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REVIEW SERIES
Short Subjects
Psychiatry
For PG Medical Entrance
–Especially made for
NIMHANS—
CONTENTS
Chapter - 01: GENERAL PSYCHIATRY
Chapter - 02: PSYCHOLOGY
Chapter - 03: SCHIZOPHRENIA AND
OTHER PSYCHOTIC DISORDERS
Chapter - 04: MOOD DISORDERS
Chapter - 05: NEUROTIC DISORDERS
Chapter - 06: ORGANIC MENTAL
DISORDERS
Chapter - 07: SUBSTANCE USE
DISORDERS
Chapter - 08: MISCELLANEOUS
QUESTIONS BANK
Important Topics
1. Classification in Psychiatry
2. Epidemiology of psychiatric
disorders
3. Examination in psychiatry
4. Basic Terminologies
CLASSIFICATION IN PSYCHIATRY
ICD-10 DSM IV
(International (Diagnostic
Classification and statistica
of Diseases) manual)
Disorders Mental
All
covered disorders
Limited to few
Acceptability Universal
nations
APA
(American
Published by WHO
Psychological
Association)
Multi-axial
approach
AXIS I: Clinica
Psychiatric
Diagnosis
AXIS II:
Personality
Disorders and
Mental
Retardation
AXIS III:
Commonly Single axis General
used as diagnosis Medical
Conditions
AXIS IV:
Psychosocial
and
Environmenta
Problems
AXIS V: Globa
Assessment o
Functioning:
Current and in
past one year
Points to remember:
1) DSM 5 is latest DSM, which does
not recommend multi-axial
approach to diagnosis
2) In India, both ICD and as well as
DSM are followed in routine
practice.
3) There is no GAF score (Axis 5) in
DSM 5.
Psych
syndro
Normal to resu
Age
No. Stage Development from f
Range
(gratification) (and
regres
to this
1. Dep
person
traits a
Major site of disord
gratification is 2.
the oral Schizo
region. 3. Seve
1. Oral 0-1.5y
i. Oral erotic mood
phase (sucking) disord
ii. Oral sadistic 4. Alco
phase (biting) depen
syndro
and dr
depen
Major site of
gratification is
the anal area;
1. Obs
It consists of 2
compu
phases:
person
i. Anal erotic
traits a
2. Anal 1.5-3y phase
disord
(excretion)
2. OCD
ii. Anal sadistic
sadisti
phase
phase)
(’holding’ and
’letting go’ at
will)
Major site of
gratification is
the genital
area;
According to
Freud, this
development is
different
in both sexes.
Male
development
The boy
develops
castration
anxiety (fear
of castration
at the hand of
his father in
retaliation
for the boy’s
desire to
replace his
father in his
mother’s
affections).
This leads to
formation of
the Oedipus
complex
(aggressive
impulses
directed
towards the
father; named
after the Greek
tragedy
Oedipus rex in
which Oedipus
unknowingly 1. Sexu
kills his father deviat
3. Phallic 3-5y and marries his 2. Sexu
mother, dysfun
unaware of 3. Hys
their true
identities).
Oedipus
complex is
usually
resolves by
identification
with father,
attempting to
adopt his
characteristics.
Female
development
The girl
develops penis
envy
(discontent
with female
genitalia
following a
fantasy that
they result
from loss of
penis). This is
theorised by
Freud to
lead to a wish
to ’receive’ the
penis and to
bear a child.
Resolution
occurs by
identification
with the
mother. This
phase has
been called as
Electra
complex.
Oedipus (and
Electra)
complex is
usually
resolved at the
beginning of
this stage. This
is a
stage of
relative sexual
quiescence.
Super-ego is
Neuro
4. Latency 5-12y formed at this
disord
stage. Sexual
drive is
channelized
into socially
appropriate
goals such as
development
of
interpersonal
relationships,
sports, school,
work, etc.
Adult sexuality
develops.
Neuro
5. Genital >12y True self-
disord
identity
develops.
CONTRIBUTIONS OF FREUD:
1. Father of classical psychoanalysis
2. Gave models of mind
3. Dream analysis (He said “dream is
a royal road to unconsciousness”)
4. Coined the terms transference,
countertransference, neurosis
5. Gave concept of hysteria
6. First description of defence
mechanisms (Later the classification
of defence mechanisms was given by
George Valliant)
Narcssistic defenses:
1) Denial involves blocking external
events from awareness. If some
situation is just too much to handle,
the person just refuses to
experience it.
2) Projection, involves the tendency
to see your own unacceptable
desires in other people
Immature defense:
1) Regression is a movement back in
psychological time when one is faced
with stress. When we are troubled
or frightened, our behaviors often
become more childish or primitive
2) Introjection, sometimes called
identification, involves taking into
your own personality characteristics
of someone else, because doing so
solves some emotional difficulty.
3) Acting Out: Conflicts are
translated into action with little or
no intervening reflection. The
unconscious fantasy is lived out
impulsively in behavior, thereby
gratifying the impulse, rather than
the prohibition against it.
Neurotic defenses:
1) Repression, is just that: not being
able to recall a threatening
situation, person, or event. Most
basic defence mechanism and is
mother of all other defence
mechanisms.
2) Reaction formation, is changing
an unacceptable impulse into its
opposite.
3) Displacement is the redirection of
an impulse onto a substitute target.
If the impulse, the desire, is okay
with you, but the person you direct
that desire towards is too
threatening, you can displace to
someone or something that can
serve as a symbolic substitute.
4) Rationalization is the cognitive
distortion of "the facts" to make an
event or an impulse less
threatening. We do it often enough
on a fairly conscious level when we
provide ourselves with excuses. But
for many people, with sensitive
egos, making excuses comes so easy
that they never are truly aware of it.
In other words, many of us are quite
prepared to believe our lies.
5) Undoing involves "magical"
gestures or rituals that are meant to
cancel out unpleasant thoughts or
feelings after they've already
occurred.
Mature defenses:
1) Asceticism, or the renunciation of
social needs; Eliminating the
pleasurable effects of experience.
2) Altruistic surrender is a form of
projection that at first glance looks
like its opposite: Here, the person
attempts to fulfill his or her own
needs vicariously, through other
people.
3) Sublimation is the transforming of
an unacceptable impulse, whether it
be sex, anger, fear, or whatever, into
a socially acceptable, even
productive form.
4) Anticipation: Realistically
anticipating or planning for future
inner discomfort
5) Humour: Emphasizing the
amusing or ironic aspects of the
conflict or stressors.
6) Suppression: The conscious
process of pushing unacceptable
thoughts into the preconscious.
Discomfort is acknowledged but
minimized.
TOPIC 6 : LEARNING THEORIES
There are three types of learning:
(1) In classic conditioning, learning is
thought to take place as a result of
the contiguity of environmental
events; when events occur closely
together in time, persons will
probably come to associate the two.
Classic (also called respondent)
conditioning results from the
repeated pairing of a neutral
(conditioned) stimulus with one that
evokes a response (unconditioned
stimulus), such that the neutral
stimulus eventually comes to evoke
the response. (CLASSICAL PAVLOV
EXPERIMENT)
(2) In operant conditioning, learning
is thought to result from the
consequences of a person's actions.
It is a form of learning in which
behavioural frequency is altered
through the application of positive
and negative consequences
(3) Social learning theory
incorporates both classic and
operant models of learning, but also
considers a reciprocal interaction
between the person and the
environment.
Prevalence of Schizophrenia in
Specific Populations
Prevalence
Population
{%)
General population 1
Non-twin sibling of a
8
schizophrenia patient
Child with one parent with
12
schizophrenia
Dizygotic twin of a
12
schizophrenia patient
Child of two parents with
40
schizophrenia
Monozygotic twin of a
47
schizophrenia patient
Neurotransmitters in schizophrenia:
1) Dopamine Hypothesis:
Schizophrenia results from too much
dopaminergic activity.
2) Serotonin: Current hypotheses
posit serotonin excess as a cause of
both positive and negative
symptoms in schizophrenia.
3) Norepinephrine: A selective
neuronal degeneration within the
norepinephrine reward neural
system could account for anhedonia
in schizophrenia.
4) GABA: patients with
schizophrenia have a loss of
GABAergic neurons in the
hippocampus.
5) Neuropeptide: substance P and
neurotensin
6) Glutamate: Glutamate has been
implicated because ingestion of
phencyclidine, a glutamate
antagonist, produces an acute
syndrome similar to schizophrenia.
7) Acetylcholine and Nicotine:
Postmortem studies in schizophrenia
have demonstrated decreased
muscarinic and nicotinic receptors
DIAGNOSTIC CRITERIA OF
SCHIZOPHRENIA (DSM- IV TR)
A. Characteristic symptoms: Two (or
more) of the following, each present
for a significant portion of time
during a 1-month period (or less if
successfully treated):
1. delusions
2. hallucinations
3. disorganized speech (e.g.,
frequent derailment or incoherence)
4. grossly disorganized or catatonic
behavior
5. negative symptoms, i.e., affective
flattening, alogia, or avolition
Note: Only one Criterion A symptom
is required if delusions are bizarre or
hallucinations consist of a voice
keeping up a running commentary
on the person's behavior or
thoughts, or two or more voices
conversing with each other.
B. Social/occupational dysfunction:
For a significant portion of the time
since the onset of the disturbance,
one or more major areas of
functioning such as work,
interpersonal relations, or self-care
are markedly below the level
achieved prior to the onset (or when
the onset is in childhood or
adolescence, failure to achieve
expected level of interpersonal,
academic, or occupational
achievement).
C. Duration: Continuous signs of the
disturbance persist for at least 6
months. This 6-month period must
include at least 1 month of
symptoms (or less if successfully
treated) that meet Criterion A (i.e.,
active-phase symptoms) and may
include periods of prodromal or
residual symptoms. During these
prodromal or residual periods, the
signs of the disturbance may be
manifested by only negative
symptoms or two or more symptoms
listed in Criterion A present in an
attenuated form (e.g., odd beliefs,
unusual perceptual experiences).
D. Schizoaffective and mood disorder
exclusion: Schizoaffective disorder
and mood disorder with psychotic
features have been ruled out
because either (1) no major
depressive, manic, or mixed
episodes have occurred concurrently
with the active-phase symptoms; or
(2) if mood episodes have occurred
during active-phase symptoms, their
total duration has been brief
relative to the duration of the active
and residual periods.
E. Substance/general medical
condition exclusion: The disturbance
is not due to the direct physiological
effects of a substance (e.g., a drug of
abuse, a medication) or a general
medical condition.
F. Relationship to a pervasive
developmental disorder: If there is a
history of autistic disorder or
another pervasive developmental
disorder, the additional diagnosis of
schizophrenia is made only if
prominent delusions or
hallucinations are also present for at
least a month (or less if successfully
treated).
NOTE :
1) IN DSM 5, THERE ARE NO
SUBTYPES OF SCHIZOPHRENIA
2) DSM-5 raises the symptom
threshold, requiring that an
individual exhibit at least two of the
specified symptoms. (In DSM-IV, that
threshold was one.)
3) ICD-10 CRITERIA SPECIFIES
MINIMUM SURATION TO DIAGNOSE
SCHIZOPHRENIA AS 1 MONTH
SUBTYPES OF SCHIZOPHRENIA
Single, divorced,
Married
or widowed
Family history of Family history of
mood disorders schizophrenia
Good support Poor support
systems systems
Negative
symptoms
Neurological signs
and symptoms
Positive symptoms History of
perinatal trauma
No remissions in 3
years
Many relapses
Treatment Of Schizophrenia:
Antipsychotics (1st generation and
2nd generation)
ACUTE DYSTONIA:
• Slow, sustained painful muscular
contraction one group of muscle.
• Spasm of muscles of trunk, head
and neck.
• Risk Factor--- young male, high
potency dopamine receptor
antagonist.
• Treatment: Anti – Parkinsonism
drugs.
PARKINSONISM
• Symptoms like rigidity,
bradykinesia, shuffling gait and
tremor,
• Treatment: Anti – Parkinsonism
drugs.
NEUROLEPTIC MALIGNANT
SYNDROME –
• Life threatening
• Main features,
Hyperthermia
Muscular rigidity
Autonomic instability including
hyperthermia, tachycardia, increased
blood pressure,’ tachypnea and
dipahoresis,
Changing leves of sensorium;
• Often CPK Creatinine
phosphokinase increased
• Treatment:
1. Dantrolene iv.
2. orally Bromocriptine and
Amantadine
TARDIVE DYSKINESIA
• Delayed painless peri-oral
movements
• Movement disorders that may
occur following long – term
treatment with anti – psychotic
medication. Mainly mouth and
tongue movements. Rabbit
Syndrome
• Risk Factors : Increasing age,
mainly elderly female; Mood
disorder patients, Dosage and
duration of medication.
• Perioral tremor is uncommon S/E
which is called as rabbit syndrome
• Treatment- Clozapine may be
started. It carries minimal risk of TD.
DELUSIONAL DISORDERS
Delusion A false belief based on
incorrect inference about external
reality that is firmly sustained
despite what almost everyone else
believes and despite what
constitutes incontrovertible and
obvious proof of evidence to the
contrary. The belief is not one
ordinarily accepted by other
members of the person's culture or
subculture (e.g., it is not an article of
religious faith).
TYPES :
• Erotomanic type: delusions that
another person, usually of higher
status, is in love with the individual.
• Grandiose type: delusions of
inflated worth, power, knowledge,
identity, or special relationship to a
deity or famous person
• Jealous type: delusions that the
individual's sexual partner is
unfaithful
Persecutory type: delusions that the
person (or someone to whom the
person is close) is being
malevolently treated in some way
• Somatic type: delusions that the
person has some physical defect or
general medical condition
Schizoaffective disorder :
Schizoaffective disorder has features
of both schizophrenia and affective
disorders (now called mood
disorders).
Neurotransmitters in mood
disorders:
Of the biogenic amines,
norepinephrine and serotonin are
the two neurotransmitters most
implicated in the pathophysiology of
mood disorders.
1) Norepinephrine: Clinical
antidepressant responses is
probably the single most compelling
piece of data indicating a direct role
for the noradrenergic system in
depression.
2) Serotonin: Depletion of serotonin
may precipitate depression, and
some patients with suicidal impulses
have low cerebrospinal fluid (CSF)
concentrations of serotonin
metabolites and low concentrations
of serotonin uptake sites on
platelets.
3) Dopamine: The data suggest that
dopamine activity may be reduced in
depression and increased in mania.
4) Other Neurotransmitter
Disturbances: Cholinergic agonist
and antagonist drugs have
differential clinical effects on
depression and mania. Agonists can
produce lethargy, anergia, and
psychomotor retardation in healthy
subjects, can exacerbate symptoms
in depression, and can reduce
symptoms in mania.
5) Reductions of GABA have been
observed in plasma, CSF, and brain
GABA levels in depression.
DEPRESSIVE EPISODE
DSM-IV-TR Criteria for Major
Depressive Episode
A. Five (or more) of the following
symptoms have been present during
the same 2-week period and
represent a change from previous
functioning; at least one of the
symptoms is either (1) depressed
mood or (2) loss of interest or
pleasure.
Note: Do not include symptoms that
are clearly due to a general medical
condition, or mood-incongruent
delusions or hallucinations.
1. depressed mood most of the day,
nearly every day, as indicated by
either subjective report (e.g., feels
sad or empty) or observation made
by others (e.g., appears tearful).
Note: In children and adolescents,
can be irritable mood
2. markedly diminished interest or
pleasure in all, or almost all,
activities most of the day, nearly
every day (as indicated by either
subjective account or observation
made by others)
3. significant weight loss when not
dieting or weight gain (e.g., a change
of more than 5% of body weight in a
month), or decrease or increase in
appetite nearly every day. Note: In
children, consider failure to make
expected weight gains.
4. insomnia or hypersomnia nearly
every day
5. psychomotor agitation or
retardation nearly every day
(observable by others, not merely
subjective feelings of restlessness or
being slowed down)
6. fatigue or loss of energy nearly
every day
7. feelings of worthlessness or
excessive or inappropriate guilt
(which may be delusional) nearly
every day (not merely self-reproach
or guilt about being sick)
8. diminished ability to think or
concentrate, or indecisiveness,
nearly every day (either by
subjective account or as observed by
others)
9. recurrent thoughts of death (not
just fear of dying), recurrent suicidal
ideation without a specific plan, or a
suicide attempt or a specific plan for
committing suicide
B. The symptoms do not meet
criteria for a mixed episode.
C. The symptoms cause clinically
significant distress or impairment in
social, occupational, or other
important areas of functioning.
D. The symptoms are not due to the
direct physiological effects of a
substance (e.g., a drug of abuse, a
medication) or a general medical
condition (e.g., hypothyroidism).
E. The symptoms are not better
accounted for by bereavement, i.e.,
after the loss of a loved one, the
symptoms persist for longer than 2
months or are characterized by
marked functional impairment,
morbid preoccupation with
worthlessness, suicidal ideation,
psychotic symptoms, or
psychomotor retardation.
Cognitive Distortions
Drawing a specific
Arbitrary inference conclusion without
sufficient evidence
Focus on a single
detail while ignoring
Specific
other, more
abstraction
important aspects of
an experience
Forming conclusions
based on too little
Overgeneralization
and too narrow
experience
Over- or
Magnification and undervaluing the
minimization significance of a
particular event
Tendency to self-
Personalization reference external
events without basis
ATYPICAL FEATURES
Patients with atypical features have
specific, predictable characteristics:
overeating and oversleeping. These
symptoms have sometimes been
referred to as reversed vegetative
symptoms, and the symptom
pattern has sometimes been called
hysteroid dysphoria.
The patients with atypical features
are found to have a younger age of
onset, more severe psychomotor
slowing, and more frequent
coexisting diagnoses of panic
disorder, substance abuse or
dependence, and somatization
disorder. The high incidence and
severity of anxiety symptoms in
patients with atypical features have
sometimes been correlated with the
likelihood of their being
misclassified as having an anxiety
disorder rather than a mood
disorder. Patients with atypical
features may also have a long-term
course, a diagnosis of bipolar I
disorder, or a seasonal pattern to
their disorder.
MANIC EPISODE
DSM-IV-TR Criteria for Manic
Episode
A. A distinct period of abnormally
and persistently elevated, expansive,
or irritable mood, lasting at least 1
week (or any duration if
hospitalization is necessary).
B. During the period of mood
disturbance, three (or more) of the
following symptoms have persisted
(four if the mood is only irritable)
and have been present to a
significant degree:
1. inflated self-esteem or grandiosity
2. decreased need for sleep (e.g.,
feels rested after only 3 hours of
sleep)
3. more talkative than usual or
pressure to keep talking
4. flight of ideas or subjective
experience that thoughts are racing
5. distractibility (i.e., attention too
easily drawn to unimportant or
irrelevant external stimuli)
6. increase in goal-directed activity
(either socially, at work or school, or
sexually) or psychomotor agitation
7. excessive involvement in
pleasurable activities that have a
high potential for painful
consequences (e.g., engaging in
unrestrained buying sprees, sexual
indiscretions, or foolish business
investments)
C. The symptoms do not meet
criteria for a mixed episode.
D. The mood disturbance is
sufficiently severe to cause marked
impairment in occupational
functioning or in usual social
activities or relationships with
others, or to necessitate
hospitalization to prevent harm to
self or others, or there are psychotic
features.
E. The symptoms are not due to the
direct physiological effects of a
substance (e.g., a drug of abuse, a
medication, or other treatment) or a
general medical condition (e.g.,
hyperthyroidism).
Note: Manic-like episodes that are
clearly caused by somatic
antidepressant treatment (e.g.,
medication, electroconvulsive
therapy, light therapy) should not
count toward a diagnosis of bipolar I
disorder.
Features of
Features of mania
hypomania
Present for at least Present for at least
4 days 7 days
Core features mild Core features
or moderate marked
Mild or moderate Substantial
dysfunction dysfunction
Partial insight Minimal or absent
preserved insight
Psychotic
No psychotic
symptoms may
features
occur
DEPRESSION:
The range of initial treatment
modalities includes psychotherapy,
pharmacotherapy, or a combination
of the two.
OTHER THERAPIES
• Vagal Nerve Stimulation
The use of left vagal nerve
stimulation (VNS) using an electronic
device implanted in the skin, similar
to a cardiac pacemaker. Preliminary
studies have shown that a number
of patients with chronic, recurrent
major depressive disorder went into
remission when treated with VNS.
• Sleep Deprivation
Mood disorders are characterized by
sleep disturbance. Mania tends to
be characterized by a decreased
need for sleep, whereas depression
can be associated with either
hypersomnia or insomnia. Sleep
deprivation may precipitate mania
in patients who are bipolar I and
temporarily relieve depression in
those who are unipolar.
Approximately 60 percent of
depressive disorder patients exhibit
significant but transient benefit from
total sleep deprivation
• Phototherapy (light therapy)
Used as treatment for SAD (mood
disorder with seasonal pattern).
Phototherapy typically involves
exposing the afflicted patient to
bright light in the range of 1,500 to
10,000 lux or more, typically with a
light box that sits on a table or desk.
Patients sit in front of the box for
approximately 1 to 2 hours before
dawn each day, although some
patients may also benefit from
exposure after dusk.
Somatoform disorders
Hypochondriasis
Body Dysmorphophobia
Somatization disorder
Somatoform Pain disorder
Conversion disorder
Other somatoform disorders
Points to remember:
1) There are certain common
symptoms of anxiety seen in many
of these neurotic disorders.
2) Neurotransmitters
The three major neurotransmitters
associated with anxiety on the bases
of animal studies and responses to
drug treatment are norepinephrine
(NE), serotonin, and GABA.
(From Kaplan Textbook, important
chart to remember basic clinical
manifestations of some important
neurotic disorders) : will help in
clinical questions
TREATMENT PHOBIAS:
Behavior therapy:- Systemic de-
sensitization ( treatment of choice) ;
Flooding also used
Pharmacological: - SSRIs,
benzodiazepines (alprazolam &
clonazepam) and buspirone
TREATMENT OCD:
Behavior Therapy :
• Exposure and response prevention
• Thought stopping
• Modeling
Drug of choice—SSRI (fluoxetine,
fluvoxamine preferred)
Treatment resistant—ECT and
psychosurgery (cingulotomy) may be
considered
Treatment : Psychotherapy is
treatment of choice
SOMATOFORM DISORDERS
Repeated physical symptoms,
together with persistent request for
medical investigation, in spite of
repeated negative findings and
reassurances by the doctor that the
symptoms have no physical basis.
Seven somatoform disorders are
listed in the revised fourth edition of
the Diagnostic and Statistical
Manual of Mental Disorders (DSM-
IV-TR):
(1) somatization disorder,
characterized by many physical
complaints affecting many organ
systems
(2) conversion disorder,
characterized by one or two
neurological complaints
(3) hypochondriasis, characterized
less by a focus on symptoms than by
patients' beliefs that they have a
specific disease
(4) body dysmorphic disorder,
characterized by a false belief or
exaggerated perception that a body
part is defective
(5) pain disorder, characterized by
symptoms of pain that are either
solely related to, or significantly
exacerbated by, psychological
factors
(6) undifferentiated somatoform
disorder, which includes
somatoform disorders not otherwise
described that have been present
for 6 months or longer
(7) somatoform disorder not
otherwise specified, which is the
category for somatoform symptoms
that do not meet any of the
somatoform disorder diagnoses
mentioned above
Clinical clues for TYPES
1) Somatization disorder: -
• Usually female of age less than 30
yrs, duration should be more than 2
yrs
• Multiple somatic symptoms
involving multiple organ system
Symptoms are recurrent and chronic
changing symptoms
• Refusal to accept the advice or
reassurance of doctors not
explained by another mental illness
e.g. Depression.
2) Hypochondriacal disorder
• Persistent pre occupation with fear
or belief of having serious disease,
based on their misinterpretation of
physical signs and sensations.
• The belief must last 6 months
• Fear or belief is not a delusion
• Belief persists even after showing
normal reports
5) CONVERSION DISORDER
It is a disturbance of bodily
functioning that does not conform
to current concepts of anatomy and
physiology of the central nervous
system.
Visceral Symptoms
Psychogenic vomiting
Pseudocyesis
Globus hystericus
Swooning or syncope
Urinary retention
Diarrhea
TREATMENT :
Psychiatric interviewing
Drug assisted interviewing or
narcoanalysis
Hypnosis
Strong suggestion
Aversion therapy
Factitious Disorder:
Dissociative Disorders
TYPES OF DEMENTIA
CORTICAL SUBCORTICAL
Sub cortical
Site Cortex grey matter
Mild to
moderate,
Severe, recall recall helped
Memory
helped very partially by
loss
little by clues clues and
recognizable
tasks
Dysarthria
dystonia,
chorea,
Motor Usually normal rigidity,
System tremors’,
ataxia, flexed
or extended
posture
Aphasia,
apraxia,
Executive
Complex
functionally,
delusions,
Others agnosia,
depression,
acalculia,
mania
bradyphrenia,
dyslexia simple
delusions
SCREENING TESTS
CAGE: an acronym for 4 questions
used to assess those with alcohol
problem (FASTEST AND EASIEST)
MAST: Michigan Alcohol Screening
Test
DAST: Drug Abuse Screening Test
AUDIT: Alcohol Use Disorder
Identification Test
TREATMENT OF WITHDRAWAL:
Benzodiazepines can be given either
orally or parenterally;
Drug Therapy for Alcohol Intoxicatio
Clinical
Drug Route
Problem
Tremulousness
and mild to
Chlordiazepoxide Oral
moderate
agitation
Diazepam Oral
Extreme
Chlordiazepoxide Intraveno
agitation
Withdrawal
Diazepam Intraveno
seizures
Delirium
Lorazepam Intraveno
tremens
Special notes:
In alcoholic hallucinosis, a heavy
drinker experiences recurrent
auditory hallucinations, usually of a
threatening or derogatory nature.
The hallucinations occur in clear
consciousness (cf. withdrawal
hallucinations). The syndrome is an
example of a drug - induced
psychosis
Will
precipi
severe
Hepatitis; optic
withdra
neuritis;
patient
peripheral
depend
Serious Adverse neuropathy;
on opio
Reactions psychotic
hepato
reactions.
(uncom
Pregnancy
at usua
Category C.
doses).
Pregna
Catego
Nausea
abdom
pain;
Metallic after-
Common Side constip
taste;
Effects dizzine
dermatitis
headac
anxiety
fatigue
Amitryptyline;
anticoagulants
Opioid
such as
analges
warfarin;
(blocks
diazepam;
action)
isoniazid;
Examples of drug yohimb
metronidazole;
Interactions (use wi
phenytoin;
naltrex
theophylline;
increas
warfarin; any
negativ
nonprescription
drug ef
drug containing
alcohol
OPIOIDS
DSM-IV-TR Diagnostic Criteria for
Opioid Intoxication
A. Recent use of an opioid.
B. Clinically significant maladaptive
behavioral or psychological changes
(e.g., initial euphoria followed by
apathy, dysphoria, psychomotor
agitation or retardation, impaired
judgment, or impaired social or
occupational functioning) that
developed during, or shortly after,
opioid use.
C. Pupillary constriction (or pupillary
dilation due to anoxia from severe
overdose) and one (or more) of the
following signs, developing during,
or shortly after, opioid use:
1. drowsiness or coma
2. slurred speech
3. impairment in attention or
memory
D. The symptoms are not due to a
general medical condition and are
not better accounted for by another
mental disorder.
3) Buprenorphine
• As with methadone and LAAM,
buprenorphine is an opioid
agonist approved for opioid
dependence in 2002. It can be
dispensed on an outpatient basis
but prescribing physicians must
demonstrate that they have
revived special training in its use.
Buprenorphine in a daily dose of
8 to 10 mg appears to reduce
heroin use.
• Buprenorphine also is effective
in thrice-weekly dosing because
of its slow dissociation from
opioid receptors. After repeated
administration, it attenuates or
blocks the subjective effects of
parenterally administered
opioids such as heroin or
morphine. A mild opioid
withdrawal syndrome occurs if
the drug is abruptly discontinued
after chronic administrations.
4) Opioid Antagonists
Opioid antagonists block or
antagonize the effects of opioids.
Unlike methadone, they do not
exert narcotic effects and do not
cause dependence. Opioid
antagonists include naloxone,
which is used in the treatment of
opioid overdose because it
reverses the effects of narcotics,
and naltrexone, the longest-acting
(72 hours) antagonist. The theory
for using an antagonist for opioid-
related disorders is that blocking
opioid agonist effects, particularly
euphoria, discourages persons
with opioid dependence from
substance-seeking behavior and,
thus, deconditions this behavior.
The major weakness of the
antagonist treatment model is the
lack of any mechanism that
compels a person to continue to
take the antagonist.
CANNABIS
ACUTE INTOXICATION:
Dysfunctional behaviour or
perceptual disturbances which
include at least one of the following:
(1) euphoria and disinhibition;
(2) anxiety or agitation;
(3) suspiciousness or paranoid
ideation;
(4) temporal slowing (a sense that
time is passing very slowly, and/or
the person is experiencing a rapid
flow of ideas);
(5) impaired judgement;
(6) impaired attention;
(7) impaired reaction time;
(8) auditory, visual or tactile
illusions;
(9) hallucinations with preserved
orientation;
(10) depersonalisation;
(11) derealization;
(12) interference with personal
functioning.
At least one of the following signs:
(1) increased appetite;
(2) dry mouth;
(3) conjunctival injection;
(4) tachycardia.
WITHDRAWAL
This is an ill-defined syndrome for
which definitive diagnostic criteria
cannot be established at the present
time. It occurs following cessation of
prolonged high-dose use of
cannabis. It has been reported
variously as lasting from several
hours to up to seven days.
Symptoms and signs include anxiety,
irritability, and tremor of the
outstretched hands, sweating, and
muscle aches.
AMOTIVATIONAL SYNDROME
A controversial cannabis-related
syndrome is amotivational
syndrome. Whether the syndrome is
related to cannabis use or reflects
characterological traits in a
subgroup of persons regardless of
cannabis use is under debate.
Traditionally, the amotivational
syndrome has been associated with
long-term heavy use and has been
characterized by a person's
unwillingness to persist in a tasks be
it at school, at work, or in any
setting that requires prolonged
attention or tenacity. Persons are
described as becoming apathetic
and anergic , usually gaining weight,
and appearing slothful
Suspiciousness Tachycardia
Expectations of (or Bradycardia at
harm high doses)
Sensation of slowed
Light headedness
time
(Postural
Social withdrawal
hypotension)
Impaired judgement
Illusions & halluc
inations with insight
COCAINE
ADVERSE EFFECTS
• A common adverse effect
associated with cocaine use is
nasal congestion; serious
inflammation, swelling, bleeding,
and ulceration of the nasal
mucosa can also occur. Long-
term use of cocaine can also lead
to perforation of the nasal septa.
• Freebasing and smoking crack
can damage the bronchial
passages and the lungs.
• The IV use of cocaine can result
in infection, embolisms, and the
transmission of HIV.
• The major complications of
cocaine use are cerebrovascular,
epileptic, and cardiac.
• About two thirds of these acute
toxic effects occur within 1 hour
of intoxication, about one fifth
occur in 1 to 3 hours, and the
remainder occurs up to several
days later.
The most common
cerebrovascular diseases
associated with cocaine use are
non-hemorrhagic cerebral
infarctions due to
vasoconstriction.
• Cocaine is the substance of abuse
most commonly associated with
seizures; the second most
common substance is
amphetamine. Cocaine-induced
seizures are usually single
events, although multiple
seizures and status epilepticus
are also possible
• Myocardial infarctions and
arrhythmias are perhaps the
most common cocaine-induced
cardiac abnormalities.
Cardiomyopathies can also
occur.
WITHDRAWAL:
Dysphoric mood (for instance
sadness or anhedonia)
Any two of the following symptoms
and signs:
(1) lethargy and fatigue;
(2) psychomotor retardation or
agitation;
(3) craving for cocaine;
(4) increased appetite;
(5) insomnia or hypersomnia;
(6) bizarre or unpleasant dreams
STAGES OF CHANGE
(Motivation Cycle)
CHARACTERISTIC
SUBSTANCE
FEATURES
Magnus Symptoms
Cocaine (cocaine bugs or
tactile hallucination)
Cannabis Run Amok
Alcohol Morbid jealousy
LSD Bad Trips
flash backs;
Paranoid
hallucinatory
Amphetamine Syndrome (like
paranoid
schizophrenia)
Phencyclidine(Angel Dissociative
dust) anesthesia
ANOREXIA NERVOSA
A. Weight loss, or in children a
lack of weight gain, leading to a
body weight of at least 15%
below the normal or expected
weight for age and height.
B. The weight loss is self-induced
by avoidance of "fattening
foods".
C. A self-perception of being too
fat, with an intrusive dread of
fatness, which leads to a self-
imposed low weight threshold.
D. A widespread endocrine
disorder involving the
hypothalamic-pituitary-gonadal
axis, manifest in the female as
amenorrhoea, and in the male as
a loss of sexual interest and
potency
E. Does not meet criteria A and B
of Bulimia nervosa
Physical symptoms
Sensitivity to cold
Gastrointestinal symptoms —
constipation, bloating
Dizziness
Amenorrhea
Poor sleep
Physical signs
Emaciation
Cold extremities
Dry skin, sometimes orange
(hypercarotenaemia)
Downy hair (’lanugo ’) on back,
forearms and cheeks
Poorly developed or atrophic
secondary sexual characteristics
Bradycardia, postural hypotension,
arrythmias
Peripheral oedema
Proximal myopathy
Abnormalities on investigation
Low LH, FSH, estradiol, T3,
somatomedin C
Increased cortisol and CRH, growth
hormone
Hypoglycaemia
Hypokalaemia, hyponatraemia,
metabolic alkalosis
ECG: prolonged QT interval (serious)
Hypercholesterolaemia
Osteopenia and osteoporosis
Delayed gastric emptying
Acute gastric dilatation (due to over
- rapid refeeding)
GENERAL PRINCIPLES OF
TREATMENT:
• Weight restoration is the
cornerstone of treatment for low
weight patients.
• Most patients are treated as
outpatients at varying levels of
intensity (e.g., partial hospital,
intensive outpatient, individual
treatment).
• Consider specialized eating
disorder hospitalization in patients
with markedly low weight or with
medical or psychiatric instability (see
criteria below).
• A multidisciplinary team approach
is the standard of care and includes
a psychiatrist, psychotherapist,
dietitian, and primary care
physician.
• Psychotherapy—There is no strong
evidence for any psychotherapeutic
approach. Family therapy is
recommended for children and
adolescents. CBT may be helpful for
adults.
• Pharmacology—No evidence of
efficacy for any medication to
ameliorate core symptoms of AN.
SSRIs may be useful for managing co-
morbid anxiety and/or depression in
weight-restored patients only, but
the evidence is weak. Some evidence
that second-generation
antipsychotics may decrease
obsessional thinking and anxiety in
low- weight patients.
REFEEDING SYNDROME:
• A potentially lethal consequence
of refeeding characterized by
cardiovascular decompensation
(myocardium weakened in
starvation) and serious electrolyte
disturbances (including
hypophosphatemia, which produces
abnormalities in cardiac
contractility) that can lead to heart
failure, severe fluid retention, and
multiorgan system collapse. Risk is
highest in early refeeding and when
using TPN.
• General inpatient refeeding
guidelines
• Controlled weight gain of 1-
1.5kg/week in hospitalized patients
and 0.25-0.5kg/week in outpatients.
• Intake levels begin around
35kcal/kg/day and increase by 200-
300kcal every 3-5 days (working with
a nutritionist).
• Medical monitoring with daily
attention to vital signs,
cardiovascular status (including
edema), and gastrointestional
symptoms.
• Electrolyte and mineral level
monitoring frequently during early
refeeding.
Anorexia nervosa has one of the
highest mortality rates (~5.6% per
decade of illness) of any psychiatric
disorder. Women with anorexia
nervosa are 12 times more likely to
die and have a suicide rate 57 times
higher than women of a similar age
group in the general population.
Poor prognostic factors include:
• Late age of onset.
• Chronicity of illness.
• Lower initial minimum weights.
• Bulimic features (vomiting,
purgative abuse).
• Obsessive-compulsive personality
features.
BULIMIA NERVOSA
A. Recurrent episodes of
overeating (at least two times
per week over a period of three
months) in which large amounts
of food are consumed in short
periods of time.
B. Persistent preoccupation with
eating and a strong desire or a
sense of compulsion to eat
(craving).
C. The patient attempts to
counteract the fattening effects
of food by one or more of the
following:
(1) self-induced vomiting;
(2) self-induced purging;
(3) alternating periods of
starvation;
(4) use of drugs such as appetite
suppressants, thyroid
preparations or diuretics. When
bulimia occurs in diabetic
patients they may choose to
neglect their insulin treatment.
D. A self-perception of being too
fat, with an intrusive dread of
fatness (usually leading to
underweight).
Patients with eating disorders have
in common the core
psychopathology of extreme
concerns about body shape and
weight.
EPIDEMIOLOGY
Estimates of bulimia nervosa range
from 2 to 4 percent of young women
bulimia nervosa is significantly more
common in women than in men
(10:1),history of obesity maybe
present
but its onset is often later in
adolescence than that of anorexia
nervosa.
TREATMENT:
General Principles
• Assessment: Full psychiatric and
medical evaluation
• Management: Outpatient
management is typical. Hospital
admission may be indicated for
acute medical instability, extremely
refractory symptoms, suicidality, or
severe co-morbid psychiatric illness.
• Nutrition counseling: Includes the
development of a structured,
balanced meal plan to reduce
dietary restriction and urges to
binge and purge.
• Psychotherapy (the cornerstone of
treatment):
o CBT has a strong evidence base
and is effective in addressing the
core symptoms of bulimia
nervosa.
o Interpersonal Therapy (IPT)
appears to be effective long-
term, but acts less quickly
“Guided self-help” may be a
useful first step (e.g.,
bibliotherapy, on-line programs)
in the absence of available CBT.
PHARMACOTHERAPY
Antidepressants are effective in
reducing binge eating and purging
behaviors, with SSRIs considered to
be the safest. Fluoxetine (at doses of
60mg) is the best studied and
currently is the only FDA approved
medication for bulimia nervosa.
There is some initial evidence
supporting topiramate.1
Prognosis
Short term reduction of binge eating
and purging behaviors for patients
treated with psychosocial or
pharmacological interventions is
approximately 50-70%. There are
high rates of relapse (30-85%),
reflecting a frequently waxing and
waning course of the illness.
Long-term prognostic data are
limited, but in clinical studies more
than 50% of patients do not meet
criteria for bulimia nervosa at the
end of study. Onset of illness in
adolescence is associated with a
better outcome, while co-morbid
depression is associated with a
poorer outcome. Bulimia nervosa
does not appear to be associated
with increased relative mortality.
DSM-5 CHANGES
DSM-5 criteria reduce the frequency
of binge eating and compensatory
behaviors that people with bulimia
nervosa must exhibit, to once a
week from twice weekly as specified
in DSM-IV.
SLEEP DISORDERS
NARCOLEPSY
• There are repeated attacks of
daytime somnolence usually leading
irresistibly to sleep.
• It usually begins in the second
decade and is associated with
cataplexy (abrupt loss of muscle
tone), hypnagogic hallucinations and
sleep paralysis (the patient wakes
but is unable to move).
• An autoimmune origin is
suspected as 98% have the DR15
variant of HLA - DR2.
• Pathologically, there is a loss of
hypothalamic hypocretin -producing
neurons. Stimulants (amphetamines
or modafinil) are the main
treatment. (Modafinil is DOC)
NREM parasomnias :
Somnambulism, somniloquy, night
terrors, bruxism and enuresis
REM Parasomnias : Narcolepsy and
Nightmares
SEXUAL DISORDERS
The sexual disorders can be
classified into four main types:
1. Gender identity disorders
(Transexualism and Dual Role
Transvestism)
2. Psychological and behavioural
disorders associated with sexual
development and maturation.
3. Paraphilias (disorders of sexual
preference).
4. Sexual dysfunctions
Transexualism
Transexualism, the severest form of
gender identity disorders, is
characterised by the following
clinical features:
1. Normal anatomic sex.
2. Persistent and significant sense of
discomfort regarding one’s anatomic
sex and a feeling that it is
inappropriate to one’s perceived-
gender.
3. Marked preoccupation with the
wish to get rid of one’s genitals and
secondary sex characteristics, and to
adopt sex characteristics of the other
sex (perceived-gender).
4. Diagnosis is made after puberty.
Dual-role Transvestism
Dual-role transvestism is
characterised by wearing of clothes
of the opposite sex in order to enjoy
the temporary experience of
member ship of the opposite sex,
but without any desire for a more
permanent sex change (unlike
transexualism).
PARAPHILIAS
• Paraphilias (sexual deviations;
perversions) are disorders of sexual
preference in which sexual arousal
occurs persistently and significantly
in response to objects which are not
a part of normal sexual arousal (e.g.
nonhuman objects; suffering or
humiliation of self and/or sexual
partner; children or nonconsenting
person).
• These disorders include: Fetishism;
fetishistic transvestism; sexual
sadism; sexual masochism;
exhibitionism; voyeurism;
frotteurism; pedophilia; zoophilia (
bestiality); and others.
SEXUAL DYSFUNCTIONS:
PHASES DYSFUNCTION
1. Desire
Hypoactive sexual desire
Or
disorder; sexual aversion
Appetitive
disorder
Phase
Female sexual arousal
disorder; male erectile
2.
disorder (may also occur in
Excitement
stages 3 and 4); male erectile
and
disorder due to a general
Plateau
medical condition;
Phase
Female orgasmic disorder;
3.
male orgasmic disorder;
Orgasmic
premature ejaculation;
phase
Postcoital dysphoria;
postcoital headache
4.
Resolution
Phase
Communication
Usually poor Fair
skills
Circumscribed Variable Marked
interests (mechanical) (facts)
Family history-
similar Sometimes Frequent
problems
Seizure disorder Common Uncommon
Head growth
No No
decelerates
Severe MR Mild MR to
IQ range
to normal normal
Fair to
Outcome Poor to fair
good
ATTENTION-DEFICIT/HYPERACTIVITY
DISORDER
Attention-deficit/hyperactivity
disorder (ADHD) is characterized by a
pattern of diminished sustained
attention and higher levels of
impulsivity in a child or adolescent
than expected for someone of that
age and developmental level.
CORE FEATURES
• Hyperactivity
• Poor attention and concentration
• Impulsivity
• Present for at least 6 months
• Evidence for impaired functioning
in two or more settings
• Onset by age 7, usually by 3
OTHER FEATURES
• Distractibility
• Poor at planning and organizing
tasks
• Learning difficulties
• Clumsiness
• Low self - esteem
• Socially disinhibited
• Unpopular with other children
• Non - localizing neurological signs
• Conduct disorder coexists in 50%,
TREATMENT
• Pharmacologic treatment is
considered to be the first line of
treatment for ADHD. Central nervous
system stimulants are the first
choice of agents in that they have
been shown to have the greatest
efficacy with generally mild tolerable
side effects.
• The US Food and Drug
Administration (FDA) approved the
use of dextroamphetamine in
children 3 years of age and older
and methylphenidate in children 6
years of age and older. These are the
two most commonly used
pharmacologic agents for the
treatment of children with ADHD
PERSONALITY DISORDERS
CLUSTER B (DRAMATIC)
EMOTIONALLY LABILE AND INTENSE
• Callous
• Unstable, transient
relationships but forms
relationships easily
• Low frustration
threshold
• Irritable and impulsive
• Failure to learn from
experience
Dissocial (= • Failure to accept
psychopathic, responsibility
antisocial) • Lack of guilt/remorse
• Tend to be young men
• History of conduct
disorder in childhood
• Extremely manipulative
& gives plausible
rationalization for
irrational behaviors
• Defense mechanisms:
Conversion
• Multiple, turbulent
relationships
• Impulsivity
• Recurrent emotional
crises
• Variable, intense mood
• Stress - related psychotic
- like symptoms
• Tend to be young
Borderline (= women
emotionally • Chronic feeling of
unstable) emptiness
• Anxiety and unstable
mood
• “confused personality”
• Defense mechanisms:
Splitting, acting out,
projective identification,
dissociation
• Dialectical behavior
therapy (DBT) is the
treatment of choice
• Exaggerated, theatrical
displays of emotion
• Attention seeking
• Vain
Histrionic • Suggestible
• Shallow, labile mood
• Crushes and fads
• Defense mechanisms:
Dissociation, repression
• Grandiose self –
importance
• Exaggerates
achievements and
abilities
• Exploits others
• Arrogant
Narcissistic • Expects special praise
and respect
• Defense mechanisms:
Acting out, idealization,
symbolization
• Psychotherapy is therapy
of choice though lithium
maybe added
• Excessive orderliness
• Preoccupation with detail
• Perfectionist
• Excessively adherent to
Anankastic social customs
(= • Inflexible and dogmatic
obsessional) • Humourless
• Miserly spending style
toward both self and
others
• Defense mechanisms:
Isolation
• Persistent tense and
apprehensive feelings
• Avoid personal contact
• Hypersensitivity to
rejection by others
• Afraid to speak up in
public or to make requests
of others
• Desire to make social
Anxious (=
interactions
avoidant)
• Views self as inept and
inferior
• Defense mechanisms:
Introjection
• Individual or group
psychotherapy are both
effective
• Anti-depressants or
anxiolytics may be added
• Encourage others to make
decisions.
• Excessive need to be
taken care of
unrealistically preoccupied
with fears of caring for
Dependent
self.
• More likely to have “foli a
deux” i.e. shared
delusional disorder.
• Defense mechanisms:
Identification
ELECTROCONVULSIVE THERAPY
CONTRAINDICATION:
No absolute contraindications
SIDE EFFECTS:-
• Headache
• Delirium &confusion 10%
• Memory loss 75%
• Mortality 0.01 each patient
Practice Questions
Answer Key
1 D 61 C
2 A 62 D
3 B 63 B
4 B 64 B
5 B 65 D
6 A 66 C
7 D 67 D
8 C 68 C
9 B 69 B
10 C 70 D
11 C 71 B
12 D 72 D
13 A 73 D
14 D 74 B
15 A 75 C
16 C 76 A
17 B 77 C
18 D 78 A
19 A 79 C
20 D 80 B
21 D 81 B
22 D 82 C
23 C 83 A
24 C 84 C
25 D 85 C
26 D 86 A
27 A 87 C
28 C 88 B
29 B 89 C
30 C 90 B
31 C 91 B
32 C 92 B
33 B 93 B
34 B 94 A
35 B 95 D
36 A 96 A
37 B 97 B
38 C 98 C
39 B 99 B
40 A 100 A
41 D 101 B
42 B 102 C
43 A 103 A
44 C 104 C
45 B 105 A
46 B 106 C
47 A 107 B
48 A 108 C
49 D 109 C
50 B 110 C
51 D 111 C
52 D 112 C
53 C 113 A
54 A 114 C
55 D
56 D
57 C
58 D
59 B
60 D