PSYCHIATRY PATIENT PREREQUISITES

PSYCHOTHERAPIES
1. High motivation
2. Ability to form a relationship
DECEMBER 2020 3. Psychological mindedness and capacity for insight
4. Ego strength
PSYCHOANALYSIS GOALS
1. Gradual removal of amnesias rooted in early childhood
• Founded by Sigmund Freud 2. To achieve some measure of self-understanding or insight
• “classic” or “orthodox” psychoanalysis 3. Total personality change
• Based on theory of sexual repression; traces the unfulfilled 4. Greater ego strength
libidinal wishes in the individual’s unconscious memories 5. Resolution of the transference neurosis
• Discover the meaning and motivation of behavior, esp. the
unconscious elements that inform thoughts and feelings. STRUCTURE
• involves bringing to the surface repressed memories and
feelings by means of a scrupulous unraveling of hidden § DYADIC ARRANGEMENT: “individual”
o “neurosis is an intrapsychic phenomenon
meanings of verbalized material and of the unwitting ways in
which the patient wards off underlying conflicts through o Must be internally resolved
defensive forgetting and repetition of the past. o Memory and perception of repressed past are
pivotal
PROCESS: § FREQUENT
o 4 interval should be avoided
§ LONG TERM
RECOLLECTION REPETITION WORKING
o Changes occur slowly
THROUGH
• Early childhood • Emotional replay of • Affective and
SETTING
events former interactions cognitive
• Time when core of with significant integration
§ USE OF COUCH
neurosis was individuals • Patient is gradually
formed set free
ADVANTAGES DISADVANTAGES
§ Reclining position is relaxing § The reclining position with
because it is associated with analyst nearby can also
STAGES:
sleep and so eases the generate threat and
patient’s conscious control of discomfort as it recalls
STAGE 1 STAGE 2 STAGE 3
thoughts anxieties from the earlier
• Becomes familiar • Transference • Termination § Minimizes intrusive influence parent-child configuration
with methods, neurosis phase of the analyst, thus curbing that it physically resembles.
routines, and substitutes actual • Dissolution of unnecessary cues § Personal meanings:
requirements of neurosis (wish for analytical bond § Permits analyst to make § Portent of dangerous
analysis health vs emotional • Irrational observation of patient without impulses
• Realistic gratification from attachment interruption § Submission to authority
therapeutic analyst) subsided § Holds symbolic value for both figures
alliance formed • Gradual surfacing • Greater mastery party, a tangible reminder of § A relief from confrontation of
• Basic rules of unconscious and more the Freudian legacy that analyst
established conflicts mature gives credibility to the
• Patients • Increased irrational adaptation analyst’s professional
describes attachment to the • Has to continue identity, allegiance, and
problems analyst working through expertise.
• Initial relief and • Developmental outside the
sense of security return to earlier therapy without
§ FUNDAMENTAL RULE
through catharsis forms of relating the analyst
o free association
• Primarily • Repetition of • May need
o Requires patient to tell analyst everything that
motivated by wish childhood patterns intermittent
comes into their heads however disagreeable,
to get well • Recall of traumatic assistance after
unimportant or nonsensical
memories analysis
o The patient is asked to reveal those very thoughts
and events that are objectionable precisely
INDICATIONS/CONTRAINDICATIONS because of being averse to doing so
o Examine when flow of association is diminished or
INDICATIONS CONTRAINDICATIONS comes to a halt
§ Non-psychotic conditions § Absence of suffering o Elicits recall of deeply hidden early memories
§ Significant suffering § Poor impulse control o Reflects analytical priority placed on verbalization
§ Genuine wish to § Inability to tolerate o Prohibits action
understand self frustrations, anxiety and
§ Can withstand anxiety, other strong emotions § PRINCIPLE OF EVENLY SUSPENDED ATTENTION
frustrations and other § Low motivation to o requires analyst to suspend judgment and give
strong emotions understand impartial attention to every detail equally.
§ Reasonable, mature § ASPD (dishonesty) o Making no effort to concentrate on anything
superego § Concrete thinking (not specific, while maintaining a neutral, quiet
§ Average intelligence psychological minded) attentiveness to all that is said.
§ Abstract and symbolic § Midst of a major upheaval or
thinking life crisis
§ Serious physical illness
§ Low intelligence
§ Close relationship with
analyst

Page 1 of 7
 § ANALYST AS MIRROR STAGE 2 § ACTUAL
o Reflect only what is shown § ransference § As analysis proceeded, Ms. M became
o The analyst should be impenetrable to the patient neurosis quite focused on analyst: became curious
o Neutral blank screens substitutes actual of analyst’s life
o Not to bring their own personalities into the neurosis (wish for § Analyst’s appointment book “slotted in”;
treatment; not to bring own values or attitudes or to health vs “like an assembly line” = feeling slotted in
share personal reactions or mutual conflicts with emotional by parents as they ran from one activity to
patient gratification from another.
o Bringing in of reality and external influences can analyst) § Resistance : >1 min late in sessions she
interrupt or bias the patient’s unconscious § Gradual surfacing didn’t want analyst to think she was “too
projections of unconscious eager”
o Neutrality allows analyst to accept without censure conflicts § She needed to devalue her analyst as a
all forbidden or objectionable responses. § Increased defense against overwhelming positive
irrational and even erotic transference
§ RULE OF ABSTINENCE attachment to the § Conflicts with sexual orientation : central
o Does not mean corporal or sexual abstinence analyst preoccupation bec father was
o Frustration of emotional needs and wishes that the § Developmental homophobic
patient may have toward the analyst or part of the return to earlier § Began to date men, inc a male
transference. forms of relating psychologist
o Allows the patient’s longings to persist and serve as § Repetition of § Transference interpretation: a date with
driving forces for analytical work and motivation for childhood patterns the male psychologist seemed as if it were
change § Recall of traumatic a date with analyst and sleeping with him
o Analyst is in state of renunciation memories would be equivalent to sleeping with the
analyst
DREAM INTERPRETATION § Ms. M was able to see that her transient
§ Dream choice of dating a male psychologist was
o royal road to the consciousness a defensive compromise
o manifest content – what a dreamer reports § Part of her conflict about homosexuality
o latent content – unconscious meaning after the stemmed from her relationship toward her
condensations, substitutions and symbols are father. It was a means of securing his
analyzed attention as well as infuriating him
§ According to Freud
o dreams arise from day residue (events preceding STAGE 3 ACTUAL
the day which stimulated the patient’s unconscious § Termination phase § Over the course of 4 years, began to do
mind) § Dissolution of well at work and was promoted
§ Analysts use patient’s association to find clue to the meanings analytical bond § Able to deal better with parents,
of the dreams – the workings of the unconscious mind. § Irrational particularly father about her sexual
attachment orientation
LIMITATIONS subsided § Has a relationship with a female
§ ECONOMIC : time and money § Greater mastery professional
§ Restricted and more mature § Considering adoption
§ Use and misuse of stringent rules adaptation
§ Long term risk of interminability § Has to continue
§ May interfere with a more open and flexible application of its working through
tenets to meet changing needs outside the
§ May obstruct comprehensive view of patient care that therapy without
includes a greater appreciation of other treatment modalities the analyst
in conjunction with, or as an alternative to, psychoanalysis § May need
intermittent
CASE STUDY assistance after
§ Ms. M, 29 y/o, single, clerk at a magazine analysis
§ considerable sadness and distress; working far below her
potential
§ parents’ negative reaction when they found that she had a
homosexual relationship
§ Clearly intelligent, sensitive, self-reflective, and insightful
§ 4 days/week’ 40min session

STAGE 1 ACTUAL
§ Becomes familiar § oldest of 3 children; only girl
with methods, § father a successful professional, very
routines, and demanding and intrusive ; never thought
requirements of “anything was good enough”
analysis § Ms. M was however proud of her father’s
§ Realistic accomplishment
therapeutic § Mother was homemaker, weak,
alliance formed acquiescent to the powerful father;
§ Basic rules woman in her own right: community
established volunteer work and powerful public
§ Patients describes speaker
problems § prior to first session, Ms. M’s wallet was
§ Initial relief and stolen
sense of security § “completely new identity”
through catharsis § dream analysis and association
§ Primarily § initially hesitant to use couch bec she
motivated by wish wanted to see analyst’s reaction
to get well

Page 2 of 7
 PSYCHOANALYTIC PSYCHOTHERAPHY § Warm, friendly, strong
leadership
§ Partial gratification of
§ derived from classic psychoanalysis dependency needs
§ use of insight-oriented method § Establishment of § Support in the ultimate
§ duration shorter and more variable than psychoanalysis therapeutic alliance development of
§ BRIEF TREATMENT: for selected problems or highly focused § Early recognition and legitimate
conflicts interpretation of independence
§ LONGER TREATMENT: more chronic conditions or negative transference § Help in
intermittent episodes that require ongoing attention to deal Major
§ Only limited or developingpleasurable
with pervasive conflict or recurrent decompensation Approach
controlled regression activities
§ rarely uses couch; and
is encouraged § Adequate rest and
§ face to face to help prevent regression because it encourages Techniques
§ Positive transference diversion
the patient to look on the therapist as a real person from whom left unexplored unless § Removal of excessive
to receive direct cues, even though transference and fantasy they are impending strain
will continue. therapeutic progress § Hospitalization when
§ free association method rarely used except when the therapist indicated
wishes to gain access to fantasy material or dreams to § Medications to
enlighten a particular issue. alleviate symptoms
§ 2 techniques: EXPRESSIVE AND SUPPORTIVE § Guidance and advice

INDICATIONS § Problem of emotional § Viewed as superficial

integration of § Less interpersonal
EXPRESSIVE SUPPORTIVE Limitations cognitive awareness commitment
Mild to moderate ego § Overintellectualization § more demanding,
weakening; neurotic § Acting out erratic and frustrating
Poor ego strength;
conflicts, symptom
decompensation high
complexes, reactive SPECIFIC TECHNIQUES FOR SUPPORTIVE PSYCHOTHERAPY
§ In acute crisis or
conditions, nonpsychotic
temporary state of
character disorders TECHNIQUE DESCRIPTION EXAMPLE
disorganization and
(narcissistic and PX: I took my insulin
inability to cope (grief § may reinforce
borderline) every day last week.
reactions, illness, accomplishments
§ Fairly well integrated MD: Good. You said you
divorce, job loss or PRAISE or positive were going to do this – not
egos
who were victims of changes in skip a single dose – and
§ Capacity to both
crimes, abuse, natural behavior. you did it. What do you
sustain and detach
disasters or think?
from a bond of
accidents) PX: Whenever I go
dependency and trust anywhere, I have this fear
§ With chronic severe
Indications § Psychologically of losing control.
pathology with fragile
minded § based on MD: I don’t think you will
or deficient ego
§ Self-motivated understanding of lose control. You have
functioning had this fear for a long
§ Ability to manage unique situation
(psychosis, impulse REASSURANCE time and you have always
rearousal of painful of patient;
disorder or severe been able to maintain
feelings outside unconditional
character good self-control.
therapy hour w/o concern (Reassurance based on
disturbance)
additional contact the PX’s history and
§ With cognitive deficits
§ Capacity for reinforcement of adaptive
and physical behavior).
introspection
symptoms PX: Maybe its all in my
§ Impulse control
§ Psychologically head.
§ Cognitive distinction
unmotivated MD: Everyone from time
b/w fantasy and
to time wonders that. Its
reality what we do when we don’t
have the answers about
§ a form of
General aim is the NORMALIZING these kinds of symptoms.
reassurance.
amelioration or relief of MD: It might be interesting
symptoms through for you to know that
§ Overall goal is to 40%of college students
behavioral or
increase the patient’s experience a classic
environmental
self-awareness and to panic attack during the
restructuring within the four years of college.
improve object
existing psychic § can be powerful
relations through
framework bec. people want MD : I think its great that
exploration of current
§ Helping patient adapt to believe that you want to apply for
interpersonal events ENCOURAGEMENT courses at the community
better to problems their small efforts
and perceptions. college. I think you should
and live more will lead to
§ Major thrust is to deal do it.
comfortably with his something
Goals with preconscious or
psychopathology bigger.
conscious derivatives
§ To suppress or MD: I can see how you
of conflict as they
control § looking at are disappointed. You
become manifest in
symptomatology something in didn’t get to try out for the
present interactions. team with that sprain. I
§ To stabilize patient in different light or
§ Greater emphasis is can also see how you
a protective and different angle.
on clarifying recent might use this semester to
reassuring benign § Positive
dynamic patterns and REFRAMING focus on your academics
atmosphere connotation instead of sports and get
malda
§ Relabelling of all ahead there.
negatively MD: Yes your son’s
expressed behavior is challenging.
feelings or He seems to be testing
every limit in the book. At
Page 3 of 7
 behavior as the same time it shows
GROUP PSYCHOTHERAPY
positive that he is a really secure
kid and is right on track § uses therapeutic forces within the group, constructive
developmentally. interactions between members, and interventions of a trained
MD: You do seem to be leader to change the maladaptive behavior, thoughts, and
experiencing more
anxiety. It looks like that is feelings of emotionally distressed individuals.
a result of trying new § Support group, skills training group, psycho-education group
things.
MD: This is the third time THERAPEUTIC FACTORS
Ive seen you for bronchitis
in two months. Im worried FACTORS DEFINITION
ADVICE AND § based on about the effect that
Process by which repressed materials,
cigarettes is having on
TEACHING professional your lungs and how well particularly a painful experience or conflict, is
expertise Abreaction
they can fight off lung brought back to consciousness. Not only recalls,
infection. I think its time to but relives the experience
enroll in a smoking Feeling of being accepted by other members of
cessation program. Acceptance
the group
CAREFUL USE OF “why…” “why didn’t Altruism Act of one member helping another
§ Expression of ideas, thoughts and suppressed
LANGUAGE you….”
Catharsis materials acco.by emotional response that
produces a state of relief.
CORRECTIVE EMOTIONAL EXPERIENCE Sense that group is working together toward a
Cohesion
common goal
§ The relationship between therapist and patient gives Universalization Awareness not person is not alone
therapist an opportunity to display behavior different Expression of suppressed feelings, ideas or
from the destructive or unproductive behavior of a Ventilation events toother group member; sharing; self-
patient’s parent.
disclosure
§ Neutralizes or reverses parent’s mistake
Confirmation of reality by comparing one’s own
§ Gives patient an opportunity to adjust, be led by, and Consensual conceptualization with those of other group
identify with a new parent figure. validation members
Expression of emotion by one member stimulates
BRIEF PSYCHODYNAMIC PSYCHOTHERAPY Contagion
awareness of similar emotion in another member.
Corrective Re-creation of the family of origin for some
§ time-limited; based on psychoanalysis and psychodynamic familial members who can work through original conflicts
theory experience psychologically through group interaction
§ depression, anxiety and PTSD Capacity of a group member to put self into the
§ BASIC CHARACTERISTICS: Empathy psychological frame of reference of another
o designed to put patient at ease, to manipulate the member
transference and to use trial interpretations flexibly; Incorporation of qualities of another person into
o corrective emotional experience Identification
own ego system
BRIEF FOCAL TIME-LIMITED SHORT- SHORT-TERM
Imitation Conscious emulation or modeling
PSYCHOTHERAPY PSYCHOTHERAPY TERM ANXIETY- Conscious awareness and understanding of
DYNAMIC PROVOKING
McGill
Insight one’s own psychodynamics and symptoms of
Boston University,
University in maladaptive behavior
early 1970’s; James
Balint team at Canada; Massachusetts
Mann Imparting sense of optimism to group members;
ORIGIN
Tavistock Clinic in
12 interviews
Habib Gen. Hosp in Inspiration
London, 1950’s;
focusing on
Davanloo Boston; instillation of hope
David Malan Predominant Sifneos 1950’s
specified central
oedipal Interaction Free and open exchange ofideas and feelings;
issue
conflicts Group leader formulates meaning and
Circumscribed
Ability to chief complaint Interpretation significance of one’s resistance, defenses and
interact Meaningful or symbols;
emotionally give-take rel
with evaluator during Acquire knowledge about new areas; advice and
Determine patient’s Learning
central conflict
Hx of give- childhood guidance
take rel. Ability to
Same as in Explore a young
Ability to interact flexibly Consensual validation; ability to evaluate
SELECTION psychoanalysis person’s Reality testing
CRITERIA *response to maturational crises
experience w/evaluator objectively
and tolerate Ability to
interpretation with many
anxiety express Projection of feelings thoughts and wishes into
psychological and Transference
somatic complaints
Psychological feelings therapist
minded appropriately
*Ability to Above average
respond to psychological PSYCHODRAMA
interpretation sophistication
Contract § Originated by Jacob Moreno
Serious suicide § personality make up, IPR, conflicts and emotional problems
attempts;
Substance
are explored by means of special dramatic methods;
dependence; MDD; acute § Roles:
Chronic alcohol psychotic states; o DIRECTOR – therapist
CONTRA abuse; desperate patients
INDICATIONS Incapacitating chronic who need, but o PROTAGONIST- patient in conflict
phobic cannot tolerate, o AUXILIARY EGO – another group member
symptoms;(Davanloo) object relations.
Gross destructive or o GROUP – audience
self-destructive acting
out
ETHICAL AND LEGAL ISSUES
ISSUES
Confidentiality Group members are not legally bound
May occur within or outside the group
Violence and Patients with history of assaultive behavior and
aggression psychotic patients who pose potential for
violence should not be placed in a group
Sexual behavior Issues of pregnancy, rape and HIV
Page 4 of 7
 FAMILY THERAPY STRUCTURAL MODEL
§ Families are viewed as single, interrelated systems assessed
§ any psychotherapeutic endeavor that explicitly focuses on in terms of significant alliances and splits among family
altering the interactions between or among family members members, hierarchy of power, clarity and firmness of
and seeks to improve the functioning of the family as a unit, boundaries between the generations, and family tolerance for
or its subsystems, and the functioning of individual members one another
of the family § Use concurrent individual and family therapy
§ Presence of relational difficulty
§ Once a week; at most 2 hours GENERAL SYSTEMS MODEL
§ Families are systems and that every action in a family
TECHNIQUES produces a reaction in one or more of its members.
§ Every member play a role(spokesperson, persecutor, victim,
INITIAL INTERVIEW FREQ AND TERMINATION rescuer, symptom bearer, nurturer) which is relatively stable,
CONSULTATION TECNIQUE LENGTH which member fill each role may change
§ Specific § “Whatever § No more § Can § Scapegoat : identified patient
request by transpire in than once complete
families with therapy a week transactions
COUPLES/ MARITAL THERAPY
high levels of session is § At most 2 § Can interpret
conflict; known to all.” hours hostility
§ Pretreatment § Therapist § Flexible § Can see how § designed to psychologically modify the interaction of two
work when must schedule others see persons who are in conflict with each other over one
initial complaint carefully § Length of them parameter or a variety of parameters-social, emotional,
is about an channel treatment § Can see how sexual, or economic.
individual family catharsis of variable they see § a trained person establishes a therapeutic contract with a
member anger by one depending themselves patient-couple and, through definite types of communication,
§ Underlying member twd on model § One member attempts to alleviate the disturbance, to reverse or change
resistance: another; use can tell maladaptive patterns of behavior, and to encourage
§ Fears by § Free others how personality growth and development.
parents that association they manifest
they may be is themselves § INDICATIONS:
blamed inappropriate § One member o when individual therapy has failed to resolve
§ Entire family be bec it can tell relationship difficulties
pronounced encourages others what o when onset of distress in one or both partners is
sick one person is hoped, clearly a relational problem
§ A spouse will to dominate feared, and o When couple’s therapy is requested by a couple in
object expected of conflict
§ Negative them o problems in communication in couple are prime
influence on § Can disagree indications
other siblings § Make o conflict in one or several areas , such as sexual life
choices
§ Learn § CONTRAINDICATIONS:
through o severe forms of psychosis
practice o when one or both partners really want a divorce
§ Can free o One spouse refuses to participate because of
themselves anxiety or fear
of harmful
effects of TYPES
past models
§ Can give TYPES DESCRIPTION
clear INDIVIDUAL Partners consult different therapists; Goal is to
messages THERAPY strengthen each partner’s adaptive capacities

INDIVIDUAL Each partner in therapy; concurrent, same

MODELS COUPLES therapist, or collaborative with different
therapists
PSYCHODYNAMIC-EXPERIENTIAL MODELS CONJOINT Joint sessions
§ Emphasize individual maturation in the context of the family THERAPY
system and are free from unconscious patterns of anxiety and
FOUR-WAY Each partner seen by different therapist, with
projection rooted in the past
SESSION regular joint sessions in which all four persons
§ Clarity of communication and honestly admitted feelings given
participate; used for sexual dysfunction
high priority
§ Family sculpting GROUP Three to four couples
§ Feedback loop of self-observation and change PSYCHOTHERAPY
COMBINATION

BOWEN MODEL
§ Murray Bowen
§ “family systems”
§ HALLMARK: persons’ differentiation from family of origin;
ability to be their true selves
§ Emotional triangle: role of therapist is to stabilize or “shift” the
hot triangle
§ Genogram

Page 5 of 7
 DIALECTICAL BEHAVIORAL THERAPY

§ DBT; to help create a life worth living for patients who often
suffer tremendously from chronic and pervasive problems
across many areas of their lives
§ Originally developed for chronically self-injurious patients with
borderline PD and parasuicidal behavior.
§ Patients are seen weekly
§ Techniques: advise, metaphor, storytelling, and confrontation
§ Developed by Marsha Linehan

§ FUNCTIONS OF DBT:
o to enhance and expand the patient’s repertoire of
skillful behavioral patterns
o To improve patient motivation to change by PROCESS
reducing reinforcement of maladaptive behavior,
inc dysfunctional cognition and emotion PROCESS EXAMPLE
o to ensure that new behavioral patterns generalize Eliciting automatic thoughts PATIENT: “I won’t get a job. No one
from the therapeutic to the natural environment (cognitive distortions) will hire me.”
o to structure the environment so that effective Testing automatic thoughts THERAPIST: “Have you tried to apply
behaviors are reinforced for a job?”; “Have you prepared a
o to enhance motivation and capabilities of the resume?” “When you were not hired
therapist so that effective treatment is rendered before, is it because they don’t like
you or there was no more vacancy?”
§ GROUP SKILLS TRAINING Identifying Maladaptive PATIENT: “If I don’t get hired, they
o Observations about others in the group are Assumptions: patterns, rules don’t like me, Im not competent.”
discouraged
o Specific exercises from a skills training manual
Testing the Validity of The therapist reviews the entire
§ INDIVIDUAL THERAPY Maladaptive assumptions situation with the patient and helps
o Weekly; skills learned in group training are reassign the blame or cause of the
reviewed and life events from previous week unpleasant events
examined
o Record thoughts, feeling and behaviors on diary BIOFEEDBACK
cards
• Involves the recording and display of small changes in the
physiological levels of the feedback parameter
§ TELEPHONE CONSULTATION
• Patients are instructed to change the levels of the parameter,
o Available 24 hours
using the feedback from the display as a guide
o CONSULTATION TEAM
• Based on the idea that the ANS can come under voluntary
o Weekly meetings; review and provided support
control through operant conditioning (Neal Miller)
• For example, a patient can learn to raise the
COGNITIVE BEHAVIORAL THERAPY temperature of his or her hands to reduce the
§ Altering cognitive process frequency of migraines, palpitations or angina
§ Active, directive, time-limited pectoris.
§ Structured
METHODS
§ A central feature of the cognitive theory of emotional disorders I. INSTRUMENTATION
is its emphasis on the psychological significance of people's • Most effective instruments are : EMG, EEG,
beliefs about themselves, their personal world (including the galvanic skin response gauge, and thermistor.
people in their lives), and their future the "COGNITIVE TRIAD’ • EXAMPLE: treatment of bruxism: an EMG is
attached to masseter muscle. High tone if muscle is
COGNITIVE DISTORTIONS: contracted; low tone if at rest
§ Overgeneralizing - “if its true in one case, it applies to ay I. The patient can learn to alter the tone to
case that is even slightly similar” indicate relaxation.
§ Selective abstraction – discounting the positives II. Patients receive feedback about the
§ Excessive responsibility – masseter muscle, the tone reinforces
§ Jumping to conclusions the learning, and the condition
§ Catastrophizing – always think of the worst “what if….” ameliorates.
§ Personalization
§ Dichotomous thinking – all or none II. RELAXATION THERAPY
• Characterized by:
I. 1) immobility of the body;
II. 2) control over the focus of attention;
III. 3) low muscle tone;
IV. 4) cultivation of specific frame of mind
(contemplative, nonjudmental, detached
or mindful)
• PROGRESSIVE RELAXATION: developed by
Edmund Jacobson in 1929
I. isolate and contract specific muscles or
muscle group at a time

Page 6 of 7
III. AUTOGENIC TRAINING
• A method of self-suggestion that originated in
Germany.
• Patient directs attention to specific bodily areas and
hear themselves think certain phrases reflecting a
relaxed state

THEME EXAMPLES OF SELF STATEMENT

Heaviness “My left arm is heavy”
Warmth “My left arm is warm”
Cardiac regulation “My heartbeat is calm and regular”
Breathing adjustment “It breathes me”
Solar plexus “My solar plexus is warm”
Forehead “My forehead is cool”

IV. APPLIED TENSION

• Can be used to counteract the fainting response;
opposite of relaxation
• FIRST PHASE:
I. Patient learns to tense the muscles of the
arms, legs, and torso for 10 to 15 sec.
The tension is maintained long enough
for a sensation of warmth to develop in
the face. The patient then releases the
tension, but do not progress to a state of
relaxation. This is repeated five times at
half-minute intervals
• SECOND PHASE:
I. The patient is shown a series of slides
that are provocative (mutilated
bodies).They are coached in identifying
early warning signs of fainting, such as
queasiness, cold sweats, dizziness, And
in applying the learned muscle tension
response quickly.

V. APPLIED RELAXATION

TECNIQUE INSTRUCTIONS
Session 1: hands, arms, face, neck, and
PROGRESSIVE shoulders
RELAXATION Session 2: back, chest, stomach, breathing,
hips, legs and feet
RELEASE-ONLY as with progressive relaxation, except that
RELAXATION the tension phase is omitted
CUE-CONTROLLED A stimulus (the word ”relax”) is presented
RELAXATION just before exhalation
Can remain relaxed and move at the same
DIFFERENTIAL time by differentially keeping muscles
RELAXATION unrelated to the movement in a relaxed
state
Patient relax by taking 1-3 breathes with
RAPID RELAXATION slow exhalations, thinking the work “relax”
before each exhalation
Patient relax before entering the target
APPLICATION situation; stay in the situation for 10 to 15
TRAINING min

Page 7 of 7
 PSYCHIATRY § Synergistic with lithium or
ANXIETY & carbamazepine to treat mania
§ Schizophrenia and tardive dyskinesia
ADVERSE EFFECTS § Clonidine patch for hypersalivation and
dysphagia caused by Clozapine
OF PSYCHOTROPICS § Hallucinogen-persisting perceptive
HYACINTH MANOOD, MD disorders
JANUARY. 9, 2021
PRECAUTIONS AND ADVERSE REACTIONS:
SCOPE OF THE LECTURE:
§ Most common: dry mouth and eyes, fatigue,
i. α2- adrenergic Receptor Agonists (Clonidine and sedation, dizziness, nausea, hypotension and
Guanfacine) constipation.; 10% discontinuation of therapy;
ii. Benzodiazepines tolerance develop except for sedation.
iii. Buspirone § Uncommon CNS A/E: insomnia, anxiety,
iv. Β-adrenergic Receptor Antagonists ADVERSE
depression
v. Medications used in treatment for Adverse Effects of EFFECTS:
§ Rare CNS a/E: vivid dreams, nightmares,
Psychotropics hallucinations
o Dantrolene § Local skin irritation –transdermal patch
o Dopamine receptor agonists § Fluid retention – treat with diuretics
o Anticholinergics § Guanfacine with milder adverse effect profile
o antihistamines § Shld not be taken with BP <90/60 or with
o α- adrenergic Receptor Antagonists - cardiac arrythmias, esp. bradycardia.
o Sildenafil § If with bradycardia, tapered discontinuation
PRECAUTIONS
§ Should be avoided in pregnancy and lactation;
I. α2- ADRENERGIC RECEPTOR AGONISTS Elderly more sensitive; children more
susceptible to A/E
(Clonidine and Guanfacine) § Coma and constricted pupil (similar to opioid
overdose)
OVERDOSE
GUANFACINE CLONIDINE § Dec. BP, PR and RR; Guanfacine overdose
milder
Mode of action Agonist on presynaptic α2- adrenergic
receptors in the sympathetic nuclei of the brain
WITHDRAWAL, DRUG INTERACTION, LABORATORY
Effects Reduces plasma NE; inhibits sympathetic
INTERFERENCE
outflow; vasodilation of BV: antihypertensive
Reset body sympathetic tone at lower level
and decrease arousal. § Anxiety, restlessness, perspiration,
tremor, abdominal pain, palpitations,
Potency Less potent; more
headache, dramatic increase in BP
selective
§ -appear 20 hours after last dose of
Absorption;peak Well absorbed fm GIT; peak plasma level:1-3
Clonidine; also seen if 1 or 2 doses are
plasma level hours WITHDRAWAL
skipped
Half-life 10 to 30 hours 6 to 20 hours § -2 to 4 days after discontinuation of
Sedation + +++ Guanfacine,
hypotension + +++ § -usual course is gradual return to baseline
BP over 2 to 4 days
THERAPEUTIC INDICATIONS § Potential additive sedative effects when
combined with other centrally active
§ effective in reducing autonomic depressants
symptoms of rapid opioid withdrawal; § Dose reduction when combined with B
DRUG
WITHDRAWAL Clonidine 0.1-0.2 mg bid –qid before blockers Ca channel blockers and digitalis
INTERACTIONS
FROM OPIODS, detoxification, tapered off 1-2 weeks ; the combination increases the risk of AV
ALCOHOL, BDZ, OR § reduce craving, anxiety and irritability of block and bradycardia
NICOTINE nicotine w/drawal § TCAC’s -inhibit hypotensive effects of
§ transdermal patch with better long-term Clonidine
compliance LABORATORY § NO known laboratory interference
§ For children, starting dose Clonidine INTERFERENCE
.05mg/day, increase to .3 mg/day in
TOURETTE’S
divided doses CLINICAL GUIDELINES
DISORDER
§ 3 mos. To see beneficial effects;
response rate 70% 1. Begin at a dose of 1mg/day, and adjust in increments of no
OTHER TIC more than 1mg/week, for both monotherapy and adjunctive
§ Reduce frequency and severity
DISORDERS therapy to a psychostimulant.
§ Clonidine .05mg/day, increase to .3 2. Maintain dose w/in the range of 1-4 mg once daily, depending
mg/day in divided doses on the clinical response and tolerability, for both monotherapy
HYPERACTIVITY
§ efficacy diminishes over several months and adjunctive therapy
AND AGGRESSION
of use 3. In monotherapy trials, clinically relevant improvements were
IN CHILDREN
§ combined with Methylphenidate or observed beginning at doses in the range of 0.05- 0.08 mg/kg
Dextroamphetamine OD. If well tolerated, doses up to 0.12 mg/kg/day may provide
POSTTRAUMATIC additional benefits. Doses above 4 mg/day have notbeen
§ Hyperadrenergic symptoms of PTSD
STRESS DISORDER systematically studied in controlled clinical trials.
§ Panic disorders, phobias, OCD, 4. In the adjunctive trial, the majority of subjects reached optimal
OTHER DISORDERS generalized anxiety d/o doses in the 0.05- 0.12 mg/kg/day range.

Page 1 of 7
 DRUG PREP
CHILD
Starting Dose
ADULT
Starting Dose
ZOLPIDEM and ZALEPLON and ESZOPICLONE
dose range dose range § Benzodiazepine agonists at BZ2 site; Selective on subunits
Clonidine 0.1, Up to 0.3
0.3-1.2
of GABA receptor
mg/day in 0.1 -0.2 § Rapidly and well-absorbed, although can be delayed for as
tabs 0.2, 0.05mg/day
divided mg bid-qid
mg/day,
(Catapres) 0.3 mg doses
bid-tid much as 1 hour if taken with food;
Up to 0.3 § Zolpidem t1/2= 2.6 hrs; Zaleplon t1/2= 1 hour
Clonidine 0.1,
mg/day 0.1 mg/day § No active metabolites; selective sedative effects; no muscle
patch patch per
transdermal 0.2, every 5
0.1 mg/day
week
relaxant and anticonvulsive effects like BZD
0.05mg/day every 7 § solely indicated for insomnia.
(Catapres- 0.3 days (max
days
0.6mg/day
0.5mg/day every 7
TTS mg/day every 5 days
days
THERAPEUTIC USES
1, 2 1-2 mg 1-2 mg
Guanfacine 1 mg/day 1 § LORAZEPAM and DIAZEPAM are the
mg HS
HS(3mg
mg/dayHS
HS(3mg
(Tenex) max) max) most commonly used BZD for seizure
tabs
disorder.
§ Diazepam is longer-acting than Lorazepam
II. BENZODIAZEPINES STATUS however very lipid-soluble and highly-
EPILEPTICUS protein bound and very large distribution of
unbound drug hence shorter duration of
PHARMACOLOGIC ACTIONS: action.
§ Acts by binding to GABA A receptors which opens chloride § Lorazepam has a more prolonged duration
channels and reduces the rate of neuronal and muscle firing. of action
§ Act as hypnotics in high doses and as sedative in low doses
§ Drug of choice for management of acute anxiety and agitation. ANXIETY
§ Risk for psychological dependence DISORDERS
§ CNS effects on anxiety and sleep
§ Inhibit spinal polysynaptic afferent pathways making them § Highly effective; should be treated for a
Generalized
effective muscle relaxants. predetermined, specific and relatively brief
Anxiety D/O
§ Anticonvulsants period.
§ All BZD are completely absorbed unchanged from the GIT § Alprazolam and Clonazepam (high
except for CLORAZEPATE. potency); have advantage of working
§ Absorption, peak concentrations and onset of action are quickly and no significant sexual
Panic Disorder
quickest with the following: dysfunction and weight gain.; for acute
o Diazepam (Valium) panic symptoms; Shld be tapered after 3-4
o Triazolam (Halcion) wks
o Lorazepam (Ativan) Social Phobia § Clonazepam effective
o Estazolam(Esilgan) Other Anxiety § Adjunct for adjustment d/o w/ anxiety,
o Alprazolam (Xanor) disorders anxiety asso with life events
§ Rapid onset of action important for single dose to calm an
Anxiety asso. W/
episodic outburst or to fall asleep rapidly.
depression
§ Only LORAZEPAM and MIDAZOLAM have rapid and reliable
absorption following IM administration. § Clonazepam, lorazepam and alprazolam
§ Longest-acting BZD: Bipolar 1& 2
for acute manic episodes; adjuvant to
o Diazepam Chlordiazepoxide disorders
maintenance therapy
o Clonazepam Clorazepate § Lorazepam; definitive treatment for
o Flurazepam Prazepam Catatonia
catatonia is ECT.
o Quazepam Halazepam Akathisia § First line is betablocker
§ with plasma half-lives of 30 to >100 hours
§ Long term use of Zolpidem with reduced
§ Half-life of between 8 – 30 hours = LORAZEPAM, Parkinson’s dse
bradykinesia and rigidity
OXAZEPAM, TEMAZEPAM and ESTAZOLAM
Alcohol § Chlordiazepoxide(Librium) and
§ ALPRAZOLAM has half-life of 10 – 15 hours
withdrawal Clorazepate (Tranxene)
§ TRIAZOLAM has shortest half-life = 2 – 3 hours
§ QUAZEPAM shares final metabolite with Flurazepam – Substance induce
o DESALKYLFLURAZEPAM- T1/2 100 HOURS. psychosis and § IM Lorazepam
Quazepam is associated with daytime impairment agitation
when used for a long time. Drug assisted
§
interviewing
LONG HALF-LIFE BENZODIAZEPINES: § Clonazepam has serotonergic effects and
ADVANTAGES DISADVANTAGES OCD and PTSD is effective in treating the anxiety
§ LESS FREQUENT DOSING § DRUG ACCUMULATION component of OCD.
§ LESS VARIATION IN PLASMA § INCREASED RISK OF DAYTIME § mild – Flurazepam. Quazepam, Estazolam;
PSYCHOMOTOR IMPAIRMENT mod– Midazolam; severe- Triazolam,
§ LESS SEVERE WITHDRAWAL § INCREASED DAYTIME Temazepam
PHENOMENA SEDATION Insomnia § Flurazepam – longest half-life; minor
cognitive impairment
SHORT HALF-LIFE BENZODIAZEPINES: § Triazolam – shortest half-life; mild rebound
ADVANTAGES DISADVANTAGES anxiety
§ NO DRUG ACCUMULATION § MORE FREQUENT DOSING
§ Clonazepam augmentation may accelerate the
§ LESS DAYTIME SEDATION § EARLIER AND MORE SEVERE antidepressant effects of Fluoxetine.
WITHDRAWAL SYNDROMES
§ IM Lorazepam used to manage substance-induced (except
§ REBOUND INSOMNIA AND methamphetamine) and psychotic agitation in ER.
ANTEROGRADE AMNESIA § Flumazenil is used to reverse BZD Overdose
MORE COMMON

Page 2 of 7
 o Flumazenil 0.2mg (2 ml) IV over 30 seconds; after
30 seconds, 0.3mg IV over 30 seconds; 0.5mg at 1
minute interval up to cumulative dose of 3 mg.
ADVERSE EFFECTS
§ Drowsiness – most common; residual daytime sedation
§ Dizziness and ataxia
§ Most serious is when taken with another CNS depressant
such as alcohol – marked drowsiness, disinhibition,
respiratory depression.
§ Anterograde amnesia – high-potency BZD
§ Triazolam – associated serious aggressive behavior with
doses greater than 1 mg.
PRECAUTIONS
§ Hepatic disease
§ Elderly patients
§ COPD and Sleep Apnea
§ History of Substance Abuse
§ Renal disease
§ Cognitive disorders
§ Porphyria
§ Myasthenia Gravis
§ Breastfeeding
§ Pregnancy
DRUG INTERACTIONS
§ Alcohol and other CNS depressants – cause synergistic
adverse effects with possible increase in depression and
suicide
§ Antacids and anticholinergics –may slow down absorption of
BZD
§ Clonazepam + Lithium + antipsychotics – ataxia and
dysarthria
§ BZD + Clozapine = delirium
§ Oral contraceptives and INH – increase plasma conc.
§ Nefazodone and Fluvoxamine – inc. plasma conc. of
Triazolam and Alprazolam to potentially toxic levels.
§ Smoking – increase metabolism of BZD
§ Rifampicin, Phenytoin, Carbamazepine and Phenobarbital –
increase metabolism of Zaleplon
§ BZD increase plasma conc. Of phenytoin and digoxin.
§ SSRI’s may prolong and exacerbate the severity of Zolpidem-
induced hallucinations.
III. BUSPIRONE
§ Azapirone
§ High affinity for 5-HT1A (agonist or partial agonist)
§ Moderate affinity for the D2 receptor (both agonist and
antagonist)
§ Better alternative to benzodiazepines
§ No anticonvulsant and muscle relaxant effect
§ Low potential for abuse; lacks euphoric effect
§ Not associated with withdrawal phenomena or cognitive
impairment
§ No significant effects on the respiratory, cardiovascular,
Muscular and auntonomic nervous systems.
PHARMACOLOGICAL ACTIONS
§ Well absorbed from GIT; delayed by food ingestion
§ Peak plasma level 40-90 min after oral ingestion
§ 10-40 mg = linear pharmacokinetics are observed
§ After multiple doses= non linear pharmacokinetics
§ Half life: 2-11 hours
§ 1-pyrimidinylpiperazine(1-PP) –active metabolite; 20%less
potent but 30% more concentrated in the brain; half life is
6hours.
THERAPEUTIC INDICATIONS
Narrow spectrum anxiolytic for GAD only; not
effective for panic disorder, OCD, or social phobia;
Generalized
less effective for somatic symptoms of anxiety,
Anxiety
equally effective for psychic symptoms
Disorder
>30 mg/day = full benefit 2-4 weeks for full clinical
response
Anger and
hostility
If serotonin is very low or depleted from
Augmenting
serotonergic neurons in depression, there would
agent for
not be much of it released for an SSRI to block its
SSRI for
reuptake . Thus, buspirone may be able to "kick
treatment
start" the desensitization process directly. Initially,
resistant
buspirone also slows neuronal impulses, which
depression
may also help the neuron to replete its serotonin.
Beneficial against increased arousal and
PTSD
flashbacks
Aggression and anxiety asso. With Traumatic brain
OTHERS
injury or organic brain disease
SSRI induced bruxism and sexual dysfxn, nicotine
craving, ADHD
ADVERSE EFFECTS AND PRECAUTIONS
§ Most common adverse effects are headache, nausea,
dizziness, and insomnia
§ No deaths reported from overdoses; median lethal dose is
160-550 times the recommended daily dose.
§ Should be used with caution by persons with hepatic and renal
impairment, pregnant women and nursing mothers.
§ Can be used safely in the elderly
DRUG INTERACTION
§ It increase blood concentration of Haloperidol
§ With MAOI – hypertensive episodes
§ Erythromycin, Itraconazole, Nefazodone, and grapefruit juice
= raise plasma concentration of Buspirone.
LABORATORY INTERFERENCES
§ Single doses of Buspirone can cause transient elevationsin
growth hormone, prolactin and cortisol concentrations,
although the effects are not clinically significant.
DOSAGE AND CLINICAL GUIDELINES
§ Treatment is usually initiated 5 mg TID or 7.5 mg BID, raised
to 5 mg every 2 to 4 days; up to 15 – 60 mg/day.
§ Should not be used in patients with past hypersensitivity to
buspirone, in cases of diabetes-associated metabolic
acidosis, or in patients with severely compromised liver or
renal function.
SWITCHING FROM A BENZODIAZEPINE
§ Not cross-tolerant with benzodiazepines, barbiturates or
alcohol
§ Two alternatives:
o Start buspirone treatment gradually while the
benzodiazepine is being withdrawn
o Start buspirone treatment and bring the person up
to a therapeutic dosage for 2-3 weeks while the
person is still receiving regular benzodiazepine
dosage and then slowly taper the benzodiazepine
dosage.
Page 3 of 7
 § depression asso. with propanolol – rare
IV. β-ADRENERGIC RECEPTOR § nausea, vomiting, diarrhea and constipation;
ANTAGONISTS: § agitation, confusion, hallucinations - rare

Cardiovascular
PHARMACOLOGIC ACTIONS § Hypotension
§ 5 most commonly used β-receptor antagonist in psychiatry: § Bradycardia
o Propanolol § Dizziness
o Nadolol § Congestive failure (in patients with compromised
o Metoprolol myocardial fxn)
o Pindolol
o Atenolol. Respiratory
§ When CNS effect is desired: more lipophilic drug; When § asthma (less risk with B1-selective drugs)
peripheral effect is desired: less lipophilic drug
§ Pindolol also has sympathomimetic effects Metabolic
§ Pindolol, propranolol and nadolol also has some antagonistic § worsened hypoglycemia in diabetic patients on insulin
activity at 5-HT1A receptors. or oral agents
§ NO KNOWN LABORATORY INTERFERENCE
Gastrointestinal
INITIAL
NAME
LIPO METAB SELEC T1/2
DOSE
MAX.DOSE § nausea, diarrhea, abdominal pain
PHILIC OLISM TIVITY (HRS) (MG.)
(MG)
10-20 30-140 Sexual
PROPANOLOL Yes hepatic β1=β2 3-6
BID/TID BID § impotence
14- 30-240
NADOLOL No renal β1=β2 40 OD
24 OD Neuropsychiatric
5 60 § lassitude
PINDOLOL Yes hepatic Β1>β2 3-4
TID/QID BID/TID § fatigue
75-150 § dysphoria
METOPROLOL Yes hepatic Β1>β2 3-4 50 BID
BID
§ insomnia
50-100
ATENOLOL No renal Β1>β2 6-9 50 OD § vivid nightmares
OD
§ depression (rare)
§ psychosis (rare)
THERAPEUTIC INDICATIONS
Other (rare)
§ Propanolo l- social phobia primarily the § Raynaud’s phenomenon
performance type; Panic disorder, PTSD § Peyronie’s disease
and GAD
ANXIETY
§ 10-40 mg 20-30 min before the anxiety- Withdrawal syndrome
DISORDERS
provoking situation § rebound worsening of angina pectoris when
§ - Less effective than BDZ and SSRI for discontinued
panic disorder
§ Initial approach: loweing Lithium, eliminate
LITHIUM-INDUCED
aggravating factors such as caffeine and PRECAUTIONS
POSTURAL
administering Lithium at bedtime; § Contraindications:
TREMOR
§ Propanolol 20-160 mg a day 2-3x a day o Asthma
NEUROLEPTIC- o insulin-dependent diabetes
§ More effective than anticholinergics and
INDUCED ACUTE o congestive heart failure
BDZ
AKATHISIA o significant vascular disease
§ Aggressive and violent outbursts in o persistent angina
impulse disorder, schizophrenia, o hyperthyroidism
AGGRESSION AND
aggression associated with brain injuries
VIOLENT
such as trauma, tumors, anoxic injury, DRUG INTERACTIONS
BEHAVIOR
encephalitis, alcohol dependence and § increased plasma concentrations of antipsychotics,
degenerative disorders anticonvulsants, theophylline, and levothyroxine -
§ Pindolol used to augment and hasten (Propanolol)
ANTIDEPRESSANT andtidepressants § Barbiturates, Phenytoin and cigarette smoking increase the
AUGMENTATION § May shorten the usual 2-4 weeks latency elimination of b-antagonists that are metabolized by the liver
§ Schizophrenia, mania § co-administration with MAOI’s = hypertensive crisis and
OTHERS bradycardia
§ Stuttering
§ Propanolol as adjuvant to BDZ but not as § co-administration with Calcium channel inhibitors= depressed
sole agent myocardial contractility and A-V nodal cond.
ALCOHOL
§ No propranolol for PR< 50bpm; 50 mg for
WITHDRAWAL DOSAGE AND CLINICAL GUIDELINES
PR 50-79 bpm; and 100 mg of PR 80 and
above.
§ 10,20, 40, 60, 80 AND 90 MG TABS; 4, 8 and
ADVERSE EFFECTS 80 mg/ml sol; 60, 80, 120 and 160 mg SR caps.
§ Antagonize the normal physiological response to § For tx of chronic disorders, Propanolol initiated
hypoglycemia; at 10 mg TID or 20 mg BID; can be raised by 20
PROPANOLOL
§ Worsen A-V conduction defects and lead to complete A-V to 30 mg a day until therapeutic effect
heart block – death § For aggressive behavior – up to 80 mg/day
§ Produce bradycardia § For social phobia- 0 to 40 mg 20 to 30 min
§ Blocks bronchodilating effects of epinephrine before performance
§ hypotension and bradycardia most common; test dosage of NADOLOL § 20, 40, 80 and 160 mg tabs
20 mg PINDOLOL § 5 and 10 mg tabs
Page 4 of 7
 § 50 and 100 mg tab; 50, 100 and 200 mg SR
METOPROLOL
tabs
ATENOLOL § 25, 50, and 100 mg tabs ANTIHISTAMINES

§ Pulse and BP should be taken regularly META ONSET

DURA
TION
GENERIC BRAND USE IN
§ Drug use shld be temporarily discontinued if it produces NAME NAME
B MOA OF OF
PSYCHIATRY
OLISM ACTION ACTIO
severe dizziness, ataxia or wheezing. N
§ Treatment should never be discontinued abruptly. IM=15-
Neuroleptic
30 min
§ Propanolol tapered by 60 mg/day until dose of 60 mg/day is (antiparki
induced
parkinsonism;
reached, then tapered 10-20 mg/day every 3 to 4 days. DIPHENHYD
Benadryl H1 ant;
nsonian)
4-6 neuroleptic
RAMINE Sedative
induced acute
antimusc effect
Liver arinic dystonia;
MEDICATIONS USED IN TREATMENT FOR
peaks 1-
cholinerg hypnotic
3 hours
HYDROXYZI Atarax, ic
ADVERSE EFFECTS OF PSYCHOTROPICS NE Vistaril 20-60
min
6-24 anxiolytics
PROMETHA Sedative;
Phenergan 4-6
ZINE anxiolytic
H1 and
ANTICHOLINERGIC AGENTS
Anorexia
5-HT2
nervosa;
CYPROHEP ant;
inhibited male
Periactin Kidney antimusc 4-6
TADINE and female
arinic
orgasm caused
§ Block the actions of atropine cholinerg
ic
by SSRIs
§ Anti-muscarinics because specific for muscarinic receptors.
§ Well absorbed in GIT; lipophilic THERAPEUTIC INDICATINS
§ IM administration is preferred because of low risk for adverse
effects NEUROLEPTIC-INDUCED-
§ Trihexyphenidyl is the most stimulating; Benztropine is the PARKINSONISM, ACUTE § Alternative to anticholinergics and
least stimulating. DYSTONIA AND Amantadine
§ No known laboratory interferences. AKATHISIA
SAFE HYPNOTICS § Not superior to benzodiazepines
THERAPEUTIC INDICATIONS
ANXIOLYTIC § Not proven for long term therapy
SSRI-INDUCED IMPAIRED § Cyproheptadine, esp. delayed
§ Benztropine 1-3 mg OD/BID for 4-8 weeks,
ORGASM orgasm
then d/c to assess if person still requires the
NEUROLEPTIC- § Cyproheptadine promotes weight
drug. EATING DISORDERS
INDUCED gain
§ Prophylaxis usu not indicated
PARKINSONISM § Cyproheptadine can reduce
§ In young men, prophylaxis may be indicated PTSD
esp if given high potency DRA recurrent nightmares
§ Benztropine 1-2 mg IM, repeated 20 to 30 min
as needed PRECAUTIONS AND ADVERSE REACTIONS
NEUROLEPTIC- § Laryngeal dystonia is an emergency – § Commonly associated with dizziness, sedation and
INDUCED Benztropine up to 4 mg in a 10 min period, hypotension and can be severe in the elderly
DYSTONIA followed by 1-2 mg of Lorazepam slow IV. § Anticholinergic effects- dry mouth, urinary retention, blurred
§ Prophylaxis: high risk persons (with prev vision, and constipation
episode or young age) § Paradoxical excitement and agitation
§ Poor motor coordination can result in accidents
AKATHISIA § Anticholinergics not the drug of choice
§ Central anticholinergic syndrome with psychosis -
Cyproheptadine or Diphendydramine
PRECAUTIONS AND ADVERSE EFFECTS
§ Weight gain –cyproheptadine
§ Potential for abuse
§ Prostatic hypertrophy, Urinary retention, and narrow-angle
§ Persons should be warned about driving and operating
glaucoma
dangerous machinery.
§ Adverse effects: anticholinergic intoxication *
§ Should be used only at very low doses, if at all, by persons
o delirium, coma, seizures, agitation, hallucinations,
with narrow-angle glaucoma or obstructive GI, bladder or
severe hypotension, supraventricular tachycardia,
prostate conditions;
peripheral manifestations such as flushing,
§ Coadministration with opioids can increase euphoria
mydriasis, dry skin, hyperthermia and decreased
experience
bowel sounds.
§ Overdoses can be fatal
§ Tx: Physostigmine (Antilirium) 1-2 mg IV or IM every 30 or 60
§ Excreted in breastmilk
minutes.
§ Potential for teratogenicity
PREPARATIONS AND DOSAGES
DRUG INTERACTIONS
GENERIC NAME BRAND PREPARA USUAL PARENTERA
§ Add to sedative property of CNS depressant
NAME TIONS DOSAGE L DOSE § Add to anticholinergic effects resulting in severe
.5,1,2 mg
1-4 mg OD- anticholinergic intoxication
BENZTROPINE Cogentin tab; 1 1-2 mg. § Cyproheptadine may antagonize the beneficial effects of
TID
mg/ml
SSRI’s.
2 mg tab; 2 mg OD-
BIPERIDEN Akineton 2 mg
5mg/ml TID
10, 50 mg 50-100 mg LABORATORY INTERFERENCES
ETHOPROPAZINE Parsidol -
tab OD-TID § May eliminate the wheal and induration that form the basis of
100 allergy skin tests.
50-100 mg 60mg IV over
ORPHENADRINE Norflex mg;30
mg/ml
TID 5’ § Promethazine may interfere with pregnancy test and increase
2.5-5 mg blood glucose concentration.
PROCYCLIDINE Kemadrin 5 mg tab - § Diphenhydramine may yield a false-positive urine test for
TID
2.5mg PCP.
2-5 mg § Hydroxyzine can falsely elevate certain tests for 17-
TRIHEXYPHENIDYL Artane elixir; -
BID-QID
2mg/5ml hydroxycorticosteroids.
Page 5 of 7
DOSAGES AND GUIDELINES PHARMACOLOGICAL ACTIONS/ INDICATIONS

§ Diphenhydramine 25-50 mg IV effective for acute dystonia. DRUG ABSORPTN

T½
(hrs)
RECEPTOR
AFFINITY
THERAPEUTIC INDICATIONS
§ Diphenhydramine 25 mg TID up to 50 mg QID for Well
Augments Medication-
absorbed;
parkinsonism, akinesia and buccal movements. AMANTADI
excreted
12- dopaminergic induced
Cotard’s Syndrome
NE 18 neurotransmiss parkinsonism
§ Diphenhydramine 50 mg OD- mild transient insomnia unmetaboliz
ion in the CNS;
ed in kidney Extrapyramidal
§ Hydroxyzine shouldnot be given IV bec. It is irritating to BV Rapid; peak symptoms
§ Hydroxyzine 50-100mg QID for long term treatment of LEVODOPA plama level 1½ D3>D2(20x)
30-120min Akinesia
anxiety; 50 -100 mg IM every 4 – 6 hours for short-term Hyperprolactinemia
treatment of anxiety. BROMOCRI
D2, D3, 5-HT1, Rabbit Syndrome Neuroleptic malignant
Rapid; 1st 5-HT2, α-1, α- (focal perioral syndrome
§ CYPROHEPTADINE 4-16 mg a day 1-2 hours before PTINE
pass metab; 2, β tremors of Medication-resistant
30-55% choreoathetoid Bipolar 2 dep
anticipated sexual activity to reverse SSRI-induced bioavailable type Restless leg syndrome;
ROPIRINOL
anorgasmia E
6 D3>D2(20x) Antidep-induced sexual
Augmentation for dysfunction;
antidep therapy in Treatment of depression in
PRAMIPEX Rapid; little treatment resistant
8 D3>D2(20x) Parkinson’s dse.; reduce
α-ADRENERGIC RECEPTOR ANTAGONISTS OLE 1st pass dep. anhedonia in Parkinson’s

ADVERSE REACTIONS
YOHIMBINE PRAZOSIN
§ α-2 adrenergic receptor § α-1 adrenergic receptor DRUG
antagonist antagonist § CNS: mild dizziness, insomnia, and impaired
§ For idiopathic and medication- § Suppress nightmares concentration (5 – 10%); irritability,
induced sexual disorders particularly those asso with depression, anxiety, dysarthria and ataxia (1-
§ A/E: anxiety, inc. BP/HR, inc. PTSD 5%) seizures, and psychotic symptoms;
psychomotor activity, § A/E: dizziness, headache, AMANTADINE
§ PERIPHERAL: nausea (most common),
irritability, tremors, headache, drowsiness, lack of energy, headache, loss of appetite, blotchy skin spots;
flushing, dizziness, urinary weakness, palpitations and § Livedo reticularis (purple discoloration of the
frequency, nausea , vomiting, nausea skin caused by dilation of BV)
sweating. § No adverse drug interactions LEVODOPA § Dosage dependent;
§ No known laboratory § No known laboratory § nausea, vomiting, orthostatic hypotension,
BROMOCRIPTINE
interferences interferences headache, dizziness, and cardiac arrythmias.
ROPIRINOLE
§ Long term use, particularly in elderly:
DANTROLENE PRAMIPEXOLE
§ Choreiform and dystonic movements,
psychiatric disturbances – hallucinations,
delusions, confusions, depression and mania
§ Direct-acting skeletal muscle relaxant; directly affects
contractile response of the muscles at the site beyond the PRECAUTIONS
myoneural junction.
§ May cause muscle weakness, slurring of speech and drooling, DRUG
diarrhea, headache and depression, elevated liver function § Relative contraindication: Renal disease and
tests. seizure d/o
§ Primary indication : muscle rigidity in neuroleptic malignant § Should be used with caution in persons with
syndrome edema and cardiovascular disease;
§ Direct-acting skeletal muscle relaxant; directly affects AMANTADINE
§ May be teratogenic; Excreted in milk
contractile response of the muscles at the site beyond the § Overdosage: toxic psychoses (confusion,
myoneural junction. hallucinations, aggressiveness),
§ May cause muscle weakness, slurring of speech and drooling, cardiopulmonary arrest.
diarrhea, headache and depression, elevated liver function § Contraindicated in pregnant women and
tests. LEVODOPA
nursing mothers.
§ Primary indication : muscle rigidity in neuroleptic malignant
§ Long-term use of Bromocriptine and
syndrome
Pergolide can produce retroperitoneal and
BROMOCRIPTINE pulmonary fibrosis, pleural effusions and
DOPAMINE RECEPTOR AGONISTS pleural thickening.; Contraindicated in
pregnant women and nursing mothers.
ROPIRINOLE § may cause irresistible sleep attacks;
§ Symmetrel; Antiviral used in Influenza A and Contraindicated in pregnant women and
AMANTADINE Cotards syndrome; Beneficial to elderly PRAMIPEXOLE
nursing mothers.
persons prone to anticholinergic side effects;
§ Parlodel; Neuroleptic Malignant Syndrome DRUG INTERACTIONS
BROMOCRIPTINE
and hyperprolactinemia
§ L-dopa, Larodopa; false elevated serum and DOPAMINE RECEPTOR
urinary uric acid conc, urinary glucose test AMANTADINE
LEVODOPA AGONISTS
results, urinary ketone test, and urinary § Amantadine + MAOI = increase in § With TCAC’s = neurotoxicity
cathecholamine conc. resting BP § With diuretics and Anti-HPN=
ROPINIROLE § Requip § Amantadine + CNS stimulants = potentiate effects
insomnia, irritability, nervousness, § BZD, Phenytoin, Pyridoxine =
§ Mirapex; Most widely prescribed as
possible seizures, and irregular interfere with therapeutic effects
PRAMIPEXOLE augmenter of antidepressants; possible heartbeat. § Bromocriptine + ergot alkaloids
increased risk of heart failure § Should not be co-administered with = hypertension and myocardial
APOMORPHINE § Apokyn anticholinergics because adverse infarction
§ Permax; Removed from market in 2007 bec effects may be exacerbated. § Progestin, estrogen and OCP
PERGOLIDE of increased risk of serious damage to heart (confusion, hallucination, may interfere with effects of
nightmares, dry mouth, blurred Bromocriptine and raise plasma
valves
vision concentrations of Ropinirole
§ Cimetidine may raise plasma
conc of Pramipexole
Page 6 of 7
 SILDENAFIL
§ PDE5, regulates cGMP which acts on arteriolar smooth
muscle of corpus cavernosum
§ Inhibits PDE5, allowing blood to fill the corpus cavernosum
and cause erection;
§ For erectile dysfunction
§ Most potential adverse effect in Myocardial infarction
§ Contraindicated in patients taking organic nitrates
§ No laboratory interferences

Page 7 of 7
 PSYCHIATRY
ANTIDEPRESSANTS
HYACINTH C. MANOOD, MD
JANUARY 2021

BIOLOGY OF DEPRESSION HISTORY OF ANTIDEPRESSANTS

§ CATECHOLAMINE HYPOTHESIS - Schildkraut (1960’S)

o deficiency of the neurotransmitter norepinephrine
(also known as noradrenaline) in certain areas of
the brain was responsible for creating depressed
mood.
o However, research results also tell us that not all
people experience mood changes in response to
decreased norepinephrine levels. Some people
who are depressed actually show more than normal
within the neurons that produce norepinephrine.
o More current studies suggest that in some people,
low levels of serotonin trigger a drop in
norepinephrine levels, which then leads to
depression.

§ MONOAMINE HYPOTHESIS
o depression is the result of underactivity of
monoamines, especially 5-HT.
o Reserpine, a monoamine antagonist, which was
used to treat things like high blood pressure, is
rarely used at the present time due to the fact that
depression is a common side effect.
o Dopamine plays an important role in controlling our
drive to seek out rewards, as well as our ability to
obtain a sense of pleasure. Low dopamine levels
may, in part, explain why people with depression
don't get the same sense of pleasure out of
activities or people that they did before becoming
depressed.

§ AUTORECEPTOR SUBSENSITIVITY THEORY

o Autoreceptors, typically located on the presynaptic
or axonal membrane, serve a feedback function;
inhibitory effect;
o Presumably, the initial effect of the monoamine
agonists is to stimulate these autoreceptors such
that they inhibit the increased release of
monoamines resulting from the drug. After two or
three weeks, however, the autoreceptors become
subsensitive due to continued stimulation, and quit
sending their inhibitory signal, so the monoamine
agonists then have the effect that we would expect.

§ STRESS
o Elevates glucocorticoids (cortisol) - failure of the
negative feedback of the HPA axis and following
continuous elevation of GC may be strongly
associated with MDD.
o Stress decreases hippocampal volume - elevated
GC decrease the volume of the hippocampus, the
decreased volume of the hippocampus may induce
the failure of the negative feedback of the HPA axis,
and subsequent further elevation of the levels of GC
and aggravation of the failure of the HPA axis result
in MDD.
CLASSES OF ANTIDEPRESSANTS
§ MAOI’S – Monoamine Oxidase Inhibitors
§ TCA’S – Tricyclic and Tetracyclic Antidepressants
§ SSRI’S – Selective Serotonin Reuptake Inhibitors
§ SNRI’S – Serotonin – Norepinephrine Reuptake Inhibitors
§ Atypical Antidepressants
o Norepinephrine-Dopamine Reuptake Inhibitors
(NDRI) - Bupropion
o Serotonin Antagonist and Reuptake Inhibitors
(SARI) – Trazodone, Nefazodone
o Mirtazapine

Page 1 of 6
 MONOAMINE OXIDASE INHIBITORS
(MAOI’S)

§ Two functional forms of MAO:

o MAO-A
§ metabolized norepinephrine and
serotonin selectively
o MAO-B
§ metabolizes benzylamine and ß
phenylethylamine PRECAUTIONS
§ Contraindicated in pregnancy and lactation
§ Discontinuation Syndrome – arousal, mood disturbances,
somatic symptoms; gradual tapering over several weeks
when discontinuing
§ Intoxication: agitation, hyperthermia, hypertension,
tachypnea, dilated pupils, hyperactive deep tendon reflexes,
coma.
o There is often an asymptomatic period of 1 to 6
hours after ingestion
o Treatment: acidification of urine to hasten the
excretion of MAOI; dialysis

§ Phenelzine, Isocarboxacid, Tranylcypromine
o Readily absorbed; peak plasma conc = 2 hours; half
lives: 2-3 hours
o Because of irreversible action, therapeutic effect of
a single dose may persist for as long as 2 weeks.
§ Moclobemide (RIMA) – selective, reversible inhibitors of
MAO-A
o Rapidly absorbed; half-life of .5 to 3.5 hours
o Briefer clinical effect; reversible
§ TYRAMINE-INDUCED HYPERTENSIVE CRISIS
o Headache, stiff neck, sweating, nausea and
vomiting
o Treatment: alpha adrenergic antagonist eg.
Phentolamine and Chlorpromazine – lowers BP
within 5 minutes
§ Diuretics
§ Beta adrenergic receptor antagonist –
control tachycardia
§ Don’t use Nifedipine – hypotensive shock
THERAPEUTIC INDICATIONS
§ Depression
§ Panic Disorders
§ PTSD
§ Eating Disorders
§ Social Phobia
§ Pain Disorders
ADVERSE EFFECTS
§ Management of orthostatic hypotension
o Avoidance of caffeine
o Intake of 2L of fluids per day
o Addition of dietary salt or adjustment of
antihypertensive drugs
o Support stockings
o Fludrocortisone0.1 to 0.2 mg per day
§ Rare effect: Non-tyramine induced hypertensive crisis
(tranylcypromine) – should avoid MAOI’s
§ Paresthesias ( secondary to MAOI-induced pyridoxine
deficiency), myoclonus, and muscle pains
DRUG INTERACTION
§ Potentiates action of CNS depressants, inc. alcohol and
barbiturates;
§ With SSRI and Anafranil – triggers serotonin syndrome
§ Fatal reactions when combined with Meperidine or fentanyl
§ When switching to another type of antidepressant, wait for at
least 14 days from last dose of MAOI to allow replenishment
of body’s MAOs.
§ Cimetidine and Fluoxetine – reduce elimination of
Moclobemide.
LABORATORY INTERFERENCES:
§ Lowers blood glucose concentration
§ False-positive test results for pheochromocytoma or
neurobastoma
§ Minimal false elevation in thyroid function test
TRICYCLIC AND TETRACYCLICS
ANTIDEPRESSANTS (TCA’S) :
§ TRICYCLICS: three-ring nucleus
o Tertiary amines - Imipramine, amitriptyline,
clomipramine, trimipramine and doxepin
o Secondary amines- Desipramine, nortriptyline and
protriptyline
§ TETRACYCLICS: four-ring side chain and bridge
o Amoxapine- derivative of antipsychotic drug
Loxapine
o Maprotiline
o Mianserine
MECHANISM OF ACTION
§ All tricyclics block reuptake pumps for both 5HT and NE and
dopamine at nerve terminal, thus increasing NE, 5HT and DA
at extracellular and more of its action at the receptor site
§ Some have more potency for inhibition of 5HT uptake pump
o (e.g. clomipramine, imipramine, amitryptyline)
§ Others have more potency for inhibition of NE uptake pump
o (nortriptyline, desipramine)
§ Tricyclics also block Na+channels, thus may cause cardiac
arrythmia
§ Competitive antagonists at muscarinic acetylcholine,
histamine H1, and alpha-1 and alpha-2 receptors (causes side
effects, e.g., weight gain, drowsiness, blurred vision)
§ Doxepine has the most antihistaminergic effects
§ Clomipramine is the most serotonin-selective

Page 2 of 6
PHARMACODYNAMICS
§ Completely absorbed, with significant first pass metabolism by
CYP 450 enzyme system
§ Peak plasma conc. = 2 – 8 hours
§ Half life = 10 to 70 hours; nortriptyline, maprotiline and
protriptyline has longer half-lives;
THERAPEUTIC INDICATIONS
§ Major Depressive Disorder
§ Mood Disorder due to general medical condition with
depressive symptoms
§ Panic Disorder with Agoraphobia - Imipramine
§ Generalized Anxiety Disorders - Doxepin
§ Obsessive Compulsive Disorders – Clomipramine
§ Eating Disorders – Imipramine and Desipramine
§ Pain Disorders
§ Childhood enuresis – Imipramine
§ Peptic ulcer disease – Doxepin
§ Narcolepsy; Nightmare disorders
§ PTSD
§ Premature ejaculation, Movement disorders –
Clomipramine
ADVERSE EFFECTS
§ induce manic episode
§ Anticholinergic effects – dry mouth, constipation, blurred
vision, urinary retention; Amitryptiline, Imipramine
trimipramine and doxepin are the most anticholinergic drugs;
§ Sedation – Amitryptiline, Trimipramine and Doxepin are the
most sedating agents;
§ Orthostatic hypotension, profuse sweating, palpitations and
inc. BP
§ Tachycardia, flattened T waves, prolonged QT intervals,
depressed ST segments
§ Psychomotor stimulation – Desipramine and protriptyline –
myoclonic twitches and tongue tremors
§ Parkinsonian symptoms and impotence – Amoxapine
§ Should be avoided in pregnancy and lactation
§ Should not be administered during ECT
PRECAUTIONS
§ Should be avoided in pregnancy and lactation
§ Should not be administered during ECT
§ No reported laboratory interference
§ Overdose = agitation, delirium, convulsions, hyperactive DTR,
bowel and bladder paralysis, BP and temp. dysregulation,
mydriasis, coma
DRUG INTERACTIONS
§ Block antihypertensive effects of guanethidine, propanolol
and clonidine
§ With methyldopa – behavioral agitation
§ Antipsychotics add to the anticholinergic effects of TCAs.
§ Additive effects on CNS depressants and over-the-counter
cold medications
§ With sympathomimetic drugs – serious cardiovascular effects
§ Birth control pills decrease plasma conc. Of TCAs.
§ TCA plasma conc. Inc by acetazolamide, aspirin, thiazide,
cimetidine, fluoxetine and sodium bicarbonate
§ TCA plasma conc. Dec. by ascorbic acid, ammonium chloride,
barbiturates, cigarette smoking, chloral hydrate, lithium and
primidone
SELECTIVE SEROTONIN REUPTAKE
INHIBITOR (SSRI)
§ Specific activity in inhibition of serotonin reuptake without
effects on norepinephrine and dopamine reuptake
§ Essentially devoid of agonist and antagonist activity on any
NT receptor
§ 5 available SSRI’s : Fluoxetine (Prozac), Sertraline (Zoloft),
Paroxetine (Paxil), Fluvoxamine (Luvox); Citalopram (lupram)
§ Fluoxetine has longest half-life (2 – 3 days) and its active
metabolite has a half life of 7 to 9 days; Other SSRI has about
20 hours without any active metabolites;
§ All SSRI’s are well-absorbed after oral administration; food
does not have a large effect on the absorption
§ Peak concentrations reached in 4-8 hours
§ All SSRI’s are metabolized in the liver.
o Paroxetine and Fluoxetine metabolized by CYP
2D6
o Fluvoxamine inhibits CYP 3A4 - should not be
given with Terfenadine and Astemizole
THERAPEUTIC INDICATIONS
§ Depression
o First line agents for depression in general
population, the elderly, medically ill, and those who
are pregnant
§ Anxiety disorders
o OCD – over age 18: Fluvoxamine, Paroxetine,
Sertraline and Fluoxetine; in pediatric OCD:
Fluvoxamine and Sertraline
o Panic Disorder – Citalopram, Fluvoxamine, and
Fluoxetine
o Social Phobia – Paroxetine
§ Eating Disorders:
o Fluoxetine - Bulimia Nervosa.
§ Not that effective for Anorexia Nervosa
o May be used for Obesity. However, SSRIs may
cause initial weight gain
§ Premenstrual Dysphoric d/o
§ Premature Ejaculation - Fluoxetine and Sertraline
§ Paraphilias: SSRI reduces the obsessive-compulsive
behavior in persons with paraphilias
§ ADHD
§ OC symptoms in Autistic Disorder
§ Chronic Pain Syndromes – neuropathic pain, fibromyalgia
§ Psychosomatic Conditions – syncope
ADVERSE REACTIONS
§ Most adverse effects appear with the first 1 to 2 weeks and
generally subside or resolve spontaneously
§ The most common AE of SSRI is sexual inhibition – inhibited
orgasm and decreased libido; does not resolve spontaneously
but usually continues as long as the drug is taken.
§ Treatment: decrease dosage; may add Bupropion switch to
Bupropion or Nefazodone Yohimbine, cyproheptadine or
dopamine receptor agonist Sildenafil
§ Gastrointestinal – Sertraline, Fluvoxamine and Citalopram
has the highest rates of GI effects;
o Nausea, diarrhea, anorexia, dyspepsia, weight gain
§ Headaches – Fluoxetine; on the other hand, all SSRIs are
effective prophylaxis against both migraine and tension-type
headaches;
§ CNS
o anxiety – Fluoxetine
o Insomnia – Fluoxetine is taken during the daytime
because of this adverse effect;
o Sedation
o Vivid dreams and nightmares
o Seizures
o Extrapyramidal symptoms: tremors; closely
associated with Fluoxetine
Page 3 of 6
 § Anticholinergic effects: Paroxetine increased twofolds and threefolds,
§ Hematological – increased bruisability (platelet function); respectively.
Paroxetine and fluoxetine cause reversible neutropenia § Raises concentrations and may increase the
§ Decreased glucose concentration; hyponatremia and SIADH activity of clozapine, carbamazepine,
§ Increase prolactin levels (mammoplasia and galactorhea) methadone, propanolol and diltiazem.
§ Allergic rashes § No significant interactions with lorazepam and
§ SSRIs do not interfere with any laboratory tests digoxin
§ Cimetidine increases its concentrations by
PRECAUTIONS 40%
§ Serotonin Syndrome: concurrent adm. with MAOIs, § Increases plasma concentrations of
tryptophan, lithium or other antidepressants – metoprolol by twofolds with no significant
o Diarrhea, restlessness, extreme agitation, CITALOPRAM
effects on blood pressure or heart rate.
hyperreflexia, autonomic instability, myoclonus, § -Does not significantly affect the metabolism of
seizures, hyperthermia, uncontrollable shivering,& warfarin, digoxin, lithium, carbamazepine or
rigidity, delirium, coma, status epilepticus, cadio- imipramine.
vascular collapse and death
o Treatment:
§ Remove offending agents;
§ Nitroglycerine; cyproheptadine; SEROTONIN NOREPINEPHRINE REUPTAKE
methysergine INHIBITOR (SNRI)
§ Cooling blankets
§ Chlorpromazine , dantrolene, § Concomitant blockade of neuronal serotonin and
benzodiazepines, anticonvulsants norepinephrine uptake transporters
§ Mechanical ventilation § Sometimes referred to as “dual reuptake inhibitors”
§ Paralyzing agents § Relative lack of affinity for other receptors, esp. muscarinic,
§ Serotonin withdrawal syndrome – abrupt withdrawal of SSRI, histaminergic, α- and β-adrenergic receptors
especially one with shorter half-life. § Duloxetine formulated as a delayed-release capsule to reduce
o Dizziness, weakness, nausea, headache, rebound the risk of severe nausea
depression, anxiety, insomnia, poor concentration,
upper respiratory symptoms, paresthesias, and VENLAFAXINE / DESVENLAFAXINE
migraine-like symptoms.
o Persons who experience transient adverse effects Therapeutic Adverse Drug
during the first weeks of taking SSRI are most likely Precautions
indications reactions interactions
to experience discontinuation symptoms. 1. Depression § Nausea is the § Sustained § metabolized
o Paroxetine is most likely to cause discontinuation – currently most hypertension – primarily by
syndrome, because plasma concentration drop the only frequently dose related CYP2D6, but
rapidly in the absence of continuous dosing. reported weak
FDA- treatment- § Discontinuation inhibitor of
o Fluoxetine is less likely to cause discontinuation approved emergent AE Syndrome- enzyme
syndrome because of the long half-life of its active indication for dizziness, dry
metabolite which effectively tapers itself. DVS; § Sexual: mouth, insomnia, § C/I in
decreased nausea, patients
DRUG INTERACTIONS 2. Generalized libido and nervousness, taking
Anxiety delayed sweating, anorexia, MAOI’s
SSRI DRUG INTERACTION orgasm or diarrhea,
Disorder – ejaculation somnolence and § No available
§ decreases the metabolism of Carbamazepine, extended sensory data for
anti-neoplastic agents, Diazepam and release § headache, disturbances. laboratory
phenytoin formulation insomnia, interferences
FLUOXETINE § Significant interactions with benzodiazepines, of somnolence, § ECG changes, -
antipsychotics and lithium Venlafaxine dry mouth, prolonged QT and
§ no interactions with warfarin, tolbutamide or dizziness, QRS int, BBB,
chlorothiazide constipation, tachy/bradycardia,
3. Social asthenia, hypo/hypertension,
§ May displace Warfarin from plasma proteins Anxiety D/O sweating and coma, seizures
SERTRALINE and cause increase prothrombin time. nervousness;
§ Cimetidine may increase its concentration 4. Others – noradrenergic § Serotonin
§ Cimetidine may increase concentration of OCD, Panic agonism syndrome
paroxetine disorder,
ADHD, with § Fatal overdoses
§ Phenobarbital and Phenytoin may decrease with other drugs,
its concentration dual alcohol, or both
PAROXETINE diagnosis of
§ Increase anticoagulant effect of Warfarin
§ Coadministration with Tramadol may depression § -excreted in
precipitate a serotonin syndrome in elderly and cocaine breastmilk
persons. dependence
§ Has the most risk for drug-drug interaction
§ Metabolized by enzyme CYP 3A4 which may
be inhibited by Ketoconazole; if given
Terfenadine – cardiotoxicity
§ Should not be coadministered with
FLUVOXAMINE
alprazolam, triazolam, and diazepam because
it increases half-lives of these agents;
§ If used with Warfarin and Theophylline, levels
of these agents should be monitored and
doses be adjusted accordingly, bec. they are

Page 4 of 6
 DULOXETINE § Overdose: seizure, bradycardia and cardiac arrest in rare
cases
Therapeutic Adverse Drug § False-positive results on urinary amphetamine screens
Precautions
indications reactions interactions
1. Depression § Nausea – most § increases blood § metabolized DRUG INTERACTION
2. Neuropathic commonly lead sugar and primarily by § Should not be used with MAOI’s – hypertensive crisis; at least
pain asso. to treatment hemoglobin A1C CYP2D6, but 14 days should pass after MAOI discontinuation before
discontinuation levels during moderate bupropion is initiated;
with diabetes § Dry mouth, long term inhibitor of
– first drug to § Coadministration with dopaminergic agents (Levodopa,
dizziness, treatments; enzyme
be approved Pergolide) – delirium, psychosis, dyskinesia
fatigue, § Should not be § No available
3. Stress constipation, given with data for § With Prozac (Fluoxetine) – panic, delirium and seizure
urinary decreased substantial laboratory § Carbamazepine decreases plasma concentration of
incontinence appetite, alcohol use bec interferences bupropion
– effects in anorexia, of possible § Increases plasma conc. Of Valproic Acid
somnolence hepatic effects;
the sacral and increased § Hepatic
spinal cord, sweating insufficiency SEROTONIN ANTAGONIST AND REUPTAKE
which in turn § asso. with § End-stage renal
increase the increased in disease INHIBITORS (SARI)
activity of the BP § Uncontrolled
striated narrow angle
urethral glaucoma TRAZODONE
§ Discontinuation § Weak inhibitor of serotonin reuptake and a potent antagonist
sphincter; syndrome
awaiting of Serotonin 2A and @C receptors;
§ Pregnant and
approval nursing women – § mCPP- active metabolite; agonist of Serotonin 2C receptors ;
unless the half-life of 14 hours
potential benefits § Adverse effects are partially mediated by a1-adrenergic
justify the receptor antagonism
potential risks

MILNACIPRAN AND LEVOMILNACIPRAN Therapeutic Adverse Drug

Precautions
§ Milnacipram is only FDA-approved for the treatment of indications reactions interactions
FIBROMYALGIA. Depressive § Sedation, § Trazodone § Potentiates
§ Levomilnacipram approved in 2013 for treatment of MDD. Disorders - orthostatic overdose – CNS
§ Most common adverse reactions: nausea, constipation, main indication hypotension, lethargy, vomiting, depressant
dizziness, drowsiness, effects of
hyperhidrosis, increased heart rate, erectile dysfunction, is MDD; headache headache, other
tachycardia, vomiting and palpitations. § increase and nausea orthostasis, centrally
§ The only dose-related adverse events were urinary hesitation total sleep § neutropenia dizziness, dyspnea, acting drugs
and erectile dysfunction. time tinnitus, myalgias, and alcohol;
§ decrease in tachycardia, § Trazodone
numer of incontinence, +anti-HPN =
NOREPINEPHRINE DOPAMINE REUPTAKE awakenings shivering, coma. hypotension
§ Tx: emesis or § Trazodone
INHIBITORS (NDRI) § decrease lavage and increase
REM sleep supportive care; level of
forced diuresis digoxin and
BUPROPION Insomnia – § Priapism – phenytoin
§ inhibits NE and dopamine reuptake; it binds to dopamine first line agent intracavernosal § With caution
transporter in the brain injection of with warfarin
§ Bupropion is metabolized into its hydroxylated active Erectile Aramine or § Drug that
metabolite, which is a potent NE reuptake blocker epinephrine inhibit
disorder – can § C/I in pregnant CYP3A4 –
§ Effective for patients who can not tolerate side effects of potentiate and nursing inc level of
SSRIs such as sexual dysfunction or nonresponders of SSRIs erections women metabolite =
§ First line agent for the treatment of depression and smoking § With caution in increase s/e
§ Quite effective in combinations with other SSRI’s Others: hepatic/renal dse. § No known
severe laboratory
THERAPEUTIC INDICATIONS agitation in interference
§ Depression – does not disrupt sleep architecture; may be children with
used in hypoactive sexual desire that may accompany development
depression; disabilities and
§ May be combined with Eskalith for refractory depression elderly
§ Bipolar Disorders. persons with
§ ADHD – major second-line agent; appropriate for comorbid dementia;
depression. depression in
§ Cocaine Detoxification patients with
§ Smoking Cessation Schizophrenia;
insomnia and
PRECAUTIONS, ADVERSE REACTIONS AND LABORATORY nightmares in
INTERFERENCES PTSD
§ Headache, insomnia upper respiratory complaints, nausea
§ Restlessness, agitation and irritability NEFAZODONE
§ Rare: psychosis, delirium; euphoria at high doses § Blocks 5HT uptake selectively but in a less potent manner
§ Devoid of sexual side effects than tricyclics
§ Risk of seizure § This helps reduces depression
§ Contraindicated in persons with histories of substance abuse § However, they are powerful 5HT2Aantagonists
§ Use in pregnancy and lactation not recommended
Page 5 of 6
 § 5HT2Aantagonists are not potent antidepressants
§ But blockade of 5HT2Areceptors stimulate 5HT1Areceptors,
which may help reduce depression
§ 5HT2Aantagonism also reduces the risk of anxiety, sedation
or sexual dysfunction which is normally associated with
SSRIs

Therapeutic Adverse
Precautions Drug interaction
Indications Reactions
§ Effective in § nausea, § Should not be § Should not be
treatment of dizziness, given in given
depression insomnia, presence of concommitantly
accompanied weakness liver function with MAOI’s
by anxiety; and impairment § Triazolam and
Premenstrual agitation § Should be Alprazolam –
dysphoric used in inhibition of
disorder, pregnancy only CYP450 3A4
Chronic if benefit § May slow the
pain(both outweighs the metabolism of
neuropathic risk; it is not Digoxin and
and non- known whether Haloperidol
neuropathic, it is secreted in § Exacerbates
PTSD, chronic breastmilk. the adverse
fatigue § No known effects of
syndrome laboratory Lithium.
§ It is not interferences
effective for
OCD

SEROTONIN NOREPINEPHRINE
DISINHIBITORS (SNDIS):

MIRTAZAPINE
§ Blocks alpha 2 receptors and selectively antagonize 5HT2
and 5HT3 receptors. within CNS – net effect of increasing
synaptic levels of norepinephrine and serotonin
§ Potent antagonist of histamine receptors (H1), less alpha 1
adrenergic and muscarinic-cholinergic receptors
§ Therapeutic Indications: Depression, Sleep disturbances,
Somatic and psychological symptoms of anxiety and agitation
§ most common adverse effects: somnolence; give it at bedtime
§ Dizziness, mania and hypomania
§ Lacks the annoying anticholinergic effects;
§ Potentiates the sedative effect of alcohol and
benzodiazepines
§ Increase appetite; increase cholesterol concentration to 20%
or more above the upper limit; elevated ALT (alanine
transaminase) more than three times the upper limit
§ Drop in absolute neutrophil count; agranulocytosis
§ Not recommended to use in pregnancy and lactation
§ No laboratory interferences

SOURCE: Powerpoint 2021

Page 6 of 6
 PSYCHIATRY
ANTIPSYCHOTICS
HYACINTH MANOOD, MD
JANUARY. 9, 2021

TYPES OF ANTIPSYCHOTIC

FIRST GENERATION SECOND GENERATION

§ D2 antagonists; Dopamine
receptor antagonist
§ Can cause extrapyramidal
side effects
§ Better at treating positive
symptoms
ANTIPSYCHOTIC DOPAMINE EFFECTS:
§ D2 and serotonin receptors
antagonist; SDA
§ Also antagonize histamine and
alpha 2 receptors
§ Can cause anticholinergic and
metabolic side effects
§ Better at treating negative
symtoms
Prior to the first antipsychotic medication – Chlorpromazine - the
mode of treatment included electroconvulsive therapy, hydrotherapy,
and putting patients in an insulin coma.

MESOLIMBIC MESOCORTICAL
FIRST GENERATION ANTIPSYCHOTICS
VTA Projections to the ff: VTA Projection to:
1. Nucleus 1. Prefrontal cortex:
Dopamine receptor antagonists – better at treating positive symptoms
accumbens : cognition, working
(hallucination, etc)
(reward,desire and memory and decision
placebo effect) making
§ PHENOTHIAZINES -Chlorpromazine
2. Amygdala:emotion Decreased activity in
§ BUTYROPHENONES
3. Hippocampus: Schizophrenia/psychosis
§ THIOXANTHENES
memory formation. Negative symptoms:
§ DIBENZOXAZEPINES
Increased activity in • Flat affect
§ DIHYDROINOLES
Schizophrenia/psychosis • Poverty of speech
§ DIPHENYLBUTYLPIPERIDINES
Positive symptoms: • Anhedonia
• Delusions • apathy
LOW POTENCY HIGH POTENCY
• Hallucinations
• Disorganized § Chlorpromazine and § Haloperidol and
speech Thioridazine Fluphenazine
• Bzarre behavior § 100 mg or more/day § <10 mg/day
§ More weight gain and sedation § More likely to cause EPS
NIGROSTRIATAL TUBEROINFUNDIBULAR extrapyramidal side effects
From substantia nigra to Begins in the arcuate and
corpus striatum periventricular nuclei of Pharmacological Actions
Involved in motor planning hypothalamus and projects to the § Well absorbed after oral administration
Decreased in treatment with infundibular region of § Liquid preparation absorbed more efficiently than tablets or
first gen. antipsychotics: hypothalamus. capsules
• Dystonia Dopamine inhibits prolactin § Peak plasma conc:
• Akathisia release which in turn inhibits GnRH. o 1-4 hrs after oral adm;
• Parkinsonism Dopamine blockade –more o 30-60 min after parenteral adm.
• Tardive dyskinesia prolactin-less GnRH: § Half life approx. 24 hours
• Galactorrhea § Steady state level approx. 3-5 days
• Gynecomastia § Most are highly protein-bound
• Decrease libido § Bioavailability tenfold higher with parenteral adm
• Sexual dysfunction § Most are metabolized by cytochrome p450 enzymes
§ Long acting depot - Haloperidol and Fluphenazine; adm.
Every 1-4 weeks
ANTIPSYCHOTIC NON-DOPAMINE EFFECTS: § Can take up to months to reach steady state plasma levels,
oral therapy should be continued
HISTAMINE ALPHA 1 ADRENERGIC § Factors influencing pharmacokinetics :
§ Sedation § Orthostatic hypotension
§ Weight gain § Cardiac arrythmias § Elderly demonstrate reduced clearance
AGE
§ Sexual dysfunction rates
MUSCARINIC AUTOIMMUNE REACTIONS § Decreased hepatic blood flow can
MEDICAL CONDITION
Anticholinergic S/E: § Urticaria, dermatitis, rashes reduce clearance; hepatic disease
§ Dry mouth § Dermal photosensitivity § Carbamazepine, phenytoin,
ENZYME INDUCERS
§ Blurring of § Corneal and retinal ethambutol, barbiturates
vision pigmentation § SSRI, TCA, cimetidine, β-blockers,
§ Tachycardia § Cholestatic jaundice CLEARANCE INH, methylphenidate, ciprofloxacin,
§ Urinary INHIBITORS ketoconazoles, erythromycin,
retention triazolobenzodiazepines
§ constipation CHANGES IN BINDING § Hypoalbuminemia can occur with
§ ejaculatory PROTEINS malnutrition or hepatic failure
failure

Page 1 of 6
DRA’s Potency and Adverse Effects should be used; may
experience acute EPS
THERAP SIDE EFFECTS
DRUG NAME CLASSIF. EQUIVALE Sedation Autonomic EPS
NT ORAL § Should be reserved for patients
Fluphenazine Phenothiazine 2 mg ↑ + + +++ IMPULSE CONTROL in whom other interventions
Trifluoperazine Phenothiazine 5 mg ++ + +++ DISORDER have failed
Perphenazine Phenothiazine 8 mg ↔ ++ + ++/+++
Prochlor- Phenothiazine 1 mg ++ + +++ § Hyperactivity, screaming,
perazine PERVASIVE DEVT. agitation with
Aceto- Phenothiazine 20 mg ++ + ++/+++ DISORDER combativeness;high potency
phenazine
Triflupromazine Phenothiazine 25mg +++ ++/+++ ++
DRA
Mesoridazine Phenothiazine 50mg ↓ +++ ++ + BALLISMUS/HEMIBALLISMUS § Respond to antipsychotics
Chlorpromazine Phenothiazine 100 mg ↓ +++ +++ ++ § Nausea, emesis, intractable
Thioridazine Phenothiazine 100 mg ↓ +++ +++ + hiccups, pruritus, psychosis
Pimozide Diphenylbutyl- 1.5 mg ↑ + + +++ OTHERS
piperidine asso w, endocrine disorders
Haloperidol Butyrophenone 2 mg ↑ + + +++ and temporal lobe epilepsy
Thiothixene Thioxanthene 4mg + + +++
Chlorprothixene Thioxanthene 100 mg ↓ +++ +++ +/++
Precautions and Adverse Reactions
Molindone Dihydroindole 10 mg ++ + +
Loxapine Dibenzoxazepin 10 mg ++ +/++ ++/+++
e § POTENTIALLY FATAL; can occur at any
time during the course of treatment
Therepeutic Indications § SYMPTOMS: extreme hyperthermia,
severe muscular rigidity and dystonia,
§ Effective in both short- and akinesia, mutism, confusion, agitation,
long-term management; increase PR and BP
effective against positive § LABS: inc. WBC count, CPK, liver
SCHIZOPHRENIA AND NEUROLEPTIC
symptoms; negative symptoms enzymes, myoglobin, and myoglobinuria
SCHIZOAFFECTIVE MALIGNANT
may worsen § Symptoms evolve over 24 to 72 hrs; men
DISORDERS SYNDROME
§ After a first episode, cont meds and younger patients affected more
for 1-2 years; if multiple, 2 -5 frequently; mortality rate 20 to 30%
years § TREATMENT: D/C DRA immediately;
§ Effective for psychotic § Medical support; cooling blankets,
symptoms of acute mania; monitor vital signs, fluids and electrolytes
standard practice is to combine and renal output; treat fever; Dantrolene
MANIA (Dantrium); Bromocriptine or Amantadine.
an antipsychotic with mood
stabilizer and then gradually § Severe agitation, disorientation to time,
withdraw the antipsychotic. person and place, hallucinations,
§ Combination of antipsychotic seizures, high fever and dilated pupil;
DEPRESSION W/PSYCHOSIS and antidepressant; alternative stupor and coma
is ECT CENTRAL § TREATMENT: D/C DRA, close medical
§ Delusional disorder or paranoid ANTICHOLINERGIC supervision, Physostigmine (Antilirium) 2
DELUSIONAL DISORDER EFFECTS mg slow IV, repeated within 1 hour if
thinking in Borderline PD
§ Regardless of diagnosis; necessary
SEVERE AGITATION AND extreme irritability, § PHYSOSTIGMINE TOXICITY:
VIOLENT BEHAVIOR impulsiveness, and agitation hypersalivation and sweating. Atropine
§ Haloperidol and Pimozide most sulfate can reverse physostigmine toxicity
commonly used; Other SEIZURE § DRA may lower seizure threshold. Low
TOURETTES’S DISORDER clinicians prefer Clonidine bec THRESHOLD potency DRA more epileptogenic
of lower risk of neurological side § Blockade of H1 receptors;
SEDATION
effects Chlorpromazine is the most sedating
§ Transient psychotic symptoms § ↓ cardiac contractility, disrupt enzyme
BORDERLINE PD contractility in cardiac cells,
and aggression
CHILDHOOD § Careful considerations should § ↑ circulating levels of catecholamines,
SCHIZOPHRENIA be given to side effects prolong atrial and ventricular conduction
time and refractory periods.
§ Low doses of high potency DRA
§ Low potency DRA more cardiotoxic, part
(0.5- 1 mg/day
Phenothiazines
Haloperidol);psychotic
CARDIAC § Haloperidol IV – abnormal heart rhythm,
symptoms and agitation; toxic
DEMENTIA AND DELIRIUM EFFECTS ventricular arrythmias, Torsades de
delirium caused by
Pointes and sudden death.
anticholinergics can be
§ Pimozide, Sulpiride and Droperidone –
exacerbated by low potency
prolong QTc interval, Torsade de Pointes
DRA.
and sudden death
§ Psychosis tend to be time
§ Chlorpromazine –prolong QT and PR
limited, it is preferable to avoid
intervals, blunting of T waves, and
use of DRA unless severely
depression of ST segment.
SUBSTANCE-INDUCED agitated and aggressive. BDZ
§ May be the result of cardiac arrythmias,
PSYCHOTIC DISORDER should be used instead in cases
SUDDEN DEATH seizure, asphyxiation, malignant
of phencyclidine intoxication;
hyperthermia, heat stroke and NMS
DRAs may increase risk of
seizure in alcohol withdrawal. § Most common with low potency DRA part.
§ DRA reduce the chorea in early Chlorpromazine and Thioridazine; ;
ORTHOSTATIC
HUNTINGTON’S DSE. stages; High potency DRA adrenergic blockade.
HYPOTENSION
§ Occurs during the first few days of
treatment, tolerance develops
Page 2 of 6
 § Initial dosing lower than therapeutic dose
§ Warn patient and instruct him to rise
slowly after sitting and reclining
§ Avoid caffeine and alcohol; drink at least
2L of fluids a day;
§ TREATMENT: Trendelemburg position;
pump legs as if bicycling
§ Administration of epinephrine results in
paradoxical worsening of hypotension
and is contraindicated. Use Metaraminol
or Norepinephrine (pure α-adrenergic
pressor agents.)
§ Temporary leukopenia (WBC 3500) not
serious
§ Agranulocytosis –life threatening
§ Thrombocytopenic or
nonthombocytopenic purpura, hemlytic
HEMATOLOGIC
anemia, and pancytopenia rare
EFFECTS
§ If with sore throat and fever, do CBC
immediately
§ If blood index values low,d/c meds,
hospitalization
§ Mortality rate as high as 30%
Common with low potency DRAs.
• Constipation – treated with usual
laxatives; severe constipation may
lead to paralytic ileus; decrease
PERIPHERAL
dosage, Pilocarpine may be used
ANTICHOLINERGIC
but relief is only transitory.
EFFECTS
• Urinary retention- Betanechol
(Urecholine) 20-40 mg/day
• Weight gain –low potency DRA;
Molindone and Loxapine less likely
§ Breast enlargement, galactorrhea,
ENDOCRINE amenorrhea, inhibited orgasm in women
EFFECTS and sexual dysfunction in men,
§ Anorgasmia and decreased libido
§ 50% male = ejaculatory and erectile
disturbances
SEXUAL ADVERSE
§ TREATMENT: Sildenafil, Verdenafil and
EFFECTS
Tadalafil
§ Thioridazine – retrograde ejaculation,
decreased libido; priapism
§ Allergic dermatitis and photosensitivity
esp. with low potency DRA
§ Long term us of Chlorpromazine cause a
blue gray discoloration in sun- exposed
areas.
SKIN AND EYE
§ Irreversible retinal pigmentation –high
EFFECTS
dose Thioridazine (>1000mg)
§ early symptom may be difficulty with night
vision; result in blindness
§ Benign pigmentation of the eyes –
Chlorpromazine; resolves when d/c
§ Elevations of liver enzymes; rare; if
JAUNDICE
present should d/c Chlorpromazine
§ Typically consists of exaggerated DRA
side effects:
§ CNS depression, mydriasis, EPS, rigidity,
restlessness, ↓DTR, ↑HR, ↓BP
§ Delirum, coma, respiratory depression,
seizures
§ Haloperidol among the safest typical
antipsychotic in overdose
OVERDOSE § After overdose, EEG show diffuse slowing
and low voltage
§ TREATMENT: activated charcoal and
gastric lavage if OD is recent
§ Emetics not indicated because of
antiemetic actions of DRA
§ Seizure treated with IV Diazepam or
Phenytoin
§ hypotension treated with NE or dopamine
§ Low correlation between antipsychotic
use in pregnancy and congenital
PREGNANCY AND
malformation; still it should be avoided
LACTATION
esp in first trimester
§ Secreted in breastmilk
§ Chlorpromazine and Perphenazine: false
+/- pregnancy test; falsely elevated
LABORATORY bilirubin (reagent test strips) and
INTERFERENCES urobilinogen (Ehrlich’s reagent test)
§ False (+) results in tests for
phenylketonuria
Drug Interactions
§ CYP2D6 is the most common hepatic isoenzyme involved
§ Antacids, activated charcoal, cholestyramine, kaolin
pectin and Cimetidine = ↓ absorption when taken within 2
hours of DRA administration
§ Anticholinergics decrease absorption of DRA
§ DRA + anticholinergics + TCACs = anticholinergic toxicity
§ Digoxin and steroids increase DRA absorption
§ Phenothiazines (esp. Thioridazine) – decrease metabolism
and cause toxic concentrations of Phenytoin
§ Barbiturates increase metabolism of DRA.
§ Paroxetine, Fluoxetine and Fluvoxamine and TCACs –
increased plasma concentration of both drugs; additive
anticholinergic, sedative and hypotensive effects.
§ DRA inhibit hypotensive effects of α−methyldopa; additive
effects on some hypotensives.
§ Propanolol coadministration increases blood concentrations
of both drugs
§ DRAs potentiate the CNS depressant effects of sedatives,
antihistamines, opiates and alcohol particularly in persons
with impaired respiratory status. When taken with alcohol, risk
of heat stroke increased.
§ Cigarette smoking decrease plasma levels of DRA
§ Epinephrine has paradoxical hypotensive effects
§ DRA decrease concentration of Warfarin resulting in
decreased bleeding time
§ Phenotiazines and Pimozide should not be coadm with drugs
that prolong QT interval
§ Thioridazine is C/I in patients taking drugs that inhibit CYP2D6
isoenzyme or with decreased level of the enzyme
Contraindications
§ History of serious allergic response
§ Possible ingestion of a substance that will interact with the
antipsychotic to induce CNS depression ( alcohol, opioids,
barbiturates and benzodiazepines) or anticholinergic delirium
(scopolamine,, PCP)
§ Presence of severe cardiac abnormality
§ High risk for seizures
§ Presence of narrow-angle glaucoma or prostatic hypertrophy
if a drug with high anticholinergic activity is to be used
§ Presence or a history of tardive dyskinesia
Cautions
§ With hepatic disease
§ CBC, liver function test, ECG, esp is women >40 and in men
>30
§ Elderly persons and children are more sensitive to side effects
§ Begin at low dosage and increase as necessary
§ Maximal effects of a particular dosage may not be evident for
4 to weeks.
Page 3 of 6
Short-Term Treatment RISPERIDONE (Risperdal)
§ HALOPERIDOL
o 5 – 20 mg adult § Schizophrenia in adults and adolescents
o 1 mg elderly (acute and maintenance)
§ CHLORPROMAZINE § Short term treatment of acute manic or
o doses for IM administration are about half those mixed episode in adult and children 10-17
given orally INDICATIONS y/o
o More than 2 mg in one injection may result in § Irritability in Autistic Spectrum Disorder
serious hypotension (children 5-16 y/o) inc.aggression, self-
§ Observe for 1 hour after first dose of medication injurious behavior,, temper tantrums and
§ Possible sedatives: Lorazepam and amobarbital mood swings.
§ Rapid neuroleptization (Psychotolysis) - hourly IM doses until § Benzisoxazole; extensive first pass hepatic
marked sedation is achieved. metabolism; 9-OH-risperidone (metabolite)
§ Peak plasma level: 1 hour for parent
Early Treatment compound; 3 hours for metabolite;
§ Full 6 weeks may be necessary to evaluate the extent of 70%bioactivity
improvement PHARMACOLOGY § Half life: 20 hours combined; EPS dose
§ Agitation and excitement usually improve quickly dependent. >6mg/day
§ Psychotic symptoms continue to improve 3 to 12 months § Blocks 5-HT 2A, D2, α-1 and α−2
after the initiation of treatment adrenergic, H 1 receptor
§ Haloperidol 5 mg or Chlorpromazine 300 mg is usual § Low affinity for α−adrenergic and
effective daily dose muscarinic receptors; strong affinity for D2
§ Bedtime dosing help induce sleep and reduce incidence of § Initial: 1-2 mg HS, can be increased to 4
adverse effect, however for elderly may increase risk of falling DOSAGES mg/day; for child/adol= lower starting dose
if they get out ofbed during the night
§ Sedative effects last only for a few hours; antipsychotic effects § .25mg, .5mg, 1,2,3and 4 mg tablets; .5mg,
1 to 3 days OTHER 1 and 2 oral disintegrating tablets, 1 mg/ml
FORMULATIONS oral solution; depot (Risperdal Consta)
25mg IM
SECOND GENERATION ANTIPSYCHOTICS § EPS (dose dependent), weight gain,
anxiety, nausea and vomiting, rhinitis,
§ Serotonin-Dopamine Antagonists SIDE EFFECTS erectile dysfunction, increased
§ Atypical antipsychotics; novel antipsychotics pigmentation, dizziness, hyperkinesias,
§ Lower risk of EPS; action is broader than DRA somnolence
§ Substantial weight gain , increased potential for DM § Paroxetine and Fluoxetine block formation
§ Clozapine not considered a first line treatment DRUG of active metabolite; combined with SSRI
§ Should consider ff. factors: INTERACTIONS may result in elevated PRL with asso.
o Personal and family history of obesity, DM, Galactorrhea and gynecomastia
dyslipidemia, hypertension andCVD
o Weight and height (BMI calculated)
o BP
PALIPERIDONE (Invega)
o FBS
o Lipid profile § Acute and maintenance treatment of
Schizophrenia
SEROTONERGIC CONTROL OF DOPAMINE RELEASE: § Acute treatment of schizoaffective disorder
INDICATIONS
as monotherapy;
MESOLIMBIC MESOCORTICAL § As adjunct to mood stabilizers and
§ antagonism by serotonin of the § Serotonin 2A antagonism antidepressants
effects of dopamine in this not only reverses § Benzisoxazole derivative;; major active
pathway is not robust enough to dopamine 2 antagonism metabolite of risperidone.
cause the reversal of D2 but causes a net increase § Peak plasma level approx. 24 hours after
receptors by atypical in dopamine activity dosing; steady state conc. w/in 4- days; no
PHARMACOLOGY
antipsychotics or to mitigate the § favorable for ameliorating dose adjustment required for patients with
actions of atypical negative symptoms mild or moderate hepatic impairment
antipsychotics on positive § Dose should be reduced in patients with
symptoms of psychosis. renal impairment
NIGROSTRIATAL TUBEROINFUNDIBULAR § 6mg OD in AM; no more than 12 mg/day;
§ Serotonin 2A inhibits dopamine § antagonistic and long acting depot:
DOSAGES
release, both at the level of reciprocal relationship § 39 mg(25 mg), 78mg(50mg), 117 mg
dopamine cell bodies and at the between serotonin and (75mg), 156mg (100 mg), 234 mg (150mg)
level of dopaminergic axon dopamine in the control of § 3, 6 and 9mg tab; (Invega Sustenna)
OTHER paliperidone palmitate (t1/2 25-49 days)
terminals. prolactin, dopamine
FORMULATIONS
§ It acts as a brake on dopamine inhibits prolactin release,
release serotonin promotes § More sensitivity to extremes of temperature;
§ Blocking serotonin A2 promotes prolactin release increase QTc interval; orthostatic
dopamine release SIDE EFFECTS
hypotension, tachycardia, somnolence,
§ Reduction or absent EPS or akathisia, dystonia, EPS and parkinsonism
tardive dyskinesia

Page 4 of 6
 OLANZAPINE (Zyprexa)
§ Schizophrenia; monotherapy for manic or
mixed episodes; maintenance treatment
of Bipolar 1; may be used as adjunct to
mood stabilizers; may be used in
INDICATIONS
combination with Fluoxetine (Symbyax)
for depressive episodes in Bipolar 1;
Symbyax is also used in treatment-
resistant depression.
§ 85% absorbed in GIT; 40 inactivated by
first pass hepatic metabolism
§ Peak concentrations in 5 hours; t1/2= 31
PHARMACOLOGY
hours ave. (21-54 hours); OD dosing
§ Blocks 5-HT2A, D2, D1, D4, α1, 5-HT1A,
M1-M5, H1
§ Initial dosage: for psychosis -5-10 mg; for
acute mania-10-15mg
DOSAGES § After one week, dosage can be increased
to 10 mg/day; higher doses associated
with EPS
§ 2.5, 5, 7.5, 10, 15, 20 mg tab; 5, 10, 15,
20mg orally disintegrating tab (Zydis);
Imlong-acting injection (Relprevv);
parenteral form 10mg IM
OTHER
§ RELPEVV: deep gluteal injection; (-)IV SC
FORMULATIONS
or deltoid
§ Post-injection delirium sedation syndrome
(PDSS) black box warning: secondary to
accidental rupture of a blood vessel
§ More freq weight gain, somnolence, dry
mouth, dizziness, constipation, dyspepsia,
SIDE EFFECTS
↑appetite, akathisia, tremor; transaminase
elevation
§ Fluvoxamine and Cimetidine ↑ serum
DRUG conc.; Carbamazepine and phenytoin ↓
INTERACTIONS § Ethanol increases absorption by 25%,
leading to inc. sedation
QUETIAPINE (Seroquel)
§ Schizophrenia; monotherapy for manic or
mixed episodes; maintenance treatment of
Bipolar 1; may be used as adjunct to mood
INDICATIONS
stabilizers; monotherapy for acute
treatment of depressive episodes in Bipolar
1 § Initial dose: 10-15mg/day; Effective range:
§ Dibenzothiazepine; rapidly absorbed from
GIT; peak plasma conc 1-2 hours; t1/2:7 hrs
PHARMACOLOGY § BID to TID dosing; Blocks 5-HT2A, D2, D1,,
α1 , α2, 5-HT6,, H1; (x) M or BDZ receptors;
not associated with EPS.
§ Initial dosage: 25 mg BID, inc by 25-50mg
DOSAGES every 2 to 3 days up to 300-400 mg/day
§ 25-300 mg/day has been used for sedation
OTHER § 25, 50, 100, 200, 300, 400 mg tab; QR given
FORMULATIONS OD comparable to tab BID/TID
§ Somnolence, postural hypotension,
dizziness most common; least likely to
SIDE EFFECTS cause EPS; rare ↑PRL, weight gain, small
incin heart rate, constipation, transient ↑liver
transaminases
§ Phenytoin inc quetiapine clearance fivefold;
avoid use with drug that inc the QT interval:
DRUG Class 1A antiarrythmics (quinidine,
INTERACTIONS procainamide), Class III antiarrythmics
(amniodarone, sotalol), antipsychotics,
antibiotics (gatifloxacin, moxifloxacin.)
ZIPRASIDONE (Geodon)
§ Schizophrenia; monotherapy for acute
treatment of manic or mixed episodes;
INDICATIONS
maintenance treatment of Bipolar 1; may be
used as adjunct to mood stabilizers;
§ Benzisothiazole piperazine; should be
taken with food as it doubles bioavailability;
peak plasma conc 2-6 hours; t1/2: 5-10 hrs;
BID dosing; IM prep has peak serum conc
after approx. 1 hour with t1/2 of 2-5 hours
PHARMACOLOGY
§ Blocks 5-HT2A, D2, D3, D4, α1, 5-HT1d, 5-
HT2c ,H1;
§ Agonistic activity at 5-HT1A, also an SSRI
and a norepinephrine reuptake inhibitor
§ Antidepressant-like effect
§ Initial dose: 40 mg/day divided into BID
dosing; efficacy range 80-160mg/day
divided BID.
DOSAGES
§ IM dosage: 10-20mg every 2 hours for
20mg dose; and every 4 hours for 40
mgdose; max daily dose is 40 mg
OTHER § 20, 40, 60, and 80 mg caps; IM 20 mg/ml
FORMULATIONS vial
§ Somnolence, headaches, dizziness,
nausea, and lightheadedness most
SIDE EFFECTS common
§ No significant effects outside CNS; almost
no weight gain; (-)PRL elevation
§ Interactions w/drugs that prolong QT
DRUG complex (low potency DRA, antiarrythmics,
INTERACTIONS etc)
ARIPIPRAZOLE (Abilify)
§ Schizophrenia; acute and maintenance
treatment of manic and mixed episodes;
INDICATIONS adjunctive therapy to lithium or valproate;
adjunct to antidepressants; irritability asso.
with Autistic disorder.
§ Well absorbed; peak plasma conc 3-5
hours; t1/2: 75 hrs99% protein bound
§ Postsynaptic D2 receptors and presynaptic
PHARMACOLOGY
autoreceptors as modulator; absence of D2
blockade in striatal areas; Blocks 5-HT2A,
α1
DOSAGES
10-30mgday;
OTHER § 5, 10, 15, 20, and 30 mg tabs;
FORMULATIONS
§ Headaches, somnolence, agitation,
dyspepsia, anxiety, nausea most common
SIDE EFFECTS § Can cause akathisia-like activation,
insomnia; no significant QT interval
changes
§ Carbamazepine and valproate ↓ serum
conc; Ketoconazole, Fluoxetine, paroxetine
DRUG and quinidine ↑serum conc.; use with
INTERACTIONS antihypertensives may cause hypotension
§ Drugs that inhibit CYP2D6 activity reduce
elimination of aripiprazole
Page 5 of 6
 CLOZAPINE (Clozaril)
INDICATIONS § Patients with severe tardive dyskinesia;
those who failed standard treatment;
treatment-resistant mania, severe psychotic
depression, psychosis in idiopathic
Parkinsons dse.,Huntington’s dse and
suicidal patients w/ schizophrenia and
schizoaffective disorders; Pervasive dev
disorder, autism and OCD
§ C/I: WBC <3500; prev. bone marrow d/o; hx
of agranulocytosis w/clozapine; use of
another drug that suppress bone marrow
PHARMACOLOGY § Dibenzothiazepine; rapidly absorbed; peak
plasma level 2 hours; steady state in less
than a week in BID dosing. Blocks: 5-HT2A,
D1, D3, D4 and α1 receptors; bind loosely to
D2 receptors : “fast dissociation”
DOSAGES § 25 and 100 mg tabs; Initial: 25mg OD/BID,
increased gradually (25mg/day every 2 or 3
days) to 300 mg/day in divided doses
SIDE EFFECTS § Sedation, dizziness, syncope, ↑HR, ↓BP,
ECG changes, nausea, vomiting common
§ Fatigue, weight gain, anticholinergic effects,
muscle weakness; sialorrhea (impairment of
swallowing) ; risk of seizure 4% in doses
>600/day; leukopenia, granulocytopenia,
agranulocytosis , fever occur in 1%;
cardiomyopathy/myocarditis
DRUG § (x) With drug asso. with agranulocytosis or
INTERACTIONS bone marrow suppression (Carbamazepine,
phenytoin, PTU, sulfonamides and captopril);
(x)with Lithium in persons with ; hx of NMS;
Clomipramine can inc risk of seizure by inc
plasma conc and lowering seizure threshold;
Risperidone, fluoxetine, paroxetine and
fluvoxamine ↑serum conc.; Paroxetine may
ppt. clozapine-associated neutropenia

Page 6 of 6