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Psychiatry and Addiction Medicine Lectures

Week 1 Mood Disorders


Introduction to Psychiatry
Overview of Psychiatric Disorders
History of Psychiatry
Introduction to Addiction Medicine
Assessment of Patients with Addiction
Schizophrenia - Overview and Management
Mood Disorders - Overview and Management
Week 2 Schizophrenia
Skills - CBT
Skills - Mental State Overview and Tools
Skills - Taking a Psychiatric History
Mental State Examination
Phenomenology
Adverse Effects of Medication
Metabolic Complications and Monitoring
Extrapyramidal Symptoms
Week 3 Substance Abuse
Smoking Cessation Therapy
Cannabis
Management of Alcohol Withdrawal and Beyond
Brief Interventions for Hazardous Alcohol Use
Drug Seeking Patient
Prescription Drug Misuse
Stimulants
Management of Opioid Dependence
Week 4 Anxiety Disorders
Anxiety Disorders - Overview and Management
Anxiety disorders
Panic disorder
Generalised anxiety disorder (GAD)
Phobias
Obsessive-compulsive disorder (OCD)
Management
Overview of the Psychotherapies
Trauma, Life Events and Mental Illness
Socio-cultural Aspects of Psychiatry
Psychiatric Emergencies, Safety Issues and Management of Aggression
Personality Disorders - Overview and Management
Week 5 Child Psychiatry
Intellectual Disability
Child Psychiatry - Overview
Child Psychiatry - Emotional
Child Psychiatry - Behavioural
Perinatal Mental Illness
Skills Session - Family
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Skills Session - Interviewing the difficult adolescent


Skills Session - Behaviour management
Skills Session - Ethics Scenarios
Week 6
Older People- What is Different?
Management of Behavioural and Psychological Symptoms of Dementia
Delirium
Overlap of Physical and Psychiatric Illness
Eating Disorders - Overview
Eating Disorders - Management

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Week 1 Mood Disorders


Introduction to Psychiatry

Psychiatric disorders
Low prevalence disorders
Schizophrenia
Bipolar disorder
High prevalence disorders
Depression
Anxiety disorders
Across the whole age range
Developmental awareness
Child & Adolescent Psychiatry; Old Age Psychiatry
Interface between medicine and psychiatry (psychosocial factors)
Consultation Liaison Psychiatry

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Overview of Psychiatric Disorders

Psychiatric disorders: Illnesses or disease states, manifest by abnormalities of thinking, feeling and behaving,
that cause the individual significant distress or significantly impair their ability to work, play and love.
20% of a community in 12 months, 40% over lifetime, persisting

% of sample
1997

2007

Any anxiety disorder

9.7

14.4

Substance use disorder

7.7

5.1

Any affective* disorder

5.8

6.2

Neurasthenia

1.5

N/A

Psychosis

0.4

N/A

Personality disorder

6.5

N/A

Any disorder

20.3

20.0

7.1

*Affective = mood disorders, including depressive states and bipolar mood disorder
12-month prevalence of DSM-IV disorders in Australia
ABS National Survey of Mental Health and Wellbeing: Summary of Results 2007

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Appreciate the difference in prevalence and impact of various psychiatric disorders between males and
females
E.g. greater prevalence of substance use disorders in males vs anxiety and depression in females

Comorbidities male

Comorbidities female

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Types of Psychiatric Disorders


Organic Disorders - Delirium, dementia, acquired brain injury, medical illness presenting as psych.
Psychotic Disorders - Schizophrenia, schizoaffective disorder, delusional disorders.
Mood Disorders - Major depression, bipolar disorder (may also be psychotic), dysthymia
Anxiety Disorders - Panic, phobias, obsessive compulsive disorder, posttraumatic stress
Personality Disorders - Lifelong maladaptive patterns of interacting with the world and others & in view of
self
Somatoform Disorders - Psychiatric disorders that present as physical illness (eg conversion disorder,
hypochondriasis)
Substance Disorders - Abuse, dependence, withdrawal intoxication
Other Disorders - Sleep disorders, eating disorders, paraphilias, Munchausens, childhood disorders
Intense Reactions - Adjustment disorders, pathological bereavement
Role Problems - Abnormal illness behaviour, abnormal treatment behaviour
4 main features of sick role:
Exemption of sick person from certain normal social responsibilities
Exempted from responsibility for his own condition i.e. victim of forces beyond his control
Price of exemption is exclusion from full participation in society, deemed to be in undesirable state
Obligation to cooperate with treatment and try to get well
Signs and symptoms of psychiatric disorders
Behaviour
Observed
Reported behavioural changes
Need for corroborative hx
Impulse control
Self/other harm/suicide
Relationships
Emotion (mood and affect)
Depression
Elation
Anxiety
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Irritability
Thinking
Content
Delusions
Over valued ideas
Obsessions
Form
Perception
Hallucinations
Illusions
Cognition
Insight and Judgment

Classificatory Systems
Diagnostic and statistical manual of mental disorders (DSM-IV/5) - American
International Classification of Diseases (ICD 10 11)
Categorical
Problematic, as these conditions often exist along a spectrum rather than all patients with a
particular condition presenting with identical symptoms
Symptoms are also important in determining treatment and prognosis
Problem Formulation in Psychiatry, think in terms of:
Psychiatric Disorder
These symptoms
Undergoing these stressors
Personality
Medical illnesses
Having certain predisposing factors
Living in these circumstances
Biological

Psychological

Predisposing
Precipitating
Perpetuating
Pattern
Protective
Prognosis

Treatments are also BioPsychoSocial:


Biological
Pharmacological
ECT
Psychological
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Social

Social

Cognitive
Behavioural
Depth
Counselling

Recovery is the goal


More than just symptom control:
Reintegration into desired culture & community
Satisfying relationships
Meaningful work and leisure activity
Spiritual dimension
Goals identified by the individual
Ethical and legal dimensions
Individual rights
Freedom
Treatment
Access to services
Safety
Self
harm
exploitation
Others
Staff
Mental Health Act
The objects of this Act include:
a) to provide for the care, treatment and control of persons who are mentally ill or mentally
disordered
b) while protecting the civil rights of those persons, to give an opportunity for those persons
to have access to appropriate care
c) to facilitate the involvement of those persons, and persons caring for them, in decisions
involving appropriate care, treatment and control.
Interactional stressors
e.g. High expressed emotion - communication style that predisposes to relapse of schizophrenia
Genetic predisposition
5HTTLPR (serotonin-transporter linked polymorphic region) depression
MAO-A functional polymorphism mediating the effect of violence in childhood on an individual
Trauma
Mainly two types described, can be used to describe a single event or period of adversity
Complex - usually refers to experience of significant continuing adversity during childhood e.g. physical,
sexual abuse
?
Definition of in the Mental Health Act 2007
Mental Illness
Mental illness means a condition that seriously impairs, either temporarily or permanently, the mental functioning
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of a person and is characterised by the presence in the person of any one or more of the following symptoms:
(a) delusions,
(b) hallucinations,
(c) serious disorder of thought form,
(d) a severe disturbance of mood,
(e) sustained or repeated irrational behaviour indicating the presence of any one or more of the symptoms
referred to in paragraphs (a)(d).
Mentally ill person s.14
A person is a mentally ill person if the person is suffering from mental illness and, owing to that illness, there are
reasonable grounds for believing that care, treatment or control of the person is necessary:
a) for the persons own protection from serious harm, or
b) for the protection of others from serious harm.
In considering whether a person is a mentally ill person, the continuing condition of the person, including any likely
deterioration in the persons condition and the likely effects of any such deterioration, are to be taken into account.
not about risk, actually about protection from serious harm. very broad definition.
Mentally disordered person s.15
A person (whether or not the person is suffering from mental illness) is a mentally disordered person if the persons
behaviour for the time being is so irrational as to justify a conclusion on reasonable grounds that temporary care,
treatment or control of the person is necessary:
(a) for the persons own protection from serious physical harm, or
(b) for the protection of others from serious physical harm.
Involuntary admission s.12-13
A patient or other person must not be involuntarily admitted to a mental health facility unless an authorised
medical officer* is of the opinion that:
a) the person is a mentally ill person or a mentally disordered person, and
b) no other care of a less restrictive kind, that is consistent with safe and effective care, is appropriate and
reasonably available to the person.

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Authorised MO must inform primary carer within 24 hours


ASAP, complete form 1, first psychiatrist sees patient within 12 hours
First psychiatrist to organise review by 2nd psychiatrist ASAP

Mental Health Review Tribunal


Specialist quasi-judicial body constituted under the Mental Health Act 2007
Lawyer alone (Mental Health Inquiry)
Panel consisting of Lawyer, Psychiatrist and suitably qualified community member for most other matters.
Wide range of powers concerned with treatment and care of people with a mental illness, including:
Involuntary patient orders
Community treatment orders
Make and revoke orders for financial management by NSW Trustee for detained patients
Approve use of ECT for involuntary patients
Approve surgery on detained patients
Psychiatry Common themes
1. Psychological disorders are common
2. Aetiology is multifactorial
3. Comorbidity is the rule - with medical and psychiatric illnesses
4. Disorders commonly start early in life
5. Treatment must consider biopsychosocial domains
6. Recovery should be the goal of intervention

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History of Psychiatry

Early history
trephined skulls 5000 BCE
madness as punishment in deuteronomy
Hindi demon, Grahi - convulsions
Babylonians Mesopotamians
spirit invasion
sorcery
demonic malice
evil eye
Greek tradition
mythology
homer
characters are puppets
external forces - gods and demons
inner life is not important
philosophy
emergence of introspection
Socrates, Plato, Aristotle
life is rational
reflection on madness - not from external forces
theatre
characters contributing to outcomes
not just fate and gods
theatre becoming therapy
playing out madness, forcing the unthinkable into the open, restoring reason
collective catharsis
internal conflict as a dimension of madness
medicine
HIppocrates (5th C BCE)
all illness is natural
illness has a rational explanation
epilepsy (sacred disease) had a rational explanation
all madness was within medicines bounds
four humours
yellow bile - choler - overheats, raving, mania
black bile - melancholic - dejection, depression
blood - sanguine
phlegm - phelgmatic
providing a somatic theory for madness
late
Aretaeus (2nd C CE)
description of melancholia and furor
possible description of mania and depression
Christianity
man is not rational
man is a sinner
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mental illness is a manifestation of sin or punishment


man is the battleground of god and the devil
European witch hunt
1450-1750
uncertain numbers 100,000 - 200,000
mostly women
midwives
cooks
healers
practiced magic in society
mostly unmarried
context
urbanisation and reformation
poverty
inflation
status of women
morally and intellectually inferior
no physical or economic power
must be using sorcery
easily accused
decline
clearly out of control
The Enlightenment
scientific revolution
literacy
rise of professions and bureaucracy
capitalist centralised economies
Madness of George III
1788
bizarre behaviour of monarch
political and constitutional crisis
Reverend Dr Francis Willis
psychological bullying
morale boosting
fixing with the eye
routine medication such as blistering
mental illness could be cured
moral management
experienced therapist outwitting the deluded psych of his patient
acute intermittent porphyria
A world without psychiatry
village idiot
fool and his staff
ship of fools
chained to walls
kept in holes
hidden - avoided asylum to avoid shaming the family
Madhouses
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Priory of St Mary of Bethlehem (13th C)


bedlam
restraints
treatments
viewing
medical involvement
The Great Confinement
Foucault
the tain of unreason - hospital detention
mad
poor
petty criminals
layabouts
street walkers
beggars
Asylum
18th C
setting with orderly routines and communal spirit
England - Battie and the Tues
France - Pinel and Esquirol
Italy - Chiarugy
doctor-patient relationship - moral therapy
as distinct from the traditional madhouse
British Psychiatry
themes
moral therapy replaced chains
physical constraint replaced by moral control
little role of doctors
approach resulted in cure, optimism
concept of partial insanity, could be cured
action
medical profession frustrated about lay success
asserted right as primary diagnosticians
by 1840s had specialised journals
tried to convince others that public asylums under medical control was best
1850 Asylum Act
1850s asylums in full swing
moral therapy since as human and therapeutically sound
Criminal insanity
legal view, voluntary acts
medical, deterministic
rivalry between medicine and law
early trials
Earl Ferrers 1760
James Hadfield 1800
1800 Criminal Lunatic Act
1830s-40s psychiatry organising as a profession
McNaughtons Rules (1843)
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Daniel McNaughton and Robert Reel


Degeneration Theory (1857)
Morel (1809-1873)
Darwin and the Asylum experience
the degenerate human being, if he is abandoned to himself, falls into progressive degradation. He
becomes not only incapable of forming part of the chain of transmission of progress in human
society, he is the greatest obstacle to this progress through his contact with the healthy portion of
the population the span of his existence is limited as that of al monstrosities (Morel)
Freud (1856-1939)
if told all, using free association, unconscious repressions which were the basis of neurosis would
find release
personal background
influences
Charcot/Breuer
Darwin
what he did differently
sceptics
Emil Kraepelin (1856-1926)
influences
Morel, Bahlbaum, Hecker, Falret
emphasis on course and prognosis, not on biological psychiatry
form vs content
achievements
dementia praecox (SCZ) vs manic depressive psychosis
basis of modern Western psychiatry
Therapeutic nihilism
Heroic psychiatry
Wagner-Jauregg
1883 erysipelas - remission from psychosis
1887 suggested malaria for psychosis
experimented with tuberculin for GPI
1917 inoculated actress with blood from malaria sufferer
1927 Nobel Prize
1920s Sakel - Germany
insulin to relieve opiate withdrawal
insulin thought to help depression in diabetes
helped improve appetite
coma initially inadvertent
seizure inadvertent
tranquility
1930s - schizophrenia
1935 Moniz - Lisbon
resection prefrontal lobes 20 patients
London conference well received
Freeman and Watts - USA
Freeman took it on the road
office procedure
ice pick
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1934 Meduna - Budapest


1929 schizophrenia makes epilepsy better
biological antagonism
camphor
cardiazol
Electro-convulsive therapy
1938 Ugo Cerletti - Rome
not a cure for schizophrenia
relief of symptoms
role in depression
Modern Psychiatry
standardisation
DSM & ICD
new treatments
pharmaceuticals
talking therapies
phsychopharmacology
late 1950s
chlopromazine
imipramine
lithium (1940s)
explosion of psycho-pharmaceuticals
carein the community
decarceration since 1960s
medication
patient rights
crumbling asylums and their expense
some success

Introduction to Addiction Medicine


Neurobiological mechanisms of dependence
a. Neuronal Reward Circuits
i. Psychoactive substances initially activate reward pathways in the meso-limbic system of the midbrain and lower fore-brain, involving (in particular) pathways coursing from the ventral tegmental
nucleus to the nucleus accumbens.
ii. The two principal pathways are the dopaminergic system (especially relevant for psychostimulants
and nicotine) and the opioid system (most relevant for alcohol and opioids).
iii. With repeated use of these substances, the activity of these systems is suppressed and more
substance is required to maintain the normal state.
iv. Normal activities with rewarding effects become blunted or ineffective.
v. A negative mood and motivational state ensues.
vi. The reward system is re-set in a profound and enduring way.
b. The brain stress systems
i. With repeated substance use there is activation of brain stress pathways involving glutamatergic
transmission (glutamate is the main excitatory neurotransmitter) and corticotropin releasing factor
(CRF).
ii. There is also suppression (uncoupling) of the natural antistress systems, including the GABA and
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Neuropeptide Y circuits.
iii. This results in heightened activation from exposure to cues (triggers) for substance use.
c. Inhibition of frontal inhibitory pathways
i. With repeated substance use there is impairment of prefrontal inhibitory pathways.
ii. This is associated with deficiencies in executive functioning, decision-making, salience of substance
use and insight.
Summary of the mechanisms
Repetitive substance use induces profound and persistent changes in rewards, stress and inhibitory control
systems, the meso-limbic system.
These changes result in under-activity of the reward systems (high-jacking).
They re-set or supercharge the stress systems responses to psychoactive substances and triggers.
An internal driving force is generated, which directs and drives further substance use
This driving force is little influenced by the voluntary control, because of the impaired inhibitory system
The core syndromes are:
Hazardous use (WHO, NHMRC)
Harmful use (ICD 10) A pattern of alcohol or drug use which is actually causing physical or psychological harm
Substance abuse (DSM-IV) A maladaptive pattern of substance use leading to clinically significant impairment or distress, as
evidence by one or more of the following:
failure to fulfil major role obligations
substance use in physically hazardous situations
recurrent legal problems
continued use despite social or occupational problems
Substance dependence (ICD 10 and DSM-IV) A syndrome of repetitive substance use which reflects an internal driving force, and includes:
a strong desire to take a substance,
impaired control over its use,
a higher priority given to substance use over other activities and obligations,
increased tolerance,
sometimes a withdrawal state, and
continued use despite harm.
Substance withdrawal syndrome
Physical complications from substance abuse
1. Liver disease
2. Peptic ulcer
3. Pancreatitis
4. Gastrointestinal cancer
5. Cardiomyopathy
6. Hypertension
7. Cerebral thrombosis and haemorrhage
8. Metabolic disorder
9. Malnutrition and vitamin deficiency syndromes
10. Blood disorders
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11. Blood-borne virus Infections


12. Trauma
Neuropsychiatric complications
1. Delirium
2. Memory impairment (amnestic syndrome)
3. Frontal lobe and other brain damage
4. Cerebellar disease
5. Stroke
6. Brain contusion
7. Intracranial haematoma
8. Peripheral neuropathy
9. Rarer conditions
Domestic and Allied Problems
Loss of friends
Deterioration in marital and other significant relationships
Spouse has varied psychological symptoms e.g. stress, anxiety, tension
Domestic arguments
Domestic violence
Neglect of children
Separation
Divorce
Occupational
Absenteeism (especially Mondays)
Poor work performance
Unexplained absence during working day
Failure to gain promotion
Demotion
Dismissal
Unemployment
Financial Problems
Loss of regular income from employment
Hardship from money spent on alcohol
Gambling debts
Victim of fraud
Legal Problems
Drink-driving offences
Loss of motor vehicle licence
Property crime
Assault
Homicide
Miscellaneous
Prostitution
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CNS Depressants

CNS Stimulants

Hallucinogens

Alcohol
Benzodiazepines
Barbiturates
Other sedative-hypnotics
Cannabis
Heroin and other opioids
Antihistamines
Kava

Amphetamines
Cocaine
Betel nut
Nicotine (state-altering)
Ecstasy

LSD
Mescaline

2010 lifetime use of drugs

2010 use in past year

Alcohol
Tobacco
Cannabis
Heroin
Amphetamines 7%
Cocaine
MDMA
Any illicit drug
Injected illicit drugs

Alcohol
81%
Tobacco
Cannabis
Heroin
Amphetamines 2%
Cocaine
MDMA
Any illicit drug
Injected illicit drugs

88%
42%
35%
1%
7%
10%
40%
2%

Substance related deaths


In 2010:
72% due to tobacco
25% due to alcohol
3% due to illicit drugs rising rates related to opiates
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18%
10%
0.2%
2%
3%
15%
0.4%

Prevalence of Alcohol Use and Misuse


90% of adults drink alcohol, at least occasionally
20% of men and 8 - 10% of women drink hazardously
10% of men and 2% of women experience significant alcohol-related harm
6% of men and 2-3% of women have alcohol dependence (515,000 in Australia)
Alcohol is the attributed cause of approx 4,500 deaths per annum (5% of all deaths).
Alcohol accounts for 10% of premature years of life lost
The cost of alcohol-related problems to the national economy exceeds $6 000 million per annum.
20 - 40% of hospital inpatients have an underlying alcohol problem; in 5 - 20% it is the cause of underlying
condition
15 - 20% of general practice patients have an underlying alcohol problem
Prevalence of Tobacco Use and Misuse
Currently <20% Australians are regular cigarette smokers.
The proportion of men who smoke has decreased steadily (from 72%) since 1945, whereas there has been
a gradual increase among women (from 25%).
Tobacco causes 19,000 deaths per annum.
Cost to national economy exceeds $6 500 million per annum.
Approximately one-third of inpatients are current smokers and another third are ex-smokers
Prevalence of Sedative-Hypnotic Use and Misuse
7% of adults aged 35 years and over take sedative-hypnotics (including tranquillisers and anti-anxiety
preparations) on a regular basis
This compares with 13% in 1977
They cause approximately 350 deaths per annum, principally from overdose
Prevalence of Cannabis Use and Misuse
The most widely used illicit drug in Australia
Prevalence of use is highly dependent on age
50% of men and 40% of women aged 20 - 40 years report having used cannabis at least once
20% in this age range report use in past month
4-5 % in this age range are cannabis dependent
Prevalence of Opioid Use and Misuse
Usage of illicit opioids is highly dependent on age
Prevalence of heroin use over 1.4%
About 75,000 heroin dependent persons in Australia
Decline in heroin use since 2000 the heroin drought
The use of prescribed opioids has increased diversion to illicit use
Opioid-related deaths peaked at 1,000 per annum in 1998; has now declined
Prevalence of Psychostimulant Use and Misuse Amphetamines
Amphetamines
15% of men and 10% of women aged 20 40 yrs report having used amphetamines at least once
The most commonly used preparation is methamphetamine (crystal meth; ice)
Commonly causes aggression, violence and psychotic phenomena
One-third of regular users experience psychosis
Ten-fold increase in hospitalisations for psychosis in past decade
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Cocaine
Cocaine use remains uncommon (especially in comparison with North America and Europe)
Causes aggression, violence, mood swings, psychosis
Use results in considerable financial losses
MDMA Ecstasy
The most commonly used illicit drug after cannabis
Prevalence of use has tripled over the past decade
Inexpensive - $20-40 per tablet
Tends to be used recreationally rather than dependently
Still relatively few presentations to treatment centres specifically because of Ecstasy use
More commonly used now with other drugs (e.g. alcohol and amphetamines)
High rate of benzodiazepine use to self-medicate during the recovery phase
Hallucinogens
LSD use not as widespread as 20 years ago, but substantial pockets of use
Costs $20 per tablet or tile
Users often young - 13-16 years
A wide variety of naturally occurring substances with hallucinogenic properties

Assessment of Patients with Addiction


What is a Drug and Alcohol Diagnosis?
1. Statement of the Drug(s) used
or Class of drugs
or Polydrug use
2. Definition of the core clinical syndrome
Hazardous or at risk use
Harmful use or substance abuse
Substance dependence
Withdrawal syndrome
3. Listing of sequelae
Physical
Neuro-psychiatric and psychological
Social
4. Coexisting disorders
Physical
Psychiatric
5. Antecedent Factors
How to reach a diagnosis
1. Key indicators
Psychosocial Problems
Stress
Insomnia
Depression
Impotence
Driving under the influence charges
Family members have symptoms of neurosis
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Physical Symptoms
Loss of appetite
Morning headache
Numerous visits to general practice with non-specific symptoms
2. Alcohol and drug history
Systematic assessment of
Use
Dependence
Complications
Current status
Reason for presentation (why now?)
Time of last drug use (intoxication, withdrawal)?

Introduce substance use as part of human experience


Place onus of denial of substance use on patient
Suggest various levels of intake (top high technique)
Feedback evidence of alcohol or drug related harm
Be aware of diversionary tactics
patient may switch focus of interview (e.g. to physical symptoms)
use alternative questions
or postpone questions (but never abandon line of questioning)

3. Social History
Living circumstances
Support network
Financial status/ means e.g. sex work
Employment
Educational status; qualifications
Legal issues offences; incarceration
Current abuse physical; emotional
Prior abuse childhood; violence
Trauma usually some history
4. Physical examination
General appearance
Signs of intoxication
Features of withdrawal
Evidence of tolerance evident when little or no impairment despite recent high use of sedatives or
elevated BAC
Mental state - Anxiety and agitation
Cutaneous stigmata (alcohol)
Evidence of injecting use
Complications occur in every system look for unexpected combinations e.g. hepatomegaly and
hypertension
4. Corroborative information
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Obtain history from collaterals


spouse
accompanying persons
Obtain information from other medical sources
general practitioner
previous hospital records

5. Aids to diagnosis screening and assessment questionnaires


6. Laboratory tests
GGT most sensitive; alcohol most common cause of increase Valuable in prognosis / monitoring
AST, ALT, INR generalised liver disease (usually hepatitis)
Uric Acid marker for gout
Carbohydrate Deficient Transferrin (CDT) Similar sensitivity to GGT; higher specificity limited use (nonMedicare funded)
Urine drug screening the mainstay of testing
Bench-top kits available to screen for cannabis, opioids, cocaine and amphetamines
Fewer practical physiological markers of drug use (unlike alcohol) Hep C, B, A serology + associated
hepatic impairment related to IVDU (LFTs; albumin; coags)
7. Special procedures
Quantification of alcohol/drugs
1 Standard Drink
= 10 grams alcohol
= 285mL of Beer
= 100mL of Wine
= 60mL of Fortified Wine
= 30mL of Spirits

Benzodiazepines: diazepam equivalents per day (or number of 5mg diazepam tabs)
Cannabis: number of cones per day, grams per day, dollar amount
Heroin: dollar amount per day, weights or grams per day
Methamphetamine: number of points (0.1 gram) per day, dollar amount
Cocaine: number of lines, dollar amount
MDMA: number of tablets per occasion

Dependence
3 criteria around the same time:
1. Tolerance
2. Withdrawal
3. Using longer than intended
4. Persistent desire or attempts to control/cut down/stop
5. Excessive amount of time to get drug or recover from drug
6. Reduction in social, occupational, recreational activities
7. Use continued despite knowledge of physical and psychological effects
Abuse
Over 12 months, 1 or more of (recurrent)
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1.
2.
3.
4.

Role problems (failure to fulfill)


Hazardous situations
Legal problems
Interpersonal problems

Substance Use Disorders and Mental Health Disorders


1. Mental health disorder may be a complication of a substance use disorder
2. The mental health disorder may be a cause of the substance use disorder
3. Both may have developed simultaneously
4. Both may be due to a third disorder

Schizophrenia - Overview and Management

Epidemiology
Incidence: 15.2/100,000; RR male: 1.4; RR migrant 4.6
Prevalence: 4.6/100,000; lifetime prevalence: 7.2/100,000 i.e. 1%
less common in least developed countries
Diagnostic profile of psychotic

disorders:

Four main dimensions characterise


general psychotic
syndrome:
affective dysregulation (depression, mania, anxiety)
psychosis (delusions, hallucinations)
negative symptoms (motivational impairment)
cognitive alterations
Behavioural expressions of vulnerability: prevalence of 10 - 20%, heritability: 40%
Evidence suggests that environmental influences associated with psychotic disorder may have greater
impact on affective and psychotic dimensions, which are more common in women, whereas negative and
cognitive dimensions may be more strongly associated with developmental impairment and male sex. Gx,
geneenvironment interaction.
For example, higher levels of affective dysregulation are likely to lead to active help-seeking, whereas
psychosis may lead to clinical detection through social conflict and cognitive symptoms through reduced
social competence.
As dimensions contribute independently to clinical detection by psychiatric services, symptom dimensions
are subject to co-morbidity bias (that is, are much more correlated and co-morbid at the level of psychiatric
services), giving rise to clinical diagnostic descriptions such as schizophrenia that have a of dimensional
expression.

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Risk factors for schizophrenia (*OR>3)


Place/time of birth
winter
urban
Infection
influenza
respiratory
rubella*
poliovirus
CNS
Postnatal
famine
bereavement* ?
flood
unwantedness
maternal depression
Obstetric
Rh incompatibility
hypoxia
CNS damage*
Low birth weight
pre-eclampsia
family history*
Other factors:
no. of childhood traumatic experiences increase likelihood of developing a psychosis in
linear fashion*
psychosis proneness is best predicted by childhood adverse events*
other factors: sexual abuse affects M>F > depression >physical abuse
Drugs
Cannabis use, especially in early adolescence

Pathophysiology of Schizophrenia
Dopaminergic dysfunction
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dopamine levels in post-mortem in schizophrenia


therefore antipsychotics typically block D2/3 receptors
DRD2 gene strongly associated with schizophrenia
Glutamatergic hypofunction
?
Neuropathology of schizophrenia
pyramidal neurons become smaller and more densely packed, but are unchanged in number
reduced neurophil volume
reduced axonal and dendrites arborizations (less extensive, aberrantly located synaptic connections)
thinner cortex (laminae II & III), grey matter loss
number and function of oligodendrocytes
glia are unaffected
Structural brain changes in schizophrenia
widespread in frontal, parietal and temporal regions
worse in schizophrenia than other psychotic disorders
affects connectivity
Symptoms
Positive
hallucinations
delusion
thought disorder
lack of insight
Negative
alogia - lack or inability to speak
blunted affect
amotivation
asociality
Cognitive
attention
memory
planning
problem solving
social cognition
Anxiety/Depression
Excitement
hostility
agression
disorganisation
Illness progression
Premorbid phase > (illness onset) prodromal symptoms > (episode onset) psychotic symptoms > first
treatment (end of first episode) > residual symptoms

Risk assessment in psychiatric disorders


Dangerousness
suicide
homicide
Treatment adherence
Absconding
- 25 -

Vulnerability
to exploitation
risk taking
to further deterioration

Response to suicidal thoughts in psychiatric disorders


Safety
ensure they are in a safe place
activate support network
determine if appropriate level of observation
monitor level of suicidality
Treatment
appropriate and prompt treatment of psychosis +- mood disorder
negotiate treatment
supportive counselling / psychotherapy
review situation regularly
Examination and investigations in psychiatric disorders
1.
Exclude possible medical causes of psychosis
2.
Establish safety of giving medications
3.
Establish a baseline for possible iatrogenic and other morbidity
Physical examination- weight /BMI, neurological - movement disorder screen
Neuroimaging - MRI/CT head
FBC, TFT, EUC, LFT, ESR/ANA, CA2+
Fasting BSL
Lipids
Urine drug screen
Other possible Ix:
neuropsychological assessment
ECG
EEG
B12, ceruloplasmin (copper carrier protein, low levels suggest pathology e.g. Wilsons disease)
autoimmune inflammatory anti NMDA
prolactin
CXR
Genetics
Infections serology: syphilis, HIV. hep B, C
Depressed mood is a part of the natural history of recovery from a psychosis.
Ongoing monitoring: Weight.BMI, BSL, Lipids, Vital signs

Side effects of antipsychotics. EPSE = extrapyramidal symptoms


extrapyramidal
up to 60% may have extrapyramidal side effects
dystonia - oculogyric, torticollis, laryngeal
choreoathetosis
- 26 -

parkinsonism/akinesia
treat with anti-cholinergic e.g. benztropine 2mg
akathisia
distressing subjective sense of physical and mental restlessness accompanied by physical
manifestations of restlessness
related to depression, suicide and later poor treatment adherence
treatment - antipsychotic reduction
anticholinergic
beta blocker
benzodiazepines
tardive dyskinesia
hyperkinetic neuromuscular disorder
receptor up-regulation or hypersensitivity secondary to exposure to antipsychotic medication
(orobuccal movements often early)
4% per year for FGA. Risks - age, female, physical illness, total dose, mood disorder.
Treat by decreasing dose. Change to clozapine.
tetrabenazine or sodium valproate, vitamin E
Weight gain
comes one quickly
correlates with the duration of use
particularly a problem of SGA (although all antipsychotics cause weight gain), especially clozapine
and olanzapine
patients with psychotic illness already less likely to exercise
anticholinergic effects
Peripheral
dry mouth, blurred vision, constipation, bladder
tachycardia, hyperthermia
idiosyncratic hypersalivation for clozapine
Central
learning difficulties, delirium
sedation
cardiovascular
increased rate of metabolic syndrome
increased incidence of sudden death with typical antipsychotics and clozapine
prolongation of QTc interval
clozapine - myocarditis, cardiomyopathy
endocrine
hyperprolactinaemia (with FGA, amisulpride, paliperidone, risperidone, clomipramine)
Sx: breast enlargement, galactorrhoea, menstrual irregularity, decreased libido, acne
risks: disturbed fertility, breast cancer, bone demineralization
neuroleptic malignant syndrome
exposure to dopaminergic agents
RF: dehydration, physical illness, high doses of neuroleptics, ?lithium
sx: confusion, autonomic instability, rigidity, raised CK
Treat with drug withdrawal, supportive
blood dyscrasias
phenothiazines (<1%) and clozapine (1-2%)
agranulocytosis
- 27 -

thrombocytopenia
eosinophilia
RF: ? age, genetic, myelosuppressive agents
seizures - especially with clozapine at high dose
polydipsia and water intoxication
temperature regulation abnormalities
hepatotoxicity
dermatological
mood
cognitive

10-20% dont show much benefit


25% remit without medication
4 - 6.5% not discharged after index admission
Clozapine most efficacious

Initial treatment regimen


Initial assessment
24 hours off antipsychotics - use benzodiazepines
Treat with second generation antipsychotic (SGA)
Trial for 4-6 weeks and change if no treatment response to other SGA
If still no response than trial clozapine
Start low and slowly increase
Consider adherence strategies / comorbidity if no response
Dosing of antipsychotics:
a. Low dose
Olanzapine 5 to 10 mg/d, risperidone 2 to 3 mg/d, or
quetiapine 300 to 400 mg/d (dose adjustment within range as
clinically indicated/tolerated).
b. Full dose
Olanzapine 12.5 to 20 mg/d, risperidone 4 to 6 mg/d,
or quetiapine 425 to 800 mg/d.
c. High dose
Olanzapine 22.5 to 30 mg/d, risperidone 6.5 to 10 mg/d,
or quetiapine 850 to 1200 mg/d.

- 28 -

Longer term treatment


target hallucinations/delusions and disorganisation
recovery is multimodal
for 1st episode - treat for a minimum of 1 year after resolution of symptoms. May need to treat for 2 years.
for >1 episode treat for 5 years after resolution of symptoms with tapering dose.
General principles of using antipsychotics
use one antipsychotic at a time
increase dose slowly, minimise side effects
reasonable trial i.e. 4 weeks at maximal dose
maintain on treatment for 12-24 months after cessation of symptoms (the longer the better)
if treatment fails, consider other factors
compliance
substance abuse
depression
trial of clozapine
Clozapine
indications
treatment resistant schizophrenia
failure to respond to at least two other antipsychotics
reasonable trials
depot trial
severe side effects to other antipsychotics
severe tardive dyskinesia
aggression
pharmacology
wide range effective dose 75 - 900 mg
plasma range 200-400 ng/ml
half life is 12 hours
metabolised CYC 1A2, 3A4
wide range of receptor sensitivity
D2,3,4,1
5HT1A, 2A,2C, 3,6,7
alpha1&2
H1
M
contraindicated with any other medication that may suppress bone marrow
monitor regularly
FBC (WBC > 3.5, agranulocytosis risk)
BLood group
Temperature, HR, weight
cardiac enzymes for first 4 weeks, echocardiogram after 6 months (myocarditis risk)

Psychosocial Treatments
Case management
Assertive community treatment
Psychoeducation
Family therapy no significant effects found in
- 29 -

Communication
Problem Solving

CBT

views hallucinations and delusions as a continuum with normal phenomenon and not dissimilar to
other strongly held beliefs
Social Skills training
complex social interactions are broken down into simpler steps and subjected to corrective learning,
role playing and then applied in the real world.
Vocational Rehabilitation
places people directly into competitive employment while providing workplace support
Cognitive Rehabilitation

Mood Disorders - Overview and Management


Melancholia?
Signs:
downward gaze,
etched face,
totally unreactive faces
Experience:
psychomotor
slowing
complete
anhedonia
diurnal variation
Categories of depression
Major division
Bipolar or Unipolar
Subtypes
Non-melancholia depression = >2 weeks social impairment
TCA = SSRI ( = CBT, IPT, St Johns wort)
Placebo = 25-60%
Melancholic depression = >2 weeks social impairment + psychomotor disturbance
TCA response rate twice that for SSRIs
Placebo = 10%
Psychotic melancholia/depression = >2 weeks social impairment + psychomotor disturbance
+ psychosis
AP alone = 30-40%
AD alone = 20-30%
Placebo = approximately 5%
AP + AD = 80%
ECT = 80%
Anxiety?
Fear/apprehension
tremor
restlessness
muscular tension
palpitations
sweating
- 30 -

feeling nauseated
flushes & chills
difficulty breathing
butterflies in stomach
headache
dizziness
dry mouth

Age of onset of developing secondary depressive disorder

There is evidence of hippocampal atrophy and loss in patients with major depressive disorder.
Anxiety and Depression
comorbid depression is frequently preceded by certain anxiety disorders and anxiety states
social anxiety disorder precedes MDD in 63% of cases
generalised anxiety disorders precedes MDD in 65% of cases
panic disorder precedes MDD in 22% of cases
Management of Depression A SET PACE
Assessment
Safety
Education
Therapeutic relationship
Psychological Therapy
comparable efficacy for mild to moderate depression. Less so for severe depression.
Antidepressant treatment
1st line - SSRIs, SNRIs, NARIs, NASSAs
2nd line (more side effects despite better efficacy) - TCAs, MAOis
Combination
Combining medication and therapy
ECT
safe and effective for severe depression

- 31 -

Serotonin 5HT

Sex
Appetite
Aggression

overlapping domains

Depressed Mood
Anxiety
Irritability
Thought process

- 32 -

Noradrenaline (NA)

Concentration
Interest
Motivation

- 33 -

Bipolar Disorder
affects 1% of the worlds population
disease onset at 12 to 25 years of age
accurate diagnosis may take 5 to 10 years
equal incidence in men and women
attempt suicide
1 in 5 of untreated bipolar individuals commits suicide (10-15%)
low proportion of patients in treatments (30%)
high recurrence rate (90%)
high economic burden
Bipolar Type I - one or more lifetime episodes of mania and usually episode of depression. Often may result
in hospitalisation
Bipolar Type II - both hypomanic and depressive episodes. No mania. Usually do not require hospitalisation.
6 key features of mania/hypomania
High energy levels
Positive mood
Irritability
Inappropriate behaviour
Creativity
Mystical experiences.

Bipolar and other disorders


OCD - 21% of bipolar patients , 15.7% among OCD are bipolar
Panic disorder - 37.1% of bipolar patients, 19% among panic disorders have bipolar
Psychosis - common in both bipolar and schizophrenia
Alcohol and substance abuse
ADHD
Dramata cluster PD?
Bulimia
Management of bipolar disorders
Bipolar mania
Acute symptoms of mania - antimanic agent ECT
Antimanic agents
1st line: olanzapine, lithium, valproate, risperidone, quetiapine, ziprasidone, aripiprazole
2nd line: carbamazepine, haloperidol
- 34 -

Combination therapy: valproate + atypical, lithium + atypical


Behavioural disturbance - short term benzodiazepine or antipsychotic ECT
Cognitive disturbance (psychosis) - antipsychotic ECT
Bipolar depression
Pharmacological
1st line: lithium, olanzapine, lamotrigine, quetiapine
2nd line: valproate, or combination therapy (adj risperidone, Li + valproate, OLZ + fluoxetine,
Li + lamotrigine, adj antidepressant)
Psychological
CBT, IPSRT, FFT
Physical
ECT
Maintenance agents
Lithium
Olanzapine
Aripiprazole
Ziprasidone
Risperidone
Clozapine
Valproate
Quetiapine
Lamotrigine

Lithium
Patients who respond to lithium are likely to have classic episodic pattern of illness characterised by
recurrent and recognizable episodes followed by remission.
Initial lithium dose (for both mania and depression) 0.6 - 0.8mmol/L
Maintenance Lithium Dose
Mania Li dose: 0.6 - 1.0mmol/L
Depression Li dose: 0.4 - 0.8mmol/L

- 35 -

Week 2 Schizophrenia
Skills - CBT

How we think and behave determines how we feel


It is one type of psychotherapy
Comprises of cognitive and behavioural components
amalgam of cognitive and behaviour therapies
cognitive therapy changing unhelpful thinking
behaviour therapy changing unhelpful behaviour
based on the premise that how we think and behave determines how we feel
Major psychotherapy framework
psychodynamic psychotherapies
behaviour therapy - rewards, punishments, systematic desensitisation, relaxation training
non-directive psychotherapy
cognitive therapies (eg. CBT, TF-CBT, DBT, IPT, ACT) - about thinking. e.g.
acceptance/thinking/interpersonal thinking/directed therapies
family therapies
attachment-orientated therapy
Recent evidence reveals underlying mechanisms of psychotherapy, which can:
promote growth of neurons and integration of neural networks
neural plasticity, growth and integration enhanced by:
the establishment of a safe and trusting relationship
mild to moderate levels of stress
activating both emotion and cognition
the construction of new personal narratives
Indications for CBT:
Ordinary human suffering
Acute psychological stressors (stressful events, losses, disappointments)
Mental disorders, as:
Primary treatment - mild-moderate depression, anxiety, eating disorders, personality
disorders, substance use disorders. Also in most child to adolescent mental health
diagnoses.
Adjunctive treatment - more severe depressive illness, schizophrenia, bipolar disorder,
personality disorder
Transtheoretical Stages of Change model
Precontemplation - There is nothing wrong with my behaviour
Contemplation - I am seriously thinking about changing my behaviour
Preparation - I have a plan to change my behaviour
Action
Maintenance - I have made the change permanent..
Assesses an individuals readiness to act on a new healthier behaviour and can help guide treatment
planing
[insert slide diagram?]
Hx might be important - SMP likes their random facts that dont really add much to our education :D
Beck = psychiatrist, lives in new york, talks a lot and developed cognitive theory.
Fundamental Principles of CBT
- 36 -

A-C relationship [add slide image]


Activating event that presents a behavioural and emotional consequence
Beliefs and thoughts - how we interpret the activating event, leads to. (based on a summed total of
our life experiences)
Consequences (Behavioural and emotional response)
real case = Activating event Beliefs and thoughts Consequences
Humans have biologically-based tendences to create deeply held:
Learned beliefs core tendencies eg:
world is benevolent a good, kind and helpful place
world is meaningful predictable/reliable rules & principles of safety
self is worthy i try to be good, moral, well-intentioned (im OK)
Modes of thinking (Kahneman, 2011):
1. System 1 is fast, instinctive, and emotional i.e. pattern recognition, automatic
thinking
2. System 2 is slower, more deliberative and more logical
each system has associated cognitive biases but generally too much
influence is placed on system 1 judgements.
CBT aims to correct system 1 thinking
Behavioural strategies employed in CBT
Progressive muscular relaxation
Hyperventilation control
Exercise - is good for you, promotes the release of hormones and neurotransmitters
Graded exposure (imaginal and in vivo) - recreation of an exposure?
Exposure and response prevention
Behavioural elements
Activity scheduling
Interoceptive exposure - exercise that bring about the physical sensations of panic e.g.
hyperventilation and muscle tension
Social skills training
Sleep-wake cycle management
Meditation
Cognitive strategies
Socratic dialogue/guided discovery
**Cognitive challenging ** (most important, can forget the rest)
e.g. get the patient to question their thinking: how helpful is it to think this way? what is the
evidence? how rational is it to think this way?
Cognitive errors:
catastrophizing
black and white thinking
personalisation
generalizing
perfectionism
mindreading
fortune telling
Worry control
Structure problem solving
Schema-focused work
Cognitive exposure and response prevention
- 37 -

Assertiveness training
Values clarification
Use of probability and decision theory
Anger management (RAGE!!!)
CBT - Putting it together tailor to the individual patient
Assessment of problems (physical, emotional, psychological, behavioural)
Diagnosis
Psycho-education (re. causes, treatments, prevention of recurrence. Empowering the patient with
the right knowledge)
Evidence-based strategies selected to target symptoms
Strategies are practiced by the patient
Outcome measured
Relapse prevention strategies are planned
Changing automatic thoughts
Identify automatic thoughts
identifying emotional and behavioural consequences of these thoughts helps to motivate
the individual to change, as well as realise the relevance of their thinking to how they feel
and act
Identify the activating events, beliefs/interpretation, consequences/emotions/behaviours
CBT Skills
psychoeducation
sleep wake cycle management
structured problem solving
behavioural activation
de-arousal strategies

Skills - Mental State Overview and Tools

https://129.78.46.33/fmi/webd#MSE_1211014
http://bit.ly/1xEU?????
Username: Concord, Password: 1234
Description
Appearance
Weight - obese; overweight; normal; underweight; emaciated
Hair - clean and tidy; dirty; unshaven; coloured; unusual style; bizarre style
Grooming - well-groomed; unusual makeup; soiled clothing; disheveled appearance; dirty
skin, nails; body odour; halitosis
Dress - unremarkable; undressed (part/full); under-dressed; over-dressed; sexualised;
militaristic; eccentric; bizarre
Other Features - nil of note; glasses; jewelry; dental braces; tattoos; scars; wounds
Behaviour
Walking: unremarkable, slow, march, limp, shuffle, assisted, limp shuffle, directionless
Repetitive: nil of note, gestures, twitches, stereotypical, automatism, mimicry, echopraxia,
ambitendance
EPS: nil observed, parkinsonian, akathisic, dystonic, dyskinetic, tic-like
Catatonic: nil observed, catalepsy, excited, stupor, rigidity, posturing, cerea flexibilitas,
negativism
Other: agitated, aggressive, hyperactive, hypervigilant, compulsions, sleepwalking, epileptic
Speech
Rate: pressured, accelerated, normal, slowed, staccato
- 38 -

Intelligibility: normal, slurred, mumbled, cluttered, stammered, accented


Loudness: scream/shouting, louder, normal, quiet, whispered, mute
Quality: unremarkable, hesitant, emotional, monotonous, stereotypical, unspontaneous,
echolalia, verbigerative
Quantity: garrulous, talkative, responsive, taciturn, mutism
Special disorders: non observed, poverty of amount, poverty of
content,
pressure/accelerated,
distractability,
tangentiality,
derailment,
incoherence,
changing/punning, neologisms, word approximation, circumstantiality, loss of goal,
perseveration, echolalia, blocking, skilled speech, slef-referential, paraphasia-phonemic,
paraphasia semantic
Attitude to examiner - seductive; playful; ingratiating; friendly; cooperative; interested; attentive;
frank; indifferent; evasive; defensive; hostile
Ideation can have multiple
Form - delusion; over-valued idea; magical thinking; misidentification; obsession; preoccupation;
suicidality; aggressivity; phobias
Theme - persecutory; self-referential; sexual; religiose; grandiose; guilty; nhilistic; worthlessness;
self-accusatory; somatic; cleanliness; control; erotomanic; infidelity; bizarre; not assessed
Congruity - mood congruent; mood in-congruent; not assessed for congruity
Frequency - never in last week; occasionally; once or twice a day; frequently during day; almost all or
most of the day; unceasingly; was not assessed
Behaviour - has no affect on behaviour; occasionally affects behaviour; frequently affects behaviour;
is almost totally preoccupying; was not assessed
Duration - less than 1 week; less than 1 month; less than 6 months; greater than 6 months; an
unknown period; was not assessed
Severity - 1 = normal (not at all); 2 = borderline ill; 3 = mildly; 4 = moderately; 5 = markedly 6 =
severely; 7 = extremely; 0 = not rated
Description what the px actually says
First-rank symptoms
Audible thoughts
Voices debating or disagreeing
Voices commentating
Somatic passivity
Thought withdrawal
Thought insertion
Thought broadcasting
Made feelings
Made impulses
Made acts
Delusional perception
Perception
Form: illusion, hallucination, pseudo-hallucination, pareidolia, eidetic imagery, delusional
perception, bodily experiences, fantasy, dream-like
Modality: auditory, visual, olfactory, gustatory, tactile
Congruity: mood congruent, mood in-congruent, not assessed for congruity
Frequency: never in last week, occasionally, once or twice a day, frequently during the day, almost
all or most of the day, unceasingly, was not assessed
Intensity: has no effect on behaviour, occasionally affects behaviour, frequently affects behaviou, is
almost totally preoccupying, was not assessed
- 39 -

Onset: <1 week, <1 month, < 6 months, > 6 months, an unknown period, was not assessed
Severity: 1 = normal, 2=borderline , 3=mild, 4=moderate, 5=markedly ill, 6=severely ill, 7=extremely
ill, 0 = not rated
Description

Mood
What has been the predominant feeling state (mood) described by the patient now, and over the
last five or six days?
Patients description of mood
Interviewers description of main mood
euthymia, depression, guilt, worthlessness, dysphoria, euphoria, anger, anxiety,
apathy, alexithymia, fear
Stability - Has the predominant feeling state (mood) been present throughout the last week?
Stable: 0 hardly ever present (stable) to 7 always present (unstable)
Intensity - To what degree has the predominant feeling state (mood) been felt throughout the last
week?
0 normal to 7 pathologically reduced/relaxed
Fluctuation - Independent of the overall mood, is there a sense that there is a fluctuation of intensity
over shorter (eg diurnal) periods?
0 normal to 7 fluctuating patterns
Any shorter-term feeling states spontaneously divulged by the patient
Affect
fatuous, labile, blunted, guarded, irritable, angry, sad, anxious, elevate
specify how often: once or twice, occasionally, often, frequently, continuously in the
interview or in the last week but not in interview
Spontaneity: 0 normal to 7 impaired
Reactivity: 0 normal to 7 impaired
Appropriateness: 0 normal to 7 impaired
Cognition
Orientation:
Time (weekday, date)
Place (ward, hospital, street, suburb, state, purpose)
Person (own name, physician's name, nurses name, roles of staff
Attention
Digit span - repeat number forwards or backwards
WORLD - spell forward and then spell backwards
Serial 7s - start off with a different number
+ behaviour indicating concentration stress what are you seeing
+ how many times did the instructions have to be repeated
Conscious level
?
Memory - rate each domain as intact/marginal/impaired
Registration
Short
Recent
Remote
Confabulation - present or absent
Information - estimate the patients general knowledge store easier ones at the beginning, harder
ones at the end. Sample questions:
- 40 -

How many days are there in a week?


What must you do to water to make it boil?
How many things are there in a dozen?
Name the four seasons of the year.
What do we celebrate on Anzac day?
How many centimetres are there in a metre?
What does the stomach do?
What is the capital of Greece?
Where does the sun set?
Who invented the airplane?
Why does oil float on water?
What do we get turpentine from?
When is Labour Day?
How far is it from Sydney to Melbourne
What is an hieroglyphic?
What is a barometer?
Who wrote Paradise Lost?
What is a prime number?
What is Habeas Corpus?
Who discovered the South Pole?
Vocabulary
Ask the patient the meaning of as many words as possible. The patient might put the word in
a sentence to indicate the meaning.
Abstraction - assess as either abstract or concrete
For example: "People in glass houses should not throw stones." A few common interpretations
include: concrete (e.g. "Don't throw stones because it will break the glass"); abstract (e.g. "Don't
judge others")
Similarities

Proverbs

Judgement
Judgement/Comprehension

Insight
Awareness - defined as the acknowledgement of the presence of a symptom or sign
rate each as 1 = full awareness; 2 = moderate awareness; 3 = impaired awareness;
4 = flat denial of symptoms
Past
Present
Attribution - patients explanatory model for the cause of any signs and symptoms of
the disorder rate as 1 = correct attribution; 2 = probably not real, 3 = possibly not
real, 4 = completely incorrect
Past
Present
Global Insight
All things considered how likely is it you have a mental disorder?
Do you think that treatments you receive are helpful/necessary to treat your
- 41 -

condition?
Do you think that the condition has influenced the way your life has gone?

Miscellaneous
Test drawing a clock face.
Others

Other notes
Often only get formication from organic disorders e.g. usually from substance intoxication/abuse.

Skills - Taking a Psychiatric History

Try to focus on key features that help discriminate between diagnoses or which have important clinical
indications
blunted affect schizophrenia
flattened affect parkinsonism, complete absence of emotional expression
flight of ideas mania
third person auditory hallucinations schizophrenia
disorientation and inattention delirium
frontal lobe signs important clinical implications
A snapshot in time
Descriptive, not interpretive (you don't want to dig a hole for yourself)
Does not contain historical information
Appearance
apparent age related to stated age
tattoos - where did they get them? the worse they are usually done in prison
clothing - ragged, well dressed?
hair - colour, ornaments etc
body habitus
etc
Behaviour
Attitude
social appropriateness
guardedness, evasiveness, suspiciousness,
rapport
degree of cooperation: mute, hostile, forthcoming
hostility
Psychomotor activity
agitation OR hyperactivity (schizophrenia)
retardation (slowing of movements) OR hypoactive (purposelessness - schizophrenia
Abnormal involuntary movements
Catatonic phenomena - dysregulation of the motor system, patients alternate between psychomotor
retardation and purposelessness to hyperactivity/echolalia, responds to ECT,
Compulsions (obsessional motor acts) - e.g. tapping table certain number of times, lining things up
on table for symmetry
Behavioural manifestations of subjective experience
(autistic) preoccupation - more interested in their own world than what's happen externally
responding to internal stimuli - patients responding to internal voices
inattentiveness
distractibility - inability to filter out irrelevant stimuli
Mood
subjective, use the patients own words
- 42 -

may describe how the patient feels over a period of time


Affect
objective expression of the patients internal state, how the patient feels currently at that point in
time
quality - what is being expressed?
intensity - the volume knob
range - restricted vs labile
reactivity - influence of external circumstances, e.g. in severe depression, patients will not
be affected by good news. in mania, patients can get very angry at the smallest
interruption.
congruence (with thought content) - refers to relationship between emotional state and
thought content
appropriateness ( with expressed mood) - refers to relationship between mood (how
patients describe how they feel) and affect
Speech
rate - how fast their speaking
amount - e.g. poverty of speech
spontaneity - how often the patient will initiate speech, some patients only respond
latency - how long it takes patients to reply, could be due to psychomotor retardation, distractibility
volume - manic patients can be really loud
prosody - emotional quality of the speech, robotic speech in ??
interruptibility Thought form
Do you find yourself forgetting the question after youve asked it?
Does the patient answer the question?
If the answer are Yes or No respectively, the patients is likely to be thought disordered.
circumstantiality - patient gets to the point but takes a round about way to get to it, not necessarily
pathological, you see it in lots of geriatric patients
tangentiality - oblique or irrelevant immediate response to questions, fails to answer the question
derailment - patient answers questions but then spontaneously jumps to another loosely related
topic until they go completely off topic
flight of idea - associated with mania, pressure of speech PLUS thought disorder
loose associations - preferable to use the term derailment instead. derailment is like a series of loose
associations.
Poverty of content / poverty of thought -patient talks so vaguely that little information is provided
despite the number of words.
word salad (mmm, tasty) schizophasia or incoherence: usually makes no sense whatsoever.
disorder at the level of the clause/individual thoughts rather than relating to the link between
clauses/individual thoughts. Completely irrelevant thought content and flow
vs derailment
Thought-blocking: unexpected cessation in the flow of thought, often associated with perplexity
and/or passivity experiences in the subject. Resembles absence seizures
Neologisms: made up words associated with schizophrenia
Clang associations: association of words based on sound rather than meaning.
Thought content
must ask about suicidal and self harming ideation (Otherwise will fail if you dont ask!!!!)
delusion: irrational belief.
as delusions may be true it is more useful to assess how the patient arrives at the belief than
- 43 -

its truth or falsity


ask patient if they think they deserve punishment or not and if so, what type of punishment
Knowledge as justified true belief
Delusions have the force of knowledge. To the patient, it is a fact.
Delusion vs overvalued ideas vs obsessions
Primary delusions - comes out of nowhere
Secondary delusions - e.g. hallucinations (voices) telling you this is the truth
Types of delusions:
Persecutory - being following, under surveillance
Delusional jealousy e.g. patients may keep thinking the their partner is cheating on them,
although it may be true, how they arrive at the conclusion is faulty and irrational.
hypochondriac / somatic - patient think their body is abnormal or changed
religious delusions
delusions of reference - thinks newspapers/TV are sending special secret messages to them
delusions of infidelity - HIGH RISK
delusions of misidentification - Capgras (familiar person suddenly is an imposter) = HIGH
RISK, Fregoli (stranger suddenly is a very close person to the patient)
delusions of sin or guilt
belief that a terrible sin or action has been committed
may manifest as excessive or inappropriate guilt, or feeling of responsibility for some
action with which the patient is not connected
punishment by god or society is felt to be deserved
nihilistic or cotard delusions - related to the concept of nothing, that they stopped
existing, that the universe stop existing
delusions of poverty / bankruptcy
grandiose delusions - mood congruent in mania or schizophrenia, often linked with
persecutory delusion. patient believes in special powers, abilities, talents, or that they are
someone powerful or famous.
"Self, world, and future" - Becks triad
Beliefs characteristic:
Depressive states
hopelessness
helplessness
guilt
low self-esteem
mood-congruent delusions
delusions of sin or guilt:
Mania
grandiose delusions
Obsessions and overvalued ideas
Obsession - thought that persists and dominates an individuals thinking despite the
awareness that the thought is either entirely without purpose or else has persisted beyond
the point of relevance or usefulness
very often anxiety and/or guilt provoking
ego-dystonic vs ego-syntonic
Overvalued idea - solitary, abnormal belief that is neither delusional nor obsessional but
dominate the patients life.
Anxiety
- 44 -

fear for no adequate reason i.e. disproportionate


patient keeps asking what ifs
Phobias
fear restricted to one objection,situation or idea
specific phobia
social phobia / social anxiety - fear of negative evaluation in public
agoraphobia - fear of situations where escape is difficult, often associated with panic
disorder
Useful questions for psychosis
Do you feel safe?
Is there anyone out to get you? Giving you a hard time?
Do you feel you are being followed, watched or pursued?
Do you feel you are undersurveillance?
Do you feel you deserve to be treated in this way? Do you think you might be punsihed?
Everyone is special, what is special about you?
What is your relationship with God like?
**Remember, the essential clarification question is: how do you know?
Can also ask:
Do other people share your beliefs? How does it make you feel when people dont
believe you?
Explore inconsistencies eg If youre so worried that your sister is going to kill you,
why do you let her into your house?
Explore possible behavioural consequences e.g. avoidance, withdrawal, safety
behaviours
Suicidal ideation
Active suicidality
ongoing plan, intention or recurring impulse to end life
assess elaborateness of plan and determine the degree of ambivalence
intent vs lethality
some people might want to really die, but their concept of lethality doesnt
fit with that eg taking something quite benign and thinking it would kill
them; flip side is somebody who is quite meh about killing themselves, but
takes something quite lethal
risk vs rescue ratio - determine if patient is trying to conceal the fact they are trying
to commit suicide whereas some people dont try to conceal it at all (which would
be easier to rescue)
Passive suicidality
Life isnt worth living
Id be better off dead
May range from eg. vague feeling of wishing not to wake up in the morning to
tormenting wish to be killed in a violent accident or crime
Ways to ask about suicidal ideation:
Given everything that's been happening, have you been thinking of ending your life
recently?
Many people in your situation may think about suicide - is this something you have
thought of in the past?
What did you think would happen when you did x?
- 45 -

What did you hope would happen when you did x?


How do you feel now about [the attempt]?
How do you see a way out of your current situation?
How do you think other people view this?
Self-harming ideation and behaviour
Functions of self-harming behaviour
To relieve distress - the sense that one is being emptied of distressing emotions or
experiences
To distract from distressing emotions
To feel physical as opposed to emotional pain
To feel something - during times of emotional numbness
To self-punish
To manipulate others
may not have any underlying suicidality
could be protective against suicide, may not be an effective way to do so,
but it can work
Homicidality
Assessed in an analogous manner to suicidality
Active vs passive
Intent
Elaborateness of planning
Relationship to psychotic symptoms:
delusions: persecutory, grandiose, erotomanic, jealousy/infidelity
hallucinations, especially command
passivity experiences
experience of doing things, but youre not in control of them essentially
like youre being controlled from the outside
Perception
Hallucinations: perceptions without an adequate external stimulus
no relation to the outside world
modalities
auditory
elementary eg noises, whispers music
voices
second or third person
single vs multiple
delusion elaboration
content
command
abusive/derogatory
arguing (Schneiderian first rank symptom)

running commentary (first-rank symptom)


helpful/comforting
visual - often associated with organic states e.g. delirium tremens, dementia with
lewy bodies
tactile - often associated with substance intoxication or withdrawal (formication),
may be associated with secondary delusional elaboration (bugs under the skin)
- 46 -

olfactory
sometimes difficult to distinguish from a delusions eg the olfactory
reference syndrome
temporal lobe epilepsy
somatic
gustatory - often associated with medications, esp. lithium
Pseudohallucinations:
when insight is partially retained
image lies in the inner rather than outer perceptual space
Illusions: misinterpretations of stimuli arising from an external object
Intrusive mental imagery (obsessional images): vivid mental imagery, usually of a distressing natures,
that occupies the patients mind
Flashbacks: sudden intrusive memories associated with cognitive and emotional experiences of a
traumatic event
Schneiderian Symptoms (German Psychiatrist) thought to be associated with psychotic disorder
(originally schizophrenia, but now research has not found this to be always true)
somatic passivity experiences
thought withdrawal
thought insertion
made feelings, impulses and volition acts
delusional perception: normal perception is delusionally interpreted and regarded as being
highly significant to the patient
audible thoughts; patient hears own thoughts spoken out loud
voices arguing: two or more hallucinatory voices quarrelling or discussing with each other, in
which the patient usually figures in the third-person
voices commenting: commentary on the patients thoughts, feelings and actions that may
take place before, during or after what is commented upon
Cognition
Tests for frontal lobe impairment (particularly in head injury, alcohol dependence, impulsive or
poorly judged behaviour) - this is most important in determining the patients functional
impairment and clinical implications.
Get patient to draw a clockface
poor planning found in frontal lobe impairment, e.g. when patients don't manage to
fit all the numbers in.
drawing half the clock in parietal lobe disorders, neglect
Trails B
Lurias three-step test (fist, edge, palm)
useful screening test for frontal lobe
fist, edge, palm demonstrate to patient and get them to demonstrate back to you
Word generation
Proverbs
Similarities and differences
Insight
basically the extent to which the patient understands that they have a mental illness, how it was
caused.
Judgement
encompasses a variety of phenomena, including:
illness behaviour (as opposed to illness beliefs, which are assessed as part of insight)
- 47 -

the wisdom of recent decisions


ability to make socially/ethically appropriate judgements in hypothetical situations

Mental State Examination

Phenomenology

Adverse Effects of Medication

Metabolic Complications and Monitoring

Psychotic illness is a barrier to all forms of effective medical care and is associated with increased mortality
and morbidity
Patients with schizophrenia die 15 -15 years prematurely
Metabolic syndrome is more prevalent in patients with schizophrenia than population controls and is a
predictor of early CHF and premature mortality. Schizophrenia is a independent intrinsic risk for CHD.
Second Generation (atypical) Antipsychotics are most associated with weight gain
Patients with schizophrenia have a 10x chance of committing suicide and 2x chance of dying of CHD than
normal population
Patients with mental health illness tend to experience or report reduced physical symptoms.
Cardiometabolic RF in patients with chronic psychotic disorders
obesity/overweight 1.5-2x
abnormal lipid metabolism 5x (esp low HDL)
smoking 2-3x (at least 80-90% of patients with mental illness smoke)
physical inactivity
unhealthy eating
hypertension 1.4x
pro-inflammatory states seen in schizophrenia
age, race, gender, family history 2-3x
Diabetes Mellitus
Antipsychotic use 10% increase
schizophrenia 2 to 3 fold increase
may be associated with the accelerated ageing process in schizophrenia
SGA > FGA
Weight gain in SGAs
*High risk of metabolic disorders : clozapine
less clearly different: olanzapine, quetiapine, risperidone amisulpride
low risk: aripiprazole (associated with weight loss in some individuals), ziprasidone (difficut to dose
and hence problems with adherence)

Extrapyramidal Symptoms

NIEPS - neuroleptic induced extrapyramidal symptoms


Associated with almost all antipsychotics, with the exception of clozapine.
Signs with use of SGA may be less subtle than with FGA.
Antipsychotics affects the D2 receptor (dopamine antagonists), particularly affecting the basal ganglia
at 65 -75% occupancy needed to be therapeutic in treatment of psychotic disorders
- 48 -

once 80% of D2 occupancy you get Parkinsonism.


Tardive dyskinesia are less in SGA than in FGA.
Haloperidol particularly associated with tardive dyskinesias.
Types of NIEPS check lecture notes again!!!
Acute
Parkinsonism: 4 cardinal sx - rigidity, bradykinesia, tremor, postural stability, bradyphrenia
Akathisia inability to sit still, restlessness
three components
subjective (feelings of inner restlessness)
objective (motor signs)
akathisic distress (subjective)
Dystonia
twisting, pulling or queesing: involuntary, often within 96hrs of rx; variable sustain
Dyskinesia
chorea
athetosis - snake like
mix of tardive akathisia and dystonia
Tardive
Dyskinesia
Akathisia
Although all antipsychotics affect D2 receptors, they can also have an affect on other receptors in the brain:
virtually all SGA are 5HT2A antagonist
Orobuccal dyskinesia
Peripheral dyskinesias

- 49 -

Week 3 Substance Abuse


Smoking Cessation Therapy

Neuronal nicotinic arc


configurations of alpha and beta types in a pentameric shape
combinations, distribution and position of them determine role in brains effect
e.g. a4b2a5 responsible for dependence, a3b4 for appetite, b4 for cognition, a7 for memory
and attention.
types and subtypes are heritable
Metabolism of nicotine
genetic racial variation of liver enzyme P450 CYP2A6 range from fast to slow
fast metabolisers smoke more, are more addicted, have higher risk of lung cancer,, do less
well on NRT, inhale more deeply than slow metabolizers
mediterranean, europeans faster metabolisers than asians, african americans
women slower metabolisers than men
Smoking anything polycyclic aromatic hydrocarbons affects liver enzyme induction ~ CYP1A2
caffeine and alcohol intake is double in smokers
nicotine may reverse cognition and incoordination effects of alcohol
alcohol alters the metabolism of nicotine in humans
ADH (alcohol dehydrogenase) and CYP2E1 metabolises alcohol in humans
caffeine toxicity is common in withdrawals
tolerance to alcohol drops in withdrawal
smokers need more drugs to take same effect, while quitters need less and must be monitored
nicotine withdrawals
cravings, urge to smoke
anxiety
tension
aggression
inability to concentrate
sleepiness/sleeplessness
depression
hunger
mouth ulcers
constipation
withdrawals last from days to weeks and are worse within the first week of quitting
62% of smokers relapse due to withdrawal within the first 2 weeks of quit attempt
Nicotine replacement therapy
patches may take hours to peak
no evidence that weaning off is required or that there is a need for lower doses
evidence that combination is better (e.g. patch and gum/lozenges?)
smoking while using NRT is safe , therefore can alternate pulsatile NRT and smoking
best to apply 24 hour 21mg patch before bed to peak in the morning
Varenicline (champix)
targets a4b2 nAch receptor which responds to nicotine
combining with NRT or bupropion is safe and effective

- 50 -

Cannabis

30% of population have used ever


Any use in the past year: 10% general population, 20% in 20-29 year olds, 23% indigenous australians

THC = terahydrocannabinol
acts on our natural cannabis receptors
Agonization of the receptors in the amygdala increases anxiety, fear, and paranoia.
Agonization of the receptors in the hippocampus inhibits short-term memory, learning, cognition,
motivation, and concentration. gonization of the receptors in the limbic system causes the emotional
distortion that cannabis causes.

CB1 mediates inhibition of release of:


Ach, NAd
DA, 5HT
GABA, Glu
d-aspartate (D-AA), cholecystokinin (CKK)
CB2, expressed by mainly immune cells
affects secretion of cytokines by immune cells
modulate immune cell trafficking
Anandamide
endogenous cannabinoid neurotransmitter
Agonises receptors in
amygdala - anxiety, fear, paranoia
hippocampus - inhibits short term memory, learning, cognition, motivation,
concentration
limbic system - emotional distortion

Routes of use
smoked: bong / joint
onset of effects: 5- 10 minutes (peak effects 30-60min)
duration of subjective intoxication: varying between 2 - 6 hours
Joints - made by mixing cannabis with tobacco. ~3 x increased tar ~5 x CO than a typical
tobacco cigarette (thus a joint is thought to equal 3 cigarettes).
Bongs - use water to filter the smoke, tends to filter out proportionally more THC than
nicotine and tar so depositing more harmful products deep in the lung.
orally: cookies / tea
bypasses the lung damaging effects of smoking and the potential carcinogens.
Use is complicated by a biphasic process (due to the different breakdown products that arise
- 51 -

when cannabis is eaten as opposed to cooked) which alters and delays onset of effects.
Effects tend to be more intense, longer acting but unpredictable and difficult to titrate.
others: vapourised / inhaled / topical
Vaporisers (constructed by combining a heating element to an enclosed vessel such as a
glass jar or plastic bag) heat cannabis to the point where the THC vaporises (creating an
aerosol) but not so much that it combusts which produces harmful by-products.
Cannabis intoxication
sedated, psychomotor impairment for up to 24 hours after use (most over within 406 hours of use)
munchies, gets hungry for carbs
blood shot eyes - vasodilation in association with lowering BP
glazed appearance, ptosis
red eye conjunctival injection
reduced coordination, balance
slurred speech
antiemetic, for those undergoing chemotherapy
antispasmodic + analgesic, seen in users with arthritis, MS, spastic disorders
mild heart rate, BP
light headed, tingling
Cannabis effects
Causes a sense of relaxation, euphoria and heightened sensory awareness.
At higher doses it causes sensory perceptual distortion.
It may be used to assist sleep and has significant analgesic properties.
As the dose of a drug increases, the role of the environment in drug effect becomes less noticeable
whilst the pharmacologically mediated ones of arousal or sedation become more marked.
At higher doses users become drowsy.
Good: relaxation, euphoria, heightened senses, altered thinking, sedation. reduced
inhibitions, relieves withdrawal
Bad: short term memory loss, anxiety and panic, exacerbate mood/mental illness, paranoia,
hallucinations (rare)
Long term physical effects
cancer of oropharynx, ?lung cancer (risks greater if use tobacco)
mild cognitive impairment
gynaecomastia
Long term psychological effects
triggering schizophrenia
2x risk of schizophrenia
earlier (adolescent) use risk of later schizophrenia
acute toxic psychosis - confusion, amnesia, hallucinations, delusions, anxiety,
remits after cessation of use.
may precipitate a first episode of a schizophrenic illness
more positive symptoms
dependence
?depression
? daily use associated with 5x in anxiety/depression
anxiety/panic disorder
paranoia
makes mental health problems worse
lower educational/work performance
- 52 -

subtle attention/memory changes


Cannabis dependence
occurs in ~10-20% of users, usually presents with loss of control over use, continued use despire
problems, tolerance, cravings
Cannabis withdrawal
irritable / restless
anxiety
appetite
sleep problems, strange dreams
anger/aggression
other: fatigue/yawning, chills/sweating, stomach pain/nausea, depressed mood, tremors, stuffy
nose, muscle pain, headaches, muscle pain, headaches, underlying mental illness
more than half of dependent cannabis users do experience several symptoms on cessation
of regular use
Managing cannabis withdrawal
diazepam for 3-7 days: one 5 mg tablet 2-4x daily
CBT for relapse prevention
Cannabis hyperemesis
intractable vomiting
repeating showering
may need hospitalisation
settles with abstinence
Cannabis Hx
Identify the amount of cannabis used, the frequency of use and the duration at which they have
been consuming at present level. Dependent users may smoke between 1 - 7 gms/day whilst for
many recreational smokers a gram may last for months.
Inquire about the use of other drugs and alcohol/ tobacco.
Identify the mode of administration and whether the drug is mixed with tobacco.
Offer health information at this point to support a reduction in smoking or a change to a safer route.
Assess the impact of smoking on role competency and interference with task such as work, study,
child care or driving should be assessed.
Identify the amount of money spent. Saving money may be a potential motivator for reducing use.
Cannabis usually costs between $10 20 per gram. Dealers may offer discounts for larger amounts
with an ounce (28gm) costing between $200-350 depending where you are in Australia.
It is useful to ask about how long after waking the first smoke occurs, as this provides a good clue to
identifying dependence and to what happens if they are unable to obtain any cannabis. Do they
worry? And do they experience withdrawal?
The severity of withdrawal is not typically severe with many experiencing a withdrawal
severity similar to that experienced by people quitting tobacco.
slow cannabis clearance from body (as lipophilic)
2-3 months for clean urines for a regular user

Management of Alcohol Withdrawal and Beyond

Alcohol withdrawal
shakes
cant sleep
sweating
vomiting, diarrhoea
seizures (EARLY 6 -48 hours) but need to be vigilant monitoring for it in the first week
- 53 -

even in high blood alcohol


2-9% alcohol dependent
delirium tremens (autonomic hyperactivity (diaphoresis, HR, RR), tremors, insomnia,
psychomotor agitation/anxiety, N/V, tonic clonic seizures, hallucinations, persecutory delusions)
later (3-5 days)
treatment is largely supportive
diagnosis of exclusion
death
Neurobiology of alcohol
alcohol increases activity at GABAa
with time, this is balanced out by increased glutamate activity (NMDA)
with no alcohol, increased NMDA, puts patient into withdrawal
Alcohol withdrawal Hx
Past withdrawals:
What was it like last time you stopped?
Ever had a seizure when you stopped drinking?
What are you like before the first drink of the day?
Based on this you will decide:
Is diazepam needed?
Where is the safest spot for the drinker to dry out?
Home detox - if never had seizures, DTs, no benzo abuse, relatively healthy, supportive/safe environment
Diazepam for withdrawal
Indications
hx of seizures or DTs
withdrawal pushed drinker back to drinking
unpleasant symptoms
Regime for moderate withdrawal
days 1 & 2: 10mg qid
day 3: 10mg tds
day 4: 10mg bd
day6 10 mg nocte
For out patients
dispensed daily
stop within a week
don't take if sleepy/drinking
avoid driving
Alcohol withdrawal scale (mild <4, moderate 5-14, severe >15)
Sweating
Tremor
Anxiety
Agitation
Temperature
Hallucinations
Orientation
Thiamine Vitamin B1
any heavy drinker should take it
at least 1 IM thiamine ideal for anyone detoxing, more if poor nutrition/severe dependence
IV thiamine
- 54 -

confusion or recent onset ataxia


severe dependence
poor nutrition
clotting problems
Agents to reduce craving
start after withdrawal except naltrexone. Goal is abstinence. 3 -12 month therapy. use combination
therapy if possible.
acamprosate (campral)
reduces the increase NMDA activity found in alcohol dependence
naltrexone (revia)
decreases in incidence of relapse
baclofen
GABAb agonist
safe in cirrhosis, 10mg tds usually
Disulfiram (Antabuse)
severe aversive reaction - flushing, palpitations, hypotension, vomiting, headache
blocks aldehyde dehydrogenase activity

Group based approach


Alcohol anonymous
SMART recovery
mens/womens groups
CBT

Brief Interventions for Hazardous Alcohol Use

Risky drinking is common:


1 in 4 (28.4%) has > 4 drinks in a session monthly
1 in 5 (20.3%) has > 2 drinks /day on average
1 in 5 (19.5%) drink alcohol after knowing they are pregnant
alcohol is the 3rd greatest reversible cause of disease and disability
FAREs 2012 Annual Alcohol Poll found that:
31% of people correctly identified the number of standard drinks in a full strength beer (1.4 standard
drinks).
26% of people correctly identified the number of standard drinks in a bottle of spirits (18.1 standard
drinks).
12% of people correctly identified the number of standard drinks in a bottle of red wine (7.7
standard drinks).
Routine alcohol screening questions
how often do you drink?
- 55 -

how much do you drink?


how often do you have more than 6 drinks?
FLAGS: Feedback, Listen, Advice, Goals, Strategies
NHMRC Alcohol guidelines
to reduce the risk of harm over a lifetime to < 2 s.d. on any day
to reduce the risk of injury on a single occasion < 4 s.d. per occasion
not drinking if under 18 years old, pregnant or planning pregnancy or breastfeeding
children <15 years are at greatest harm from drinking
Cancer risk attributable to alcohol
22% breast cancer
A significant increase of the order of 4% in the risk of breast cancer is already present at
intakes of up to one alcoholic drink/day. Heavy alcohol consumption, defined as three or
more drinks/day, is associated with an increased risk by 4050%.
7% bowel cancer
40% mouth/throat cancer
51% oesophageal cancer
Alcohol effects and pregnant women
~1% of births
ADHD type symptoms in child
reducing drinking at any point improved outcomes thereon

Drug Seeking Patient

Definition
Drug seeking behaviour - The attempt to obtain prescriptions for psychoactive drugs by making false
or deliberately exaggerated claims of pain or distress
Prescription shopper - In a 3 month period persons who are supplied prescription drugs by 6 or more
different prescribers, or who have been prescribed a total of 24 target phrmaceutical benefits or >50
pharmaceutical benefits in total.
Inappropriate prescriber behaviour - Inappropriate prescriber behaviour refers to te persistent
prescribing of opioids or other psychoactive drugs, despite the absence of a sustained improvement
in the patients function, a deterioration in function and/or development of unacceptable side
effects.
Reasons for drug seeking
Dependent on the drug they are seeking
Chronic pain with secondary opioid dependence
Dependent on illicit opioids and use prescription drugs to relieve symptoms of withdrawal or to
enhance other drugs
Dependent on illicit drugs, and sell prescription drugs to support their habit.
Professional drug dealers (financial gain)
Recreational drug use without dependence
Legals issues for doctors
Should not fear disciplinary action for appropriate prescribing, however...
Illegal to prescribe or administer a drug of addiction (Schedule 8 drug) to a person who is known or
suspected to be drug dependent without first obtaining written authorisation from NSW Health.
Where person not drug dependent NSW Health authorisation is required to prescribe a drug of
addiction for > 2 months, except for sustained release long acting oral opioids
if a doctor appears to be prescribing inappropriately then may be investigated by NSW
health PBS/MEdicare Australia/Director Professional Services Review, counselling, education
and monitoring, relinquish S8 prescribing and administration rights, health care complaints
- 56 -

commission referral for professional misconduct, suspension/conditional registration by


medical board, suspension/deregistration by medical tribunal h
Section 28 of the Poisons and Therapeutic Goods Act 1966, authority of Department of Health is
required
to prescribe for or supply to a drug dependent person any drug of addiction (schedule 8)
to prescribe for or supply to any person any preparation of dexamphetamine or
methylphenidate
to prescribe for or supply to any person other than a drug dependent person, for therapeutic
use by that person continuously for more than two months, any of the following drugs of
addiction - buprenorphine (excluding transdermal patches), flunitrazepam, hydromorphone,
methadone or any injectable drug of addiction.
Clinical presentations of drug seekers:
sx: pain (acute or chronic), insomnia, emotional distress, lost scripts or medication, drug withdrawal
other: difficulty obtaining a clear medical hx/confirm story, state he/she is travelling through or just
moved to the area, exaggerates/feigns medical problems, declines physical examination or signs not
consistent with symptoms, medications lost/stolen/forgotten, asks for their drug of choice by name,
refuses other therapeutic options, pressures the doctor by eliciting sympathy or guilt or by direct
threats.
in some instances, drug seeking patient admits they are drug dependent but may not be completely
honest about their situation: awaiting admission to hospital/drug treatment program, on bail/bond
following conviction, needs medications to treat withdrawal sx, on program and needs interim
takeaway supply.
regular drug seeking patients: aggressive, acquiring similar drugs from other medical sources,
unsanctioned dose escalation, unapproved use of drug to treat other symptoms.
Drugs sought
Commonly - benzodiazepines, opioids
less commonly - other sedatives, stimulants, anticholinergics (artane = trihexyphenidyl)
When drug seeking is suspected
establish early whether or not the visit is a request for a drug
take accurate D&A hx
look for signs of intoxication or withdrawal (look for track marks)
medicare australia prescription shopping program 1800 631 181
patient consent not required
number of doctors who prescribed over the most recent 3 months
items prescribed
number of items prescribed
number of doctors prescribing each item
Personal PBS hx
needs patient consent
name of prescribing dr, item, date of supply, qty, dispensing pharmacist
Management
refuse to prescribe
empathise but be firm, politely refuse to prescribe and give reasons
discuss dx and treatment options: withdrawal management, admission for detox, D&A
referral, pain clinic referral, refer opioid treatment program patients to their
prescriber/treatment centre
prescribe
be aware of legal responsibilities and appropriateness of prescribing
- 57 -

form contract (one dr, one pharmacy treatment plan), including what happens if
management not adhered to
establish patient commitment
consult with specialist in addiction/pain mgmt before prescribing
communicate with other prescribers
obtain NSW health authority if necessary
control drug use with limited amounts supplied e.g. daily dispensing
regular follow up
prescriptions
record the amount to be dispensed in both words and numbers
put several lines through unused space
limit supply
monitor compliance with treatment agreement and dr shopping hotline
keep unused prescriptions in a secure location
Acute pain in opioid dependents
opioid dependent people are hyperalgesic to pain, have high tolerance to opioids, often
undertreated for pain, non-opioid analgesia can be used.
if opioid analgesia necessary, may need to be used at higher doses due to tolerance
if on methadone/buprenorphine maintenance, usually continue regular dose and add other
analgesia on top.

Prescription Drug Misuse

Prescription drug misuse: use of any drug in a manner other than how it is indicated or prescribed
Aberrant drug related behaviours: behaviours that suggest the presence of substance abuse or addiction,
implying that the behaviours are pathologic
Rates of non-prescribed stimulant use in USA
0.5% past month use in age 12-17
0.8% adults >26 years used in last year
4.1% college students used in last year
Australian prescription opioid misuse
2.5% australians reports recent use of painkillers for non medical purposes
4.45% report lifetime use
15.4% had opportunity to use painkillers for non-medical purposes
rising opioid misuse (especially tramadol oxycodone morphine)
Australian Tranquilizers / Sleeping Pill Misuse
3.3% ever used non medically
1.45 used in last year
Most common performance enhancing drugs
1. anabolic agents e.g. steroids (by far), 2. stimulants, 3. cannabinoids, 4. B2 agonists, 5.
diuretics/masking agents, 5. glucocorticoids etc
Risk of opioid misuse in chronic pain patients (Fishbain et al, 2008, Pain Med,9)
overall abuse/addiction rate 3.27%, overall aberrant drug related behaviour (ADRB) 11.5%
if no prior/current hx of abuse/addiction, abuse/addiction rate 0.19%, ADRB rate is 0.59%

Stimulants
Categories of psychostimulants:
1.
Synthesised: pseudoephedrine,
amphetamine, MDMA etc.

dexamphetamine,
- 58 -

methylphenidate,

diethylpropion,

phentermine,

2.

Natural: tobacco, adrenaline, cocoa, caffeine, cocaine, guarana etc.

Stimulant intoxication
anxiety, nervousness common
often with: tachycardia, palpitations
may be chest pain: fear of MI
panic; fear of going mad common
high doses: OCD-like behaviour
pull objects apart & reassemble
compulsive foraging for things
Stimulant Psychosis
usually with chronic use
may be with 1 or more large doses
resembles PARANOID SCHIZOPHRENIA
PSYCHOSIS CLEARS RAPIDLY
within days to a week
or a MONTH at the most
with abstinence
Suspiciousness, paranoid delusions
Auditory hallucinations (voices)
Tactile hallucinations (formication
or cocaine bugs)
Visual (snow lights), gustatory, olfactory
Repetitive, compulsive behaviour common
Mood - fearful, agitated, often labile
Orientated but no insight
Violence not uncommon
Stimulants & Chronic Psychosis
precipitate psychosis in
predisposed individuals
schizophrenia, mania
trigger relapse or exacerbate illness
despite medication
low level use can have major impact
behavioural sensitisation can occur
smaller amounts trigger major reaction
Stimulants crash / come down
EXHAUSTION
FATIGUE
OVERSLEEPING
OVEREATING
DEPRESSED MOOD
LOSS OF ENJOYMENT
CRAVINGS LOW
SUICIDE
- 59 -

{CAN BE ANXIOUS, IRRITABLE WITH INSOMNIA}

Stimulant withdrawal

Methamphetamine
Powdered methamphetamine (speed, goey, whiz, uppers, louee, pep pills)
Fine to crystallised coarse powder
Looks white to yellow, orange or pink
Route of use: snorted, swallowed (with drinks), injected
Base methamphetamine (base)
Often most attempts to make ice end up with base.
Looks damp, oily, sticky, gluggy, waxy form of damp powder, paste or crystal.
Looks white, yellow, red or brown
Route of use
Typically injected (need heat to heat dissolve) and sometimes swallowed
Sometimes snorted or smoked
Crystalline methamphetamine (Ice, crystal, P, shabu, glass, batu, christy, hot ice,)
Chemical composition - high purity crystalline form of methamphetamine HCl, can be made from
reduction of ephedrine using red phosphorus and iodine.
Route of use
Injected or smoked in glass pipe (risk of dependency doubled for those who inject or smoke)
Bong - mixed with cannabis or tobacco and smoked
Chase - heated on aluminium foil and inhale vapour
snorted or swallowed
shafted - anal
Methamphetamine pills (fake ecstasy)
Liquid methamphetamine
Ox blood, red speed, leopards blood
Usually red in colour
Not widely available
Terminology confusion
Speed all methamphetamines OR powdered methamphetamine
Ice all crystal meth OR very close to 100% purity methamphetamine (ie. smokable)
Purity of methamphetamine
powder ~ 5 - 20%
base ~ 40%
ice 80-90% - 4 to 5x as expensive as speed
Typical dose is:
a point of base or ice
gram speed powder
taken 1-2x over a day or night
MDMA (3,4 - methylene-dioxymethamphetamine) Ecstasy, E, Eccy, eggs, love, doves, XTC, Adam
MDMA is generally classed as a stimulant with mild hallucinogenic properties. very easily accessible price
$30 NSW to $50 NT
Derivative of amphetamine, synthesised in clandestine labs by altering the structure of amphetamine
molecule. Often not pure and contain a mixture of other chemicals.
- 60 -

MOA:
1. Affects the SEROTONIN neurons and pathways
inhibits serotonin transporters
increases serotonin in synapse
more serotonin receptors activated
2. Affects DOPAMINE pathways
inhibits dopamine transporters
increases dopamine levels in synapse
Forms: pills (most common), capsules, powder, liquid although:
Liquid E is actually gamma-Hydroxybutyric acid (GHB)
Many pills sold as ecstasy have no MDMA in them
Pills have a variety of colours and brandings, an attempt to indicate that
they are MDMA not MA, but branding is NOT a reliable method of determining quality
Routes of use:
oral (majority)
crushed then snorted
anal shelved
inserted into vagina shafted
some IV use
Duration of effects:
single dose of methamphetamine lasts for 6 to 8 months
hour coming up
may feel rush, lasts 5-20 minutes, nausea, churning stomach, vomiting, feeeling hot,
palpitations
1-1 hour peaking
3 -4 hour plateau
stimulant: alertness, confidence. energy to dance, talkativeness
hallucinogenic: heightens sensations (sight, touch, sound), significant distrotions,
lasts longer if swallowed than if snorted or injected
coming down
residual fatigue and depression can last several days
Hyperthermia , caused by a combination of:
MDMA has direct effects on hypothalamus
hot environment, sustained physical activity
inadequate fluid replacement
causes: seizures, DIC, rhabdomyolysis, renal failure, liver impairment, >41.5 degrees = risk of
death
Hyponatraemia
MDMA causes inappropriate release of ADH, capacity to excrete fluid = water retention
Excess water consumption from MDMA induced thirst, repetitive stereotyped actions from MDMA,
advise < 500ml/hour
Hypertension
amphetamines may increase risk of cerebral haemorrhage or ischaemia
Pre-existing cardiac/respiratory disease
cardiac arrhythmias, infarction, respiratory difficulties, complicated by contaminants in illicit drugs
Neurotoxicity
damage to brain cells which produce serotonin
depression, anxiety, impulsivity, decreased cognition
- 61 -

Cocaine (coke, charlie, snow, okey doke, blow, nose candy, toot)
Alkaloid from the Erythroxylon coca plant chewed by South American Indians for its stimulant effects, is
primarily available in Peru and Bolivia
Cocaine is extracted from the coca leaf and imported into Australia in the form of a salt, cocaine
hydrochloride. The salt is a white, odourless, crystalline powder with a bitter taste
Cocaine base is extracted from the powder to form rocks or crystals known as crack or freebase (rarely
available in Australia
Users tend to be middle age well educated professionals or IVDUs
Route of use
snorted - adverse effects nosebleeds, sinusitis, tear of nasal wall
injected - breathing difficulties, chronic cough, chest pain, lung damage
Quantification
grams (NSW $280)
caps (NSW $50)
Duration of effects
Single dose of cocaine lasts only 8 to 20 minutes
5 minutes Initial rush
ultimate orgasm
hear shell noise in ears and echoes
lose all inhibitions
much more intense than speed
30 - 60 minutes
feel highly energised
fades slowly
Come down
2-3 days to recover
like a bad hangover
Polydrug use is the norm (88%) for amphetamine users
Use of nicotine, benzodiazepines, analgesics, alcohol is common
Most ecstasy users use methamphetamine & visa versa
Cocaine and concurrent alcohol use is popular because their combination creates cocaethylene which has an
extended half-life (from 30 minutes to 2 hours)
Most psychostimulant users tend to use other drugs to medicate the come down (CNS depressants)
Amphetamine like substances - pharmacology
Cocaine, MDMA & amphetamine stimulate neurotransmitter release & prevent reuptake to activity of:
a. Dopamine
b. Noradrenaline
c. Serotonin
causing CNS effects & SNS effects
Cocaine & amphetamine primarily releases DA pleasure burst
MDMA primarily releases 5HT
Amphetamine like substances - usual effects
energy, hyperactivity
appetite
- 62 -

dry mouth, nausea, dilated pupils


jaw clenching & teeth grinding
BP & pulse; sweating
euphoria
sense of well-being
confidence
alertness
sexual arousal - sexuall compulsive, increse in need and urgency for sex, disregard for risks
disinhibition: risk-taking
talkativeness

Amphetamines - adverse effects when taken at high doses


Hypertension
Serious cardiac toxicity
arrhythmias
myocardial infarction
heart failure
aortic dissection
Haemorrhagic & non-haemorrhagic stroke
Dehydration
Hyperthermia
Inappropriate ADH + xs water: water intoxication with hyponatraemia
Seizures
Serotonin syndrome
Agitation, Psychosis, Delirium
Amphetamines like substances - Adverse mental health effects
Dependence
Insomnia
Anxiety states
Delirium
Psychotic symptoms
Violence
Profound mood swings
mania
withdrawal depression
? neurotoxicity

- 63 -

Amphetamine like substances - Management


Acute intoxication consequences
Delirium, dehydration, cardiac, skin, kidney, injury etc
Psychosis, agitation, risk assessment
Other substances
Detoxification environment (safe, support), meds, links
STDs, BBVs, other addictions
Brief Intervention ENGAGE, risks/harms, motiv to change, goals, strategies (good for harmful use/abuse)
Co-morbid mental illness - mood, anx, chronic psychosis, ADHD, Pers Dis
Residential Rehab
Family based
Group based
Individual psychotherapy
Drug and alcohol counselling
Motivational Interviewing
Long term meds? Disulfram, dexamphetamine, vaccines, modafinil
POOR EVIDENCE at this time

Management of Opioid Dependence

Agonists
Heroin
Morphine, pethedine
Methadone
Buprenorphine
Partial opioid agonist with high affinity
Naltrexone, Naloxone
Opioid antagonists
Pain killers Codeine, Endone, Fentanyl

Opioid Effects
Nervous system
- 64 -

Analgesia, euphoria, sedation, respiratory depression, pupil constriction, low PR/BP


Gastrointestinal
Nausea/vomiting, constipation, biliary spasm
Endocrine
Menstrual changes, decreased libido, galactorrhoea
Other
Dry mouth/skin/eyes, urinary hesitancy

Opiate Withdrawal
Flu symptoms
Sweating, goosebumps, hot and cold flushes, yawning
Dilated pupils
Agitation, irritability, dysphoria
Loss of appetite
Stomach cramps, diarrhoea, nausea, vomiting
Pains back, joints, arms and legs, headache
Cravings
Poor sleep
Tiredness, fatigue
Increase in Vital signs

1st to 3rd day symptoms onset


Duration up to a month (methadone)

Opioid Harm
Overdose
Mortality of 1-2% each year (10 times greater than matched age)
Most deaths occur following use of opioids with other drug
Overdose (accidental, intentional), liver, HIV, trauma
Injecting
Infection, trauma, thrombosis
Sepsis, endocarditis, pneumonia, osteomyelitis, renal problems, immune
Blood-borne viruses (HIV, HCV, HBV)
Psychological
Depression, anxiety, suicide, cognition
Social
Financial, forensic, work, parenting, friendships, economic/community
10 year outcomes (for dependence)
40-50% still using/imprisoned
30-40% abstinent
10-20% dead
Overdose Prevention Strategies
Use with others around
Avoid IVDU
Dont drive or use machinery
No polysubstance use
Small dose to begin
- 65 -

Clean equipment,
Maintain hydration
Seek medical help if problems
Caution around loss of tolerance
Watch impurities, reliable source

Principles of effective treatment


Long duration of treatment
Adequate dose of medication
Quality of therapeutic relationship
Psycho-social supports for the patient
regular review, supervision & monitoring
participation in counselling
environment, family, friends, employment
Bio-psycho-social model for chronic condition
Opioid Treatment options
DETOX
Detox is not a cure for heroin dependence
Most heroin users relapse after withdrawal
Need long-term treatment to achieve long-term changes
Short-term intervention that aims to:
Interrupt a pattern of heavy & regular drug use
Alleviate withdrawal discomfort
Prevent complications of withdrawal
Facilitate post-withdrawal treatment linkages
Symptomatic medications
Clonidine
BZDs, NSAIDS, antiemetics, antidiarrhoeal agents etc
Methadone or buprenorphine
reducing doses over days / weeks
minimises severity of withdrawal symptoms
buprenorphine increasingly used internationally
Antagonist assisted (rapid detox)
Use naloxone / naltrexone as prelude to longer term antagonist treatment
Harm reduction strategies
Needle exchange
Supervised Injection Rooms
Overdose risk reduction
HBV Vaccination
Substitution/ Maintenance Programs
Provision of a long-acting prescribed opioid enables patient to cease / reduce heroin use & related
behaviors
Long term approach: opportunity for client to distance themselves from drug-using lifestyle
Combines medication with psychosocial services
Medication options: methadone and buprenorphine
Issues of pain management, pregnancy, missed doses, unexpected circumstances, holidays, what to
do if used, vomited, legal requirements for prescribing, urine testing
- 66 -

Supportive counselling, vocational, mentor, groups, co-morbid, accommodation, case management, family
Naltrexone
Relapse preventer. Dose 25-50mg daily
Opiate antagonist blocks/decreases effects of heroin
Can cause acute withdrawal if used too quickly after last opiate (can use naloxone challenge for all
except Bup)
Can decrease tolerance to opiates once ceased (risk of OD)
Long acting depot (implant)
Short acting rapid detox (with light and heavy anaesthetic)
Enforced treatment MERIT
Rehabs

Heroin
Route of use
IV or subcutaneous injection due to high first pass metabolism, short acting
increasingly smoked/snorted
skin popping vs mainlining
Duration of use
effects occur within minutes, 3-6 hours duration
Dependence
Difficult to sustain for most people as expensive
2 to 4 injections a day is common
Highly stigmatised
Polydrug use common (eg. 50% use THC, 33% use benzos)
Heroin Withdrawal

- 67 -

Despite considerable variation between programs, almost all patients reduce heroin use
~ 1/2 of patients stop using heroin
~ 1/3 of patients use heroin infrequently
~ 1/6 of patients continue to use heroin frequently
Mortality rates
Heroin users not in treatment = 1 - 2% per annum (p.a.)
Methadone maintenance treatment = 0.5 to 0.75 % p.a.
HIV transmission
lower risk practices than users not in treatment (placebo or wait list controls);
lower rates of HIV transmission
Criminality
Reduced crime in most patients after treatment

Methadone
Full opioid agonist
Onset 30 - 60 min after dose, Peak after ~ 2 - 6 hrs
Long-acting: t1/2= 24-30 hrs: one dose / day
Opioid toxicity with too much methadone: sedation, respiratory depression, death
1 dose of 20-40mg can kill child repeated doses of 3040mg can kill an adult (opiate nave)
1 dose of 70mg can kill an adult (opiate nave)
widespread diversion & methadone related deaths where no supervision (e.g. UK)
daily supervised dispensing at clinics / pharmacies
Dosing
Induction
Require slow induction (start low & go slow)
20-30mg / day & increase dose by 5-10mg every 3 days until reach target dose (over 2-6
weeks)
Maintenance
Doses of 20 40mg prevent opiate withdrawal
Doses >60mg most effective in reducing heroin use
Withdrawal
Gradual dose reductions (at rate of 10mg / month)
Methadone Side Effects
Teeth
Sleep
- 68 -

Decreased Libido and sexual dysfunction


Lethargy
Constipation

Buprenorphine (subutex)
Partial agonist at the opiate receptor
Low intrinsic activity only partially activates receptors
High affinity for the receptor
- Binds more tightly to receptors than other opiates (including naloxone, naltrexone)
High first pass metabolism (so sublingual)
Less risk of overdose c/w full opiate agonists
Less respiratory depression & sedation than methadone
Bup tolerated by individuals with low levels of opiate dependence
Potential concerns re: safety
Bup related deaths reported in combination with other sedatives (EtOH, BZDs) BUT less of a
concern than other opiates (e.g. methadone , heroin)
Scope for takeways, and multi-day dosing
Pharmacology
Sublingual tablets
0.4, 2 & 8 mg tablets available
3 to 10 minutes to dissolve
Time course
Onset: 3060 min, peak: 14 hours
Duration of action dose-related (1 dose / day)
Side Effects
Typical for opioid class: less sedating than methadone
Withdrawal syndrome
Milder than full agonists
Dosing
Induction
Delay first dose of Bup until early opiate withdrawal
Commence 4 to 8 mg daily
Frequent and rapid dose increases possible (by 2 to 8mg/day)
Maintenance
Daily doses: 8 16mg (max 32mg) required initially
Alternate day dosing possible for many clients
Withdrawal
More rapid dose reductions possible than methadone (e.g. 2 4 mg / week usually well
tolerated)
Bup-Naloxone tablet (Suboxone)
Sublingual tablet in 4:1 ratio (BPN:NLX)
Naloxone (antagonist) poorly absorbed sublingually & inactive
Naloxone produces antagonist (withdrawal) effects if tablet injected by heroin user
Enables takeaway doses with greater convenience for patients & less risk of tablet misuse
Bup vs Methadone
Methadone

Buprenorphine
- 69 -

More clinical experience


More opiate-like (sedation, pain)
More range

Safer in overdose
May need to be taken less often, easier logistics
Easier to divert (not if Suboxone)
Less stigma

When to stop maintenance Rx


Chronic condition needs long term treatment
Premature cessation of treatment usually results in relapse to dependent heroin use
Consider ending treatment when
no illicit drug use for months / years
stable social environment
stable medical / psychiatric conditions
patient has a life that does not revolve around drugs
patient informed consent

- 70 -

Week 4 Anxiety Disorders


Anxiety Disorders - Overview and Management

Normal vs Pathological anxiety


criteria for differentiation
intensity
duration
quality of the experience
flooding/overwhelming anxiety
loss of control over anxiety
context and appropriateness of response
true alarms - presence of real danger
false alarms - absence of true danger
negative/disabling effects on behaviour and functioning

Anxiety disorders

Main features
pathological anxiety - dominant emotional characteristic
other emotions may also be present eg disgust, shame, guilt, anger
no organic aetiology of anxiety
not related to substance use
absence of psychosis
Cognitive factors common to all anxiety disorders
exaggerated perception of threat and danger
Most common group of psychiatric disorders
lifetime prevalence for all anxiety disorders
best estimate = 16.6% (range from 9.2% Korea to 28.7% Switzerland)
Australia 1-year prevalence = 9.7%
typical 2x more common in women (exceptions in OCD, SAD)
Often lead to secondary depression + drug abuse
Associated with increased rates of attempted suicide
Some (esp panic disorder) associated with cardiovascular morbidity + mortality
Disabling high personal and social costs
- 71 -

Often misdiagnosed/unrecognised
Aetiology
genetic component 40-60%
common vulnerability factors
negative affectivity (temperament factor with genetic component)
overestimation of probability and cost of harm (cognitive)
?hyperactivity of noradrenergic systems (biological)
more specific factors
behaviour inhibition
specific heritable component
SAD
learning may play a role eg specific phobias

Panic disorder

unexpected panic attacks triggers often identified over course of therapy


physical symptoms symptoms of autonomic hyperactivity (eg cardiac, respiratory,
dizziness/fainting feeling) may masquerade as medical conditions
often one or more symptoms especially distressing perceived similarity to serious physical
illness
racing heart, chest pain heart disease
breathlessness heart and pulmonary disease
dizziness vestibular and neurological conditions
trembling, numbness and tingling sensations (pins and needles) neurological
conditions
sweating, hot and cold flushes endocrinological (esp thyroid) disease
nausea, stomach churning, diarrhoea gastrointestinal conditions (esp IBS)
psychological symptoms fears of dying suddenly, fainting/collapsing, losing control, going mad,
depersonalisation/derealisation
peak of attack within 10mins

anticipatory anxiety
fear of another panic attack fear of fear
fear of/preoccupation with symptoms of panic attack and/or their anticipated consequences
physical/bodily consequences (eg dying)
psychological consequences (eg loss of control)
- 72 -

social consequences (eg embarrassment, shame) not not the major concern
with agoraphobia (PDA)
phobic avoidance present panic driven: main purpose is to avoid/prevent panic attacks
fear and avoidance of the cluster of situations
when alone and/or outside ones own safety zone (eg travelling far away from home), where
immediate medical or other help might not be available
where it might be physically difficult or impossible to escape immediately (eg crowded
places, public transport)
where it might be awkward or embarrassing to escape immediately but fear of physical
harm trumps embarrassment
probably higher level of negative affectivity (temperamental sensitivity) in Pan/Ag cd Panic alone
without agoraphobia (PD)
phobic avoidance not present
epidemiology
lifetime prevalence in different countries: 0.4 -2.9%
lifetime prevalence for AG (best estimate rate): 3.8%
M:F = 1:1.5/2.5
+AG M:F = 1:2.5/4
typical age of onset: 3rd decade
high prevalence in primary care, hospital emergency departments, certain medical settings
(cardiology, otolaryngology, gastroenterology)
course
recovery 30-35%
complete or almost complete remission
no impairment in functioning
no need for treatment
chronic, with fluctuations 50%
mild and/or occasional symptoms
minor and/or occasional interference with functioning
occasional, sometimes a prolonged need for treatment
chronic, without fluctuations 15-20%
continuous and moderate to severe symptoms
complications of panic disorder more likely
continuous interference with functioning
continuous need for treatment
SSx
hypersensitivity to CO2 of brainstem chemoreceptors
lower threshold for activating the suffocation alarm mechanism
hypersensitivity of the presynaptic 2 receptors
failure of the GABA system to inhibit the locus coeruleus
inhalation of CO2
hyperventilation
abnormally sensitive anxiety-regulating mechanism, originating in the amygdala
Cognitive factors relatively specific for panic disorder
threat is perceived to originate within ones body
hypervigilance about physical sensations and bodily functioning
fear of anxiety and its (physical) symptoms because of beliefs that anxiety and its (physical
symptoms) are dangerous
- 73 -

misinterpretation of physical sensations as a sign of an impending catastrophe

Agoraphobia without history of panic disorder

Generalised anxiety disorder (GAD)

pathological worry - range of concerns


excessive, out of proportion to the actual problem
pervasive, present most of the time
several themes - everyday life circumstances + remote future
uncontrollable
often repetitive, with intrusive quality
causes much distress, interferes with functioning
symptoms of tension
psychological aspects
nervousness, feeling keyed up/on edge, unable to relax
restlessness
hypervigilance, exaggerated startle response
irritability
difficulty with concentration
physical (somatic) aspects
muscle tightness/stiffness
stiff neck
back pain
shoulder pain
tension headache
muscle spasms, tic-like movements, jerks, fine tremor, difficulty swallowing
consequences
sleep disturbances
agitation
fatigue
exhaustion
various physical symptoms (less prominent than in panic disorder)
chronic course, with some fluctuations

Epidemiology
lifetime prevalence: 1.9-9.2%
best-estimate rate: 6.2%
- 74 -

rarely occurs alone (usually co-occurs with depression, SAD and panic disorder)
relatively high prevalence in all age groups
most common anxiety disorder in elderly
typical age of onset: 15-25
M:F = 1:2
long period between onset of GAD and time of seeking help
help usually sought for a disorder that complicates the course of GAD (eg depression)
Cognitive factors
worry as cognitive avoidance (by means of worry one avoids unpleasant somatic symptoms that
accompany strong emotional states)
beliefs about benefits of worry may maintain worry
avoid danger
be prepared
cope better if worst happens
interpretation of a wide variety of ambiguous stimuli and information as threatening - intolerance of
ambiguity and uncertainty

Phobias

fear of known objects, situations, activities or phenomena phobic stimuli


phobic stimuli generally do not pose a realistic threat
if they do, the anxiety response is irrational or excessive out of proportion
preserved insight that the fear is irrational or excessive
exposure to phobic stimuli elicits an immediate anxiety response
avoidance of phobic stimuli or endurance of phobic stimuli with great distress and/or anxiety
impaired functioning or significant distress about having the fear

Social anxiety disorder/social phobia (SAD)


excessive and persistent fear of:
performance-type situations performance anxiety
speaking in public
eating or writing in front of other
performing work duties under observation
using public toilets in the presence of others
social interactional situations
interpersonal communication
speaking with authority figures, expressing an opinion
asking for directions, returning purchased goods
avoidance of social situations of their endurance with much anxiety/distress
- 75 -

chronic course, often significant impairment/disability


underlying fears in SAD
fear of being under scrutiny
fear of negative evaluation
fear of making a mistake
fear of having visible physical symptoms that would reveal anxiety
especially blushing, sweating, trembling
anticipation of the interference with performance or of generally performing poorly
epidemiology
lifetime prevalence rates vary
best estimate rate: 3.6%
M:F ~1:1.3-1.7 in community
M=F in clinical situations
more likely to be single, unemployed, in lower SES with lower levels of education =
consequence of SAD
higher risk of alcohol abuse than in people with other anxiety disorders
secondary depression common
age of onset: usually mid-teens to early 20s
usual period between onset and time of seeking help: >10years
aetiology
genetic predisposition
behavioural inhibition to the unfamiliar = component of inborn temperament, observable during the
1st year of life manifests as:
difficulty sleeping in unfamiliar surroundings
irritability in novel situations
avoidance of contacts with unfamiliar people, places and objects
cognitive model
low self-esteem + perception of the social environment as hostile = expectation to be
evaluated negatively in social situations

Specific (isolated) phobias


Epidemiology
prevalence rates vary
lifetime best-estimate: 5.3%
more common among women
M:F = 1:2/2.5
except for blood-injection-injury phobia
usual age of onset
animal phobias: (early) childhood
blood-injection-injury phobia: (later) childhood
situational phobias: adolescence, early 20s
natural environment type of phobias: variable
very few persons with specific phobias seek professional help and treatment
Aetiological factors
genetic predisposition (esp blood-injection-injury phobia)
acquisition through learning
traumatic conditioning direct aversive experience with phobic stimulus
vicarious learning observation of the fear in others
- 76 -

transmission of the relevant information (eg information on dangerousness of certain


objects or situations)
innate fears (not a product of learning; fears with evolutionary survival value)

Animal phobia
clearly a fear reaction (eg phobia of dogs)
appraisal of danger posed by some animals vs disgust elicited by these same animals
especially snakes and some insects eg spiders
clearly a disgust reaction (eg phobia of cockroaches)
Blood-injection-injury phobia
related to excessive disgust (at the sight of blood, injured tissues, mutilation of the body or needle
penetrating the skin body envelope violation)
unique pathophysiology, with 2 phases
initial tachycardia
subsequent vasovagal reaction, with bradycardia, hypotension and fainting
treatment: applied tension
Situational phobias
similarities with agoraphobia
fear of flying
fear of enclosed places (claustrophobia)
driving phobia
Natural environment type of phobias
fear of heights (acrophobia)
water phobia
fear of storms
Other phobias
illness phobia
phobia of choking/vomiting
dental phobia

Obsessive-compulsive disorder (OCD)


Components of OCD
OBSESSIONS
causing anxiety or distress and/or
experienced as alien and/or harm-portending

NEUTRALISATION
alleviation of anxiety or distress and/or
undoing of obsessions and/or
prevention of harm associated with obsessions

behavioural

overt compulsions
avoidance
reassurance seeking

Epidemiology
similar prevalence in different countries
- 77 -

mental (cognitive)
covert (mental, cognitive) compulsions

lifetime: 1-2%
best-estimate: 1.3%
M:F = 1:1
age of onset earlier in males
mean age of onset 21-22yrs
many have onset in childhood
average period between onset and time of seeking help: 7.5 years

Course
lasting remission or recovery
max 20%
fluctuating chronic course
2-47%
exacerbations and periods of complete or partial remission
steady (constant, continuing)
15-61%
chronic course, without significant fluctuations (no clear-cut exacerbations and remissions)
progressive, deteriorating course
5-14%
Aetiology
biological factors
dysfunction of the serotonin neurotransmitter system
increased dopaminergic function in some patients
implicated brain structures
limbic system: orbitofrontal cortex, cingulate, amygdala, thalamus
basal ganglia: striatum (caudate nuclei)
dysfunction in the orbitofrontal (limbic)-basal ganglia circuits or cortico-striato-thalamocortical circuits
certain forms of OCD in childhood: postulated autoimmune process after an infection with
group A beta-haemolytic streptococci (PANDAS)
Obsessions
Characteristics
thoughts, impulses, and/or images
recurrent/repetitive
uncontrollable
not just excessive worries about real-life problems
cause marked anxiety or distress
usually experienced as alien, intrusive, strange, crazy, senseless, inappropriate and/or portending
harm
compel the person to attempt to suppress or neutralise obsessions or resist them in some other way
Common types (frequency)
multiple obsessions
72%
contamination
50%
pathological doubt
42%
somatic
33%
need for symmetry
32%
aggressive
31%
sexual
24%
Compulsions
Characteristics
overt behaviours or unobservable mental acts (covert/mental/cognitive compulsions) that the
person feels driven to perform in response to an obsession and often according to strict rules
(rituals)
- 78 -

repetitive
compulsions are performed in an attempt to achieve one or more of the following goals:
alleviation of anxiety or distress that is caused by the obsession
undoing of obsession
prevention of harm associated with the obsession
Common types (frequency)
checking
61%
multiple compulsions 58%
washing, cleaning
50%
counting
36%
need to ask or confess 34%
need for symmetry or precision, rearranging objects
28%
hoarding
18%

Posttraumatic stress disorder (PTSD)


exposed to a traumatic event
persistently re-experienced
recurrent or distressing recollections
distressing dreams
acting or feeling as if the event was recurring
intense psychological distress at exposure to cues that symbolise/resemble an aspect of the event
persistent avoidance of stimuli, numbing of general responsiveness

Management

General goals of treatment


significant decrease in the intensity and frequency of anxiety and its manifestations (especially
physical symptoms of anxiety)
significant decrease in behaviours (eg escape, avoidance, compulsions) that are related to or are a
consequence of anxiety, which cause distress and functional impairment
better coping with anxiety
decreased vulnerability and prevention of recurrences
prevention of complications
improved functioning and quality of life
Psychoeducation
most important treatment
provide alternative hypothesis to explain cause of symptoms
anxiety symptoms instead of serious illness symptoms
provides information about how problems can be overcome
provides information about realistic and appropriate goals of treatment
Treatment goals and treatment modalities
where is agreement?
reducing the negative impact of anxiety
where is disagreement?
how do we go about it?
Main treatment modalities
pharmacotherapy
advantages over CBT
- 79 -

faster onset of therapeutic effects (possibly)


more obvious and/or greater effects on physical symptoms and symptoms of
tension
greater suitability in some clinical contexts
when the disorder is more severe and more disabling
when patients cannot tolerate symptoms, anxiety and distress, and quick
relief is needed
in the presence of co-occuring psychiatric conditions (eg depression)
generally greater ease of administration
generally wider availability
relatively lower cost

SSRIs

SNRIs
Fine print
OCD - only serotonergic ADs (ie SSRIs and clomipramine [a TCA])
GAD - buspirone
PD - imipramine (a TCA); MAOIs
GAD - probably all TCAs
SAD - MAOIs
performance of pharmacotherapy in various anxiety disorders
PD

4-5

very good to excellent

GAD

3-4

good to very good

SAD

2-4

mediocre to very good

OCD

1-3

marginal to good

specific phobias

0-1

marginal at best

using pharmacotherapy effectively


start low and go slow
SSRIs may cause initial anxiety; patients cope better when warned about
this and allowed to start slowly
use medication long enough
6 weeks or more to see an effect is common (ie longer than with depression)
only OCD shows a clear dose-response relationship with antidepressants, so try
usual doses before moving to higher doses
if an adequate trial with one medication fails, the patient should be switched to
another medication (same class OK)
if several failures, consider augmentation
benzodiazepines
many authors argue that they are safe and effective treatments with low potential
for abuse
current recommendations reserve benzodiazepines for treatment resistant cases
arguments for use
consistent efficacy, especially in an acute setting
rapid onset of action
possibility of prn use
good tolerability (often better than that of SSRIs and TCAs)
- 80 -

some patients will need benzos long term


in long-term use of benzo, tolerance to their anxiolytic effects usually does
not develop and there is usually no escalation of doses and no loss of
therapeutic benefit
arguments against use
side effects
sedation
cognition problems (anterograde amnesia)
impaired psychomotor performance
disinhibition
improved symptoms but not function in SAD
only one small study in PTSD - only modest effect and antidepressants
probably superior
no evidence for effectiveness as monotherapy in OCD
interaction with alcohol
relapse the rule on discontinuation - plus problems of withdrawal symptoms
no sense of mastery; no reduction of future vulnerability
withdrawal symptoms
paradoxical dread of the benzo withdrawal symptoms
most of these symptoms resemble a recurrence of an anxiety
disorder
unpleasant but not life-threatening
seizures most serious, but very rare
last from several days to two weeks
leave no sequelae
often abate without specific treatment
risk minimisation
very gradual benzo tapering schedule
booting patients ability to cope with the anxiety and withdrawal
symptoms by means of CBT and supportive psychoterapeutic
interventions
psychological therapies (psychotherapy)
behaviour therapy
exposure-based treatments
changing and eliminating behaviours (eg avoidance, compulsions) which help
maintain pathological anxiety pathological anxiety will greatly diminish or
disappear with disappearance of these behaviours
most effective in those anxiety disorders that are characterised by pathological
behaviours (eg avoidance in phobias and certain compulsions in OCD)
Principles
in vivo exposure is most effective
stay in the situation until anxiety is diminishing (eg SUDs 50% less)
do not escape, use distraction or safety behaviours
confront the situation frequently and repeatedly
Graded Exposure
create a step ladder or hierarchy of difficulty
eg use SUDs to rate
aim for about 75% expectation of success
- 81 -

too easy better than too hard


example Pan/Ag
catch the bus four stops not in peak hour
catch the bus to local shops, not peak hour
catch the bus to the city on a Saturday
catch the bus home from work - leave a bit early
catch the bus home from work in peak hour
catch the all-stops bus to work in peak hour
catch the express bus to work in peak hour

SUDs
40
50
55
70
75
85
95

cognitive therapy
changing of unhelpful and/or unrealistic thinking patterns in order to decrease or
eliminate pathological anxiety
based on the A B C model
A = situation, event, object, phenomenon, behaviour, person
B = the way in which one thinks about A (appraisals, interpretations)
target of cognitive therapy (changing thinking in order to change feelings)
C = feelings in relation to A (eg fear)

eg.
techniques
identifying erroneous thinking patterns (interpretations, assumptions,
beliefs), and demonstrating how they maintain pathological anxiety
socratic dialogue
when you feel afraid,
what goes through your mind?
what do you think would happen?
uncovering of automatic patterns of thinking that cause, maintain
- 82 -

or amplify anxiety and undermine problem-solving (what if


thinking)
one phobia, many underlying fears

challenging the basis and correctness of such thinking patterns - searching


for evidence pros vs cons
convincing patients that changing their thinking would lead to improvement
patients acceptance of rational alternatives
cognitive-behavioural therapy (CBT)
advantages over pharmacotherapy
brings about changes in dysfunctional patterns of thinking and maladaptive
behaviours, which decreases vulnerability to anxiety and risk of relapse
fosters a more active attitude towards treatment (sense of ownership of
treatment gains)
longer duration of therapeutic effects (relapse the rule when medication
ceased in anxiety cf depression)
decreases likelihood of relapse following cessation of treatment
absence of medication-related side effects and therapeutic drug
dependence
cognitive aspects of anxiety
cognitive distortions
overestimation of likelihood of harm
overestimation of cost of harm
mindfulness/acceptance
psychodynamic psychotherapy, marital therapy, supportive psychotherapy
symptom control (de-arousal) techniques
relaxation techniques (eg progressive muscle relaxation, meditation, tai chi)
breathing retraining (slow, controlled breathing)
pharmacotherapy + psychological treatment
CBT + pharmacotherapy
no clear advantages for simultaneous treatment, but some evidence of superior
outcome if CBT added to pharmacotherapy (eg sequential)
if used simultaneously, potential problems with motivation, attribution of effect to
medication?
Possible ways to reduce the negative impact of anxiety
by attempting to control/suppress the symptoms:
- 83 -

pharmacotherapy
breathing retraining, muscle relaxation (no longer preferred as a primary approach)
by controlling behavioural responses to anxiety
exposure-based (behaviour) therapy
by changing maladaptive patterns of thinking and beliefs (eg anxiety symptoms are dangerous) and
developing more adaptive coping strategies
cognitive therapy (cognitive restructuring)
by attempting to learn to live with the anxiety instead of trying to control it
mindfulness/acceptance

PD; GAD; SAD pharmacotherapy


1st line: SSRIs, venlafaxine
2nd line: other antidepressants
TCAs (imipramine) for PD and GAD
3rd line: antidepressant + benzodiazepine
sometimes used in combination, given for initial few weeks to minimise SE from Ads
usually not necessary with good pscyhoeducation and start low and go slow
irreversible MAOIs for SAD
4th line: benzodiazepines only
high-potency benzodiazepines (clonazepam, alprazolam) for PD
clonazepam for SAD
further down the line
classical MAOIs, mirtazapine and reboxetine for PD
buspirone and hydroxyzine for GAD
-adrenergic blockers (propranolol, atenolol) often used for performance anxiety
NOT effective in generalised SAD
PD psychotherapy
cognitive therapy
more realistic and likely interpretations of physical sensations and symptoms
changing threat and danger appraisals
learning not to be afraid of anxiety/panic and its symptoms
most recent developments - move away from trying to suppress or control symptoms to panic
surfing
behaviour therapy for agoraphobia
exposure (hierarchy-based, gradual, self-directed, in vivo) to phobic situations
GAD psychotherapy
reduce arousal (eg progressive muscle relaxation)
cognitive therapy
- 84 -

improve decision-making and problem solving process


coping better with uncertainty
imagery exposure to the content of worries
identifying specific beliefs about the benefit of worrying + challenging these beliefs
behavioural
resist urge to seek certainty (eg reassurance-seeking)
SAD psychotherapy
exposure (imaginal and in vivo, often in-session, therapist-assisted, with role-play) to relevant social
situations
social skills training: if there is a marked deficit in social skills (not usual)
cognitive therapy
most effective when target beliefs about the cost of negative evaluation
Specific phobias psychotherapy
various techniques of behaviour therapy, based on exposure, are most effective
exposure
gradual vs flooding
imaginal (guided imagery) vs in vivo
self-directed vs therapist-assisted
OCD pharmacotherapy
only medications with specific serotonergic effects (clomipramine, SSRIs) efficacious
longer duration of treatment (>12wks) and (often) higher doses are needed for response to occur
only 40-60% respond to clomipramine or SSRIs
1st and 2nd line: SSRIs
3rd line: clomipramine
augmentations and combinations
SSRI/clomipramine + antipsychotic
SSRI + clomipramine
SSRI/clomipramine + clonazepam
OCD psychotherapy
behaviour therapy
exposure (to the obsession- and compulsion-related cues) and
response prevention (abstaining from performing the compulsion)
cognitive therapy, which targets
beliefs that patients are responsible for having obsessions
beliefs that having unacceptable/repugnant thoughts is the same as acting in accordance
with such thoughts

Overview of the Psychotherapies

Self regulation
an overarching goal of therapeutics is to restore, or change/develop self regulation and self
organisation
self is relational
trauma breaks down connections
self develops or is restored in positively connected relationship
Definition of psychotherapy
treatment that relies primarily on the therapists ability to mobilise healing forces in the sufferer by
psychological means
e.g. verbal communication, specific therapeutic procedures and techniques, patienttherapist relationship (holding in mind, collaboration)
- 85 -

Why do we need psychotherapy?


We learnt how to think/feel/be/do a certain way that back then was helpful/the best we could
come up with (defence/schema/adaptation/ distorted cognition/ stress regulation). It is now no
longer useful or is actively causing us harm = symptoms, syndrome. We need to change, and,
because it has become so practiced, changing is at best hard, at the worst terrifying (resistance)...
that was then, this is now
Body-mind-brain integration
Attachment theory is a true biopsychosocial model, developmental and evolutionary based,
proposing that human beings develop physically, mentally and socially in relationship.
It predicts the mal/adaptations to development, self-regulation and the stress response that
arise if a person is not safely and comfortably supported and if experience becomes acutely
or chronically traumatic.
Attachment theory and a working understanding of self-regulation, stress systems and
dissociation then offer guides to different recovery pathways and can direct psychotherapy.
Polyvagal theory and stress
The stress response in mammals and primates has evolved to make use of social regulation of stress.
This is intimately tied to the parasympathetic and sympathetic arms of the autonomic nervous
system as well as the 2 arms of the vagal nerve (myelinated and unmyelinated).
The hierarchy is:
Social (soothing accessible socially via the PS)
Flight/fight (removal of the vagal brake and SNS activation)
Withdrawal/ freeze (the unmyelinated vagal)
Mammals use social soothing and attachments to soothe and manage stress
Attachment states of mind
A. Dismissive
I have do it myself AS others are no helpful/reject me. I am shameful/contemptible when
needy. I avoid/minimise feeling. I focus on being independent/strong,
achievements/fun/things, material success.
B. Secure
I am free to ask for help BUT I am lovable, others are useful and reliable. I am free to value
relationships, express emotion openly and directly, express myself, remember clearly.
C. Preoccupied
I cant do it myself BUT others are unreliable, I am untrustworthy, I feel
anxious/angry/blaming, lost in memories, helpless/hopeless/useless. If I scream they might
hear. I remember too vividly.
D. Disorganised
I cant do it BUT others will make it worse! Those who should help are
frightened/frightening. I feel dreadful/disconnected/confused, bad/fragmented/afraid.
Outcomes of development are patterns of homeostasis
Ways that the child, then adult, learns to manage stress using the possibilities of regulation by self or
others. They include procedural aspects a sense of the way things are
initially implicit, unconscious, or at least out of conscious awareness
much being laid down before autobiographical memory
Later in life, self-regulation may be challenged, forcing it to reorganise in ways that optimize or limit it
making the person more resilient or more prone to stress.
Early disruption shifts organisation patterns and changes epigenetics with possible consequences
e.g. depression, chronic complex PTSD, anxiety, somatoform disorders, substance use disorders
- 86 -

Goals of psychotherapy
1. Movement towards a more secure attachment state of mind, and a robust self with reflective
capacity that fosters development of interpersonal skills through
Cohesiveness and Collaborativeness
Autonomy and Flexibility
Mindfulness of self and others (Mentalization and reflective functioning)
In doing so leads to symptom reduction and relief from disorders
2. Coherence and Collaborativeness as outcomes
of a single, internally consistent working model of attachment (Main et al, 2002, AAI
Research)
of a secure/autonomous/flexible attachment state of mind
the narrative of self becomes coherent and collaborative
as coherence increases so does playful flexibility (Meares,2005) and reflective functioning
all aspects of experience are allowed access to consciousness without distortion or contradiction
(Slade,1999). Sounds like a successful therapy.
An ideal psychotherapy patient
Is aware of his/her distress or pain or dysfunction
Cannot cope with it or its effects
Wishes to change the situation and is MOTIVATED to change!
Therefore asks for or accepts help
Believes in the ability of another to help
An ideal psychotherapist
has the Skills/Knowledge/Attitudes about a theoretical system or model that:
Provides an explanation for the symptoms, problems and/or maladaptive behaviours
Prescribes a procedure and techniques for alleviating/resolving/eliminating these
Who has a robust, flexible and collaborative mind with empathy and respect for human beings and
the life of the mind
An understanding of trauma-informed care and recovery
An ideal healing (therapeutic) setting
A place/space/relationship that provides safety. Is a quiet, predictable and trustworthy environment,
in which there is freedom to speak and to feel (without negative consequences)
A place/space that raises patients hopes and expectations from their psychotherapeutic investment
The therapeutic relationship
the patient and therapist has a very intimate relationship that is still has very firmly set boundaries
of verbal dialogue/conversations/interactions/frame.
is asymmetrical.
the patient reveals his/her problems and confides
whereas the therapist should not normally disclose to the patient his/her personal details
Main psychotherapy models
1. Psychodynamic
2, Behaviour/ Cognitive
3. Experiential/ humanistic/ systemic
Freuds topography of mind
conscious
preconscious (dream state, recent experiences)
unconscious (instincts, traumas, fears, passion etc)
Main principles of early psychodynamic theory
unconscious
- 87 -

conscious - is fragile and restricted by trauma


conflicts e.g different thoughts/feelings/actions that conflict
defences/resistances against feeling/knowing this conflict
this resistance originates from external reality or from the persons own conscious (moral
standards) or a difficult feeling of dissonance
developmental - origins of conflict are often in childhood relationships/experiences
psychic determinism - mental phenomena and behaviours are not chance occurrences but at
linked/related to what comes before. Consequently these links mean these phenomena and
behaviours are subject to repetition.
Main goals of early psychodynamic therapy
to make the unconscious conscious
insight leads to therapeutic change, insight = cure, insight oriented therapy
***Models of technique in contemporary psychodynamic therapy (LEARN!!!!)
Reliance on transference:
unconscious repetition of early attachments still crucial e.g. important relationship from
patients past e.g. a female patient relates to her male therapist in the way she did to her
father by expecting disapproval
opportunity to understand and rework the relational template
Notions of Unconscious informed by modern understanding of neurobiology, attachment, trauma
and memory eg memory systems
Implicit procedural / associative
Explicit semantic / episodic / autobiographical
Fostering a reparative relationship
the psychotherapist acts as the mirror, blank screen
The analyst is to remain relatively removed/detached, a deliberately dispassionate
observer of the patients feelings
but not cold or unresponsive!!
The therapist helps develop the kind of relationship and conversation that builds and repairs
mind and allows the old expectations to be revealed and explored
Fosters development of self and processes trauma (Meares, 2005)
To encourage a free, spontaneous and new response
Modern understanding of affect (Le Doux, Damasio, Porges)
affective experiencing
facilitated expression of feelings
abreaction
catharsis
direct and open emotional expression
***Contemporary Dynamic Therapy Technique 1
Transference
Organises the therapeutic interaction.
Needs to be monitored and understood
Will be both the old/archaic and the new
Experienced as backgrounded or foregrounded
Affect
Underlies the transference, organises much cognition
Say what you feel/mean, mean/feel what you say
Follow it, track it, down the associative paths (depression case)
Disjunction and Repair
- 88 -

Failures of affective attunement reproduce the old experience


Repair of these disjunctions build the new experience, the new transference and new self
structure
***Contemporary Dynamic Therapy Technique 2
Focus on affect and expression of emotion
Exploration of attempts to avoid distressing thoughts and feelings (defence/adaptation mechanisms,
behaviours)
Identification of recurring themes and patterns
Discussion of past experience i.e developmental focus
Focus on interpersonal relationships
Focus on the therapy relationship
Exploration of fantasy life (dreams, wishes)
***Range of dynamic interventions
Expressive to Supportive (top to bottom)
*Interpretation
*Confrontation
Clarification
Encouragement to Elaborate
*Empathic Validation
*Advice & Praise
Affirmation
Main principles of the behavioural/cognitive model
All behaviour and mental phenomena are a product of what we have learned or not learned =
Learning theory
Symptoms of mental disorders are learned habits
Involuntarily acquired (e.g., through a traumatic experience)
Repeated responses to specific stimuli in the environment, which reinforce (maintain) the
symptoms
Humans are manipulable and therefore controllable by external events
Main goals of CBT
Elimination of symptoms and maladaptive behaviours
Elimination of maladaptive patterns of thinking
Whatever maintains the problem
i.e abnormal behaviour, pattern of thinking, disorder
Treatment goals are specific, somewhat limited in scope but achievable within allocated time frames
e.g., alleviation of symptoms, better coping with problems at work
formulated in collaboration between the patient and the therapist at the beginning of
therapy
Means of achieving goals of CBT
Direct teaching and learning of new associations (e.g., induction of anxiety + relaxation)
The patient is taught alternatives that must be repeated and practiced
Skills need practice, homework!
Educative, teacher-pupil relationship (Hollander, 1975)
The patient-therapist relationship is important only to the extent that it can secure patients
cooperation with the treatment plan and agreed-upon treatment goals
Actually all good therapists are aware of transference eg clinically relevant behaviour ( see
Shedler, 2006)
Main techniques of CBT - Directive techniques
- 89 -

Patient and therapist are generally more overtly active


Systematic desensitization + muscle relaxation
Relaxation
*Exposure and response prevention
Flooding (Implosion)
Assertiveness training
Positive or negative reinforcement
Token economy
Aversion therapy
Shaping/modeling
*Cognitive restructuring
Problem solving
Stress management
Issues in psychotherapy
Roles and responsibilities
Clarifying what the therapists can and cannot do
Understanding requires two
I cannot make decisions instead of you, but I can help you in the decision-making
process by drawing your attention to the options that you might not have
considered (vs Woody Allens view)
Reliance and dependence: the patient can rely on the therapist temporarily, but reliance on
the therapist must not turn into inappropriate dependence
Boundaries
Strict observance of the boundaries ensures the integrity of psychotherapy
Limit-setting from the very beginning and consistency about it, as some patients have a
tendency to test boundaries in many different ways
Be aware (Beware!) of potential boundary violations!
Sexual
Non-sexual
Communication and empathy
Listening to patients takes the priority over talking to them
Careful, reflective (empathic) listening
Empathy: The power of understanding things outside ourselves
Knowing what its like to feel and think the way the patient does
Being in the others shoes
Some basic psychotherapy tips
Engaging patients by:
Listening carefully
Creating an atmosphere of expression
Not critical or judgemental
Validating
I see why youre upset when everyone keeps telling you that you should just get
over it
Clarifying the collaborative relationship
Fostering trust and interpersonal consistency
Elucidating patients expectations and goals, with an emphasis on
the HERE and NOW, and on
where to go from here/what needs to be done next
- 90 -

What made you decide to seek help NOW?


What do you expect to achieve through therapy? How do you see your future?
How do you think I could help you with your CURRENT problems? How do you
see we could work on these together?
Providing support by
Emphasising patients strengths
Encouraging patients to be more self-reliant in longer term
Teaching patients the specific skills and techniques
Psychotherapy is all about growth and change, and usually entails:
Better understanding, especially of:
causes/antecedents/underlying motives/ consequences
Examining problems from a different perspective
Looking for the alternatives and broadening the options
Coping with problems more effectively
Emphasising the patients responsibility for his/her behaviour (there is nobody else to
blame, but I am also empowered)
Develops flexibility of mind and a sense of agency
Mechanism of change across various psychotherapies
Mastery of Cognition/Affect/Self/Behaviour
Correcting problems by explaining them rationally and empathically
Acquiring and integrating new perceptions, thinking patterns and/or self-awareness
Understanding myself and others (mentalizing, mindfulness, theory of mind, reflective
capacity
Empathic attunement of therapist (and patient!)
Self/Behavioural Regulation And Change
Optimal length of therapy
Variable: from several sessions (CBT/brief psychodynamic) to several years (long-term
psychodynamic or CBT for personality change)
Tendency globally towards shorter courses of psychotherapy (e.g., 8-16 weekly sessions), with
clearly set goals at the beginning
Rigid adherence to a pre-determined time frame may be counterproductive, but duration is often
part of contract
Outcome of psychotherapy
Generally favourable, depending on the type and application
Difficulties in:
Applying the currently favoured scientific methodology of EBM
Good therapy is absolutely specific, not random.
Knowing exactly what goes on during the therapy (manualised v non-manualised therapies,
adherence to a model)
Evaluating patient-therapist relationship
Assessing outcomes (in view of the different goals of different therapies) : often measuring
apples not oranges!
Psychotherapy research is one of the most challenging areas in psychiatry and clinical psychology
Current good meta-analyses, supporting both CBT and psychodynamic approaches, but need more
work on what works for whom and process
Required reading (still need to take notes!!!)
*Leichsenring, F et al. (2006) Cognitive-Behavioural Therapy and Psychodynamic therapy: Techniques,
Efficacy , and Indications. American Journal of Psychotherapy, 60(3), 233-259.
- 91 -

*Shedler J. (2010). The efficacy of Psychodynamic psychotherapy. American Psychologist, 65(2), 98-109.

- 92 -

Trauma, Life Events and Mental Illness

Life events
Stressful events - vs - Hassles
Life events that exceed persons capacity to regulate them and maintain homeostasis associated
with onset of mental health problems and stress system disorders - stress diathesis model
Salience of event
Effort after meaning
Stress
An environmental challenge that challenges the organisms ability to cope
primary appraisal, scope of the challenge, secondary appraisal, available coping resources
Stress-diathesis model

Stress trauma and mental health


traumatic stress best defined as overload for an organism
subjective perception of stress is often more important than some objective reality
US population studies indicate that 89% of the population met PTSD DSM-IV Criteria A1 and A2
A1: experienced/witness event that involved actual or threatened death or serious injury
A2: response involved intense fear, helplessness or horror
Types of trauma
A single isolated event outside the realm of ordinary human experience
An accumulated set of circumstances or events that an individual is exposed to, and that can have
consequences that would not have occurred in the absence of such circumstances - cumulative
trauma
Where such cumulative trauma is relational and often occurs early in development: chronic complex
trauma
Massive trauma in the form of violence, terrorist acts, wars, deprivation, torture and natural
disasters, forced migration, retention, slavery
Repeated microtrauma, not just macrotrauma, is damaging to the developing self
Trauma causes states of disconnection
Trauma breaks down self, attachment organisation and relationships
It breaks down links between parts of self, self and other, and the community
It breaks down links between brain states and body states and mind-body-brain states
Trauma destroys trust and assumptions about safety
Trauma calls into question basic human relationships, their safety, continuity and meaningfulness
Effects of trauma
Impedes development of self
- 93 -

Disrupts the sense of self if formed


Interrupts continuity - stream of consciousness
Overthrows self-reflectivity
Dissociates aspects of experience, sensation, feeling and cognition
Alienates (alones) us
The autonomic nervous system
Balance in stress management between the sympathetic and the parasympathetic (newer paradigm)
vs sympathetic alone (older paradigm)
Porges model posits that humans have a social nervous system evolved to manage stress in a
hierarchy of
Social soothing (myelinated vagal)
Flight and fight (sympathetic)
Withdrawal response (unmyelinated vagal)
Aim to promote social processing, decrease arousal, promote rest and digest
Traumatic stress
How to define trauma?
Subjective experience vs objective reality
The perception of threat to self or others
Embodied experience of threat
Attribution of meaning to events
Pre-trauma variables
post-trauma variables
Growing breadth of the stress-diathesis
Evidence growing for gene-environment interactions and epigenetic influences on mental health and
mental illness
Now biological disorders such as Schizophrenia influenced by the newer models that acknowledge
the role of stress and trauma in mental illness
Predisposition
Precipitating/triggering
Causal
Comorbid
Complicating/perpetuating
Terrs typology of trauma
Type I trauma - acute or one-off traumas characterized by full, detailed memories, omens and
misperceptions eg. car accident
Type II trauma - recurrent and chronic traumatic stress characterized by denial and numbing, selfhypnosis and dissociation, and RAGE eg. Repetitive physical or sexual abuse
Development
Important role of trauma in family and for individual in development
Acknowledged that stress/trauma in mother or previous generations can influence stress
vulnerabilities in children
Epigenetics (Meaney et al)
Attachment-related transgenerational transmission of trauma/disorganised state of mind
The nature of post traumatic mental health - watch this space!
...WTF?!
Post traumatic disorders
Depression 44%
Anxiety 39%
PTSD 16%
- 94 -

Other 1%

- 95 -

Post

PTSD

traumatic stress and


disorder

12 month prevalence estimated at 1.3%


Lifetime prevalence up to 5%
Symptoms:
Reexperiencing
Arousal
Avoidance/dissociation

- 96 -

Probability of persistence in terms of months from onset of PTSD


Female and event to self
Female and event to other
Male and event to self
Male and event to other
Screening for PTSD

- 97 -

Comorbidity in post-traumatic mental health

Cluster C: avoidance; Cluster D: arousal


The biology of psychological trauma
Important concepts
Physiological responses to stress, the ANS
Neurotransmitters - catecholamines, opioids, neuropeptides
The role of glucocorticoids
Kindling
Limbic system structures - amygdala, hippocampus
Genetic and epigenetic influences
Kindling hypothesis
Borrowing from analogy of campfire
Goddard (1969) found that repeated subthreshold electrical stimuli leads to full blown seizures
A pathophysiological model of Bipolar Disorder
In PTSD, repeated traumatisation, eg chronic sexual abuse or repeated trauma or intrusive reexperiencing of traumatic stress might kindle limbic nuclei like the amygdala or hippocampus leading
to behaviour change such as startle reflex and differences in cognitive and emotional processing i.e.
affect regulation
Glucocorticoid cascade hypothesis
Excess glucocorticoid secretion is associated with alterations in the hippocampus - due to spikes
Glucocorticoids damage CA4 neuronal layer of hippocampus
altered glucose metabolism
excitotoxicity mediated by glutamate
inhibited long term potentiation
impaired neurotrophin synthesis
- 98 -

Glucocorticoids and opioids alter the manner in which memories are laid down - state dependent
Does prophylactic glucocorticoid administration prevent PTSD???
Parental PTSD, a putative risk factor for PTSD, appears to be associated with low cortisol levels in
offspring, even in the absence of lifetime PTSD in the offspring
The Frontal Lobes
Van der Kolk and other have shown that the frontal lobes become disengaged from processing by
trauma which becomes locked in subcortical and lower centre processing
Significantly lower benzodiazepine receptor binding was found in the pre-frontal cortex of PTSD
patients
The Hippocampus

Genetic aspects
Examined 4042 Vietnam veterans MZ and DZ male twin pairs to determine the effects of heredity,
shared environment, and unique environment on the liability for 15 self-reported PTSD
After adjusting for differences in combat exposure genetic factors account for:
13 - 30 % of the variance in liability for symptoms in B symptoms
30 - 34 % for symptoms in the avoidance cluster C symptoms
28 - 32 % for symptoms in the arousal cluster D symptoms

Treatment for PTSD - the evidence base


Acute and one-off trauma
Guideline for recovery from acute trauma from Australian Centre for posttraumatic Mental Health
(http://guidelines.acpmh.unimelb.edu.au/__data/assets/pdf_file/0008/851489/ACPMH_Full_ASD
_PTSD_Guidelines.pdf)
Trauma-informed care for chronic complex trauma
(adults surviving child abuse) ASCA practice guidelines
(http://www.asca.org.au/About/WHATWEDO/ASCAsPracticeGuidelinesforTreatmentofComple.as
px)
Psychological first-aid after a trauma: safety, security, social support, practical assistance and information;
monitor mental state
Trauma-focused psychological treatment is the mainstay
If patient too unwell to undertake psychological treatments alone, addition of medication can be considered;
SSRI is first line
- 99 -

Psychological treatments for acute and chronic PTSD


Most evidence exists for structured treatments
Most supported treatments are those based upon arousal reduction and exposure based therapies
Many patients avoid these treatments
Many apparently helpful therapies have little empirical support
Most therapeutic approaches are long-term and supportive in nature
Approaches to build up the self and affect regulation needed in chronic complex trauma
Sequential approach to psychotherapy of PTSD
Education and deal with comorbidity
Arousal reduction - progressive muscle relaxation, deep breathing, mycalmbeat (HRV biofeedback),
safe place etc
In-vivo exposure
Imaginal exposure
Interpersonal approaches eg IPT
Longer term supportive approaches
Dealing with medicolegal aspects
Key aspects of structured psychological interventions
Confronting the traumatic memory in a controlled and safe environment (eg imaginal exposure)
Identifying, challenging and modifying biased or distorted thoughts and interpretations about the
event and its meaning (cognitive therapy and emotional processing)
In-vivo exposure
Most evidence for CBT and EMDR (Eye movement desensitisation and reprocessing)
EMDR
Originally comprised only eye movements while accessing memories and sensations associated with
the trauma
Now includes many elements of stabilization, stress regulation and CBT
Long term outcomes < exposure therapy unless this is included
Debriefing
Controversial
Cochrane analysis found no supporting evidence
Some evidence of increase risk of subsequent psychopathology
Not support as a routine intervention
Modalities
Behaviour therapy
Stress-innoculation therapy - superior to no treatment, less effective than CBT/EMDR
Cognitive behaviour therapy
EMDR
Brief eclectic psychotherapy - insufficient data
Mindfulness psychotherapy - insufficient data
Supportive counselling - not effective as stand alone
Acceptance commitment therapy - insufficient data
Interpersonal psychotherapy
Hypnotherapy - not effective as stand alone
PTSD - treatment effect sizes
Psychotherapy r = 1.16
Control r = 0.4
Medication r = 0.6
PTSD treatment drop-out rates
Medication 30%
Psychotherapy 12%
Control 15%
Medications
SSRIs the mainstay for acute
SNRI and other dual acting agents with more depressive component and where PTSD more chronic
Benzodiazepines
Anticonvulsants eg topirimate
Antipsychotics - esp quetiapine, olanzapine, respiridone
Beta-blockers
Clonidine
Buspirone
Chronic complex trauma
Longer term treatments that build up self and self-regulation and process trauma in borderline personality
disorder and other outcome of CCT (client centered therapy), repair chronic dissociation and negativity bias
eg. dialectical behavioural therapy, conversational model, mentalisation, transference-focussed
psychotherapy
change the attachment template and the theory of mind
Summary
PTSD is reasonably common with a 12 month prevalence of 1.3%
Women are affected more commonly than men
- 100 -

The risk of PTSD is greater after some types of traumatic events (


Premorbid factors increase the risk of PTSD
Psychological treatments are first-line; antidepressants may be used as adjunctive treatment
Chronic complex trauma an important factor in mental health
Trauma an important factor in psychiatric and related stress system disorders

Socio-cultural Aspects of Psychiatry

Refugees vs migrants

Migrants

Refugees

choose their new country carefully and find out


all they can about it before they leave

take the quickest way out of their country,


often not knowing where they will finish up

plan their move carefully in advance

leave hastily, often to escape from midnight


raids and soldiers with guns

take time to get their passport and visas ready

leave secretly, often not daring to advertise


their intention of leaving by arranging travel
documents

pack all their belongings up and organise for


everything to be sent to their new home

leave with whatever they can carry often no


more than the clothes on their backs

say goodbye to their family and friends

often cannot tell anyone that they are leaving,


for fear that their friends or family will be
tortured to reveal the information

can go home if things dont work out in their


new country

often dare not get in touch with anyone in their


home country, for fear that they will be
suspected of having the same beliefs and then
be tortured or held at ransom - will probably
never be able to go home

first migrants Indigenous


oldest continuous culture in the world
psychological trauma of the stolen generation
consecutive Fed Govt policies during 20th C until 1970s
European settlers from 1788
1938 150th celebrations initial refusal for convict and aboriginal floats, later reversed
decision for convicts only
egalitarian society
no colonial ruling class
disdain for authority in peacetime and in world wars
The immigrant experience
Immigration is an unending brutal workout for the adult brain, requiring a massive rewiring
of vast amounts of cortical real estate
The migrant and refugee experience
Enormous focus on loss.family, friends, contacts, job, financial situation
Sometimes worsened by Western govt. policies.
Could have a severe impact on YOU as the clinician involved in their health..
What do you know of refugee problems, torture and dislocation stressors..?
YOU will feel a sense of helplessness and may even risk burnout in your caring roles.
Some migrant/refugee health issues include psychiatric disorders, drug and alcohol-related
- 101 -

problems, TB, HIV/AIDS, tropical diseases, suicide risk.


Cultural awareness
You need to be culturally competent and therefore aware of your own inheritance and
potential prejudices.
Knowledge of anothers language and their background could be vital for the
migrant/refugee and yourself when meeting them.
Refugees
A refugee is a person who (Article 1A, 1951 Convention on the Status of Refugees)
has a well-founded fear of persecution because of his or her
religion
nationality
race
membership of a particular social group or political opinion
and is outside of his or her country
or does not have nationality and is outside his or her country and is unwilling or
unable to return to it.
re-settlement in Australia
offshore vs onshore
13799 places for refugees and humanitarian entrants for 2010-2011
Top 10 country of birth

Healthcare
50,000 refugees/asylum seekers between 2006-2012
inadequate funding for research health problems of asylum seekers
many are in good health, but many have range of health needs
psychological disorders
PTSD
anxiety, depression
psychosomatic disorders
physical consequences of torture such as
musculoskeletal pain or deafness
hypertension, diabetes
poor dental hygiene
TB or intestinal parasites
delayed growth or development in children
Refugee background
- 102 -

may have experienced


torture
prolonged harrassment by authorities
imprisionment without trial
loss of loved ones through violence
deprivation while fleeing or in exile
separation from family during flight
loss of home, possessions, job, status and future
long periods of settlement in refugee camps
Psychological effects of trauma
PTSD
complex PTSD
dissociation
personality change
poor relationships
aggression
self harm
loss of meaning in life
cognitive impairment
somatisation
anxiety disorder
depressive disorders
grief (may be chronic)
psychosis
substance abuse
Socio-cultural psychiatry: general approach in primary care
among immigrants, prevalence of common mental health problems initially lower, but increases
over time to become similar to that in the general population
refugees who have had severe exposure to violence often have higher rates of trauma-related
disorders including PTSD, chronic pain or other somatic syndromes
assessment of risk for mental health problems includes
consideration of premigration exposures stresses and uncertainty during migration
postmigration resettlement experiences that influence adaptation and health outcomes
clinical assessment and treatment effectiveness can be improved with the use of trained interpreters
and culture brokers when linguistic and cultural differences impede communication and mutual
understanding
Adolescents and children - immigrants or refugees
wide variation in rates of mental health problems
some studies show higher risk for psychopathological disorders
others show rate is no higher than that of native-born children
many do exceptionally well
many children coping with a history of exposure to war and political violence manage to
have relatively good mental health
Women - immigrants
2-3x risk for post-partum depression
do not proactively seek help though
barriers to seeking help
lack of knowledge about treatment options or disease
- 103 -

reluctance to discluse emotional problems outside the family


unwillingness for medical treatment for what is perceived to be a psychosial
problem
concern that maternal mental illness will burden or stigmatise family
feelings of shame at being labelled mentally ill
fear of losing ones children to authority
Seniors - immigrants or refugees
Risk factors for psychological distress
female
less education
unemployment
poor self-rated health
chronic diseases (heart disease, diabetes, asthma)
widowhood or divorce
lack of social support or living alone
Issues
slower rates of learning the language or acculturation
separation from extended family peers and familiar surroundings
decreased social support and isolation (family + community networks are lost)
increased dependency on others because of language and mobility difficulties
fewer opportunities for meaningful work and productivity
loss of status as respected elder in new cultural context
Place of origin can affect exposure to endemic diseases, childhood immunisation, and health care
experiences
Culture can affect
interpretations and reactions to symptoms
explanations of illness
patterns of coping, of seeking help and response
adherence to treatment
styles of emotional expression and communication
relationships between patients, their families and healthcare providers
Any patient who has limited proficiency in the languages known by the clinician should be
encouraged to use a medical interpreter
Interviewing working with interpreters
Before
meet with interpreter explain goals of interview
discuss whether the interpreters social position in country of origin and local
community could influence the relationship with the patient
explain the need for especially close translation in the MSE (eg to ascertain thought
disorder, emotional range and appropriateness, suicide risk)
ask the interpreter to indicate when a question or response is difficult to translate
discuss any relevant etiquette and cultural expectations
arrange seating in a triangle so that the clinician is facing the patient and the
interpreter is to one side
During
introduce + explain roles
discuss confidentiality + ask for consent for interpreter
look at and speak directly to the patient
- 104 -

After

use clear statements in everyday language


slow down pace; speak in short units
do not interrupt interpreter, keep looking at the patient while the interpreter is
speaking
clarify ambiguous responses (verbal and non-verbal) and ask the patient for
feedback to make certain that crucial information has been communicated clearly
give the patient the chance to ask questions or express concerns that have not been
addressed
discuss interview and ask the interpreter to assess the patients degree of openness
or disclosure
consider translation difficulties and misunderstandings and clarify any important
communication that was not translated or was unclear (including non-verbal
communication)
whenever possible work with the same interpreter for the same patient

- 105 -

Psychiatric Emergencies, Safety Issues and Management of Aggression

Types of psychiatric emergency


Aggression
Suicidality assessment
Other psychiatric assessment
Illicit substance emergencies
Sudden cardiac death
Neuroleptic malignancy syndrome
Serotonin syndrome
Lithium toxicity
Clozapine
Movement disorders
Considerations in presentation
History taking not straight-forward
Stigma, shame
Degree of co-morbidities
Heightened emotions
Resources difficulties, hospital differences
Impact on life/career if things go wrong
Cuts across all systems (all wards, legal, police, DOCS, NGOs, media)
Less certainty in aetiologies, how treatments work
Guidelines unclear, interdisciplinary measures required, common sense and creativity
Clients can be good at manipulation, pushing buttons, reeking havoc, highlighting system/personal
weaknesses
Aggression and Violence
People with mental disorders are more likely to be violent vs general community
Vast majority of people with mental disorders are not violent
Increased risk of violence mediated in part by active psychotic symptoms
MAJOR Risk factors
Past hx of violence
Drug alcohol intoxication/withdrawal
Demographic factors
Acute mental illness
Brain injury, neurological conditions w/ disinhibition
Personality disorder
Threats of violence
RF Violence in PSYCHOSIS
Delusions of persecution
Delusions of control
Command auditory hallucinations
Drug alcohol intox.
Past hx of violence
Approach to patient work-up w/ potential violent behaviour
Consider attitudes, preconceived ideas
Self-awareness (physiology), take a deep breath, get focused
Corroborative, use of trusted relative/friend
Consider approach, plan
- 106 -

May differ between hospital


Consider security/staff support/presence
Proximity
Low stimulation environment
Alarms
Consider patient access to objects, potential weapons
Level of agitation
Observe closely! Be aware of other signs of aggression
Body position at the same level as the patient
Shake hand if possible
Sit/stand close to the door, but do not obstruct
Beware of pride
Engagement strategies
Explain role
Simple, clear language (avoid medical lingo where appropriate)
Stay calm
Try to empathise
Listen to why angry/having thoughts of violence - let rant if possible
Dont interrupt
Open questions
Use neutral themes, general chat if appropriate
Explain actions, explain delays
Offer blanket, food, drink
Use medical problems as a way in (pain, sleep problems, rash, flu symptoms)
Consider eye contact, hidden hands, distance, angle
Dont argue/challenge
Set limits/give choices
Dont drop guard
Dont turn back
Dont make promises that cannot be kept
Depersonalise
as explanation to patient
to manage own feelings
History considerations
Must consider medical causes/co-morbidities
e.g. organic brain causes, hypoglycaemia
Contraindications/cautions for sedation
Mental Health Act
Documentation - use quotes
Golden rules of engagement
Trust your gut!
Never feel you are over-cautious
Safety over rapport, time limits, logistics, pride
Debrief
Rapid sedation
Get a tea
Get organised, medication ready, other equipment
Someone nominated to do talking
- 107 -

Plan B and C
Observations, 1 to 1 supervision
Individual emergency dept, hospital policy and protocols
Cautions/adverse effects
Sudden cardiovascular collapse
Respiratory depression
Brain injury
Hypotension
Irregular, slow pulse
Acute dystonic reaction (past history)
Limited history
Unknown ingested/injected substances
History/presentation not making sense
Agents for rapid sedation
Oral: diazepam, olanzapine, haloperidol (with benztropine)
IM: lorazepam, midazolam, haloperidol, olanzapine
IV: Anaesthetics, benzos, antipsychotics

Suicidality
Key assessment/management issues?
Assessing severity of suicidality
Physical assessment
Engagement
Risk - immediate, short term
Mental state
Next step - specialist review, discharge/admission
IMPORTANT TO BE THOROUGH!
Poor/incomplete assessments increase risk of repetition by 3x
Asking about suicidality does not increase suicide risk
Patients who threaten to leave must be detained
General considerations
Risk factors
Stressors/triggers
Supports
Mental illness
D&A
Suicide intent/plan and severity
RF
Background
Demographics, past history, family history, mental illness, physical illness
Current mental state
Intox, mood, psychosis, hopelessness, active suicidal thoughts, insight
Future
Access to harm, supports, no change to circumstances that created trigger/stressor
A layered approach suicide risk
General opener - life not worth living, better off dead. dark thoughts
Duration, intensity, frequency, distress
Thoughts/plans to harm/kill self
- 108 -

Specific plans, access


Preparations (wills, belongings, notes)
Suicide-protective measures
Post-suicide attempt
How found/sought help
What was felt would happen (vomit, never wake up)
Current feelings (shame, regret, anger, disappointment, ambivalence)
Still suicidal? Whats changed
Potential for change
Illicit substance emergencies
Substance-related deaths
72% tobacco
25% alcohol
3% other drugs
Specific substances
Methamphetamine
High dose: hypertension, serious cardiac toxicity (arrhythmias, myocardioa infarction
heart failure, aortic dissection), haemorrhagic/non-haemorrhagic stroke,
dehydration, hyperthermia, inappropriate ADH + hypervolaemia (water intox +
dilutional hyponatraemia), seizures, serotonin syndrome, agitation, psychosis,
delirium

Ecstasy Lucky Dip


Effect unpredictable
May contain:
amphetamine
PMA (amphetamine analogue)
Caffeine
Glucose
Bicarbonate of soda
Benzodiazepines
Ketamine
Agricultural chemicals
Bleach, cleaning fluids
Opiates
Mortality 1-2% per year
Deaths occur following use of opiates with other drugs
- 109 -

Signs/symptoms:
Drowsy, slurred speech, N/V, miosis, flushed warm, sweaty skin
Severe - decreased respiratory rate, PR, BP, seizures, pulmonary oedema
Reverse with naloxone

IVDU
Infection, nerve trauma, emboli, thrombosis
Sepsis, endocarditis, pneumonia, osteomyelitis, renal problems
Other specific psychiatric emergencies
Sudden cardiac death
Increased risk in schizophrenia
cardiovascular disease, suicide/accidental
Cardiac/cardiovascular factors
Sedentary lifestyle
DIet
Smoking
Alcohol
Substance abuse
MEDICATIONS - large contributor
Cardiac death associated with prolonged QT
Torsade de Pointes ventricular fibrillation sudden cardiac
death
Unpredictable
Difficult to manage
Medications have been withdrawn due to risk
All
Lithium toxicity
Signs/symptoms
Impaired consciousness
Dysarthria
Ataxia
Course tremor
Muscle twitches
Vomiting
Increased tone, reflexes
Myoclonus
Seizures
Arrhythmias, prolonged QTc
Usually occurs with Li > 2 (less in elderly, physically frail)
Occurs with poor fluid intake, fluid loss (vomiting diarrhoea, excessive
sweating), use of diuretics, other medications affecting renal function
Neuroleptic malignancy syndrome
Life threatening
Mortality 10-20%
Has decreased due to greater awareness, earlier diagnosis, more
aggressive treatment
Incidence 0.02-3% (population dependent)
Most associated with typical high potency neuroleptics
All classes implicated, and antiemetics. Higher doses are a RF
- 110 -

Other RF include
Rapid dose escalation
Switching neuroleptics
Parental administration
Extreme agitation
Acute catatonia
?dehydration, lithium, depot, acute medical illness
Symptoms develop within first 2 weeks of neuroleptic therapy, BUT can
occur after a single dose, AND also after many years of the same agent at
the same dose. Suspect NMS if 2/4 symptoms
Muscle rigidity
Extreme, generalised
Lead-pipe rigidity
Superimposed tremor - cogwheel rigidity
Less commonly opisthotonus, trismus, chorea, sialorrhoea,
dysarthria, dysphagia
Mental state change
Initial symptom in 82% of patients (agitated delirium w/
confusion
Catatonic signs and mutism may be prominent
Evolution to profound encephalopathy, eventual coma
Hyperthermia
>38C (>40C common)
Autonomic instability
Tachycardia
Labile/High blood pressure
Tachypnoea
Dysrhythmias, diaphoresis
Diagnostic testing
CK
typically > 1000 (up to 100000)
Elevated (<1000) in IM injections
Severity related to degree of elevation
WCC - elevated
Increased LDH, ALP, AST/ALT (mild)
Electrolyte imbalances inc. metabolic acidosis, low Na, Mg,
Ca
Renal function impairment (inc. proteinuria, myoglobinuria)
Low serum iron (sensitive but not specific)
Often need LP/CT for exclusion of DDx
Rx
Stop causative agent +/- contributors
Supportive care (ICU)
Rehydrate, renal function, cardiac, DIC, hepatic
failure
Benzos to control agitation
Prognosis
Usually resolves within 2 weeks
- 111 -

Mortality greatest in D&A co-morbidities, renal impairment,


organic brain disease
Serotonin syndrome
Consider whenever antidepressants, stimulants, opiates,
psychedelics, anti-migraine) medications are being used
SIGNS/SYMPTOM TRIAD
Cognitive effects: headache, agitation, hypomania, mental
confusion, hallucinations, coma
Autonomic effects: shivering, sweating, hyperthermia,
hypertension, tachycardia, nausea, diarrhoea
Somatic effects: myoclonus, hyperreflexia, tremor
Clozapine
Neutropaenia
Cardiac - myocarditis, arrhythmias
Respiratory depression
Movement disorders
Acute dystonias
Usually IV/IM antipsychotics
Dopaminergic blockade
Face, neck, trunk
Laryngeal spasm can be lethal
Treat with benztropine
Manifestations
Oculogyric crisis - extraorbital muscle spasm, upward and
outward deviation of eyes
Torticollis - head turned to one side
Opisthotonus - painful forced extension of the neck. When
severe the back is involved and the patient arches off the
bed
Macroglossia - tongue protrudes and feels swollen, but does
not swell
Laryngospasm - uncommon but frightening

Conditions
Hyperthermia
MDMA - direct effect on hypothalamus
Hot environment
Sustained physical activity
Inadequate fluid replacement
Hyponatraemia
MDMA - inappropriate release of ADH
Decreased capacity to excrete fluid
Xs water consumption from
MDMA induced thirst
Repetitive stereotyped actions from MDMA
Trying to manage adverse effects
Advise <500mL per hour

- 112 -

Personality Disorders - Overview and Management

Personality
Enduring patterns of inner experience and behaviour
Enduring ways of thinking about self, others, the world
Patterns of perceiving, thinking about and relating to the inner and outer world
Durable and consistent pattern evident by early adulthood (or earlier)
Some personality styles can be adaptive in one context but not another
Different strengths and vulnerabilities of different personality styles
Cloninger model (Biosocial model), personality is influenced by:
Temperament (innate genetic factors, often identifiable within weeks of birth)
novelty seeking, reward dependence, harm avoidance, persistence
Character (learned psychosocial influences, effective bonding, cognitive development, family
relationships, learning, body build)
self-directedness, transcendence, cooperativeness
Five factor model (Costa & McCrae) (Psychological model) (OCEAN)
Derived by 5 factor analysis of existing models of personality
closednessness/openness - willingness to adapt/adjust to new ideas/situations
agreeableness/antagonism - interpersonal compatibility
intraversion/extraversion - keen interest in other people and external events, confidence
neuroticism - sensitivity, reactivity, proneness to negative emotional states
conscientiousness - doing the right thing, considering others
Stone (biopsychosicial model, mixture of the above two)
Personality traits are concordant in MZ, not DZ
Overview of personality disorders
Enduring pattern of inner experience and behaviour that deviates markedly from the expectations of
the individuals culture, manifested by:
cognitive patterns,emotional response, interpersonal functioning, impulse control
Pattern is inflexible and pervasive across a range of situations
Leads to clinically significant distress or impairment in social, occupational, role or other important
areas of functioning
Stable and of long duration, can be traced back to at least adolescence or early adulthood
Not better accounted for by another mental disorder
May be diagnosed in children if patterns evidence for at least 1 year (except anti-social personality
disorder)
Epidemiology
10% general adult population - at least mild PD
Each specific type of personality disorder is about 1%
20% general practitioner population
30% psychiatric outpatients
40% psychiatric inpatients
some types decrease with age
consistently assoc with lower s/e class
Treatment of personality disorders
Basic Premises of Treatment
effective treatment will recognise biopsychosocial formulation of personality
assessing amenability to treatment critical to success
nature of PD e.g. impulsivity
motivation
- 113 -

level of function
barriers to treatment
e.g. D&A
Treatment must be tailored to the individual
The lower the level of treatability the more modalities are likely to be required and
integrated into treatment e.g. individual/couple/family therapy, CBT, pharmacotherapy
The basic goal of treatment is to move from personality disordered functioning to
personality style functioning
Pharmacotherapy
cognitive / perceptual distortions in schizotypal - recommend low dose neuroleptics
anxiety / inhibition in avoidant personality disorder - serotonergic antidepressants
Psychodynamic psychotherapy
based on the principle that personality development is determined by a dynamic of
childhood experiences (especially with significant others) +- continues throughout life
reliance on transference - unconscious repetition of an important relationship from the
patients past in the course of psychotherapy (e.g. female patient relates to her male
therapist the way she did to her father)
The analyst is to be like a mirror to the patient, reflecting back only what the patient shows,
without bringing in any of his/her personality
The analyst is to remain relatively removed/detached, a deliberately dispassionate observer
of the patients feeling.
Specific personality disorders
Cluster A (eccentric, problems relating to others) = MAD
Paranoid - fear of being taken advantage of so protect self by not trusting, distructing,
suspicious, generally malevolent perception of others
hypervigilant, constantly alert to threats, guarded, defensive, litigious,
argumentative, distrustful, secretive, isolative, suspicious of others motives
attack is the best form of defence
cognitive bias, interpret ambiguous cues as actively threatening (unlike anxious
personality who view world as passively threatening shit happens)
SUSPECT: Spousal infidelity suspected, Unforgiving, Suspicious, Perceives attack,
Enemy or friend, Confides minimally, Threats innocuous
Treatment
responds better to coping oriented, behavioural and supportive therapy
finds it difficult to tolerate emotional probing or close relationships with
therapist
Schizotypal - eccentric, unusual experiences and beliefs, perceptual distortions
odd thinking, speech, behaviour or appearance that is eccentric or peculiar
increased prevalence in first degree relatives of individuals with schizophrenia
cognitive deficits in working memory, verbal learning and cognitive task with high
context dependency
social deficits in labelling emotions, displaying and selecting appropriate social
behaviours and strategies
prevale 2-3%, M= F
discomfort with intimacy, erratic, occupationally dysfunctional, loners,
superstitiousness, telepathy, depersonalisation, ideas of references, cold, aloof,
unemotional with constricted affect, humourless, suspicious look, fearful-dismissing
attachment style.
- 114 -

ME PECULIAR = Magical thinking and odd beliefs, Experiences perceptual


disturbances, Paranoid ideation, Eccentric behaviour or clothing, Constricted affect,
Unusual odd thinking and speech, Lacks close friends, Ideas of references, Anxiety in
social circumstances, Rules out developmental disorder/psychosis
Treatment
low dose neuroleptics shown to be useful, more effective that
antidepressants at lifting mood
Schizoid - not interested in other people, may be a way of protecting self from emotional
harm
social detachment, restricted emotional range, cool aloof, vague in thinking style,
low, negative view of others, positive view of self (unlike in avoidant PD)
neither desires nor enjoys close personal relationships
prevalence <1%, M>F,
usually come to treatment due to change in environment e.g. work restructure
now work with more people
DDx avoidant personality disorder
DISTANT = Detached affect, Indifferent to criticism/praise, Sexual experiences of
little interest, Task in solitary manner preferred, Absence of close friends, Neither
desires nor enjoys close relations, Takes pleasure in few activities
Relationship to schizophrenia
Strong for schizotypal
Reasonable for paranoid
Weak for schizoid
Cluster B - dramatic = BAD
Antisocial - disregard for and violation of others rights
CORRUPT - conformity to law lacking, obligations ignored, reckless disregard for
safety of self or others, remorse lacking, underhanded (deceitful, lies, cons others),
planning insufficient (impulsive), temper (irritable, aggressive)
Prevalence 2-13%, M:F - 3:1
20 - 70% of prisoners
increased risk for somatisation and substance use disorders in first degree relatives
link with conduct disorder in childhood
Histrionic - attention seeking, excessive emotionality
PRAISE ME = provocative seductive behaviour, relationships perceived as more
intimate than they are, attention centre, influenced easily, speech vague
(impressionistic, lacks detail), emotions rapidly shifting and shallow, made up
(physical appearance used to draw attention to self), emotions exaggerated
Narcissistic - grandiosity, exhibitionistic, lacking empathy
SPEECIAL = special self conception, preoccupied with fantasies, entitled, envious,
excessive admiration required, conceited, arrogant, lacks empathy
Borderline - unstable interpersonal relations, self image/affect, impulsivity
avoids real or imagined abandonment
unstable, intense idealise/devalued relationships
impulsivity in more that 2 self harming behaviours (substance abuse, sex, binging,
spending, driving)
recurrent suicidal behaviour/gestures/threats/self mutilation
affective instability
chronic emptiness
- 115 -

intense inappropriate anger


transient stress related paranoid or dissociation
I DESPAIR = Identity disturbance idealises or devalues, disordered mood-affect
instability, suicidal, paranoid, ideation under stress, abandonment fears, impulsivity,
rage, relationships intense
Treatment
crisis management
management of countertransference
supportive psychotherapy
psychodynamic psychotherapy
dialectical behaviour therapy
problem solving, cognitive change, managing self harm and suicidal
urges, mindfulness, interpersonal effectiveness, emotion regulation,
distress tolerance
stresses the fundamental interrelatedness or wholeness of reality
based on the theory that emotion dysregulation is a core feature of
borderline PD
Cluster C = high neuroticism + introversion + harm avoidance = SAD
Avoidant - sense of inferiority and extreme fear of rejection leads to social avoidance
CRINGES - certainty before relationships, rejection preoccupations, intimate
relationships avoided, new relationships avoided, gets around occupation activties
that involve interpersonal contact, embarrassment potential prevents new activities,
self viewed as unappealing, inept, inferior.
excessive sensitivity to negative evaluation, feelings of inadequacy, social inhibition
22-84% of person with social phobia
comorbidities include depression, alcohol misuse, anxiety disorders.
Dependent - lack of faith in own ability leads to clinging and excessive need for reassurance
prevalence approximately 1-2%, F > M
submissive, clinging, needy, interpersonal style clinging, reassurance-seeking, please
others at all costs, sacrifice own needs/wants
anxiety, depression result when dependent relationship is threatened or demands
for self-sufficiency made (or threatened)
RELIANCE = reassurance required, expressing disagreement difficult, life decisions by
others, initiating projects difficult, alone (difficulty being this), nurturance and
support sought, companionship sought after breakdowns, exaggerated fears of
being left to care for self
Obsessive compulsive - fear of losing control leads to preoccupation with control and detail,
orderliness, perfectionism
LAW FIRMS = Losses point of activity, ability to complete tasks compromised,
worthless objects kept, friendships/leisure excluded due to preoccupation with
work, inflexible, reluctant delegators, miserly, stubborn
prevalence about 2%, M>F
Personality disorder not otherwise specified is:
1. the individuals personality pattern meets the general criteria for personality disorder and
traits of several different PD are present, but criteria for specific PD not met
2. the individuals personality pattern meets the general criteria for a PD, but the individual is
considered to have a PD that is not included in the classification (e.g. passive-aggressive
personality)
- 116 -

DDx of personality disorder


Psychotic disorders
Mood disorder
Anxiety disorder
Post-traumatic stress disorder
Substance related disorder
Personality changed due to general medical condition
Personality traits
Overview of therapy (Biopsychosocial)
Bio - meds (SSRIs, low dose tranquilisers)
Psycho - therapy especialyl CBT, DBT, psychodynamic
Social - FAVER = finances, accommodation, vocation (career), education, relationships

- 117 -

Week 5 Child Psychiatry


Intellectual Disability

How is the assessment of someone with intellectual disability different from other assessments in general
psychiatry?
Communication problems
Cognitive capacity to understand symptoms
Developmental level Eg self talk, imaginary friends
Unusual symptom profiles Restricted range of experiences
Reliance on corroborative information
Need to be holistic in diagnostic formulation and assessment
Diagnostic overshadowing
Diagnostic schemes rely on good understanding of patients experience
People with ID may be more acquiescentduring an interview and pretend to understand
How can we overcome these difficulties?
Use language appropriate to the patients developmental level and speak clearly
Allow time for response
Maximise your chances of being understood: use body language, gestures, facial expressions
Admit when you do not understand
Check understanding (the patients; your own)
Establishing rapport: follow the lead in terms of eye contact, personal space; warmth and positive
regard
Locate time to an event, eg Birthdays
Dont suggest the answer
Get corroborative information
What is intellectual disability?
Significantly sub-average intellectuaL functioning (IQ <= 70)
Mild: IQ 50-55 to 70 (9-<12)
Moderate: IQ 35-40 to 50-55 (6-<9)
Severe: IQ 20-25 to 35-40 (3-<6)
Profound: IQ <20-25 (<3)
Around 3% of general population
Impairments in adaptive function in at least 2 of: communication, self-care, home living,
social/interpersonal skills, use of community resources, self-direction, functional academic skills,
work, leisure, health and safety
Onset before age 18 years
Learning disability
Mental retardation
Developmental disability
Mental handicap
Not: dyslexia, learning difficulties, ADHD, mental illness, autism
The relationship between intellectual disability and mental health problems
People with ID are at risk of emotional and behavioural problems
40% point prevalence of mental ill-health (Coopers et al 2007)
Point prevalence mental and behavioural disorders 10% (WHO)
11.4% 2 year incidence mental ill health (Smiley et al 2007)
- 118 -

Population census: 8% in 18 months


Cross reference intellectual disability and psychiatric registers in WA
32% of people with ID had a psychiatric disorder
1.6% of people with psychiatric disorder had ID
People with ID at greater risk of schizophrenia and other psychoses but not bipolar or unipolar
depression
People with dual diagnosis appeared to have a more severe psychiatric disturbance
The relationship between intellectual disability and mental health problems
20-25% have epilepsy, increases with severity of ID
Sensory impairment: 25-40%
Weight: extremes of obesity/ malnutrition
Dental: 10-25%
Respiratory: 50% of deaths
Cardiac
Gastrointestinal: H.Pylori
Osteoporosis/fractures
Thyroid: Downs Syndrome
How to assess someone with intellectual disability and suspected mental health problem
Seeking and gaining substitute consent
Guardianship Act
A person cannot give valid consent if they: cannot understand the nature and effects of the
proposed treatment; or cannot communicate whether or not they consent to the treatment.
The Guardianship Act establishes:
who can give valid substitute consent for treatment on behalf of a patient who is
incapable of consenting (ie. who can be a substitute decision maker)
when treatment can occur without consent
Substitute consent
For the purposes of the Act, treatment is defined as urgent, non urgent, and special
Special treatment requires consent of Guardianship Tribunal; this is experimental or highly
unusual or aversive treatment
Urgent treatment (i.e. needed to save someones life, prevent significant harm to the
persons health or distress) does not require consent
People under the MHA do not need consent regardless of whether or not they have a
Guardian
People who have capacity to do so have the right to refuse treatment
Identifying the person responsible
A 'person responsible', in order of hierarchy, is:
1.a guardian or, if there is no guardian,
2.the most recent spouse or de facto spouse with whom the person has a close, continuing
relationship or, if there is no spouse or de facto spouse,
3.an unpaid carer who is providing care to the person or arranged/provided this support
before the person entered residential care or, if there is no carer,
4.a relative or friend who has a close personal relationship with the person.
Definition of ID has 3 components: low IQ, problems in adaptive function, present before the age of
18
Psychiatric disturbance is common in ID
Physical problems/illness are common in ID
As the treating doctor, you need to take a full
- 119 -

BioPsychoSocial approach to assessment


As the treating doctor it is your duty to determine who the correct person is to consent to
any treatment (ie the patient or a substitute)

Child Psychiatry - Overview

Differences in Children
size, body composition
developmental perspective crucial (physical, intellectual, emotional, social)
dependence on others (family, school, etc) so the child rarely seeks help on his/her own behalf
markers of impairment are different eg educational/peer/family instead of work/leisure/martial
Differences in Child Psychiatry
the patient rarely seeks help on his/her own behalf
engagement of the parents and an assessment of the family context is essential
developmental history is detailed and crucial
corroborative history is crucial
disorders are often chronic and have a diffuse onset
collaborative management
Issues in Assessment
What is normal and what is a disorder?
need to consider developmental norms
mental health problems in children are generally dimensional problems, that is, they involve
an excess or deficit in attributes seen in most children
disorder is therefore defined as the extreme margin of the normal distribution curve,
indexed to developmental stage
examples
a 10 year old who misses weeks of school because of severe anxiety
a teenager who needs to be with their parents all the time
a 12 year old who cant sit still in class for five minutes
temper tantrums in a teenager
Classification of Psychiatric Disorders

- 120 -

Disorders that occur across the lifespan


anxiety (including OCD)
depression
somatoform (psychosomatic)
disorders resulting from trauma and stress
delirium
sleep disorders
impulse control disorders
Disorders with onset in childhood that usually also affect adult adjustment
Attention-Deficit/Hyperactivity Disorder
Oppositional Defiant/Conduct Disorder
Tic disorders
Gender identity
Development disability (autism, mental retardation)
Learning, language and motor skills disorders
Disorders generally associated with adulthood that may start in adolescence (rarer in childhood)
eating disorders
schizophrenia and related conditions
bipolar disorder
dementias
substance abuse disorders (including alcohol)
Disorders usually confined to childhood
enuresis, encopresis
selective mutism
separation anxiety
attachment disorders
Epidemiology
psychiatric morbidity is quite common among children and adolescents
emotional problems tend to be more common among girls while behavioural problems are more
common among boys
the prevalence of some conditions such as ADHD decrease in frequency with increasing age of the
sample, while other conditions such as depression tend to increase with age
Special populations
children exposed to parental neglect and abuse
children with chronic physical illness
- 121 -

children with mental retardation


children of parents with mental illness
children in and out of home care
indigenous children
What happens if disorders are not treated?
ongoing disorder which often becomes more severe (eg anxiety, depression, psychosis)
mortality (suicide, accidents) and morbidity (self-harm, school failure, delinquency, family
breakdown, failed relationships, drug and alcohol abuse)
disorders develop into related adult equivalents (eg separation anxiety agoraphobia)
Services
26% of the population, 6% mental health funding
specialist child and adolescent mental health services can at est manage about 5% of children
affected by mental illness
Child and Youth Mental Health Services
perinatal (0-2)
child psychiatry (3-12)
community adolescent team (13-17)
early psychosis (15-25)
consultation-liaision to paediatrics
inpatient psychiatry units (eg Redbank, CHW, Rivendell)
Who treats the remaining 95%?
no treatment
paediatric services eg children with ADHD
school counsellors
community health, baby health
welfare services
juvenile justice
non-governmental services
GPs
Treatment modalities
psychoeducation
advocacy (eg schools)
parent behaviour management training
family therapy
therapy with the individual child
medication
Understanding Families as a System

Circularity: a family therapy concept


- 122 -

highlights the complexity of human interactions and the interconnectedness within


relationships

Treatment
example: anxiety
Psychoeducation
nature of anxiety (worry scale)
recognising physical signs of anxiety
cognitive-behavioural model
understanding how it became the boss
Relabel
Rewire
thought stopping
detective thinking (worry box)
deep breathing
mindful of surroundings
Refocus
what would you do if you were in charge
physical activity
pleasant/soothing activities
distraction
Resist
stepladder of avoided situations (exposure & systematic desensitisation)
Reinforce
praise
Family Work
separate sessions with parents to explore the role of parental expectations in
influencing a childs perceptions of their ability to cope
joint sessions focused on parental support
containing parents own anxiety
sending coping messages
Relapse Prevention
identifying more ways of refocusing
how to identify if it becomes a problem again
*** good to read over/listen to the cases in the lecture properly ***

Child Psychiatry - Emotional

Internalising problems, includes:


Anxiety disorders
Types
Specific phobias
Separation Anxiety Disorder
Generalised Anxiety Disorder
Social Anxiety Disorder
Panic Disorder
Obsessive-Compulsive Disorder
Posttraumatic Stress Disorder
Aetiological factors
Anxiety disorders often run in families:
Parental modelling
- 123 -

Genetic heritability
Temperament
Early relationship between parent & child
Traumatic incidents and life events
Social adversity impacting on parents capacity to help the child with fears and
worries
Treatments
1. Engagement of parents and child (especially when both are anxious)
2. Address any co-morbidity (e.g. depression)
3. Address vulnerability factors and trigger events
Cognitive Behavioural Therapy (Group or individual)
Rapport building
Linking thoughts & feelings
Nature of anxiety
Cognitive restructuring
Child management
Graded exposure (key component of treatment)
Social skills, assertiveness, dealing with teasing
Other treatments (less evidence):
Antidepressant medications Evidence mostly for treatment of
Obsessive-Compulsive Disorder: SSRIs, clomipramine
Psychodynamic Psychotherapy
Family Therapy
Depressive and other mood disorders
Types:
Irritable mood or sad mood
Anhedonia
Social withdrawal
Hypersomnia or insomnia, loss of energy
Impaired concentration
Deteriorating academic performance, school refusal
Hopelessness
Thoughts of or attempts to self-harm
Poor appetite, weight loss, failure to gain weight
Somatic symptoms (e.g. headache)
Ask about: Manic/Hypomanic and psychotic symptoms
Treatment
Mild depression (often in primary care setting)
Watchful waiting
General advice & education
Supportive counselling (patient and parents)
CBT (older children and adolescents)
Interpersonal psychotherapy (adolescents)
Family therapy
Self-help (e.g. books, online websites)
Antidepressants usually not recommended
Moderate to severe depression
Cognitive behavioural therapy (CBT)
- 124 -

Challenge negative thoughts and assumptions


Structured problem solving
Scheduling and increasing pleasant activities
Training in relaxation, social skills, communication, assertiveness
Interpersonal psychotherapy (IPT-adolescents)
Short term psychotherapy address interpersonal problem areas such
as grief, role transitions, role disputes, or interpersonal
deficits/sensitivity
Family therapy
Pharmacological treatment
Used more commonly for adolescents than for prepubertal
children
Fluoxetine (start with 5-10 mg per day, then increasing to 20 mg per
day)
May need specialist advice if not responding to the above (further
dosage increase? or another drug?)
Concerns about SSRIs and suicidal thinking/behaviour in children &
adolescents
Psychosomatic symptoms
no slides on it in lecture
Issues to consider:
differentiating disorders from what is developmentally appropriate
comorbidities and overlaps
anxiety or depression may present as behavioural problems (e.g. non-compliance, aggression)
Ideally, assessment of children & adolescents should include:
Interviewing the parents
Individual session with the child/adolescent (if appropriate for age): may incorporate direct
interviewing, drawings, play, or other activities
Family assessment (including parenting issues)
Corroborative information (e.g. school reports, information from teacher/counsellor/principal,
paediatrician, GP, & other health professionals)

Child Psychiatry - Behavioural

Externalising disorders, includes


ADHD
symptoms
inattention
problems regulating activity
impulsive behaviour
clinically significant, is symptoms are
age inappropriate
maladaptive
commence before age 7 years
lead to significant impairment in two or more settings
associated problems
academic difficulties
aggressive and defiant behaviour
motor problems
difficulties in social relations
- 125 -

impaired self esteem


theories of ADHD aetiology
genetic
neurotransmitter dysfunction
perinatal hazard
environmental toxin
psychosocial
DDx ADHD
Age appropriate high spiritedness
Age appropriate inattention
Intellectual delay
Mismatch of intellectual ability with educational environment
Conduct problems
Mood disorder (including bipolar), anxiety disorder
Autistic syndromes
Reaction to neglect or abuse
Assessment of ADHD
History from parent, child, teacher
Behaviour checklists form parent, child teacher
Educational or psychometric assessment where indicated
Physical examination
Management of ADHD
Education of parents, child, teacher
Advocacy
Behaviour management strategies
Pharmacotherapy
Methylphenidate (Ritalin)
Immediate release effective 3-4 hrs (2-4 doses per day)
Sustained release effective 8 (LA) to 12 (Concerta) hrs
Dose range 0.3-1.2 mg/kg/day
Rebound common
Appetite suppression, initial insomnia, tics, headaches,
nausea/abdominal pain, hyperarousal
Authority required
Dexamphetamine
Similar properties to methylphenidate
Not available in Australia in long acting formulation
Cheaper than methylphenidate
Atomoxetine
Selective noradrenergic reuptake inhibitor
Delayed onset of action (weeks)
24 hour coverage of symptoms
Less likely to aggravate anxiety, depression, tics
Only non-stimulant approved for ADHD
Evidence base for pharmacotherapy for ADHD
Methylphenidate, dexamphetamine equally safe and effective in
short term trials (ES > 0.5 sd)
Long term benefit (15 months) mostly on classroom behaviour
- 126 -

Psychostimulants > behaviour therapies


Non-stimulant drugs effective (?as good as stimulants)
MTA study conclusions
Medication management superior to behaviour management and
community care
Combined treatment offers no advantage over medication for core
symptoms of ADHD but may help more with ODD symptoms,
internalizing symptoms, social skills and parent child relations
Note that behavioural treatments yielded greater parent satisfaction
than medication treatments
Remedial education where indicated
Cognitive therapy (stop think do)
Oppositional Defiant Disorder
Negativistic, hostile and defiant behaviour persisting for 6 months or more, leading to
distress and disability
Lose temper
Argue with adults
Non-compliant
Annoy others
Blame others for their misdemeanours
Irritable, angry, spiteful
Conduct Disorder
Persistent pattern of behaviour in which the rights of others are violated.
Onset in childhood (usually preceded by Oppositional Defiant Disorder) or adolescence
Aggression to people and animals
Destruction of property
Deceitfulness or theft
Absconding
Summary of treatments for oppositional defiant and conduct disorders

- 127 -

Continuum from overt to covert behaviours


Overt
Disobedient
Cheeky
Blame others
Brags
Shows off
Irritable, cruel
Loud
Temper tantrums
Demanding
Stubborn
Covert
Lies
Destructive
Steals
Set fires
Bad companions
Truants
Runs away
In a gang
Substance abuse
Aetiology of Oppositional Defiant Disorder (ODD)/Conduct Disorder (CD)
Genetic, affecting neurotransmitter systems such as monoamine oxidase
transporter gene
Intra-uterine influences
Parenting style
Social adversity
- 128 -

Modelling
The early years of life- Christchurch Health and Development Study
Developmental factors exerting independent influence were
maternal smoking in antenatal period > half packet per day
low maternal age
low parental supervision
harsh discipline
Middle childhood-Campbell, Patterson and others
Parenting style coercive, inconsistent, do not follow through to compliance,
uncommitted
reacts with temperament of child, non-shared environment
Abuse and neglect
School absence of leadership, harsh inconsistent discipline, limited
classroom behaviour management strategies, limited emphasis on academic
attainment
Neighbourhood influences
Adolescence
School
absence of leadership, harsh inconsistent discipline, limited
classroom behaviour management strategies,limited emphasis on
academic attainment
Neighbourhood influences
Peer influences that amplify deviant behaviour and increase exposure to
other pathogenic influences (substance misuse, early sexual experiences)
As a GP assessing a child with behavioural problems
Consider the precipitants to seeking evaluation
Consider general health, including hearing and vision
Consider differential diagnoses eg anxiety
Encourage the parents to contact the class teacher with a view to school counsellor
assessment
If ADHD/ODD/CD suspected refer to developmental paediatrician, child psychiatrist or
multidisciplinary child health/mental health service
Challenges to treatment include
Engagement
Attrition
Who is committed to change?
Crisis driven
Responsibility for the problem

- 129 -

Perinatal Mental Illness

A framework for perinatal psychiatry


The disorders
Gestational depression
Postnatal depression
Postpartum psychosis, circadian rhythms, relapse
Peripartum onset
DSM V definition: if onset of mood symptoms occurs during pregnancy or in the 4 weeks
following delivery
Conceptual model for understanding perinatal disorders
Maternal well being
Foetus - what goes into the mother can pass onto the foetus
Intimate relationships
Broader
social
supports

The importance of perinatal mood disorders


Time of predictable high morbidity for the woman
Regular contact with health professionals
Perinatal mood disorders often go undetected opportunity for effective screening
Impact of perinatal mood disorders on the:
developing foetus
infant
interpersonal relationships
Potential for chronicity
Early intervention
Peak prevalence of depression and anxiety is during childbearing years
Women with depression and anxiety will conceive
depression during pregnancy postnatal depression
New onsets of depression and anxiety over the postnatal period
arising as a consequence of being pregnant
hormonal changes postpartum
psychosocial in origin

Biological stress
Physical changes
Hormonal changes
Psychosocial stress
Role change to mother
loss of working role
Relationship to change
2 to 3 person relationships
Socioenvironmental stress
Financial pressure
Change in social networks
Intrapsychic stress
Coping with dependence
Own parenting experience

- 130 -

The stresses of becoming a mother


Biological stress
Physical changes
Hormonal changes
Psychosocial stress
Role change to mother
Loss of working role
Relationship change
2 to 3 person relationship
Socioenvironmental stress
Financial pressure
Change in social networks
Demands of mothering
Fatigue
Intrapsychic stress
Coping with dependence
Own parenting experiences
Mood disorders following childbirth

Postnatal depression
Postnatal depression is heterogenous
Postpartum onset - more likely to be melancholic type (characteristic personality style)
Common non-psychotic type of postnatal depression
gradual onset 2 -3 months
psychosocial causation
Less common postpartum melancholia
early onset within 4 weeks of delivery
biological type of depression
signal for subsequent bipolar disorder
requires antidepressant medication or ECT
- 131 -

An episode of major depression arising in the first six months postpartum with a similar clinical
picture to depression at other times of the life cycle
prevalence rate 10-15%
prevalence no greater than prevalence among non-childbearing women
Risk factors for postnatal depression
Early life experiences
genes
trauma, neglect, abuse
Sociodemographic
young age
social disadvantage
Social environment
Dysfunctional intimate relationship
poor instrumental and emotional support
life event stress
poor social network
Internal environment
Oestrogen sensitivity/hormonal changes
Personality style
Previous depression or anxiety
Impact of postnatal depression on the infant
month-infant relationship
maternal sensitivity dependent on
mood state
her own attachment relationsips interal working model
personality style
modulators of maternal sensitivity
intimate relationship
support networks
competing demands
medications
DSM-IV postnatal depression is not a specific type of depression
DSM-IV Postpartum specifier: Onset of episode within 4 weeks postpartum
Clinical picture same as non-melancholic major depression
Anxiety symptoms (irritability, panic, OCD)
Treatment of postnatal depression
Recognition
Clarification of risk factors
Permission to talk
Psychoeducation
prioritising activities
Non directive counselling
Specific treatments
CBT
IPT
Antidepressant medications
Safety with breastfeeding
Antidepressants
- 132 -

lack of evidence of the efficacy of antidepressants ain PND


safety with breastfeeding
balance effectiveness with tolerability
Indicated in
moderate to severe depression
comorbid panic disorder
previous good response to antidepressants
bipolar depression with mood stabilizer
patient preference

Edinburgh Postnatal Depression Scale (EPDS)


10 item self report scale
designed specifically for postnatal depression
score > 12 indicates probable major depression
needs to be followed up by clinical assessment
2
stage

screening

Depression in pregnancy implications


adverse impact on obstetric outcomes
preterm delivery
low birth weight
small for gestational age
gestational hypertension
effects on placental functioning
direct
neurobiological substrates of depression (glucocorticoids) deotus
indirect
activation of HPA axis placental hypersecretion of CRF
adverse effects on foetus
developmental delays
at
risk
of
mental
health
Rates of depression in pregnancy and postpartum according to EPDS
18 weeks pregnant 14%
32 weeks pregnant 15%
8 weeks postpartum 10%
8
months
postpartum
Assessment of depression in pregnancy
risk of overdiagnosis
somatic symptoms of depression
fatigue or loss of energy
appetite and weight change
sleep disturbance
change in libido
poor discrimination between depression and pregnancy related symptoms
cognitive symptoms
poor concentration
- 133 -

better

problems

8%

worthlessness or guilt
markers of depression
implications of depression in pregnancy
imperative to identify depression in pregnancy
screening programs
safe start
ensure accurate diagnosis
severity
type
necessary to treat depression in pregnancy
mild-moderate depression
focused psychological treatment
no efficacy trials of antidepressants in pregnancy
but they seem to be safe!

risk versus benefit of antidepressants during pregnancy

SSRIs during pregnancy


Physical malformations
*2 fold increased risk of heart defect with SSRIs
Persistent pulmonary hypertension
*SSRIs prescribed after 20 weeks gestation increased risk
withdrawal syndrome in infant
*poor neonatal adaptation syndrome
impact on pregnancy
low maternal weight gain
preterm delivery
low birth weight
*increased rates of gestation hypertension
Poor neonatal adaptation syndrome
insomnia or somnolence
agitation, tremors, jitteriness, shivering and/or altere tone
restlessness, irritability and constant crying
poor feeding, vomiting, diarrhoea
poor temperature control, hypoglycaemia
tachypnea, respiratory distress, nasal congestion or cyanosis
- 134 -

seizures

Describe the mood disorders following childbirth


The blues
Puerperal psychosis
Postnatal depression
Psychotic disorders in pregnancy and postpartum
Management of perinatal psychiatric disorders

The Blues
Common experience of > 70% of women
Onset days 3-5 post partum
Mixed anxiety and depressive symptoms
Lability of mood
Self-limiting
Social Support in mothers
Practical and emotional support is critical for new mothers
40 day rule
Need for good support networks, types of support include:
Knowledge support
Child rearing
Wisdom of elders
Practical (Instrumental support)
baby related
household chores
Emotional support
Discuss joys, disappointments
share feelings
company
shoulder to cry on

- 135 -

- 136 -

Skills Session - Family interveiwing

Reactive problems
e.g. divorce/separation of parents, abuse, neglect
role of family in the genesis and maintenance of the problem
Hard wired problems
e.g. autism, ADHD
capacity of the family to adapt, psychoeducation
Family involvement
practical issues
parents give historical info about the childs disorder and development
parents have legal power to initiate assessment and consent to treatment
parents provide financial resources
clinical issues
identify family strengths
with family involvement, patient doesnt become the sole focus of attention
!* disorders or problems of other family members can be identified
parenting style can be observed
engage family in treatment process
family factors may precipitate the problem
Attitude
presume the positive, start by assuming the family cares for the child and has areas of competency
in promoting child well being
Should ALL family members be asked to attend the clinic from the outset?
not necessary as one of the patients parents may be busy, difficult to arrange an appointment time,
family factors may be the cause of the issue, there may be an issue between parents etc.
in the end you want to see the patient, not not see them.
usually invite ALL family members of the same immediate household. Parents and siblings,
grandparents.
AACAP family interviewing practice parameters
Content
family demographics
clinical symptomatology of the child
individual parent history
parent relationship history
history of family as a unit
Structure
adaptability e.g. any changes in the family and how did they manage it? (moving homes,
changes in parents work, changes in school etc.)
cohesion, connectedness v.s. separateness e.g. how close the family is?
boundaries e.g. intergenerational boundaries, parent child interaction, children sleeping in
parents bed
Community
clarity e.g. are they clear? or is it indirect?
emotional expression
problem solving e.g. how does the family deal with and manage and problems?
Family beliefs
particularly around how child should be raised etc?
- 137 -

Family regulation of child development


responsiveness - to each family members needs
consistent
degree of regulation of the childs affect and behaviour
Advice on family interviewing from role playing from lecture
Introduce yourself
Ask each family member to introduce themselves
Zone into child patient and have a brief conversation
learn about their personality e.g. shy, outgoing
responsiveness, communication
language, range of vocabulary, do they speak appropriately for their age?
awareness of their family e.g. siblings and parents (what they do? school/work? where do
they work? what do they do for work?)
What do you hope from coming here today?
Assess family dynamics, dominant family member, personalities of family member
Techniques for interviewing children
With children and adolescents, engagement is very important (as they are often brought to the
interview by their parents, with little explanation or even against their will).
Children may not be able to express their feelings, and may find direct questions such as whats
troubling you? too hard to answer.
General questions about school, teachers, school friends, hobbies, pets, etc. are a good place to
start. These answers can be very informative (e.g. how the child answers the questions as well as the
content of the responses).
For some children, drawings may be a useful way to engage them and to obtain information, e.g.
Id like you to draw your whole family, everybody doing something (kinetic family drawing)
Draw a sad (or happy or angry or scary) picture
Draw a dream
Ask the child about the drawings
If you could have 3 wishes in the whole wide world, what would they be?
A comprehensive assessment of a child involves:
A comprehensive assessment of a child involves:
1.Interviewing the family together (often including siblings and others in the household)
2.Interviewing the parents alone
3.Interviewing the child alone (if developmentally appropriate)
4.Information from other sources (e.g. teachers, school reports, childcare centres, etc.)
Overview of mental health problems in various age groups
What are some common problems leading to patients, family or carers presenting to a child &
adolescent mental health service?
Infancy (approx. 0-2 years)
Parental mental health issues (e.g. postnatal depression)
Developmental problems
Feeding, sleeping, and other parenting concerns
Toddlers/preschoolers (approx. 2-5 years)
Oppositional Defiant Disorder (or externalising disorders)
Developmental problems
Attachment disorder
Primary school age (approx. 5-12 years)
Externalising problems (Disruptive Behaviour Disorders)
- 138 -

Oppositional Defiant Disorder


Conduct Disorder
Attention-deficit/Hyperactivity Disorder (ADHD)
Internalising problems
Anxiety Disorders (Separation Anxiety Disorder, Obsessive-compulsive
Disorder, Phobias, Posttraumatic Stress Disorder)
Depression
Psychosomatic Disorders (e.g. Conversion Disorder)
Adolescents (approx. 12-18 years)
Almost the full range of psychiatric disorders seen in adulthood:
Depression
Anxiety disorders
Disruptive behaviour disorders (e.g. Conduct Disorder)
Eating disorders
Drug and alcohol use disorders
Psychotic disorders
Psychosomatic disorders

Skills Session - Interviewing the difficult adolescent

Acknowledge patients difficult situation


Find out about family members and friend supports
open ended questions
focus on schools, hobbies, interests first
then learn about friends and families and their relationships
when asking about relationships, try to normalise and generalise it first, then ask them indirectly
Management of adolescent

Skills Session - Behaviour management

Self regulation
see handout

Skills Session - Ethics Scenarios

know mental health act and specific wording well.

- 139 -

Week 6
Older People- What is Different?

Prevalence of mental disorders in old age


Dementia
6 to 10%
Delirium + other brain syndromes
1 2%
Depression (melancholia 1%)
13%
Mania (bipolar)
0.5%
Schizophrenia & paranoid disorders
2%
Anxiety states
> 5%
Alcoholism
3%
Personality disorders
lots!
Currently: 14% >65; 2050: 27-30% >65
Whats different
cognitive impairment (acute or chronic)
capacity and decision making
multiple medical co-morbidities
functional disability
atypical presentations of common psychiatric illnesses
multidisciplinary working
integration of physical, functional, psychological, financial and sociological factors
residential care
non-English speaking background
Indigenous
rural
Cognitive testing in limited time on first interview
MMSE
impacted by age, educational background and language
weighted towards attention and short term memory
score out of 30
27 30:Normal range/ mild cognitive impairment
21-24:
Abnormal, consistent with Mild Dementia
10-20:
Moderate Dementia
<10:
Severe Dementia

or RUDAS (Rowland Universal Dementia Assessment Scale)


not influenced by language or education
score out of 30
<23: cognitive impairment likely

Clock Drawing Test


Bedside tests for more specific cognitive functions where relevant
Medical co-morbidities
Ageing
Illness
- 140 -

brain disease
pain, infirmity, disability
drugs
polypharmacy
altered pharmacokinetics ( side effects)
Medications
maybe be exacerbated or caused by drugs
confusion, anxiety, affective disturbance psychotic symptoms, falls
change in medications
compliance
dosette box/blister pack
supervision or prompting by carer
allergies
Functional assessment
Basic ADLs needs help? how much?
personal hygiene/continence
dressing
eating/drinking
Instrumental ADLs
ability to organise finances
use home appliances
drive safely
organise medication regimes
Environmental assessment
house safe, appropriate, liveable?
neighbourhood safe, supportive?
financial able to meet commitments?
services transport? home support?
Social
spouse alive? relationship?
family supportive? united?
neighbours friendly? helpful?
carer stress
formal services
society and culture attitude to older people
Elder abuse
repeated acts against, or failure to act for, an elderly person, which causes distress or damage and so
prevents the living of a full life
forms of abuse:
physical
physcological
financial
neglect
sexual
occurs in all settings
4% of older people
Risk
risks to self
- 141 -

wandering
poor judgement
gas/water taps left on
poor driving
self-neglect
vulnerability to abuse exploitation
self-harm/suicidal ideation
risks to others
murder suicide
aggression
disinhibited behaviour
poor driving
gas left on
Home based assessment
greater depth and quality of information
local environment, available support
hazards and cleanliness
expired food, burnt pans, can they make a cup of tea?
empty bottles of alcohol
carers more likely to be present corroborative information, family dynamics
medications compliance, current treatment, unused meds
can they identify people in photos around the home
less non-attendance
generally preferred by patients, especially if cognitively impaired
disadvantages:
travel
difficulties performing a physical exam
safety implications
not well supported financially in private practice
Initial assessment
introduction
make your role clear
do they know theyre seeing a psychiatrist, do they understand why theyre there
establish what they wish to be called
know the names, relationships and roles of the accompanying people
ask if the patient wants time to speak without the accompanying relatives/carers
*patient often denies problems, especially with dementia
permission to speak with the accompanying people
Information gathering
slow down speech
hearing and/or visual impairments
speak with the older adult directly
non-verbal cues from client or caregiver
discuss areas of pride
describe a typical day
Collateral history
can take history from anyone who wishes to offer it
best to get permission from the patient
- 142 -

explicit permission needed to give information back


if lacks capacity to consent, information can be given to relatives/carers if it is in their best interests
discuss with senior colleague if unsure
best to take collateral history in front of patient
may be useful to see informant alone
upsetting or embarrassing information
Common presentations
Dementia - BPSD
Delirium
Depression
Drugs
alcohol > prescription drugs
Anxiety disorders
beware early dementia!
Less common:
late-onset schizophrenia
first presentation mania
severe self neglect
Dementia
progressive neuro-degeneration
cognitive impairment
psychiatric symptoms
behavioural changes
personality changes
commoner with increasing age
co-exists with depression
makes delirium more likely
psychiatric symptoms
depression (commonest and earliest)
anxiety
paranoia
hallucinations
delusions (eg of theft)
disinhibition and mania
apathy
Late life Depression
melancholic depression common (ie with biological features)
psychotic features more likely in older age especially delusions
associated with medical conditions especially cerebrovascular
milder depressions as well: adjustment disorders, dysthymia (like young)
Differences in presentation
less likely to admit depressive symptoms spontaneously
persistent pain or other physical complaints (somatisation)
biological features
sleep disturbances
appetite disturbance
weight loss
reduced energy
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diurnal mood variation


pseudodementia
apparent cognitive impairment due to a depressive illness
may present with behavioural disturbance in dementia
+ Organic psychiatric disorders
20-30% of those with Alzheimers are depressed
delirium might look like depression
frontal lobes not working may look like depression (apathy)
+ Medical illness
drugs: alcohol, benzodiazepines
medications: eg -blockers
metabolic: eg hypothyroidism
stroke -- > 25% in the first few months
Parkinson Disease (50%)
chronic pain eg severe arthritis
Treatment
some types respond well to ECT
melancholic, Parkinson disease
confusion can be a problem
antidepressants
all anticholinergic: TCAs > SSRIs, SNRIs
more SEs
hyponatraemia esp SSRIs
confusion/falls esp TCAs
psychotherapy - can work
if cognitively OK, suits patient
right type of depression
Prognosis
mostly treatable
but, underlying vascular changes/other organic pathology
not improve? relationship conflict, isolation, chronic pain
Paranoid psychosis in old age
graduates ie chronic schizophrenia grown old
typical cognitive changes of schizophrenia (not dementia)
very late onset schizophrenia
rare (5%)
auditory and visual hallucinations
partial delusions
people, animals, objects, radiation
pass through an impermeable barrier
up to 70% of late paraphrenia vs 10% early onset
personality preserved
delusional disorder
rare
non-bizarre delusions alone
epidemiology

- 144 -

Risk factors for suicide


Psychiatric Illness
70% to 97% of completed suicides
Affective Illness
Substance Use
Prior suicide attempt
Personality
Decreased openness to experience
Obsessional and anxious
Physical Illness and Disability
But high base rates
Social Factors:
Negative life events
Bereavement (Acutely)
Reduced social networks
Financial stressors
Availability of lethal means
What is different about older people?
more complex
more things
different position in lifes journey
need more time for assessment
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need more care in assessment

Management of Behavioural and Psychological Symptoms of Dementia

What Causes Behavioural Problems in Older People?


Delirium, Dementia, Interpersonal Issues, Psychotic Disorders, Depression, Hypomania, Personality
Disorders
Definition of Dementia
Disease of the brain
Usually chronic or progressive
Consciousness not clouded
Cognitive impairment accompanied by
Deterioration in emotional control
Deterioration in social behaviour
Impaired motivation
Cognitive Impairment
Multiple disturbance of higher cortical function
Memory, Thinking, Orientation, Comprehension, Calculation, Language, Judgement
Behavioural and Psychological Symptoms of Dementia A Relatively New Term For An Old Problem
Introduced by the International Psychogeriatric Association in 1996 (Finkel and Burns)
symptoms of disturbed perception, thought content, mood or behaviour that frequently occur in
patients with dementia
3 symptom clusters:
agitation
psychosis
mood
***BPSD-Agitation
Wandering away from home
Purposeless activity (hoarding, opening & closing drawers, rummaging through possessions,
restlessness, pacing, taking clothes on & off)
Verbal aggression or persistent screaming
Physical aggression (scratching, biting, pushing, spitting, hitting, pinching)
Sexual disinhibition
***BPSD-Psychosis
Delusions (spousal infidelity, abandoned by family, possessions being stolen, intruders coming into
the house, family replaced by imposters, house is not ones house, deceased relatives are still alive)
Hallucinations (most often visual, people on TV are real, reflection in mirror is a real person)
***BPSD- Mood Symptoms
Apathy
Depression
Fear & anxiety about upcoming events
Lability of mood
**How Common Is BPSD?
Mild-moderate Alzheimers 35-47%
Advanced Alzheimers disease 66-85%
Similar rates for vascular dementia & FTD
Possibly higher rates for dementia with Lewy bodies
About half of residents in nursing homes have BPSD (most common reason for consultation)
BPSD - Natural History
Symptoms tend to fluctuate
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But usually persist


Sensitive times: evening sundowning, meal time, dressing/undressing, showering, toileting ie
when things are being done to the person
Hallucinations and mild depression may resolve
Agitation and more severe depression tend to persist
Triggers of BPSD
1.Biological
Infections: (chest, urinary tract)
Medications: (benzodiazepines, tricyclics, antiparkisonians)
Pain
Constipation
Urinary retention
Dehydration
Akathisia from antipsychotic medication
Sleep deprivation
2.Psychological
Depression*
Loneliness
Boredom
Frustration
3. Environmental
Change in usual carer eg spouse takes a break
Unfamiliar staff in nursing home
Inexperienced or pushy carer
Different resident sharing room
Change of residence, particularly move to residential care from own home
7 tiered model of BPSD (Brodaty et al)

***BPSD Management Principles


1. Initial
Exclude delirium from chest or urinary infections or medications eg benzodiazepines,
antiparkinsonians, anticholinergic acting drugs like tricyclic antidepressants
Exclude pain, constipation or urinary retention
Avoid unnecessaryy changes to carers or routine
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2. Behavioural
Should be main focus of management
ABC approach where:
A is antecedents of problem behaviours
B is problem behaviour
C is consequences of problem behaviour
Lets Look At An Example
1. Identify the problem behaviour & antecedents eg an elderly demented man who becomes
verbally abusive & hits out when his wife is trying to undress him to have a shower each evening
2. Work out the consequences eg the wife becomes angry and tries to force him into the shower
What To Do To Alter Behaviour
1. Get wife to move shower time to morning when hes more settled
2. Dress him in clothing which is easily removed eg track suit pants & replace buttons and
belts with velcro
3. Tell wife if hes getting aggressive not to persist but to stop & try again later
***Non Pharmacological Management Of BPSD
First line mild to moderate BPSD
Practical psychological interactions
Structured social interactions
Personalized music
Planned positive activities
Exercise
Reminiscence
Educating staff in Person Centred Care
Clinical psychologist where persistent or severe
Drug Treatment Of BPSD
WHEN
High risk to the individual or others
High levels of individual distress
Severe depression
Should only be used when behavioural management is not working
Doses of medication (especially antipsychotics) should be kept low & increases made slowly
Medication should be regularly reviewed & whenever possible reduced or suspended
(antipsychotics)
Target the most important symptoms
3 T Approach
Target the behaviour
Titrate the dose
Start low, go slow
Time limited (antipsychotics, mood stabilisers)
What Drugs?
Mild to moderate severity BPSD: SSRI antidepressant * or cholinesterase inhibitor*
More severe BPSD especially with agitation &/or psychosis: antipsychotic*
If fails to respond: augment with mood stabilizer
***Which Symptoms Respond To Drug Treatment?
Aggression and hostility
Agitation
+/- Psychosis
- 148 -

+/- Wandering and pacing


+/- Depression
Which Symptoms Dont Respond To Drug Treatment?
Screaming
Shouting
Swearing
Touching
Resistant behaviours eg toileting
Inappropriate voiding or spitting
Hoarding
***Pharmacological Management Of BPSD-How Effective?
Atypical antipsychotics: about 3-4 point drug/placebo difference on 78 point BEHAVE-AD Scale
Little difference in efficacy between low dose haloperidol & low dose risperidone, but typicals
associated with high risk of tardive dyskinesia
NNT for risperidone: 5 to 11
Cholinesterase inhibitors: about 2-3 point drug/placebo difference on the 144 point NPI Scale
Discontinuation of Antipsychotics
Should be incorporated into routine practice
After three of improvement in symptoms
Predictors of successful withdrawal
Lower daily doses of antipsychotics
Lower baseline severity of behavioural symptoms
Continue antipsychotics long term (>12 weeks) if:
Continuing severe BPSD
Where severe adverse consequences may or have occurred when discontinued
No alternative treatment approaches are suitable
Document
***SSRI Antidepressants
Citalopram
Equivalent efficacy to risperidone for agitation and aggression in mild to moderate BPSD
Maximum dose 20 mg
SSRIS
Indicated for severe depression (best evidence for sertraline)
Side Effects: Hyponatraemia, GIT disturbance, Akathisia, Sleep disturbance, Falls and fractures
Mirtazapine
Not that clearly helpful for depression
Reduces care giver burden
Anticholinergic
Cholinesterase Inhibitors
Greatest effects on
Anxiety
Apathy / indifference
Depression/ dysphoria
Require several weeks of treatment to become apparent
Trials of rivastigmine in Lewy Body Dementia show promise
Mood Stabilisers
Carbamazepine may be effective for agitation and aggression
Watch for side effects and interactions
- 149 -

Valproate appears less effective


Recommended Antipsychotic Doses In BPSD
Risperidone 0.5-1.5mg
Haloperidol 0.5-1.5mg
Olanzapine 2.5mg
Quetiapine 25mg (Lewy Body Dementia)
Risk Of CVA With Antipsychotics In Dementia
Increased risk of CVA with all antipsychotics
Relative risk vs placebo is 2.57
68 people need to be treated to cause one additional CVA in a 6 to 12 week period
Half of the CVAs are severe
The increased risk appears related to the first 8 12 weeks of treatment only
Risk Factors For CVA
Oldest old ( over 80)
Other risk factors (no trial evidence) - Obesity, Diabetes, Hypertension, Smoking, Cardiac
arrhythmias
Antipsychotics And Death In People With Dementia
Relative risk of all cause death is 1.4
May persist for six months after initial prescription
Remains increased for the duration of treatment
Causes of death - Heart failure, infections
Potential mechanisms - Anticholinergic mechanisms, QTc prolongation, Extra Pyramidal Side Effects
Overall Risks And Benefits Of Antipsychotic Treatment
1000 people with BPSD treated for 12 weeks:
91 to 200 show clinically significant improvement in symptoms
72 show clinically significant improvement in psychosis
10 additional deaths
18 additional CVAs (half severe)
No additional falls or fractures
70 with increased gait disturbance
167 additional deaths with treatment for 2 years
DART AD, NNH (death) at 2 years is 6
However - Aroma Therapy May Be Almost As Good!..
Lemon balm (Melissa oil)and Lavendar oil may be as effective as risperidone in reducing symptoms
of physical & verbal aggression in severely demented patients with BPSD
Produces similar improvements on total scores to donepezil
No side effects.Much cheape. Smells better!
Recent Cochrane: equivocal findings, more studies needed.

- 150 -

Delirium

Definition - A psychiatric syndrome characterised by a transient disorganisation of a wide range of cognitive


functions due to a widespread derangement of cerebral metabolism- Lipowski
Also known as: acute organic brain syndrome, acute confusional state, acute organic reaction, toxic
psychosis, exogenous psychosis.
Vague term: Confusion
Symptoms
Primarily a disorder of ATTENTION
Affects a wide range of cognitive functions
Fluctuating level of arousal and severity
Reversal of sleep-wake cycle
Hallucinations
Delusions, particularly of paranoid nature
Resultant behavioural disturbance
Onset of hours/days
Affective lability: crying, laughing, anger
Attention
Arousal: general state of responsivity and wakefulness
Sustained attention or vigilance: refers to capacity to maintain attention over time
Divided attention: refers to the ability to respond to more than one task at once
Selective attention (concentration): refers to the capacity to highlight one stimulus while
suppressing the awareness of others`
MMSE what does each part tell you?
Orientation
Short term memory
Concentration: serial 7s or WORLD backwards
Dysphasias Comprehensive/Expressive
Expressive: Reading, dysgraphia, speech
Construction apraxia with intersecting pentagons
Clock drawing often added on: frontal lobe executive functions, parietal lobe spatial awareness,
occipital lobes (optic fields)
Cognitive testing for Delirium
Concentration test
Months or weeks backwards
Being able to maintain the thread of a conversation
Temporal sequencing of history provided
Orientation to time
What time of day would you guess it is right now?
How many days have you been in hospital for?
Generally, memory registration, orientation, concentration and memory recall for all CL patients: the
first half of the MMSE.
Psychotic Symptoms of Delirium
Hallucinations: primarily visual.
Phenomenology: misperceptions and illusions
Brief, simple, environmentally based.
Secondary delusional beliefs eg I saw my mother, I must be at home in my village
Persecutory delusions result from disorientation, poor memory and attention.
- 151 -

Thought form: illogical, poverty


Importance of fluctuating course
Behavioural and sleep charts are very helpful
Patients are often at their best early in the morning, during the medical ward round!
At their most behaviourally difficult at night so nursing reports are helpful but tend to focus on
orientation.
Can be alert and orientated with staff and then an hour later, very confused and drowsy with family
DSM V Criteria for Delirium
A. A disturbance in attention (i.e., reduced ability to direct, focus, sustain, and shift attention) and
awareness (reduced orientation to the environment).
B. The disturbance develops over a short period of time (usually hours to a few days), represents a
change from baseline attention and awareness, and tends to fluctuate in severity during the course
of a day.
C. An additional disturbance in cognition (e.g., memory deficit, disorientation, language, visuospatial
ability, or perception).
D. The disturbances in Criteria A and C are not better explained by another preexisting, established,
or evolving neurocognitive disorder and do not occur in the context of a severely reduced level of
arousal, such as coma.
E. There is evidence from the history, physical examination, or laboratory findings that the
disturbance is a direct physiological consequence of another medical condition, substance
intoxication or withdrawal (i.e., due to a drug of abuse or to a medication), or exposure to a toxin, or
is due to multiple aetiologies.
Types: DSM V
Hypoactive: lethargic, drowsy, not mobile
At risk of dehydration, PE, reduced mobility, bedsores, early discharge
Usually not detected
Hyperactive: aggressive, combative, non-cooperative
At risk of injury from aggression, restraints and iatrogenic injury from over sedation
Mixed: both states at different times.
Epidemiology
Community: 1-2%
Acute hospital admissions: 14-24%
Post operative elderly patients: 15-53%
ICU elderly patients: 70-87%
Risk factors
Potentially modifiable risk factors
Sensory impairment (hearing or vision)
Immobilization (catheters or restraints)
Medications (e.g. sedative hypnotics, narcotics, anti-cholinergic drugs, corticosteroids,
polypharmacy, withdrawal of alcohol or other drugs)
Acute neurological diseases (e.g. acute stroke, intracranial haemorrhage, meningitis)
Intercurrent illness (for example, infections, iatrogenic complications, severe acute illness,
anaemia, dehydration, poor nutritional status, fracture or trauma, HIV infection)
Metabolic derangement
Surgery
Environment (for example, admission to an intensive care unit)
Pain
Sustained sleep deprivation
- 152 -

Non-modifiable risk factors


Dementia or cognitive impairment
Advancing age (>65 years)
History of delirium, stroke, neurological disease, falls or gait disorder
Multiple co-morbidities
Male sex
Chronic renal or hepatic disease
Aetiology

Fong TG, Tulebaev SR, Inouye SK. Delirium in elderly adults: diagnosis, prevention and treatment. Nat Rev
Neurol 2009, 5(4):210-20.
Cholinergeric deficiency
Anticholinergic drugs can induce delirium
Cholinesterase inhibitor drugs eg phyostigmine have been shown to reverse delirium caused
by anticholinergics
Serum acetylcholinergic activity and delirium have not been found to be correlated. Serum
not brain?
Elevated brain dopaminergic function
Anti parkinsons drugs can cause delirium
Haloperidol has been used to treat it.
Relative imbalance between the cholinergic and dopaminergic systems?
Other neurotransmitters: glutamate, -aminobutyric acid, 5-hydroxytryptamine (5-HT) and
norepinephrine
Typical Medical Causes
metabolic disorder, carcinoma, infection , neurological disorder, inflammation, pain , dehydration
(and constipation), malnutrition, urinary retention, sensory impairment , drug effects (and
interactions), drug/alcohol withdrawal syndromes
What are the common ways delirium patients are referred to psychiatry?
We think she is really depressed. She is not interested in physio or eating and drinking. She
sometimes cries out at night but she never says anything to us on the ward round..
This 80 year old woman who has come in with pneumonia is also having her first episode of
psychosis! Come quickly, I think she has schizophrenia..
- 153 -

How do I tell if someone has co-morbid dementia?


Significant deviation from baseline
Fluctuating course
Reversal of sleep-wake cycle, tricky with sundowning
Comparative poor performance on concentration tasks versus memory tasks or vice versa
Nature of the psychotic symptoms
Collateral history
What about co-morbid psychotic illness?
Deviation from baseline functioning
Fluctuating level of arousal
Primarily a deficiency in attention and concentration
In comparison, chronic psychosis leads to primary deficits in frontal lobe and executive functions.
Nature of psychotic symptoms eg visual hallucinations
Why the big deal?
Increased length of stay and institutionalisation
Twice as high costs of care
Reduced subsequent functional status
Not the reversible condition it was previously understood to be
Dementia patients do not generally return to baseline functioning, but have an accelerated
decline over the time course of the delirium
Mortality 4-65%, 62% increased in the next year
***Treatment for Delirium
First step: treat the medical cause
Non pharmacological interventions:
Reduce environmental stimulation, single room, close to nursing station, low light at night, reduce
staff changes.
Treat pain adequately, balancing with risk of opioid toxicity and constipation
Re-orientate patient often family, ward cues
Avoid restraints
Frequent turning to avoid bed sores, active physiotherapy for mobilising, DVT prophylaxis
CHARTS: sleep, behaviour, especially food and fluid. Promotes active and preventative nursing care.
***Medications
Benzodiazepines are ONLY used in cases of alcohol or benzodiazepine withdrawal when this is a
contributing factor
Anti-psychotics have limited evidence
Haloperidol is a popular choice
Largest evidence base
Number of routes: oral, liquid, IM, IV and doses largely the same for all
Quetiapine
Low potency so can titrate the dose
Fewer EPSE so better for elderly with Parkinsons
Other options include olanzapine and risperidone.
Prevention strategies
Eliminating unnecessary medication
Attention to hydration and nutrition
Adequate pain relief
Correction of sensory deficits
Early mobilisation
- 154 -

Pharmacological prophylaxis has been studied but not conclusive eg haloperidol, donepezil:
cholinesterase inhibitor
Take home messages
Serious condition with high morbidity and mortality
Common and often undetected
Primarily a disorder of ATTENTION, so test patients for this, not orientation.
Non pharmacological intervention is the best treatment and prevention. Medication is only used
when behaviour is placing patient or others at risk of physical injury or impacting on the patients
health care

- 155 -

Overlap of Physical and Psychiatric Illness

Cartesian Dualism
Descartes 18th century philosopher
Mind and body separate and discrete entities
Cartesian philosophy pervades western medical thinking and is reflected in the structure of medical
and psychiatric services
Doctors expect physical illness to be expressed in somatic terms - psychic distress and psychiatric
illness in psychic termsbut.
There is a psychic dimension to most somatic illness and physical symptoms form part of many
psychic syndromes
Functional Symptoms in Primary Care
Multisomatoform Disorder
3 or more medically unexplained symptoms
At least 2 years in duration
8.2% prevalence in primary care
1 in 5 new inceptions of illness in primary care satisfy criteria for somatization
Epidemiology of Psychological Syndromes in the General Hospital
50% of general hospital inpatients will have diagnosable psychiatric disorder (usually mild to
moderate anxiety and/or depression)
10 15% general medical patients and 25% hospital inpatients will have an organic mental disorder
(delirium or dementia) higher rates in geriatric units
Rates of psychological syndromes especially high in some units eg. HIV, oncology, renal
Epidemiology of Functional Diagnosis in Hospital Clinics
Gastroenterology - 37% organic 58% functional 5% undiagnosed
Neurology - 48% organic 47% functional 5% undiagnosed
Cardiac - 60% organic 35% functional 5% undiagnosed
Overlap of Physical and Psychiatric Illness
1. Medical disorders that produce syndromes or complicate treatment of syndromes
Medical disorders (or their treatments) that are complicated by psychological syndromes
Psychological responses to illness
Modifications to treatment required by physical illness
2. Primary psychological disorders that present somatically or alter the course of physical illness
Depression, anxiety and substance use
Disorders of illness behaviour
Medical Illnesses most commonly associated with Depression
Cancer (pancreatic, bowel, lymphoma), Stroke, Endocrinopathies (hypothyroidism, Cushings,
Addisons, hyperparathyroidism, oestrogen withdrawal), Parkinsons, Viral illnesses (EBV, hepatitis,
influenza, HIV, CMV), Pernicious anaemia, Collagen diseases (SLE)
Medications most commonly associated with depression
Corticosteroids, Interferon, Indomethacin, Levodopa, Cimetidine, Antihypertensives (propanolol,
Narcotic analgesics, Chemotherapeutic agents (procarbazine, vinca alkaloids), Amphotericin B,
Psychostimulants (amphetamines or cocaine used chronically or in withdrawal)
Diagnosing Depression in the Medically Ill
Exclusive diagnostic criteria
Vegetative symptoms of depression discounted unless disproportionate to objective measures of
illness
Emphasis on cognitive symptoms of depression (ideas of guilt / worthlessness), loss of reactivity of
- 156 -

mood, diurnal variation of mood or other symptoms, anhedonia


If in doubt trial of treatment
Organic Disorders Simulating Anxiety Syndromes
Cardiovascular (IHD, arrhythmias, mitral valve prolapse, myocarditis)
Respiratory (CAL, pulmonary embolism)
Neurological (TIAs, TLE, essential tremor, myasthenia gravis)
Endocrine (Phaeo, thyrotoxicosis, BSL, Adreno-cortical insufficiency
Intoxications (Caffeine, amphetamines, sympathomimetics)
Alcohol, benzo or barbituate withdrawal
Organic Disorders Simulating Functional Psychosis
Alcohol hallucinosis or withdrawal
Intoxication (organo-phosphates, LSD amphetamines)
Drugs esp. in toxicity (corticosteroids digitalis, L-Dopa, atropine and other anticholinergics)
Cerebral syphilis
Hypothyroidism
SLE
temporal lobe epilepsy
HIV
Encephalitis
Hydrocephalus
Cerebral neoplasm
CNS degenerative diseases (Picks, Huntingtons)
Psychotropic Medication in Medical Illness
Generally lower doses in context of medical illness especially in elderly
Care with pharmacokinetics
majority of psychotropic meds hepatically metabolized potential interactions with drugs
metabolized by a similar route (CYP system)
Renal function important for some esp Lithium, also Mirtazapine
Most protein bound care with low albumin
Care in context of cardiac disease (TCAs, atypicals), seizures (SSRIs, all antipsychotics), respiratory
illness (BZDs), stroke (atypicals)
Primary Psychological Disorders that Present Somatically
Somatization a concept originally from psychodynamic theories of illness causation - psychological
conflict transformed into bodily distress
A modern definition - The tendency to experience, conceptualize and communicate mental states
and distress as physical symptoms or complaints of altered bodily function.
Somatization is Ubiquitous
Worldwide and in western primary care somatic symptoms are the most common presentation of
psychic distress
?Somatization as psychopathology is a cultural construct egs: brain fag in West Africa, hwa-byung in
Korea, shockor nervous exhaustion in Western cultures
Somatization in Primary Care
8% present with illness worry, 17% have multiple unexplained medical symptoms
anxiety and depression most commonly present somatically eg: chest pain in panic disorder, fatigue
in depression
Screen for associated symptoms eg. sleep disturbance, loss of interest in depression
exclude D & A abuse or withdrawal
Across cultures there is significant correlation between number of somatic symptoms and anxiety
- 157 -

and depression scales and levels of total distress


Stronger relationships for symptoms of weakness, headache and palpitations
In common medical disorders somatic symptoms are at least as strongly associated with depression
and anxiety as objective physiological measures and improved depression was associated with
decreased somatic symptoms without improvement in physiological measures
Somatization vs Abnormal Illness Behaviour
Somatization is an overlapping but not identical phenomena to abnormal illness behaviour
Illness behaviour - (Mechanic 1962) describes the way in which an individual responds or does not
respond to an illness or to a symptom
Abnormal Illness Behaviour
Abnormal Illness Behaviour is an inappropriate or maladaptive mode of experiencing, evaluating or
acting in relation to ones own state of health despite a doctor offering accurate and lucid
information based on a thorough examination and taking into account the patients age, educational
and socio-cultural background (Pilowsky)
Somatization to AIB - Key Role for Attribution of Symptoms
eg. symptom of fatigue is ubiquitous
30% men & 20% women will complain of fatigue
a continuum of complaint
? CFS as a categorical entity is an artificial construct - a label thats acquired by those who present
Fatigue and psychological distress vary in parallel - more distress = more fatigue
Im tired and Im stressed Vs I have chronic fatigue syndrome
no difference in fatigue symptom profiles community vs. clinic populations
community populations attribute symptoms to stress, kids, too many comittments etc.
clinic pops attribute to CFS/ME, MCS, sick building syndrome, candida, food allergy, multiple
chemical sensitivity
those who label themselves as ill are more disabled socially and occupationally
What to do
Acute or intermittent somatizers present with stressful life events
Management - link stress with symptoms (Goldbergs reattribution)
Most resolve with time
A v. useful resource for patients with functional neurological symptoms
www.neurosymptoms.org/
Chronic somatizers see themselves as ill and are not amenable to change
Longstanding AIB and make multiple demands on medical services
Management
care vs cure harm minimization
Treat co-morbid psych illness but dont expect this will resolve the AIB
Psychiatric referral usually resisted but can be effected if the language of the referral is right

- 158 -

Eating Disorders - Overview

Eating disorder: DSM-5 (2013) and ICD (2017)


Women (post pubertal to 30 years)
*Pica
*Rumination disorder
Avoidant/restrictive food intake disorder (ARFID)
Anorexia nervosa
<1% prevalence
Bulimia nervosa
<2% prevalence
Binge eating disorder (BED)
<2% prevalence
*Other SFED (purging disorder, anorexia nervosa (AN), bulimia nervosa (BN), binge eating
disorder (BED), night eating syndrome (NES))
(Exercise disorder and ED 28%) ????
20% do not seek help
Males
1 in 10-15 AN, BN patients
1 in 2 BED
prepubertal ED male:female greater
Outcome (assessment)
5 to 10 years
40% complete recovery
40% some preoccupation, good QOL
20% chronic
Good prognosis if:
Never very low weight, early treatment, not overweight before, no vomiting, no abuse, no
comorbidity
Relapses are common especially in first 2 years
Every eating disorder patient is different
Criteria Avoidant/ Restrictive Food Intake Disorder (ARFID)
1. Persistent Restriction/Avoidance of food (range or amount) with failure to meet
energy/nutritional needs for growth, normal functioning
2. Significant weight loss or nutritional deficiencies (anaemia, BMD) or dependence on
nasogastric/alternate or supplemental feeding
4. Aware of the seriousness of the problem
3. Impaired psychosocial functioning
Can be overweight
Onset of ARFID
Fear aversion associated with discomfort ie choking incident, medical procedure ie barium swallow,
getting mouth guard, GI illness or life event (death) or other psychopathology and personality.
May be diagnosed following a GI operation if behaviour persists after cause is removed eg. achalasia
More kids :Sensory based or obsession avoid food: mixed food, appearance, color, smell,
temperature. Lack interest food- autism comorbidity
Criteria for Anorexia Nervosa (AN)
1. Restriction of energy intake needed for growth, normal functioning - BMI 17.5 18.5
2. Body image disturbed
self evaluation depends on body weight/shape
deny seriousness of low weight
3. Intense fear of gaining weight, behaviours for weight loss
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diet, starve
vomit, laxatives
excessive exercise
Subtypes:
Binge/purge
Restricting
Severity based on BMI
(preoccupied with control over food/body/exercise to control feelings/moods- transdiagnostic)
Amenorrhoea-assessment
reflects energy balance
can occur at any weight
predicted by:
exercise
amount of weight lost
BMI
age (> younger age)
cannot be determined if taking the pill
Anorexia Nervosa, Bulimia Nervosa, Eating Disorder Not Otherwise Specified (EDNOS), weight, low
weight, excessive exercise, exercise disorder
If hypothalamic amenorrhoea, also same endocrinology picture,
LH, LH pulsatility
leptin, leptin diurnal rhythm
hypoestrogenic
osteopenia, osteoporosis
Total BMD and vertebral first affected (trabecular)
malnutrition bone size, E vol,cortisol (?not responsive to OC/HRT)
BMI
Periods return by BMI 19 if no other behaviours associated with energy deprivation (Caucasian)
Pregnancy occur without menses return
BMI
postmenarche > premenarche
Caucasian > Asian (all post menarche)
depends on the amount of muscle
Physical changes (The Minnesota Study)
Emaciation
heart rate
BP
Dehydration (fluid)
Bloating
Constipation
Dry skin
Lanugo
Loss head hair
Cold feet hands
Mild anaemia
Psychological changes
Irritability
Indecisiveness
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Poor concentration
Confusion
Depressed mood
Withdrawal
Concentration improves with nutrition
Mind can function BMI>15.5
Routine tests (AN, BN, BED)
BP
ECG
Bloods
BMD
Vit D
History
eating
fluid
general
IPDE-ICD-10 International Personality Disorder Examination
Most ED do not have a PD
If present order of prevalence: avoidant-anxious>borderline>histrionic>obsessional
Risk , trigger and perpetuating factors for an eating disorder
being female
attaining menarche
losing weight (chemo, gastric sleeve)

Psychological

factors

associated

with

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being

in

negative

energy

balance

Criteria for Bulimia nervosa or bulimia nervosa-like disorders


Recurrent episodes binge eating 1/week for 3 months (2hr)
Feels out of control of overeating episodes (within 2 hours)
Methods of weight loss: starvation, vomiting (laxatives, medications), excessive exercise
Over concern of body shape or weight
Anorexia nervosa takes precedence
Severity: number episodes of inappropriate compensatory behavior/week
Criteria: binge eating disorder
1.Recurrent episodes binge eating 1/week for 3 months
2.Feels out of control of overeating episodes (within 2 hours)
3.No inappropriate methods of weight loss
4.Distress about binge eating
5.Three of: eating more rapidly, until uncomfortable full, when not hungry, alone (embarrassment),
feeling disgusted, depressed or guilty after.
AN BN takes precedence
Severity: number binge episodes /week
The
psychological
circle
of
binge
eating

Eating behaviour and pregnancy outcome


3 groups: term IUGR, prem LBW, control
Predictors IUGR; prepregnancy BMI, smoking, weekly weight gain, perception of overeating
Eating disorder women more likely in term IUGR
Reproductive outcome 10 years in eating disorder patients
If eating disorder current at time of pregnancy
> miscarriage, >hyperemesis gravidaruum, >postnatal depression
Eating disorders can be improved or worsen during pregnancy
LBW baby immediate outcome
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Low BMI ED women have low BW babies


Obese women have high or low BW babies
High and low BW babies have impaired Insulin resistance (in utero)
Grow up to develop metabolic syndrome
LBW baby long term outcome
Adults who have greater risk of having:
hypertension, insulin resistance, type2 diabetes, cardiovascular disease
RESTRICTION OF UTERINE GROWTH IMPORTANT
What is considered Normal structured eating?
Eating 3 meals and 2 or 3 snacks each day
Usually eating at approximately the same time each day
Eating a variety of different foods
Learning to eat normal food i.e. normal fat, normal energy content
Learning to eat normal amounts of food (not large amounts of low energy)
Eating foods containing protein, carbohydrate and fruit/vegetables at most eating episodes
Having no banned foods, can have a couple of dislikes that are not associated with weight control.
Being able to eat anywhere e.g. in any country around the world, home, food courts, fast food
outlets, restaurants.
Not having specific rules about eating associated with restricting food e.g. always eating with a
teaspoon, never eating fast food
Allowing flexibility in eating e.g. eating at different times with friends, eating what people normally
eat at celebrations.

Eating Disorders - Management

Eating disorders are prevalent


Biologically Based Serious Mental Illness
Comorbidity: rule rather than exception
Primary and Secondary eating disorders
Child and adolescent presentation
weight loss, food refusal, excess exercise
dehydration ketosis halitosis
syncope/collapse hypotension
standing BP down >20mmHg
standing PR up >20bpm
bradycardia ST/T waves changes
delayed puberty
stunted growth
Adult presentations
concern of others
menstrual disturbance, infertility, PCOS
low libido, erectile and ejaculatory failure
dyspareunia, atrophic vaginitis, pelvic floor
cold, fatigue, Raynauds
fractures
emaciation and collapse
fluid and electrolyte problems
Other history
secrecy
hasty trips to bathroom
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chewing gum
laxative packets
diet coke
vegetarianism
avoidance of meals
academic success then problems
mood swings
tantrums
blocked drains
hoarding
Medical complications
sudden death, hypoK, hypothermia, dehydration hypoglycemia, hypothyroidism
cardiac failure, arrhythmias (altered HRV)
pancytopenia
brain/cognitive changes, peripheral neuropathy
immune suppression, major infection
osteoporosis and infertility
dental decay, sialadenosis
upper GIT, constipation, rectal prolapse
renal failure, secondary DI, hyperaldosteronism
skin, hair, eyes, ENT, body odour, oedema
Psychiatric complications
psychosis
depression
anxiety, OCD
autistic spectrum
personality derailment
substance abuse
DSH, somatisation, suicide
duty of care
compulsory treatment
Prognosis - does anyone ever get better?
Anorexia Nervosa 80% wt 50% full
Bulimia Nervosa 70% asymptomatic
EDNOS depends on sim to AN or BN
BED prognosis of obesity/med comps
Mortality rate (ST vs 20y) AN 10-20% BN?
EDNOS ? less ? similar to AN
Long term medical complications
Psychiatric disability/comorbidity
Multigenerational problem
Acute presentation - Management see Academy for Eating Disorders guidelines
NB
rapidity of weight loss
duration of semistarvation
extent of starvation
HWE and LWE
onset
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purging behaviours
fluid intake incl caffeine and alcohol
Risk assessment in Anorexia nervosa
BMI
anorexia <17.5
medium risk 13-15
high risk <13
physical examination
low pulse, blood pressure, core temperature
muscle power reduced
Sit up-Squat-Stand (SUSS) test
blood tests
sodium low suspect water loading (<125 mmol/L high risk)
potassium low vomiting or laxative abuse (<3 mmol/L high risk)
Note: low sodium and potassium can occur in malnutrition with or without water loading or
purgin, raised transaminases, hypoglycaemia: blood glucose <3mmol/l (if present, suspect
occult infection, especially with low albumin or raised c-reactive protein)
ECG
bradycardia
raised QTc(>450 ms)
hypokalaemic changes

Energy metabolism and brain changes in AN


vicious cycle of AN
critical weight
metabolic impediments to weight gain
DIT PPY PP non-suppressed fat oxidation
stress NPT and abdominal fat
fear/anxiety and AN
choline ACC ?autocannabilisation
neurocognitive changes
Nutrutional requirements
Energy = 130% of REE + EXERCISE =XTRA DIT ?repair
Avoid high CHO 40 -50% of energy only
Adequate protein 20-30% of energy
Adequate fat 20-30% of energy
Usual supplements: Ensure, Ensure Plus, Fortisip, Osmolyte, Fibresource, Twocal, Resource
Electrolytes vitamins and minerals eg
B1 phosphate Mg Zn B complex Ca Fe
?EFAs
Fluids 30-35mls/kg per day + electrolytes as needed
1/2 NS for rehydration + oral or NG feeds
avoid 5% dextrose for hypoglycaemina
Resuscitation and Refeeding
Scenario
The patient hasnt been eating anything
Encourage half cup MILK 2-3 hourly
Family or friends to help
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Multivitamins B1
Blood tests ECG Check phosphate ?replace
Keep warm no exercise
Consider: Insurance status Hospital
MHA or Guardianship or press on as O/P
Medical risk
dehydration
electrolytes
refeedings
rest
warmth
monitoring
containment
Longer Term
team approach
A&E
medical ward
psychiatric
specialised setting
public vs private
residential/day program/outpatient
Refeeding syndrome
can be lethal (Heidelberg F/U, POWs, ICU
CCF, chest pain, MVP, QTc >470ms
delirium, ?Wernickes encephalopathy
beri beri (wet and dry) ie B1 deficiency
peripheral oedema (insulin, sodium)
putative cause = hypophosphataemia
adaptation to fluid depletion and low intake
HRV (heart rate variability), arrhythmias
Patients at risk
Anorexia nervosa
Extreme emaciation or chronic malnutrition
Less than 500kcal per day for more than a week
BMI <15
Rapid weight loss of >1kg per week for last 3 months
Prolonged QTc interval(> 450ms)
Patients with low levels of potassium, phosphate and magnesium
Be careful if dehydrated
Volume depletion
High carbohydrate intake
Low prealbumin
Management
Prophylactic supplementation:
Electrolytes especially potassium, phosphate, magnesium,
multivitamin, zinc
Thiamine
Slow reintroduction to feeding but not too slow
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Polymeric nutrition
Refeed cautiously - oral or enteral
Start at 800 -1200 Kcal/day, if low increase intake by 200-300kcal every second or
third day, ensure intake is polymeric
Adequate protein and fat must be taken if on oral diet.
Monitor electrolytes, urea and BGLs regularly-daily for first two weeks
Monitor pulse rate and ECG
Nutritional Rehabilitation
Steady
Medically supervised
Renutrition
Weight restoration
Therapeutic age appropriate milieu
Physical and psychotherapies incl skills
Social integration parent support
Discharge planning
Evidence based treatments
CBT
CBT-E
IPT
SSCM
FBT
Underrated therapies
MILIEU DBT, ACT, SELF PSYCHTX, CAT, CRT
Movemen
Creative therapies
Psychodrama gastalt
Bibliotherapy
Proposed miracle cures
Medications FLX OLZ quetiapine topirimate
Heating Jackets
Mandometer
Opioid antagonists
Endocannabinoids
EFAs
Oxytocin
How to get patients unstuck?
POSSIBLE TARGETS
Cognitive rigidity
Motivational enhancement
Perverse rewards
Deep Brain Stimulation
Dolphins?
Horses?
Parentectomy?

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