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Psychotic Disorders

Psychosis = a mental disorder causing an inability to distinguish between reality and

imagination, characterised by delusions and hallucinations.



Brief psychotic episode
Schizophreniform disorder
Schizoaffective disorder
Delusional disorder
Post-partum psychosis
Psychotic disorder NOS (Atypical psychosis)

i. Schizophrenia
A psychotic disorder or unknown aetiology and variable presentation, characterised
by positive and negative (deficit) sxs. Although not a cognitive disorder, the condition
often causes cognitive impairments.
1% of population (no gender difference)
Most common in people aged 15-35yrs; Rare in people aged <10yrs or >40yrs
Average onset younger for men than women (18-25yrs vs. 25-35yrs)
Causative or Contributory Factors
Genetics & Family Hx:
Adoptive MZ studies show ~50% concordance rate vs. 12% in DZ twins
Greater genetic loading = Greater risk (40% in child of two parents with
schizophrenia, 12% in child with one schizophrenic parent)
8% in non-twin sibling of patient with schizophrenia
10% of a patients 1st degree relatives are likely to be schizophrenia sufferers
Birth Cxs: Schizophrenia is specifically associated with birth trauma and foetal
hypoxia, but contribution is small (~5%)
Infection & Birth Season: children born in winter have a higher risk of
schizophrenia (5%). A viral cause is the suspected link.
Psychosocial Stress: first episode (precipitant) or relapse is commonly
correlated with stressful life events eg. Marriage breakdown
Low socioeconomic Class: This class has a disproportionate number of
patients. Whether this is a cause or effective of the illness is uncertain.
Dopamine hypothesis
Hyperactivity of the dopaminergic system (dopamine release, number /
hypersensitivity of receptors) is supported by:
Efficacy of dopamine D2 receptor antagonists (typical antipsychotics) in Rx
Drugs that dopaminergic activity induce psychosis eg. Amphetamines
Serotonin (5-Hydroxytriptamine)

Increasing research into the role of 5-HT given efficacy of dopamine-serotonin

antagonists (SDAs atypical antipsychotics) in Rx. Further, Lysergic acid
diethylamide (LSD) affects 5-HT levels and causes hallucinations.
Limbic System
System including many cortical and sub-cortical structures, its role is controlling
emotion, motivation, and emotion associated with memory.
Decreased size in patients with schizophrenia shown by MRI
Ventricles & Cortex
MRI and CT have consistently shown increased lateral, third and cerebral
ventricular size and reduced cortical volume. However, ventricular size are
usually still within normal limits.
DSM IV-TR Diagnostic Criteria


Nb. Only 1 Sx required if

A. 2 Characteristic (cardinal) Sxs:
delusions are bizarre, or if
1. Delusions
hallucinations consist of a
Paranoid or persecutory delusions
running commentary or two
Delusions of grandeur
or more voices conversing
Delusions of reference eg. TV talking about them
with each other.
Somatic delusions eg. of terrible illness
2. Hallucinations
3. Disorganised speech / thought (eg. frequent derailment or incoherence) aka
word salad
4. Grossly disorganised or catatonic behaviour
Variously characterized by stupor/inactivity, mania, odd posturing for an
extended time, catatonia, rigidity or extreme (waxy)flexibility of the limbs
5. Negative Sxs:
Flat or blunt affect
Marked apathy & Lack of motivation
Poverty of speech & speech content
Blocking of thought
Poor grooming
Social withdrawal
B. Social / Occupational Dysfunction for a significant portion of time since the
onset of sxs
C. Duration: Continuous signs / sxs persist for 6 months
D. Schizoaffective and Mood disorders excluded
E. Substance / General medical conditions excluded

Positive Sxs: Reflect an excess or distortion of normal functioning eg.

hallucinations, word salad
Negative Sxs: Reflect a loss of normal functioning eg. dishevelled
appearance, withdrawal

Clinical Features
No single feature is pathognomonic for schizophrenia.
Schneiderian 1st Rank Sxs
3 types of auditory hallucinations
Third person
Running commentary about the pt
Thought echo
3 types of thought disorder
Thought insertion
Thought withdrawal
Thought broadcasting (read by others)
Made Feelings & Actions: An external agency controls their feelings
Somatic passivity: Similar to made feelings, pt feels that they are a
passive recipient of bodily sensations from an external agency
Delusional perception
A real perception (such as a real objective sound) which is followed by
misinterpretation of that perception
In the absence of organic cerebral pathology, the presence of any of the above is indicative
of schizophrenia.

Pre-morbid sxs may include having few friends at school / college, being socially
withdrawn, acute onset of OCD. Often their pre-morbid personalities are quiet,
passive and introverted.
Sub-types: 4 Major DSM Types
1. Paranoid:
Characterised by the presence of delusions & auditory hallucinations, typically
Does not have any other positive sxs (incoherence, loosening of
associations, flat or inappropriate affect, catatonic behaviour, etc)
Sub-type with later onset and the best Px
2. Disorganised (hebephrenic):

Characterised by marked regression to primitive, uninhibited and

disorganised behaviour.
Marked positive & negative sxs; Inappropriate bursts of laughter and
cognitive & attention deficits
Subtype is usually early onset and a/w poor Px.

3. Catatonic:

Classic feature is marked disturbance in motor function eg. Stupor, rigidity,

excitement, posturing
Marked negative sxs. Also a/w poor Px.

4. Undifferentiated:

Marked positive sxs but does not meet the criteria for any other type

Sub-types: Type I vs. Type II

This system of classification is not accepted by the DSM, but clinically has been
significant with respect to research. It is based on whether the patient demonstrates
positive or negative sxs.
Type I patients have mostly positive (or productive) sxs, including delusions and
hallucinations, acute onset, normal brain structures on CT, and relatively good
response to Rx, good Px.
Type II patients have mostly negative sxs, chronic onset, structural brain
abnormalities on CT, poor responses to Rx and poor Px.
General Appearance & Behaviour:
Appearance may range from dishevelled to obsessively groomed
Behaviour may be unprovoked agitation and violence to catatonic
Speech may be talkative or silent
Mood & Affect:
Affect may be flat, blunted, inappropriate, labile.
Stream can be slow, normal or manic
Form Formal thought disorder ie. derailment, tangentiality, blocking,
circumstantiality, loosening of associations commonly seen (also in mania),
Content delusions characteristic
Perception: Auditory and visual hallucinations are common, but in the other
modalities it is unusual. Illusions may also occur in any phase of the illness.
Consciousness & Cognition: Consciousness may be depressed (in stupor) but
usually normal. Orientation and memory are usually normal. Attention / Cognition can
be affected. Classically, insight into their illness is poor, correlated with lack of
compliance. Judgement is poor with psychosis.
Rapport: often difficult to build rapport with patients, as agitation can occur without
i. Psychotic disorder due to a general medical condition
Hyper- / Hypothyroidism
Cushings disease or syndrome
Chest infection
Vitamin B12 or folate deficiency
Space-occupying lesions (may cause visual hallucinations)
Must always pursue an undiagnosed non-psychiatric medical condition in
patients exhibiting unusual or rare sxs or any variation in consciousness
ii. Medications / Substance Abuse
Medications (levodopa, antipsychotics, steroids, tranquilizers)
ETOH withdrawal, Lysergic acid diethylamide (LSD) usage, etc.
iii. Other psychotic disorders
Brief psychotic disorder = schizophrenic sxs lasting between 1 day and 1
Schizophreniform disorder = schizophrenic sxs lasting between 1 and 6
Schizoaffective disorder = bipolar or depressive syndrome develops
concurrently with the major schizophrenic sxs but where psychotic sxs
persist despite remission of mood disorder sxs.

Delusional disorder = non-bizarre delusions present for 1 month w/o other

schizophrenic sxs
iv. Mood Disorders with Psychotic sxs
MDD: delusions typically consistent with depressed mood (ie. mood
congruent delusions) such as guilt, worthlessness, etc.
Bipolar disorder: commonly delusions (grandiose) & manic behaviour during
episodes of mania though hallucinations are rare
MDD and antipsychotics can also cause negative symptoms
v. Seizure disorders
Mood disorders can be a feature of epilepsy post-seizure
vi. Malingering / Factitious disorders

Natural Hx
Classic course of schizophrenia is exacerbations and remissions. A further
deterioration of baseline functioning occurs after each relapse of psychosis. This
failure to return to baseline functioning is the key distinction between schizophrenia
and the mood disorders. A minority will only have one schizophrenic episode.

Rule of thirds: One third have somewhat normal lives, One third have continual
sxs but can function within society, One third are markedly impaired and require
frequent hospitalisations.4

~50% can be described as having a poor outcome, with repeated hospitalisation,

exacerbation of sxs, episodes of major mood disorders and suicide attempts.2
Factors associated with a good prognosis include:
Late and / or acute onset
Obvious precipitating factors
Good premorbid social, sexual and work hxs
Mood disorder sxs (especially depressive disorders)
Positive sxs
Good support systems
Suicide: ~50% of patients will attempt suicide, and 10-15% die by suicide.
Depression: Lifetime risk of MDD is 50% and it contributes to risk of relapse
(despite sxs of mood disorders being a good prognostic factor)
Drug & ETOH abuse: 30-50% ETOH, 15-25% cannabis, 5-10% cocaine.
STDs: Patients are statistically more likely to practice more sexually risky
behaviours (10 times increased risk of HIV)
Increased all-cause morbidity: ~double the requirement of physical healthcare
Increased all-cause mortality: 3-fold relative to normal population
Pharmacological Therapy
Dopamine receptor antagonists
[Typical antipsychotics]
Chlorpromazine, Pericyazine, Thioridazine // Haloperidol, Fluphenazine, Flupenthixol
Used as 2nd line Rx
Effective for Rx of the positive sxs & for sedation (eg. if agitated)
Often cause significant SEs: Akathisia (restlessness), EP Sxs (rigidity,
tremor), Acute dystonia, Tardive dyskinesia, Neuroleptic malignant syndrome
SEs (first 3): Marked sedation (often exploited), Anticholinergic SEs
(especially Thioridazine), Sun sensitivity & sunburn (Chlorpromazine).
Depots: Haloperidol, Fluphenazine, Flupenthixol
Tardive dyskinesia
Involuntary choreiform movements/tics of mouth, tongue, lips & face
Often irreversible & rarely occurs until after 6months of Rx
Prevention is the only way to Rx this adverse effect

Serotonin-Dopamine Antagonists (SDAs)

[Atypical antipsychotics]
Risperidone (Risperidal), Olanzapine (Zyprexa), Quetiapine (Seroquel), Aripiprazole
(Abilify), Clozapine (Clozaril)
Used as 1st line Rx for schizophrenia & psychosis
Antagonises different dopamine receptors as well as 5-HT receptors
Much more effective for ve sxs and at least as effective for +ve sxs
Minimal or no extrapyramidal sxs (except risperidone) due to looser bonding
at D2-receptor sites
Depots: Risperidal consta

Sxs (EPS)
malignant Syn.
Weight gain







0 to ++

0 to +


+ to +++
0 to +





0 to ++



+ to +++


0 to +++



+ to ++

0 to ++

0 to +

+++ (2%)

0 to +

0 to +

+++ (1%)

(Kaplan & Sadock, 2001)

1. Safety Assessment
Risk of patient to themselves (risk of repeated attempts + risk of successful
suicide) & to others must be assessed (Low, Medium, High)
2. Ix of causes & Dx (eg. Screen for medical causes of psychosis)
3. Immediate Rx
Antipsychotics (except clozapine) are remarkably safe and can be given in ER
situations w/o conducting physical or lab examinations.
4. Long-term Rx
SDAs (atypical) should be mainstay; long-term use of DAs (typical) is highly
questionable due to risk of tardive dyskinesia
> 1 antipsychotic at a time is rarely (if ever) indicated
Minimum length of antipsychotic trial is 4-6 weeks
Use lowest effective dose but monitor plasma levels [Clozapine requires
monthly FBEs to monitor agranulocytosis]
Combination with other drugs (eg. lithium, carbamazepine, BZDs) may be
indicated for resistant or complicated cases

Rx Extrapyramidal sxs and Acute dystonia with anticholinergics (eg.

benzhexol, benztropine)

Typical antipsychotics (and Risperidone) may be given together with anticholinergic

agents to prevent EPS sxs eg. Benztropine (Cogentin)

Electroconvulsant Therapy (ECT)

Efficacy << Antipsychotics, but may be indicated for those non-responsive to
antipsychotics, those with catatonia, or those with severe depressive sxs
Psycho(social) Therapy
Social / Behavioural skills training: shown to relapse rates as measured by
the need for hospitalisations
Family Therapy: most effective psycho-therapy in terms of sxs & relapse, but
efficacy depends on emotional temperature (expressed emotion). Also
educated family & patient about condition and how to best manage.
Case Management: Coordinates parties supporting the patient, efficacy
largely dependant on the individual case manager.
Other therapy such as Group, Cognitive behavioural and Individual have less
evidence for efficacy.
1. Non-responsiveness:
Lack of clinical improvement despite the use of at least 2 antipsychotic drugs
prescribed for reasonable durations (4-6wks)
2. Intolerance:
The inability to achieve adequate benefit with other antipsychotics because of
severe and untreatable neurological SEs (EP SEs or tardive dyskinesia)
Previous hypersensitivity to clozapine
Hx of granulocytopenia / agranulocytosis (from clozapine or otherwise)
BM disorders or BM suppressive drugs
Circulatory collapse and / or CNS depression due to any cause.
Alcoholic and other toxic states
Severe renal or cardiac disease (e.g. myocarditis)
Severe hepatic disease including active liver disease
Uncontrolled epilepsy
Paralytic ileus
(MIMS online, 2003)
1. Wikipedia, The limbic system, < >
2. Sadock & Sadock (2004), Concise Textbook of Clinical Psychiatry, pp. 134-153
3. FIRSTConsult, Schizophrenia, < >
4. Kaplan & Sadock (2001), Pocket handbook of clinical psychiatry, 3rd edn, Lippincott Williams & Wilkins.
5. Katona C & Robertson M (2005), Psychiatry at a glance, 3rd edn, Blackwell publishing, Australia.
6. MIMS online, 2003 < >

Disorder type

Behaviour &

Psychotic, +ve & -ve sxs
1% population; =
Genetics ( with FamHx;
MZ:DZ = 50%:10%)
Dopamine (& 5-HT)
Psychosocial stress
Ventricle size, Cortical
volume, and Amygdala
& hippocampus size

Mood disorder
20% popn; : = 1:2
5-HT, NA, DA
Psychosocial: loss of
parent or spouse,
unemployment, birth.
Genetics: Less important
than for Bipolar I; MZ>DZ
concordance but still
less than Bipolar.
Medical: eg. Thyroid

Bipolar (Manic)
Mood disorder
~1% population; =
5-HT, NA & DA levels
Psychosocial stressors
Genetics: 25% with one
parent, 50-75% with two,
MZ:DZ 60:20.
Medical: eg. Cushings

Behaviour: Variable (eg.

Agitated, withdrawn,
postured, catatonic)
Speech: Normal to

A: -motor retardation
agitation, poor eye
contact, tearful, poor
S: Slowed, soft,
monotone, long pauses,
M: Depressed, irritable,
frustrated, sad
A: Constricted or labile
Hallucinations rare

A: -motor agitation,
bizarre or colourful
clothing, excess makeup
B: Hyper-excited,
intrusive, threatening,
S: Pressured, loud,
dramatic, incoherent
M: Euphoric, expansive,
irritable, flirtatious.
A: Labile & swinging
Hallucinations less

loosening of associations

10% have sxs of Thought
disorder (blocking,
poverty of ideas)

Delusions, ideas of
reference, passivity,

Suicidal ideation (60%)

Negativity is customary,
obsessive rumination,
worthlessness, guilt.
Delusions possible.

Fast (racing thoughts)

Flight of ideas (severe
can be incoherent),
neologisms, clang-assoc.
Grandiosity, Selfesteem, mood congruent
delusions, hallucinations

(Unless catatonic)


Increased (excitable)

Difficulty concentrating
Impaired abstract

Easily distracted

Orientated, Poor
Impaired judgement
Insight: Sxs often overemphasised


Mood & Affect

A: Flat, blunted, labile,



Hallucinations, most
commonly Auditory



Attention &
Orientation &
Judgement &

Frontal lobe can be

affected, causing
cognitive deficits.


Extremely impaired
judgement and insight is
the hallmark of mania

Mood Disorders
Psychopathological conditions in which a persuasive disturbance of mood is the
primary feature, usually with a return to normal functioning in b/w episodes.
Aetiology of Mood Disorders:
Some clinicians believe stress is the primary cause of depression, whilst others
believe its role is limited. Aetiology is really a mix of genetic and environmental
factors, but depressive illnesses involve both mind and body, which are themselves
Genetic factors are much more significant in Bipolar I disorder than MDD, but no
specific gene has yet been identified.
Family Studies:
1 degree relatives of Bipolar I disorder have 8-18 times risk of Bipolar I and
2-10 times risk of MDD
If one parent has a Bipolar I, child has 25% chance of a mood disorder; if both
have Bipolar I, child has 50-75% chance.
1 degree relatives of someone with MDD have a 10% chance
Adoption Studies:
Biological children of affected parents remain at risk even if reared in nonaffected adoptive families.
Twin Studies:
Concordance rate for MDD in monozygotic twins is ~50%
Concordance rate for bipolar I in monozygotic twins is between 33-90%
Serotonin (5-HT)
Efficacy of Selective Serotonin Re-uptake Inhibitors (SSRIs)
Depletion of serotonin may precipitate depression
Noradrenaline (NA)
Down regulation of -Adrenergic receptors is associated with depression
Efficacy of clinical anti-depressants which also block NA-receptors eg.
Tricyclic anti-depressants, Setraline (SSRI)
Dopamine (DA)
Drugs that reduce DA and diseases that reduce DA concentrations (eg.
Parkinsons) are associated with depressive Sxs. In contrast, drugs that DA
concentrations (eg. amphetamines) reduce the sxs of depression.
Data suggests that dopamine activity is associated with depression and
activity with mania.
Medical / Hormonal factors:
Cortisol (Cushings Syn. / disease)
Correlation with cortisol and depression has been one of the oldest
observations in psychiatry; ~50% of depressed patients have cortisol levels
New data suggests that a +ve Dexamethasone-Suppression Test (DST) (ie.
non-suppression of cortisol) may correlate with relapse rates, but +ve results
also occur in other psychiatric illnesses

Thyroid disorders found in 5-10% of depressed patients

Physical Illness & Medications
The major cause of depression in later life
HIV, Multiple sclerosis and cancer carry an especially increased risk
L-Dopa & Interferon are medications known to precipitate depression
Psychosocial Factors:
Life Events & Environment
Stressful life events more often precede the first (rather than subsequent)
episodes of mood disorders
The life event most often a/w depression is losing a parent < Age 11
Environmental stressor most often a/w depression is loss of a spouse
Unemployed have 3 times risk of depression compared to employed
Childbirth: 45% of women who develop bipolar have their first episode in the
post-partum period
Suicide and self-harm

10-15% of depressed pts will commit suicide; 66% will have suicidal
Risk of CVS event

Major Depressive Disorder (MDD)

Synonyms: Unipolar depression, Clinical depression, Major depression.

Lifetime prevalence is 10-25% women; 5-12% men (: = 2:1)
Mean age of onset ~40yrs (50% cases between 20-50yrs);
Cases <20yrs increasing
Highest risk category = Women aged 25-44
No correlation with socioeconomic status

Lifetime prevalence is
the proportion of
people who will suffer
the illness at some
stage in their lives

DSM IV-TR Dx Criteria

Major depressive episode:
Dx by the DSM-IV-TR requires the presence of 5 (or more) of the following sxs
that last essentially without remission for 2 weeks.
i. Depressed mood for most of each day
ii. Anhedonia = Loss of interest/pleasure in normally
pleasurable activities

Either of these 2
must be one of the
5 sxs

iii. Recurrent thoughts of death or suicide (MUST ASK!)

iv. Significant Weight or Appetite
v. Fatigue
vi. Insomnia or Hypersomnia
vii. Concentration and decisiveness
viii. Psychomotor agitation or irritability
ix. Feelings of worthlessness, helplessness or guilt
Major Depressive Disorder (MDD) is the Dx with 2 depressive episodes.

Dysthymic disorder: Chronically depressed mood (for 2 years) but without

enough sxs to fulfil the DSM criteria for MDD ie. Incomplete depressive
syndrome without episodes of normal functioning.
Minor depressive disorder: Incomplete but episodic depressive syndrome
Recurrent brief depressive disorder: Complete depressive disorder lasting < 2
weeks duration
Associated Disorders
Anxiety: Anxiety is a common sx of depression (up to 90%). DSM IV has criteria
for the existence of mixed anxiety-depressive disorder
Drug & ETOH abuse / dependence (eg. cocaine or amphetamines used in MDD)
Natural Hx (MDD)
Onset: ~50% have depressive sxs before the first identified episode
Treated episodes last ~3mths; Untreated episodes last 6-13months
Withdrawal of antidepressants < 3mths almost always results in return of sxs
Over a 20yr period, the mean number of episodes is 5-6.
Mania: 5-10% with MDD have a manic episode within 10yrs of their Dx.
Prognosis (MDD)
MDD is not a benign condition it tends to be chronic and pts tend to relapse
Post-hospitalisation 25% relapse within 6mths
10-15% will commit suicide; rates of self-harm are higher
1St Line Pharm. Rx (MDD)
Antidepressants take 14days to have effect; trials should last at least 3 weeks.
Specific antidepressant-free intervals must be observed when changing between
Combinations of antidepressants have not been shown to be more effective than
monotherapy and there is a very significant risk of serious SEs. In addition, the
risk of dying in the event of OD is increased.
Selective Serotonin Re-uptake Inhibitors (SSRIs)
Citalopram (Cipramil), Fluoxetine (Prozac), Fluvoxamine (Movox), Paroxetine
(Aropax), Setraline (Zoloft)
Selectively inhibits CNS neuronal reuptake of serotonin; low affinity for - & adrenergic, dopaminergic and muscarinic receptors
Despite many SSRIs, each one can have very different characteristics and
efficacy between pts Eg. Fluoxetine has a very long life
SSRIs have a relative lack of SEs, even at high doses (eg. OD)
SE: Sexual dysfunction (commonest complaint), Sleepiness, Hyponatremia,
initial anxiety may occur (suicide risk) so must Rx with BZDs, withdrawal
reaction if stopped suddenly (as with all CNS drugs)
Serotonin-Noradrenaline Reuptake Inhibitor (SNRI)
Venlafaxine (Efexor)
Like a suped-up SSRI; efficacy with matching toxicity
Potent inhibitor of CNS neuronal 5HT and NA reuptake
Only antidepressant to cause hypertension (most cause hypotension)
Reversible Monoamine Oxidase Inhibitor (MAOI)
Moclobemide (Arima)

Reversible inhibitor of monamine oxidase A (MAO-A) to CNS monoamines

Only antidepressant that does not cause sexual dysfunction; SEs similar to
SSRIs otherwise

Mirtazapine (Avanza)
Blocks 2-receptors causing release of 5HT & NA, and also block 5HT2- and
5HT3-receptors, enhancing 5HT1 serotonergic transmission.
Have long elimination lives, allowing once daily dosing
SE: Notorious for weight gain, sedation, postural hypotension
2nd Line Pharm. Rx (MDD)
Tricyclic Antidepressants (TCAs)
Amitriptyline, Nortriptyline, Imipramine, Dothiepin
Non-selective reuptake inhibitors of 5HT & NA
Extensively metabolised in the liver
Long lives allow once-daily admin, usually in the evening
SE: Use is 2nd line due to lethal cardiotoxicity in OD, Anticholinergic SEs (dry
mouth, blurred vision, constipation, urinary retention), Alpha-adrenergic SEs
(sedation, postural hypotension, sexual dysfunction, weight gain).
C/I: Suicide intent (OD risk), CVS disease, glaucoma, bladder neck
Monoamine oxidase inhibitors (MAOIs)
Phenelzine, Tranylcypromine
These non-selective monoamine oxidase inhibitors (MAOIs) irreversibly inhibit
the enzymes MAO-A and MAO-B; results in [monoamine] in brain and other
tissues. Duration of action = 2-3 weeks while new enzymes form.
SEs: postural hypotension, dry mouth, blurring of vision, constipation,
anorgasmia, impotence, failure of ejaculation, insomnia and arousal.
Paradoxically, some patients experience sedation and fatigue.
C/I: Various foodstuffs with high amine concentrations (eg. home-brewed
alcoholic beverages, cheeses, pate) and cold & flu medications may cause
significant hypertension & CVA / CVS events
Tetracyclic antidepressant; Works identically to mirtazapine but is a 2nd line
St Johns Wart
Systematic reviews found there was no significant difference between St John's
wort (hypericin) and other antidepressants for Rx of mild-moderate depression. It
is not recommended for Rx of severe depression.

Switching Medications & Serotonin Syndrome

An appropriate interval should be observed between changing antidepressants to
avoid adverse effects, the most serious of which is the Serotonin syndrome:
Diarrhoea & Restlessness / Extreme agitation
Hyperreflexia, ataxia & tremor
Autonomic instability with possible rapid changes in vital signs
Myoclonus, seizures, hyperthermia
Delirium, coma and CVS collapse & death
SSRIs should not be co-administered with a MAOI, lithium or L-trytophan as 5HT
levels may occur and cause this syndrome.

Bipolar Disorder
Synonyms: Manic depression

Bipolar disorder is a term to describe a recurrent illness characterised by episodes of

either mania and / or depression, with a return to normal functioning in between.
~1% prevalence (: = 1:1)
Mean age of onset ~30yrs (may be as early as 5yrs old); 90% of cases are
apparent by 30yrs age
Men have more manic episodes whilst women have more depressive episodes
Higher then average incidence in upper socioeconomic groups
DSM IV-TR Dx Criteria
Manic Episode:
A. Abnormally and persistently elevated or irritable mood lasting 1 week
B. 3 (or more) of the following sxs persist to a significant degree during the
mood disturbance:
i. Inflated self-esteem or grandiosity
ii. Need for sleep (eg. feels rested after only 3hrs sleep)
iii. More talkative than usual or pressure to keep talking
iv. Flight of ideas / Subjective feeling that thoughts are racing
v. Distractibility
vi. Goal-directed activity or psychomotor agitation
vii. Excessive pleasurable activities that have high potential for detrimental
consequences (eg. buying sprees, sexual indiscretions, foolish business
C. Marked impairment in occupational or social functioning, or there are
psychotic features, or there is risk of self harm, or the episode requires
Hypomanic Episode:
All the same criteria as for a Manic episode BUT the episode is not severe
enough to fulfil criteria C (ie. less severe & no psychosis)
Bipolar I Disorder: Complete manic and depressive syndromes. 10-20% have
manic episodes only. Other psychiatric illnesses (eg. schizophrenia) have been
excluded as cause of manic episode.
Bipolar II Disorder: Recurrent major depressive episodes with hypomanic
syndromes ie. where depression predominates. Other psychiatric illnesses (eg.
schizophrenia) have been excluded as cause of hypomanic episode.
Cyclothymic disorder: incomplete depressive and manic syndromes
Associated Disorders (Bipolar):
Drug & ETOH abuse and dependence
Anxiety disorders eg. Panic disorder, social phobia
Antisocial behaviours eg. Gambling, spouse abuse, child abuse
Eating disorders eg. Bulimia nervosa
Attention deficit hyperactivity disorder (ADHD) and / or conduct disorder,
especially with juvenile onset (57-98%)
Borderline personality disorder
Natural Hx (Bipolar)

Most often starts with depression (~70% of cases) but is a recurring disorder
Most patients experience both depressive and manic syndromes, but 10-20%
have only manic episodes
Untreated manic episodes last ~3mths

Prognosis (Bipolar)
Bipolar patients have a poorer prognosis than patients with MDD
40% have a chronic disorder; 45% have > 1 episode
Early onset is a/w poor prognosis
Pharmacological Rx (Bipolar)
Getting the correct Dx of Bipolar disorder is essential to Rx. Bipolar is not Rx with
antidepressants alone as this will precipitate manic episodes and contribute to rapid
Mood Stabilisers (Mania)
Considered 1st line Rx for mania, both acute episodes and prophylaxis. Weak
antidepressant properties.
Renal toxicity is the most important SE, but thyroid and dermatological effects
can also occur
May be combined with mood stabilisers for refractory cases
Sodium Valproate (Epilim):
Alternative to Li also considered 1st line Rx for mania, both acute episodes
and prophylaxis. Additional antidepressant action in 1/3 of pts.
Many tolerate valproate better the Li and carbamazepine, and some nonresponsive to Li may respond to valproate
SE: hair loss, weight gain, tremor and sedation. Iatrogenic properties (neural
tube defects).
Carbamazepine (Tegretol):
2nd line Rx as it is a potent enzyme inducer so many drug interactions (eg.
warfarin, OCP) but can be used in acute episodes and for prophylaxis.
Additional antidepressant action in 1/3 of pts
Olanzapine (Zyprexa): Atypical antipsychotic indicated in acute mania
Lamotragine (Lamictal): a 1st line prophylactic agent, but not for acute episodes
Adjunctive antipsychotics / BZDs (Mania)
Manic episodes may require the addition of an antipsychotic or BZD, but it
depends on the primary Rx eg. If Olanzapine is the primary Rx, addition of
another antipsychotic is not recommended. Atypical antipsychotics are used first
(better SE profile), and the most common BZD used in diazepam (Valium).
Antidepressants (Bipolar Depression):
Choice of antidepressant is similar to that for MDD, but as they may precipitate
manic episodes and rapid cycling, they are:
a) Never given in an acute manic episode
b) Usually withdrawn after 1-2mths after successful resolution of bipolar
Combination Rx
Patients who fail to respond to monotherapy in acute or prophylactic settings
do benefit from combination therapy

Lithium is typically combined with mood stabilisers (sodium valproate or


Non-Pharmacological Rx (MDD & Bipolar Disorder)

Electroconvulsant Therapy (ECT)
Not 1st line Rx, but can be effective (and life saving) in refractory manic or
depressive episodes
Safe in combination with Li
C/I: MAOIs, Pts unfit for anaesthesia, raised ICP
Psychosocial Therapy
Psychotherapies may be used alone for Rx of some cases of MDD (especially
cognitive-behavioural), but they are not recommended as the only Rx for bipolar
disorder. In combination with pharmacological Rx, psychotherapy
(psychoanalytical, family & interpersonal) has been shown to reduce relapse
Mood & Affect


Sensorium &

Judgement &

Depressive Episodes
Psychomotor Retardation or
Agitation (hand wringing, pulling hair,

Manic Episodes (Bipolar)

hyperactive. Can be grossly psychotic
and disorganised, sometimes requiring
Rate & Volume
Cannot be interrupted whilst speaking.
Volume and rate increase
Single word responses
Depressed mood, though ~50% deny May be euphoric, irritable or hostile.
any depressive feelings
Often emotionally labile, from laughter
to irritability to depression in mins.
Negativity is customary. ~10% have Stream is unrestrained & accelerated
marked sxs of thought disorder Form is disturbed (eg. loosening of
(usually thought blocking or poverty of associations). Content includes themes
of self-aggrandisement.
Psychosis can occur (called MDD with 75% have delusions mood congruent
psychotic features).
(great wealth & power) typically.
Delusions congruent with a depressed Bizarre & mood incongruent delusions
mood are said to be mood congruent. & hallucinations may also occur.
Mood incongruent delusions would
Hallucinations can occur but are rare.
Most are fully orientated
Most are fully orientated with normal
50-75% have cognitive impairment memory. No obvious cognitive defects
causing poor memory (depressive but patients are often easily distracted.
pseudodementia). There is often
diurnal variation of severity.
Insight is often excessive (pts often Impaired judgement is the hallmark.
overemphasise their sxs).
Insight is often very limited also.
Most severely depressed pts lack ~75% are assaultive or threatening.
motivation / energy to act in an Pts may commit suicide but incidence
impulsive way. There is risk of suicide is unknown. Pts who threaten
as they begin to improve as they regain important people (President of USA)
have Bipolar I disorder rather than
energy (paradoxical suicide).

DDx (Mood Disorders)

i. Mood disorder resulting from general medical condition
Cushings syndrome / disease
Thyroid disorders
Neurological disease (Parkinsons disease, epilepsy, cerebrovascular
disease, tumours)
Chronic renal failure
Hypercalcemia (moans, bones, stones & abdominal groans)
ii. Substance-induced Mood Disorder
Mood disorders caused by drug or toxins
Must be ruled out in patients with depressive or manic sxs; Mood disorders
often occur simultaneously with substance abuse / dependence
iii. Other mood disorders eg. Dysthymic disorder, minor depressive disorder,
recurrent brief depressive disorder, Cyclothymic disorder
iv. Psychotic disorders
Eg. Schizophrenia, Schizoaffective Disorder
Mood incongruent psychotic features suggests schizophrenia
Rely on such factors as family hx, course premorbid hx, and response to
v. Adjustment disorder with depressed mood
Moderate depression in response to clearly identifiable stress, which resolves
as stress diminishes
vi. Bereavement
Profound sadness secondary to major loss
Differentiate from MDD by absence of suicidal ideation or profound feelings of
Usually resolves within a year but may progress to MDD
vii. Other mental illnesses
Substance-induced mood disorders (eg. cocaine, amphetamines, propranolol,
Anxiety disorders with depression
Personality disorders eg. Borderline
1. Sadock & Sadock (2004), Concise Textbook of Clinical Psychiatry, pp. 173-199
2. FIRSTConsult, Schizophrenia, < >
3. Kumar & Clarke (2002), Clinical Medicin 5th Edn, Elsevier Ltd, pp. 1243-48
4. Therapeutic Guidelines (2006), Psychotropic agents, < >

Stress Reactions

Grief / Bereavement
Adjustment disorder
Acute stress disorders (ASDs; Sxs last <1month)
Post-traumatic stress disorder (PTSD; Sxs last >1month)

Definition: A normal expression of grief or mourning from loss eg. of a loved one.
It follows a recognisable sequence of stages that last for 2 years. 2
Elisabeth Kbler-Ross Stages of Grieving
This staging series describes the typical reaction to death and dying of a patient
who is told of a terminal illness. However, it applies in general to many different
grieving stages.

1. Shock and

Initial shock, followed by denial that anything is wrong.

Pts become frustrated, irritable and angry and may displace their
anger onto others and/or themselves.
3. Bargaining: Pt may attempt to bargain with others or God for something (eg.
cure) and will in return fulfil promises
4. Depression: Pt shows clinical signs of depression either due to the current
effects on their life or in anticipation of future effects
5. Acceptance: Person comes to accept the situation eg. That death is inevitable

2. Anger:

Grief vs Depression
Bereavement / Grief
Immediate onset (at least of process)
Normal identification with deceased.
Little ambivalence with deceased.
Depressive Sxs but without suicidal
Self-blame restricted to how deceased
was treated; No global feelings of
Evokes empathy and sympathy from
Sxs self-limited; usually clear 1year
Responds to reassurance and supports
Not helped by antidepressants

Delayed onset
Abnormal over-identification with
Ambivalence and unconscious anger
towards deceased
Depressive sxs with suicidal ideation
Self-blame is global; person thinks they
are generally bad or worthless
Usually evokes interpersonal annoyance
or irritation
Sxs do not resolve and may worsen
Does not respond to reassurance and
pushes supports away
Helped by antidepressants

Normal grieving requires no specific Mx apart form support and encouragement
to ventilate feelings and accept them as normal.
Abnormal grieving reactions may respond to CBT and antidepressants.

Adjustment Disorders
Disproportional or excessive clinical sxs (emotional or behavioural) that develop in
response to an identifiable psychosocial stressor(s) 3 months of onset of the
Clinical Features:
Autonomic arousal
Depressed mood

*Dx should only be made when there

are insufficient sxs to justify a
diagnosis of another specific anxiety
or depressive disorder.

1. Psychotherapy (eg. CBT): Rx of choice, used to explore what the meaning of
the stressor was & alternative ways of coping
2. Crisis intervention: aimed at helping the person resolve the situation quickly
through any means necessary (including hospitalisation)
3. Pharmacology: Same as for anxiety disorders

1. Kaplan & Sadock (2001), Pocket handbook of clinical psychiatry, 3 rd edn, Lippincott Williams & Wilkins.
2. Katona C & Robertson M (2005), Psychiatry at a glance, 3rd edn, Blackwell publishing, Australia.

Cognitive Disorders (Organic Brain Disorders)

Consciousness = A state of wakefulness with awareness of self & surroundings

Sleep = state of normal mental and physical inactivity where the pt can be roused
Stupor = an abnormal sleepy state from which the pt can be aroused by external
stimuli, applied vigorously or repeatedly Eg. Catatonic and depressive stupor
Confusion = state of altered consciousness in which the subject is bewildered
and misinterprets his or her surroundings

The cognitive disorders are characterised by severe impairment in cognitive

functions such as memory, judgment, language and attention. They include:
i. Delirium
ii. Dementia
Dementia of Alzheimers type (DAT)
Vascular dementia

i. Delirium (Acute Brain Syndrome)

Characterised by an impairment of consciousness, usually accompanied by
global disturbances in cognitive function.
Generally associated with emotional lability, hallucinations / illusions,
inappropriate and unpredictably behaviour.
Usually acute and reversible, but may become irreversible.
10% of all hospitalised patients; 30% of ICU & AIDS patients
Very young and very old more susceptible to delirium
Delirium is a common pathway for any brain insult. Major causes include:
Systemic disease eg. Cardiac failure, renal failure, SIRS
CNS disease eg. Seizure disorders
Intoxication or withdrawal from medications or abusive substances eg. ETOH
Signs / Sxs:
Depressed conscious state
Hyper- or Hypoarousal (ie. swinging conscious state)
Agitation or fear
Prominent hallucinations (visual, auditory or tactile) and illusions
Memory (& attention) impairment
Illogical speech
Reversed sleep-wake cycle
Psychomotor disturbance
a. Dementia
b. Schizophrenia & mania

c. Dissociative disorders: may show spotting amnesia but lack global cognitive
impairment & disrupted sleep patterns
Course & Prognosis
Course is usually rapid with sxs receding 3-7 days after the cause is treated. Sx
resolution may take 2 weeks.
In some cases the delirium may spontaneously clear.
3-month mortality rate of 20-33%; 12-month mortality of 50%.
i. Find the cause: Delirium is a Medical ER and the cause must be identified as
rapidly as possible.
ii. If cause remains unknown, full medical work up should be performed
immediately (FBE, ESR, U&Es, LFT, urinalysis, ECG, CT of head, lumbar
puncture if indicated)
iii. Rx the underlying cause
iv. Agitation:
Haloperidol 1.5-10mg PO or IM, but use with caution with cardiac
conduction problems
Diazepam 5-10mg PO (do not give IM as absorption is poor and erratic)
Midazolam 2.5-5mg IM (avoid IV due to risk of respiratory depression)
Use BDZs If the most prominent symptom is Anxiety OR
If agitation is not
controlled with haloperidol
In patients with significant respiratory depression avoid all BZDs
Because of the potential of BDZs to impair hypoxic respiratory drive, use low flow
rates if O2 is required used
Monitor vital signs closely during and after giving all sedatives
Use flumazenil if necessary to reverse the BZD effect.

ii. Dementia (Chronic brain syndrome)

An acquired, generalised and often progressive loss of cognitive function that
does not affect the level of consciousness
Often associated with deterioration in emotional control, social behaviour and
Affects 10-20% of people aged > 65 years
Increasing age is the biggest risk factor
The majority of cases are due to Alzheimers disease
Alzheimers disease (60-70% of cases)
Vascular disease
Head trauma

Huntingtons and Parkinsons disease

HIV infection

Defect continually affects all higher cognitive functions
Memory (especially short term)
Planning & organising
Apraxia (ability to carry out familiar, purposeful
movements without any sensory/motor impairment)
Agnosia (ability to recognise sensory stimuli)
Abstract thinking
Marked changes in personality, affect and behaviour can occur
Hallucinations (20-30%)
Delusions (30-40%)
Sxs of depression and anxiety (40-50%)

Tasks such as
drawing &
labelling a clock
face and counting
backwards from

a. Age-related Cognitive decline (Normal ageing)
b. Depression (Pseudodementia)
May present with many features of an cognitive impairment, especially with
memory, slowed thinking and lack of spontaneity
c. Delirium / Acute Brain Syndrome
Also characterised by global cognitive impairment, and most demented pt.s
have a superimposed delirium
Course & Prognosis
Generally, the course is chronic and progressive
Often cognitive impairment is worse at night (sun-downing)
As condition progresses, they may forget familiar places and people, and
eventually become incontinent of faeces and urine
15% of dementias are reversible eg. Hypothyroidism, subdural haematoma, Vit.
B12 deficiency, uraemia, hypoxia) and cognitive impairment depends on how
soon the cause is treated
Rx is generally supportive. Avoid BZDs and barbiturates as they worsen cognition.
Agitation can be treated with low dose antipsychotic.
Dementia of Alzheimers Type (DAT)
Progressive dementia in which all known reversible causes have been ruled out
Most common cause of dementia (50-60% of all dementias)
5% over the age of 65yrs
RFs include: female, head trauma, 1st degree relative with DAT (<40% have
family Hx), Downs syndrome associated
Mean survival is 8yrs post-Dx
Rx: Anticholinesterases are used to slow cognitive decline, but do not alter the
underlying disease process
Vascular Dementia
Dementia resulting from cerebrovascular disease ie. CVAs
2nd most common cause of dementia (15-30% of all dementias)
Cognitive impairment may be patchy, with some areas intact
Rx: Identify and prevent further CVAs


Level of
Sleep cycle:



Sudden (acute)
Days Weeks
Retarded, agitated or

Slow, Insidious
Months Years

2 weeks


Depressed, sad,

common (esp. visual),

Labile but not usually

Hallucinations less
common (except



delusions possible

Anxious, irritable

No abnormalities

Fluctuating but
overall decreased
Very Poor



Less impaired



Highly disrupted

Less disrupted

Slowed, personality
Moderately disrupted




Mini-Mental State Examination

A screening tool validated, reliable, but not diagnostic
Limited to coverage to parietal and frontal lobe functions
Subject to effects of culture and education
Ceiling Effect Can be difficult to use for screening because of
the lack of difference in scores b/w those with dysfunction and
those without

Anxiety Disorders
Anxiety is a state characterised by feelings of dread and accompanied by
physical signs & sxs of hyper-autonomic nervous system function. The YerkesDodson performance/anxiety curve illustrates that anxiety is beneficial up to a point
beyond which performance deteriorates.
Aetiology of Anxiety Disorders
Biological: Sympathetic N/S hyperactivity & Noradrenaline release. GABA
causes CNS hyperactivity, 5-HT causes anxiety.
Psychoanalytic: Freud said the unconscious fear of loss / sense of danger
threatens to break through to the conscious, producing anxiety.
Cognitive-Behavioural: Classical conditioning to a specific stimulus (eg.
phobias), learned behaviour from parents (eg. inability to cope)
Existential: that anxiety is a response to profound nothingness in life to fill the
void in existence and meaning.

Panic disorder Agoraphobia

Generalised Anxiety Disorder (GAD)
Phobias (Phobic disorder)
Social anxiety disorder
Obsessive-Compulsive Disorder (OCD)
Post-Traumatic Stress disorder (PTSD)






Characterised by recurrent and spontaneous panic/anxiety attacks (PAs). It
may occur alone or be a/w agoraphobia. Typically a PA will only last a few
DSM: 3 PAs in a 3 week period where there is no discernible danger to
the pt, and where the pt is free of anxiety in b/w the discrete PAs.
Px*: Remissions & exacerbations, PAs tend to recur 2-3 times /week,
Excellent Px with Rx.
Fear of being in open spaces, outside the home, in public places or
anywhere where escape / help could be difficult in the event of a PA.
Characterised by intense resistance to leave the home. By far the most
common phobia.
Characterised by generalised, persistent and excessive anxiety about
actual circumstances, events or conflicts lasting >6 months. Sxs may
Px*: Sxs may diminish as pt gets older, but 2 depression may develop
especially if GAD goes w/o Rx.
An irrational fear or an object where exposure (or anticipated exposure)
causes massive anxiety.
Px*: May worsen or spread w/o Rx, Px is good-excellent with Rx.
Agoraphobia is the most resistant of all phobias however.
An irrational fear of public or social performance situations where the
individual will be exposed to unfamiliar people or under scrutiny. (Also
known as Social Anxiety Disorder).
Involves recurrent intrusive ideas, images, impulses or thoughts
(obsessions) and subsequent repetitive patterns of behaviour
(compulsions). The obsession is a mental event, whereas the compulsion is
a behaviour. Both obsession and compulsions produce anxiety if resisted,
and compulsions are typically designed to relieve the anxiety produced by


the obsession. Compulsions may actually anxiety & not always be

realistically connected to the obsession. Most common obsession =
Cleanliness (43%); Most common compulsion = Hand-washing (85%).2
A pt with OCD usually has insight ie. realises the irrationality & absurdity
(ego-dystonicity) of the obsession & compulsion, but still feels helpless to
resist. Often recalls facts without affect.
DSM: Obsession or compulsions cause marked distress, social dysfunction,
or take >1hr/day.
Px*: Waxing and waning of sxs, Px with Rx is fair but some cases are
refractory to all Rx modalities.
In these disorders, anxiety is produced by an extraordinarily stressful
event. Sxs include reliving the event in dreams and waking thoughts
(flashbacks), avoidance of reminders, persistent anxiety with autonomic
sxs and numbing.
DSM: Sxs 1month = PTSD; Sxs <1month = Acute stress disorder.
Px*: Trauma is re-experienced for several years, Px is worse with +ve past
psychiatric hx.

*Course is chronic for all anxiety disorders.

DSM Signs & Sxs for Panic attacks & Anxiety disorders
*A PA is a Sx not a Dx; 4 of the following must be present for classification as a PA.
Physical Signs:
Autonomic hyperactivity
Tachycardia, palpitations
Flushing & pallor
Cold hands
Dry mouth (xerostomia)
Urinary frequency
Pupil dilatation
Hyperventilation, Dyspnoea
Muscle tension
Trembling, twitching, feeling shaky

Physical Sxs:
Butterflies in stomach
Lump in the throat / Difficulty
swallowing or choking
Chest pain
Dizziness, Headache, Backache
Psychological Sxs:
Feeling of impending doom / dread
Derealisation (the experience of the
world or people in it seeming
Depersonalisation (being detached
from oneself)
Fear of going crazy, losing control
or dying


: Ratio

Age at onset

Family Hx

Twin Studies



Late 20s

50% of pts have

one affected



Variable; early

25% of 1 relatives

Concordance in
MZ twins > DZ
concordance in
MZ twins; 1015% in DZ twins

*Most common


Late childhood

May run in




Adolescence or
early adult life

35% in 1
relatives; a/w
Tourettes syn.

Concordance in
MZ twins > DZ


30% in Vietnam


Any age,



Nb: 1 = 1st Degree, MZ = Monozygotic, DZ = Dizygotic

Mood disorders
Depressive disorders (MDD)

50% of MDD exhibit anxiety or obsessive brooding, and 20-30% of primarily

anxious patients also experience depression1
Bipolar I Disorder

Massive anxiety may occur during a manic episode

Psychotic disorders

Schizophrenic patients may be anxious and have severe obsessions in addition

to or preceding the outbreak of hallucinations or delusions
Atypical psychosis (psychotic disorder not otherwise specified)

Massive anxiety is present, in addition to psychotic features

Adjustment disorder with anxiety
Patient has a history of psychosocial stressor 3 months of onset.
Medical & neurological conditions
Endocrine disorders eg. Phaeochromocytoma
Inflammatory disorders eg. SLE, Rheumatoid arthritis
Neurological disorders eg. Cerebral neoplasms, haemorrhages, migraine,
encephalitis, MS, epilepsy, etc.
+ Many many more
Substance-related disorders
Anxiety often associated with intoxication (especially caffeine, amphetamines,
cocaine, hallucinogens) and withdrawal states.

Mx of Anxiety Disorders
Rx will vary depending on the anxiety disorder. Phobias and PTSD are best treated
with psychotherapy alone, whereas the other disorders are usually combined with

Immediate Mx of PA
Isolated PAs should be treated with non-pharmacologic means & all other
medical causes should be ruled out (eg. AMI).
Breathing techniques: Deep slow breathing or Re-breathing in a paper bag
(Arterial CO2 & Sxs)
eg. Diazepam (Valium) 2-5mg PO, Oxazepam (Serepax) PO, Alprazolam
(Xanax) PO
Not usually for Rx of acute attacks, used to treat residual or anticipatory
anxiety (~30mins to enter blood stream)
BZD usage has largely been replaced by newer SSRIs but Alprazolam is
particularly good and can be used in combination

ii. Short-term Mx
SSRIs (1st Line Rx, even w/o depressive sxs)
Paroxetine (Aropax) and Sertraline (Zoloft) are currently approved but
others may be tried
Indicated for all anxiety disorders except phobias; initially a transient
anxiety may occur
Tricyclic Antidepressants (TCAs) (2nd Line Rx)
Imipramine (Tofranil) is the TCA of choice
Doses are typically higher for panic than for depression
Irreversible Monamine Oxidase Inhibitors (MAOIs) (2nd Line Rx)
Phenelzine (Nardil)
Risk of hypertensive crisis & fatal intracranial bleeding with consumption of
foods containing tryptophan or tyramine, or with co-administration of
narcotics, TCAs, or other MAOIs.
iii. Long-term Mx
Continue pharmacological Rx as required
Cognitive-Behaviour Therapy
Effective in disorders where thoughts cause behaviour eg. OCD
Insight-Orientate Psychotherapy
Goal is to insight into psychological conflicts that, if unresolved, can
manifest as symptomatic behaviour
This includes the subconscious meanings of their anxiety, symbolism,
secondary gains of the sxs, etc.
Supportive Psychotherapy
Use of psychodynamic concepts to promote adaptive coping by promoting
adaptive defences and discouraging maladaptive ones.

1. Kaplan & Sadock (2001), Pocket handbook of clinical psychiatry, 3 rd edn, Lippincott Williams & Wilkins.
2. Katona C & Robertson M (2005), Psychiatry at a glance, 3rd edn, Blackwell publishing, Australia.

Somatoform Disorders
Somatoform disorders are distinguished by physical sxs that cannot be explained
by a medical or other psychiatric condition diagnosed in the patient. These
patients physical sxs are a manifestation of their mental illness, and they are
significant enough to cause distress and functional impairment.

Somatization disorder
Conversion disorder
Body dysmorphic disorder
Pain disorder

Generally more common in low-socioeconomic & low-education groups
Less seen in psychiatric institutions; much more common in medical wards and
GP surgeries
Multi-system complaints
(pain, GIT, sexual, neuro)
that recur over several
years & are not explained by
any known medical
1 neurological sign or sx
a/w psychological conflict
or need.
Pts present with paralysis,
pseudoseizures, ataxia,
blindness & other
neurological signs/sxs.
Morbid fear or belief that
one has a serious disease
even though none exists.

1. Avoid psychotropics as pts
often become dependant.
2. Insight or Supportive
psychotherapy useful.


Imagined belief (not of

delusional proportions) of a
bodily defect.

SSRIs effective in 50%

Psychotherapy useful

Pain disorder

A preoccupation with pain in

the absence of physical
disease to account for its
intensity. Depressive sxs

Psychotherapy and counselling




Must find all medical causes

(medical disorder eventually
founding 25-50% of cases).
BZDs for anxiety
Antidepressants for obsessive
ruminating about sxs
Psychotherapy (Insight, CBT)
Anti-anxiety &
Psychotherapy (Insight, CBT)

Course & Px
Chronic course,
few remissions.
Px: Poor to fair.
Tends to recur;
episodes in b/w
are sx-free.
Px: Excellent
(except in chronic
Chronic course
with remissions.
Px: Fair to good;
waxes and wanes
Chronic course;
beliefs may
progress to
Px: Unknown
Px: Variable

Somatoform vs. Factitious vs. Malingering

Somatoform disorder = pt. actually experiences physical sxs as an expression
of unconscious conflict
Factitious disorder = conscious deception but for unconscious secondary
gains apart from assuming the sick role
Malingering = conscious deception for conscious secondary gains

Factitious Disorders
Where patients consciously produce physical or psychological sxs in order to
assume the sick role (and in most cases, be admitted to hospital). Any other gain is
unconscious (ie. no external incentive).
Clinical Presentation
Physical signs & sxs:
Nausea, vomiting, pain, seizures
Intentionally putting blood in faeces or urine
Artificially raise body temperature
Take insulin to lower BSL
Psychological signs & sxs:
Intentionally production of psychiatric sxs hallucinations, delusions,
depression, bizarre behaviour
Fabricating stories of stress & extravagant lies that the patient may believe
Stories of substance abuse
Course & Px
Course is typically chronic
Substance abuse risk is high over time
Risk of death from multiple surgical procedures over time

Avoid unnecessary tests & procedures and confront pt about diagnosis of a

Factitious disorder and feigned sxs.
Psychopharmacological therapy is useful for associated anxiety or depression.
Appropriate Mx of substance abuse.
Contact child welfare services if disorder is in a parent

Voluntary and conscious production of physical or psychological sxs in order to
accomplish a specific goal / secondary gain (eg. insurance payments, avoid jail
Clinical Presentation
Patients may have vague or poorly localised sxs that are described in great detail.
They are easily irritated if the doctor shows any scepticism to the history.
Psychosocial history usually reveals some area with a defined goal (where
secondary gain occurs).
Pt should be monitored as if real disease were present, but no Rx should be
offered. Identify areas of secondary gain and allow pt to ventilate. Help provide
ways of managing the stressor.

Substance Abuse
Abuse (DSM)
1 or more of the following within a 12 month period:
1. Recurrent use causing failure to fulfil major
2. Recurrent use in physically hazardous situations (eg. driving)
3. Recurring substance related legal problems
4. Continued use despite recurrent social or interpersonal problems
Dependence (DSM)
At least 3 of the following occurring within a 12month period:
1. Tolerance (dose for same effect)
2. Withdrawal sxs on cessation
3. Substance taken for longer or in larger amounts than expected
4. Persistent desire / failed efforts to cut down
5. Impaired social or occupational functioning
6. Substance use is continued despite knowledge of adverse physical or
psychological problems
7. Great deal of time / effort is spent on obtaining, using and recovering from
the substance
Withdrawal Syndrome
Sweating & Fever
Musculoskeletal pain
Abdominal cramps
Diarrhoea, nausea and vomiting

piloerection (goose-bumps)
Shivering or trembling
Increased blood pressure

Alcohol (ETOH)
Aetiology is very multifactorial. Incidence of abuse / dependence increases with:
FamHx of alcoholism (4 fold risk) & depression
Race eg. Low incidence in Asians
Concurrent psychiatric disorders eg. Personality disorders, schizophrenia
Psychosocial stress
ETOH is a depressant that produces somnolence and neuronal activity. It can
be categorised with the other sedative-anxiolytics such as BZDs, barbiturates
and carbamates.
These agents are cross-tolerant with ETOH (ie. tolerance to ETOH causes
tolerance to the other agents despite not actually been exposed).
It is thought to production of opioid-like alkaloids as well as act on many other
receptor pathways (eg. NMDA)
ETOH is potentially lethal when taken in combination with any agent from this
class eg. BZDs.
Cut down before (tried)?
Annoyed when others have suggested you cut down?
Guilty about amount you drink?

Eye-opener to get the day started?

Alternatively, you can use the AUDIT questionnaire (8-14 is risky of harmful usage;
>14 indicates dependence).
Low Risk
Short-term harm risk:
6 per day, up to
3 days per wk
4 per day, up to
3 days per wk
Long-term harm risk:
4 per day
28 per week
2 per day
14 per week

Medium Risk

High Risk

7-10 per day

11+ per day

5-6 on any day

7+ per day

5-6 per day

29-42 per week
3-4 per day
15-28 per week

7+ per day
43+ per week
5+ per day
29+ per week


FBE: Macrocytic anaemia

Blood Alcohol Concentration (BAC)
Rapidly rising BAC correlates with degree of intoxication; intoxication is
more pronounced with BAC is rising rather than falling
Liver biochemistry
GGT: measure of recent ETOH consumption (also with DM)
AST & ALT: if raised, 50% have fatty liver. All biochemistry will be
deranged in decompensated cirrhosis
Liver function tests (LFTs)
Serum albumin and Prothrombin Time (PT) are the best indicators
Ultrasound (Dx cirrhosis)
Serum -fetoprotein: Marker of HCC

The goal is prolonged maintenance of total abstinence. Insight is the first critically
important step but can be difficult to achieve. Patient must see that they have a
1. Detoxification and Rx of withdrawal sxs
2. Alcoholics Anonymous (AA) and Al-Anon
AA is for the patient, Al-Anon is for the patients family
3. Psychotherapy: Family Therapy is particularly useful
4. Psychopharmacology
Disulfiram (Antabuse)
Inhibits aldehyde dehydrogenase causing accumulation of acetaldehyde
Causes ETOH to taste terrible & ingestion to result in flushing, nausea
and vomiting
Compliance is the biggest problem, so use is temporary only
Naltrexone (ReVia)
Both 1st line; used for 612mths.
Decreases craving for ETOH by blocking release of
Drinking rate (66%).
endogenous opioids / receptor blockade
Very few SEs & No
One tablet per day. Compliance is good.
withdrawal state.
Acamprosate (Campral)
Cheap (relatively).
Decreases craving by other receptor system blockade

3 tablets per day

Opioids affect opioid receptors, as well as dopaminergic systems.
-opioid receptors: mediate analgesia, respiratory depression, constipation &
-opioid receptors (kappa): mediate analgesia, diureses & sedation
-opioid receptors: mediate analgesia
Heroin is more potent, more addictive, has a faster onset of action and cross the
blood-brain barrier faster than morphine.
Multiples routes; Smoked (opium), IV (heroin), inhaled (snorted), or combined with
stimulants IV (speedball).
Clinical Features

CNS depression
GIT motility
Respiratory depression
Nausea + vomiting
Bradycardia & Hypotension
Slurred speech
Pupillary constriction (pin-point

Euphoria (total body orgasm)
Swinging anxiety / tranquillity
Attention & memory
Psychomotor retardation

Mx (Long Term)
Mx Option
1. Nothing

No interventions

2. Withdrawal
3. Home Detox

Detox cold turkey, residential detox

4. Substitution

5. Abstinence

Family help Community services

Not necessarily at home eg. travel
Adjuvant BZDs effective
a. Methodone (full-agonist)
b. Buprenorphine (partial-agonist) +
Naloxone (Suboxone)
Long acting oral opioid agonists prevents
the development of withdrawal sxs,
craving, IV use, and blocks the euphoric
effects of heroin if relapse occurs.
Naltrexone (ReVia) PO
Pure long-acting opiate receptors
antagonist. Blocks opiate effects for those
committed to abstinence.

Mx (OD)
Naloxone (Narcan) 0.4mg IV or IM every 2-3mins up to 2mg

Success rates
5-10% abstinence
Mortality ~2-3% per year
5-10% abstinence (or less)

50% pt retention at 1year

25% pt heroin cessation at
4-fold reduction in
Very poor retention rates.
Risk of OD due to

Naloxone is a fast acting opioid-receptor antagonist. It reverses opioid effects

of CNS & respiratory depression within 2 mins (IV).
An acute withdrawal syndrome may occur post-adm in dependent patients

Other Drugs
Lysergic acid diethylamide (LSD)
Produces physiologic & psychologic effects but not dependence
Magic mushrooms (Psylocibin)
Have effect similar to but less intense than LSD
Ecstasy (MDMA):
Synthetic amphetamine analogue
Has mixed stimulant and hallucinogenic properties
Amphetamines (speed, crystal meth.)
Sedatives & Hypnotics
Benzodiazepines (BDZs)
Solvents (eg. glue, petrol)
Initial euphoria is followed by drowsiness
Psychological is common but not physiological
Toxic effects: Cognitive impairment, hepatorenal and cerebral damage,
Phencyclidine (PCP or angel dust)
Usually smoked
Effects include euphoria, peripheral analgesia, impaired consciousness and

Personality Disorders
Described as a persons characteristic configuration of behaviour response patterns
in ordinary life; a totality that is usually stable and predictable.
Personality Disorder (PD):
When personality traits are rigid, maladaptive and produce functional impairment
and subjective distress.
Traits are pervasive and persistent
Traits are ego-sytonic (ie. acceptable to the ego), not ego-dystonic (eg. in OCD)
Traits are alloplastic, not autoplastic (ie. pt seeks to alter the environment
rather than self)
Traits are held rigidly
Underneath the protective defensive mechanisms lies anxiety

Dx requires a Hx of long-term difficulties in social and occupational spheres

By definition PD cannot be diagnosed in 16yrs old as personality has not been

Cluster A
Paranoid PD

Schizoid PD
Schizotypal PD
Cluster B
Histrionic PD

Narcissistic PD

Antisocial PD

Odd, eccentric, and introverted
Suspicious and mistrustful; believe that everyone
is out to get them / bring them down
Often hostile, irritable or angry; often bigots
High prevalence in armed forces
High propensity to develop psychosis (schizo)
Space cadet; aloof and vague
Lives an isolated lifestyle; Love is the hardest part
of success
Connections with magical thinking and reliance
on superstition to resolve conflict.
Appear strange to others; multiple oddities
Explosive, outward, dramatic, emotional &
Hollywood / Paris Hilton / Self-centred.
Similar to narcissism but less body-orientated.
Gets bored easily so jumps from thing to thing;
very attention seeking; in .
Person is hyper-dramatic & extraordinarily
seductive but frigid & immature. Stems from
being rejected as dads little girl when she hits
Divinely right; obsessed with body and image.
Explode easily over nothing if they are crossed,
have shadow r/ships where the other fulfils their
needs. Pervasive pattern of grandiosity & overconcern with issues of self-esteem.
Attracted to solo / powerful positions; in .
Maladaptive behaviour where the pt doesnt

Fantasy (create
imaginary worlds
and friends)
feelings are
attributed to
A/w tendency for
psychotic thinking

(unpleasant affects
are repressed or
replaced with
pleasant ones)
Splitting (others
seen as all good or
all bad)
Acting out (wishes
or conflicts are
expressed in action
without awareness
of the idea or

Borderline PD

Cluster C
Avoidant PD

Dependant PD

compulsive PD
PassiveAggressive PD

recognise the rights or feelings of others.

Incapacity to feel guilt; blames others.
Very high prevalence in jails
Pt fluctuates between psychosis and reality
Self-harm (to see they are alive) is the hallmark
ie. acting out. ~50% will suicide. Splitting
invariable. Self-image / worth problems so will
follow influence of others.
Strongly a/w young sexual abuse, in .
Unstable and intense r/ships very common.
Pt pain is intense
Anxious, fearful and neurotic
Shy or timid personality; hates to confront or
discuss conflict (esp. emotional).
Easily hurt and sensitive to rejection; socially
withdrawn but desires social involvement.
in ; Has a sense of self but is submissive;
always does what the other wants.
Lack self-confidence and intolerant of being
alone. Passive, with difficulty with disagreement.
Perfectionism, orderliness (inc. rules &
regulations) and inflexibility predominate.
Procrastination over minute details; sexual
dysfunction common
Not social, very anxious, self-blaming and
introverted. Likes to get along with others but
cannot cope with anger (sublimation). Deep
seeded anger is communicated by forgetting or
omitting things to harm others.

Isolation (facts are

recalled without
(aggression towards
others is expressed
indirectly through
(where physical
sxs / illnesses are
exaggerated as a
means of evading
guilt, anger,
responsibility, etc.)

Psychotherapy choice is dependant on the PD:
Group therapy
Dialectical Behaviour Therapy (DBT) for Borderline PD
Antipsychotics may be useful for cognitive sxs
MAOIs may be helpful in Borderline PD (Rx mood)
Mood stabilisers (Lithium, valproate and carbamazepine) can help episodic
behavioural dysfunction

Risk Assessment
Typically sad, depressed and with evidence of self-neglect. Beware of those who
appear bright and elated they may ready to complete their suicide plans.
Clinical Assessment
Current state:
1. Assess suicidal plans Any thoughts of suicide?:
Detailed action plan
Means to accomplish suicide (eg. Firearms, tablets) & Intent not to get
Finalisation of affairs eg. Will
2. Assess emotional state
Do you think things will ever get better?
Do you feel like a burden on people?
Does anything give you pleasure / is anything stopping you?
History Taking (Risk Factors):
1. Male + Caucasian + >45y.o are highest risk group
2. Recent loss / Anniversary of important loss
3. Psychiatric disorders:
Mood disorders
Psychotic disorders (Schizophrenia & Schizoaffective)
Personality disorders (especially Borderline)
Drug & ETOH abuse / dependence
4. PHx of:
Suicide attempts or self-harm (para-suicide)
Chronic physical illness (especially CNS disorders, HIV, malignancy or chronic
Physical or sexual abuse
5. FamHx of suicide
6. Poor social support
Assess risk (Low, Medium or High)

High risk pts should not be left alone; Hospitalise if unsure (even in ER)

Relieve any immediate distress to the patient

Make a No Harm Contract with patient
Rx agitation with Haloperidol or BZDs if required
Commence Rx of any underlying illness eg. Depression
Continue Rx of psychiatric illness eg. ECT if required for depression

Counselling, support services & Psychotherapy (CBT, Family therapy)

Electroconvulsive Therapy (ECT)

While the effectiveness of ECT has been shown, the mechanism of action remains
unclear. It is known that the treatment has a positive effect on inducing brain
The most common treatment is high-dose right unilateral therapy with electrodes
over the right temporal region and near the vertex. Less commonly, a bilateral
approach is used
a) Acute mania or psychosis (especially if psychosis is extreme)
b) Severe depression
Postnatal depression Psychosis
Melancholic depression refractory to other Rx
Where it has been efficacious in the past
c) Schizophrenia
Refractory to other Rx
Where it has been efficacious in the past
d) Catatonia
Extreme under- (c. stupor) or overactivity (c. excitement) of motor system
Typically occurs in catatonic schizophrenia, but can occur in other
conditions eg. Bipolar Disorder, NMS
e) Rapid Rx response eg. Depressive stupor leading to self-neglect, acute
f) Medical conditions
Neuroleptic malignant syndrome (NMS)
Parkinsons disease
Raised ICP (or any condition a/w raised ICP eg. brain tumour)
Severe HTN and/or Aneurysms (BP during tonic-clonic phase)
Recent myocardial infarction (AMI)
Bradyarrhythmias (HR during shocks)
Pacemakers (low risk of electrical damage to pacemaker)
Osteoporosis (risk of # during tonic-clonic phase)
MAOI or TCA use within the last 14days
Cessation of all psychotropics, especially antiepileptics (as they raise
seizure threshold)
Pt put under GA and given muscle relaxants
Seizure is induced for typically ~30secs
Headache, nausea & myalgia (common): Last the day of the treatment
Cognitive deficits (post-ECT delirium)

Confusion & disorientation (common) in the hour after treatment, but this
subsides during the day
Short term memory loss: Usually fully regained in the weeks following
completion of the course of treatment
Nb. Depression is associated with cognitive impairment also, and this may
improve post-ECT

Risks undergoing GA
Long-term memory loss (rare) Increased risk with bilateral ECT
Medical Cxs eg. Ruptured aneurysm

Course of ECT
ECT involves a series of treatments to achieve optimum outcome
Typical course = 3 times / week, with a total number averaging between 6-12
The number of treatments will vary according to the individual
Benefits of ECT:
Clinical evidence shows that ECT will produce a substantial improvement in
around 80% of patients with severe major depression.
Speed of efficacy: ECT can show clinical effect after a few treatments,
compared to medications which can take weeks to show effect
Pregnancy: Can be used in confidence in the 2nd and 3rd trimesters, less
evidence for the 1st trimester

1. QLD Govt. Health
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