychiatric disorders.
• Medications that affect psychic function, behaviour or
experience are called psychotropic medications.
4. TERMINOLOGY
• Efficacy: It refers to the maximal therapeutic effect
that a drug can achieve.
• Potency: It describes the amount of the drug needed to
achieve that maximum effect.
• Half-life: It is the time it takes for half of the drug to
be moved from the bloodstream.
• Agonists: Drugs that activate receptors are termed as
agonists.
• Antagonists: Drugs that block the receptors are termed
as antagonists.
5. NEUROTRANSMISSION
KEY
A. Pre synaptic neuron
B. Post synaptic neuron
1. Mitochondria
2. Synaptic vesicle
3. Voltage gated ca++ channel
4. Synaptic cleft
5. Neurotransmitter receptor
6. Voltage gated ca++ channel
7. Neurotransmitter
8. Neurotransmitter reuptake
pump
7. SR
NO
AFFECTS DESCRIPTION
1. Release More neurotransmitters are released into the synapse from the
storage vesicles in presynaptic cell.
2. Blockade The neurotransmitters are prevented from binding to the
postsynaptic receptors.
3. Receptor sensitivity
changes
The receptor becomes more or less responsive to the
neurotransmitter.
4. Blocked reuptake As the presynaptic cells does not reabsorb the neurotransmitter
it is retained in the synapse & therefore enhance or prolongs
the action.
5. Interference with
storage vesicles
Either released more or less.
6. Precursor chain
interference
The process that “makes” the neurotransmitter is either
synthesized more or less.
7. Synaptic enzyme
interference
Less neurotransmitter is metabolised, so more remains available
in the synapse.
8. GUIDELINES REGARDING DRUG ADMINISTRATION IN PSYCHIATRY
• The nurse should not administer any drug unless there is a written
order. Do not hesitate to consult the doctor when in doubt about any
medication.
• All medications given must be charted on the patient’s case record
sheet.
• While giving medication.
-Always address the patient by name and make certain of his
identification.
-Do not leave the patient until the drug is swallowed.
-Do not permit the patient to go to the bathroom to take the
medication.
-Do not allow one patient to carry medicine to another.
9. CONTI…
• If it is necessary to leave the patient to get water, do not leave the
tray within the reach of the patient.
• Do not force oral medication because of the danger of aspiration.
This is especially important in stupor us patients.
• Check drugs daily for any change in color, odor and number.
• Bottles should be tightly closed and labeled. Labels should be written
legibly and in bold lettering. Poison dugs are to be legibly labeled
and kept in separate cupboard
• Make sure that an adequate supply of drugs is on hand, but do not
overstock.
• Drug cupboard should always be kept locked when not in use. Never
allow a patient or worker to clean the drug cupboard. The drug
cupboard keys should not be given o patients.
10. PATIENT EDUCATION RELATED TO
PSYCHOPHARMACOLOGY
Discussion of side effects
Discussion of safety issues
Drug interactions
Instructions for older adult patient
Instructions for pregnant or breast feeding patients
24. PHARMACOKINETICS
Absorption and distribution
The oral liquid dose produces a peak level at 1.5 hours
Intramuscular dose peaks at 30 minutes.
Highly bound to plasma as well as protein (92-98%)
Metabolized in liver, excreted through kidney.
Elimination half-lives are 10-24 hrs.
Most of this drug have therapeutic window.
If blood level is below the window, the drug is ineffective,
if the blood level is upper limit of the window, it results in
to toxicity, the drug is again ineffective.
26. ATYPICAL ANTIPSYCHOTICS
Here total 9 receptors are
affecting.
• 3 receptors (M1, alpha1, H1) same as
typical antipsychotics which
causing EPS.
• Rest of 6 receptors affecting
serotonin (5HT2, 5HT3, 5HT2C)and
dopamine (D1, D2, D4) receptors
• And due to this SDAS ( serotonin-
dopamine antagonists) there will be
no side effect after using atypical
antipsychotics.
ATYPICAL
D1
D2
D4
M1
alpha1
HT1
HT2C
HT3
29. ADVERSE EFFECTS OF ANTIPSYCHOTIC DRUGS
• EXTRA PYRAMIDAL SYMPTOMS
(EPS): (due to Antidopaminergic
actions on basal ganglia)
Neuroleptic-induced
Parkinsonism
Acute dystonia
Akathisia
Tardive dyskinesia
Neuroleptic malignant syndrome
• SEIZURES
• SEDATION (due to Alpha-adrenergic blockade)
• AUTONOMIC SIDE-EFFECTS: Dry mouth,
constipation, cyclopligia, mydriasis, urinary
retention, orthostatic hypotension,
impotence and impaired ejaculation.
• OTHER EFFECTS:
Agranlocytosis(especially for
clozapine)
Sialorrhea or increased salivation
(especially cially for clozapine)
Weight gain
Jaundice
Dermatological effects (contact
dermatitis, photosensitive reaction)
30. EXTRA PYRAMIDAL SYMPTOMS
1. PSEUDO PARKINSONISM
Symptoms may appear 1 to 5 days following
initiation of drug.
• It includes slow pill-rolling finger tremors,
masklike facial expression, weakened voice
• absence of arm swing when walking, stiff
stooped posture, and an impaired shuffling gait.
Cogwheeling rigidity, assessed frequently in the
arms, is a ratchet-like motion of the
extremities during extension.
31. CONTI…
• Mentally, the client can display bradyphrenia, or a slowed
ability to think through familiar situations.
• One unique manifestation after prolonged use of the
antipsychotic medication is the rabbit syndrome which is
tremors of the lips and a constant chewing motion.
The treatment of parkinsonism is anti cholinergic medication.
32. 2. AKATHISIA
• Agitation, restlessness, clients may demonstrate restlessness
through actions such as pacing, marching, shuffling, foot-
tapping, rocking motion, or shifting body weight from leg to
leg. Restlessness can be throughout the entire body or
confined to a section of the extremities.
• Muscle discomfort;
• Treatment:- change the antipsychotic drugs and
anticholinergic drug.
33. 3. DYSTONIA
• Intense involuntary spasm of muscles of neck,
tongue, face, jaw, eyes or trunk, affecting the
tongue and throat muscles can affect the vocal
cords, causing a hoarse voice, stiff or thick tongue
• Dysphagia, laryngeal or pharyngeal spasms, and
potential obstruction, which becomes a medical
emergency.
• Neck and trunk symptoms include torticollis,
34. CONTI…
• Twisting of the cervical spine muscles, and opisthotonos, a
severe form of back arching.
• In addition, clients may experience oculogyric crisis which is
rolling of the eyes in a locked upward position.
• Treatment is decrease dose of antipsychotic, anticholinergic
and antiparkinsonian agents are the first line of defence
during acute dystonic reactions
35. 4. TARDIVE DYSKINESIA
The symptoms are Potentially irreversible.
• Rapid, repetitive, involuntary movements of
the face, trunk, respiratory muscles, and
extremities. Facial movements, which often
occur in the oral area, can include a
protruding or rolling tongue, lip smacking,
grimacing, frowning, sucking or kissing
motions, and facial distortions.
36. CONTI…
• Stereotypic movements of the limbs can be irregular,
rapid, purposeless motions or slow movements.
• A client’s trunk may rock, twist, jerk, or thrust
forward.
The drug should be withdrawn at the first sign.
Treatment is benzodiazepines etc.
38. NURSING MANAGEMENT
Assessment: History and Examination
Implementation with Rationale
The risk of extrapyramidal symptoms
To prevent dry mouth –Sips of water &
frequent mouthwashes, use of chewing gum
Limit sun exposure, drink fluid or lozenges for
dry mouth.
Provide safety measures and seizure
precautions
High fiber diet to reduce constipation
Provide thorough patient teaching, including
39. CONTI…
• Patient receiving clozapine is at risk of developing
Agranulocytosis. Monitor TC, DC in the 1st weeks of treatment.
Stop the drug if the WBC count drops to less than 3000/mm3 of
blood.
• Teach the importance of drug compliance, side effects of drugs
and reporting if too severe, regular follow ups.
• Give reassurance and reduce unfounded fears and anxieties.
51. MECHANISM OF ACTION
• TCAS blocks the reuptake of
serotonin and norepinephrine
• SSRIS specifically blocks the
reuptake of serotonin
• MAOIS blocks the enzyme
and stopping the breakdown
of dopamine, norepinephrine,
and serotonin.
55. CLIENT EDUCATION WHO RECEIVING
ANTIDEPRESSANTS
• Continue to take the medication even though the symptoms have
not subsided. The therapeutic effect may not be seen for as long as
4 weeks. If after this length of time no improvement is noted, the
physician may prescribe a different medication.
• Not discontinue use of the drug abruptly. It might produce
withdrawal symptoms, such as nausea, vertigo, insomnia,
headache, malaise, nightmares, and return of symptoms for which
the medication was prescribed.
• Use caution when driving or operating dangerous machinery.
Drowsiness and dizziness can occur.
56. CONTI…
• Use sun block lotion and wear protective clothing when spending time
outdoors. The skin may be sensitive to sunburn.
• Rise slowly from a sitting or lying position to prevent a sudden drop in
blood pressure.
• Take frequent sips of water, chew sugarless gum, or suck on hard candy
if dry mouth is a problem. Good oral care is very important.
• Avoid consuming the following tyramin containing foods or
medications while taking MAOIs: aged cheese, wine, beer, chocolate,
colas, coffee, tea, sour cream, smoked and processed meats, beef or
chicken liver, canned figs, soy sauce, overripe and fermented foods,
pickled herring, yogurt, yeast products, broad beans, cold remedies,
diet pills.
• To do so could cause a life-threatening hypertensive crisis.
57. • Avoid smoking while receiving tricyclic therapy. Smoking
increases the metabolism of tricyclics, requiring an adjustment in
dosage to achieve the therapeutic effect.
• Avoid alcohol use while taking antidepressant therapy. These drugs
potentiate the effects of each other.
• Avoid use of other medications (including over-the counter
medications) without the physician’s approval while receiving
antidepressant therapy. Many medications contain substances that,
in combination with antidepressant medication, could precipitate a
life-threatening hypertensive crisis.
• Avoid exposing application site to direct heat (e.g., heating pads,
electric blankets, heat lamps, hot tub, or prolonged direct sunlight).
60. LITHIUM
•Lithium is an element with atomic number 3 and
atomic weight 7.
•Discovered in 1949 by FJ Cade for use in
treatment of Mania,
•Equally effective in treating and preventing
episodes of mania and depression in bipolar
disorder
61. INDICATIONS
•Treatment of acute
mania
•Prophylaxis of bipolar
disorder
•Schizoaffective
disorder
•Cyclothymia
•Impulsivity and
aggression
•OTHER:
Premenstrual dysphoric
disorders
Bulimia nervosa
Borderline personality
disorder
Episodes of binge
eating
Trichotilomania
Cluster headaches
62. PHARMACOKINETICS
• Rapidly absorbed from GI tract
• Peak level within 30 mins to 3 hours
• Not protein bound
• Distribution in total body water
• Maximum levels in thyroid, saliva and CSF
• Steady state level in 5 to 7 days
• Excreted almost entirely by kidneys
• Reabsorbed in proximal tubules and is influenced by sodium
balance.
• Depletion of sodium can precipitate lithium toxicity.
63. MECHANISM OF ACTION
•Accelerates presynaptic re-uptake and
destruction of catecholamines, like
norepinephrine
•Inhibits the release of catecholamines at the
synapse
•Decreases postsynaptic serotonin receptor
sensitivity
68. CONTRA INDICATIONS
CARDIAC, RENAL, THYROID OR NEUROLOGICAL
DYSFUNCTIONS
PRESENCE OF BLOOD DYSCRASIAS
DURING FIRST TRIMESTER OF PREGNANCY AND
LACTATIONZ
SEVERE DEHYDRATION
HYPOTHYROIDISM
HISTORY OF SEIZURES
70. CONTI…
GASTROINTESTINAL:
• NAUSEA
• VOMMITIING
• DIARRHOEA
• ABDOMINAL PAIN AND
METALIC TASTE
ABNORMAL THYROID
FUNCTION
GOITER
WEIGHT GAIN
DERMATOLOGICAL:
• ACNEIFORM ERUPTIONS
• PAPULAR ERUPTIONS
• EXACERBATION OF
PSORIASIS
71. CONTI…
SIDE-EFFECTS DURING PREGNANCY AND LACTATION:
• TERATOGENIC POSSIBILITY
• INCREASED INCIDENCE OF EBSTEIN’S ANOMALY
(DISTORTION AND DOWNWARD DISOPLACEMENT OF
TRICUSPID VALVE IN RIIGHT VENTRICLE)
• SECRETED IN MILK AND CAN CAUSE TOXICITY IN
INFANT.
LITHIUM TOXICITY:
72. SIGNS AND SYMPTOMS OF LITHIUM TOXICITY
•Ataxia
•Coarse tremor
•Nausea and vomiting
•Impaired memory &
concentration
•Nephrotoxicity
•Muscle weakness
•Convulsions
•Muscle twitching
•Dysarthria
•Coma
•nystagmus
3/19/2020
72
73. MANAGEMENT OF LITHIUM TOXICITY
•Discontinue
•Gastric lavage
•Adsorption with activated charcoal
•Ingest fluids
•Maintain fluid and electrolyte balance
•Serious manifestation of lithium toxicity,
hemodialysis.
3/19/2020
73
75. THE PRE-LITHIUM WORK UP:
•A complete physical history, ECG, blood studies
(TC, DC, FBS, BUN, creatinine, electrolytes) urine
examination (routine and microscopic)
•Assess renal function as renal side effects are
common and the drug can be dangerous in an
individual with compromised kidney function.
•Thyroid functions should also be assessed, as the
drug is known to depress the thyroid gland.
76. To achieve therapeutic effect and prevent lithium
toxicity, the following precautions should be taken:
• Lithium must be taken on a regular basis, preferably at the same
time daily (for example, a client taking lithium on TID schedule,
who forgets a dose should wait until the next scheduled time to take
lithium and not take twice the amount at one time, because lithium
toxicity can occur).
• When lithium therapy is initiated, mild side effects such as fine
hand tremors, increased thirst and urination, nausea, anorexia etc
may develop. Most of them are transient and do not represent
lithium toxicity.
77. • Serious side-effects of lithium that necessitate its
discontinuance include vomiting, extreme hand tremors,
sedation, muscle weakness and vertigo.
The psychiatrist should be notified immediately if any of
these effects occur.
• Since polyuria can lead to dehydration with the risk of
lithium intoxication, patients should be advised to drink
enough water to compensate for the fluid loss.
78. • Various situations may require an adjustment in the amount of
lithium administered to a client, such as the addition of a new
medicine to the client's drug regimen, a new diet or an illness
with fever or excessive sweating.
• In this connection, people involved in heavy outdoor labor are
prone to excessive sodium loss through sweating. They must be
advised to consume large quantities of water with salt, o
prevent lithium toxicity due to decreased sodium levels.
• If severe vomiting or gastroenteritis develops, the patient
should be told to report immediately to the doctor.
These are the conditions that have a high potential for causing
lithium toxicity by lowering serum sodium levels..
79. •Frequent serum lithium level evaluation is important.
•Blood for determination of lithium levels should be drawn
in the morning approximately 12-14hours after the last
dose was taken.
• The patient should be told about the importance of
regular follow up.
In every six months, blood sample should be taken for
estimation of electrolytes, urea, creatinine, a full blood
count, and thyroid function test.
80. CARBAMAZEPINE
• It is available in the market
under different trade names
like
• Tegretol,
• Mazetol,
• Zeptol. And
• Zen retard.
84. MECHANISM OF ACTION
• Normally sodium moves into a
neuronal cell by passing through a
gated sodium channel in the cell
membrane.
• Carbamazepine may prevent or
halt seizures by closing or
blocking Sodium channels, thus
preventing sodium entering the
cell.
• Keeping sodium out of the cell
may slow nerve impulse
transmission, thus slowing rate at
which neurons fire.
87. ROLE OF THE NURSE
•Since the drug may cause dizziness and drowsiness advise
him to avoid driving and other activities requiring
alertness.
• Advise patient not to consume alcohol when he is on the
drug.
• Emphasize the importance of regular follow up visits and
periodic examination of blood count and monitoring of
cardiac, renal, hepatic and bone marrow functions
89. INDICATIONS
•Acute mania, prophylactic treatment of bipolar I
disorder, rapid cycling bipolar disorder
•Schizoaffective disorder
•Seizures
•Other disorders like bulimia nervosa, obsessive-
compulsive disorder, agitation and PTSD
90. MECHANISM OF ACTION
•The drug acts on Gamma-aminobutyric acid
(GABA) an inhibitory amino acid
neurotransmitter.
•Anticonvulsant effect- blockade of voltage-gated
sodium channels and increased GABA level.
•GABA receptor activation serves to reduce
neuronal excitability.
94. •Explain to the patient to take the drug immediately after food
to reduce GI irritation.
• Advise to come for regular follow-up and periodic
examination of blood count, hepatic function and thyroid
function.
Therapeutic serum level of valproic acid is 50-100
micrograms/ml.
100. BENZODIAZEPINE
LONG ACTING (EFFECTIVE HALF LIFE MORE
THAN 24 HOURS )
SHORT ACTING ( HALF LIFE 5-24 HRS)
VERY SHORT ACTING ( LESS THAN 5 HRS)
108. MECHANISM OF ACTION
•Benzodiazepines bind to specific sites on
the GABA receptors and increase GABA
level.
•Since GABA is an inhibitory
neurotransmitter, it has calming effect on
the central nervous system, thus reducing
anxiety.
109. SIDE EFFECTS
• Nausea
• Vomiting
• Weakness
• Vertigo
• Blurring of vision
• Body aches
• Epigastric pain
• Diarrhoea
• Impotence
• Sedation
• Increased reaction time
• Ataxia
• Dry mouth
• Retrograde amnesia
• Impairment of driving
skills
• Dependence
• Withdrawal symptoms
111. • Administer with food to minimize gastric irritation.
• Advise the patient to take medication exactly as directed. Abrupt
withdrawal may cause insomnia, irritability and sometimes even
seizures.
• Explain about adverse effects and advise him to avoid activities that
require alertness.
• Caution the patient to avoid alcohol or any other CNS depressants
along with benzodiazepines ; also instruct him not to take any over-the-
counter (OTC)medications.
• If IM administration is preferred give deep IM.
• For IV administration do not mix with any other drug. Give slow IV
as respiratory or cardiac arrest can occur;
monitor vital signs during IV administration. Prevent extravasations
since it can cause phlebitis and venous thrombosis.
115. MECHANISM OF ACTION
It crosses into the brain
through the "blood- brain
barrier." Once it crosses, it
is converted to dopamine.
The resulting increase in
brain dopamine
concentrations is believed
to improve nerve
conduction and assist the
movement disorders
in Parkinson disease
116. DOSE
1-2 mg per day
initially, maximum
dose up to 15
mg/day in divided
dose.
118. NURSING RESPONSIBILITY
•Assess parkinsonian and extrapyramidal symptoms.
Medication should be tapered gradually.
•Caution patient to make position changes slowly to
minimize orthostatic hypotension.
•Instruct the patient about frequent rinsing of
mouth and good oral hygiene.
•Caution patient that his medication decrease
perspiration and over-heating may occur during hot
weather.
119. 6. ANTABUSE DRUGS
There are three anti-alcohol drugs available:
Antabuse (disulfiram)
Campral (acamprosate)
Revia (naltrexone)
120. DISULFIRAM
•Disulfiram is used to ensure abstinenece in
the treatment of alcohol dependence.
•Its main effect is to produce a rapid and
violently unpleasant reaction in a person
who ingests even a small amount of alcohol
while taking disulfiram.
121. METABOLISM OF ALCOHOL
ALCOHOL
ACETALDEHYDE
ACETIC ACID
Alcohol
dehydrogenase
Acetaldehyde
dehydrogenase
Under normal metabolism,
alcohol is broken down in
the liver by
the enzyme alcohol
dehydrogenase to acetald
ehyde, which is then
converted by the
enzyme acetaldehyde
dehydrogenase to the
harmless acetic acid.
122. MECHANISM OF ACTION
ALCOHOL
ACETALDEHYDE
ACETIC ACID
Alcohol
dehydrogenase
Acetaldehyde
dehydrogenase
Disulfiram blocks this reaction
at the intermediate stage by
blocking acetaldehyde
dehydrogenase.
After alcohol intake under the
influence of disulfiram, the
concentration of acetaldehyde
in the blood may be 5 to 10
times higher than that found
during metabolism of the same
amount of alcohol alone.
123. PRODUCES A WIDE ARRAY OF UNPLEASANT
REACTIONS CALLED THE
DISULFIRAMETHANOL REACTION (DER)
Symptoms include
• flushing of the skin
• accelerated heart rate
•shortness of breath
•Nausea
• vomiting,
• throbbing headache
•visual disturbance
•mental confusion
•postural syncope, and
• circulatory collapse.
124. DOSAGE AND ADMINISTRATION
•500 mg every day (single dose) initially for 1
to 2 wk.
•Maintainance dose is 125 to 500 mg every
day (max, 500 mg/day).
•Disulfiram should never be administered until
the patient has abstained from alcohol for at
least 12 hours.
125. DURATION OF THERAPY
•The daily, uninterrupted administration of
disulfiram must be continued until the patient is
fully recovered socially and a basis for
permanent self-control is established.
•Depending on the individual patient, maintenance
therapy may be required for months or even
years.
127. CONTRAINDICATION
• Patients who are receiving or have recently received
metronidazole, paraldehyde, alcohol, or alcohol-
containing preparations, e.g., cough syrups, tonics etc.
• Disulfiram is contraindicated in the presence of
severe myocardial disease, psychosis, and
hypersensitivity to disulfiram.
• Children
• Pregnant women
128. THINGS TO BE AVOIDED DURING DISULFIRAM
Cough syrups
Vitamin tonics
Ayurvedic tonics
After shave lotion
Perfumes
Sprits
Food containing alcohol content
129. SIDE EFFECTS
An allergic reaction
(swelling of your lips,
tongue, or face; shortness
of breath; closing of your
throat; or hives)
Fatigue
Dermatitis
Impotence
Optic neuritis
Acute polyneuropathy
Hepatic damage
Seizures.
Respiratory depression
cardiovascular collapse
Myocardial infarction
death
130. NURSES ROLE
•Obtain informed consent for disulfiram therapy.
•Explain the ingestion of even small quantities of
alcohol may produce DER reaction
•Warn against consuming alcohol preparation like
cough syrups, tonics, and ayurvedic medicines.
•Collect the base line values of hemoglobin and
liver function test.
131. CONT…
•Warn patient that DER may occur even one
to two weeks after the last dose of
disulfiram.
•Monitor haemogram and liver function test
every 3 months.
•Look for signs of peripheral neuropathy.
132. 7. ANTI-CRAVING DRUGS
•Used to help prevent
relapse both during the
detox phase and in
early recovery phase.
• Medications used:
• Naltrexone
• Naloxene
• Subutex
• Topiramate
• Baclofen
• Acamprosate
• Methadone
• Neurontin
133. MECHANISM OF ACTION
Through detoxification process the withdrawal symptoms
of a particular type of drug or chemical are managed as
the toxins from the drug are removed from the body.
The removal of drug from the body is accompanied by
physical, psychological and emotional cravings.
A number of stimuli can put off a craving response within
the brain.
Anti-craving drugs seem to work by blocking the
receptors associated with cues that set off relapse.