Professional Documents
Culture Documents
-2-
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
-3-
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
9.7
14.4
7.7
5.1
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
-4-
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
-5-
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
Social
Social
Cognitive
Behavioural
Depth
Counselling
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.
-9-
- 10 -
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
- 11 -
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
- 16 -
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
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%
18%
10%
0.2%
2%
3%
15%
0.4%
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
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)?
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
- 21 -
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)
- 22 -
1.
2.
3.
4.
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:
- 23 -
Pathophysiology of Schizophrenia
Dopaminergic dysfunction
- 24 -
Vulnerability
to exploitation
risk taking
to further deterioration
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
- 28 -
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
feeling nauseated
flushes & chills
difficulty breathing
butterflies in stomach
headache
dizziness
dry mouth
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.
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
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
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 -
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 -
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.
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 -
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 -
Phenomenology
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
- 49 -
- 50 -
Cannabis
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.
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 -
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 -
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 -
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: 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.
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 -
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 -
- 63 -
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 -
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
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
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 -
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 -
Safer in overdose
May need to be taken less often, easier logistics
Easier to divert (not if Suboxone)
Less stigma
- 70 -
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
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 -
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
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
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%
Management
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
GAD
3-4
SAD
2-4
OCD
1-3
marginal to good
specific phobias
0-1
marginal at best
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 -
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
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 -
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 -
*Shedler J. (2010). The efficacy of Psychodynamic psychotherapy. American Psychologist, 65(2), 98-109.
- 92 -
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
Other 1%
- 95 -
Post
PTSD
- 96 -
- 97 -
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
Refugees vs migrants
Migrants
Refugees
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 -
After
- 105 -
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 -
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 -
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
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 -
- 117 -
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 -
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 -
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 ***
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 -
- 127 -
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 -
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 -
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 -
screening
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!
seizures
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 -
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 -
Self regulation
see handout
- 139 -
Week 6
Older People- What is Different?
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 -
- 144 -
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 -
- 150 -
Delirium
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 -
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 -
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 -
- 158 -
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
- 160 -
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
- 161 -
being
in
negative
energy
balance
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
- 164 -
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
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
- 166 -
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?
- 167 -