Professional Documents
Culture Documents
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PAAM - Introduction to Psychiatry
YES
PAAM - Overview of Psychiatric Disorders
YES
PAAM - History of Psychiatry
YES
PAAM - Introduction to Addiction Medicine
YES
PAAM - Assessment of Drug and Alcohol Use
YES
PAAM - Schizophrenia
YES
PAAM - Mood Disorders - Overview & Management
YES
PAAM - Sleep wake cycle
YES
PAAM - Cognitive Behavioural Therapy
YES
PAAM - Prescription Drug Misuse
YES
PAAM - Drug Seeking Patient
YES
PAAM - Alcohol Withdrawal and Beyond
YES
PAAM - Alcohol: Brief Intervention
YES
PAAM - Stimulants & Management of Opioid Dependence
YES
PAAM - Smoking Cessation
YES
PAAM - Cannabis
YES
PAAM - Psychostimulants
YES
PAAM - Socio-cultural aspects of psychiatry
YES
PAAM - Indigenous Mental Health
YES
PAAM - Psychotherapies
YES
PAAM - Anxiety Disorders
YES
PAAM - Trauma, Life-Events and Mental Illness
YES
PAAM - Trauma and its effects on development
YES
PAAM - Psychiatric Emergencies/Safety Issues and Managem
ent of Aggression
YES
PAAM - Personality: Normal Personality Development Attac
hment and Early Adversity
YES
PAAM - Personality Disorders
YES
PAAM - Intellectual Disability
YES
PAAM - Perinatal Mental Illness
YES
PAAM - Internalising Disorders in Childhood and Adolesce
nce
YES
PAAM - Externalising Disorders in Childhood and Adolesce
nce
YES
PAAM - Delirium
YES
PAAM - Overlap of Physical and Psychiatric Illness
YES
PAAM - Eating Disorders
YES
PAAM - Taking a psychiatric history
YES
PAAM - Psychiatry of Old Age
YES
PAAM - Mental state examination
YES
PAAM - Cognitive behavioural therapy
PAAM - Ethics Scenarios
PAAM - Behaviour management
PAAM - Interviewing the difficult adolescent
PAAM - Family interviewing
PAAM - Cardio-metabolic health and general adverse effec
ts
PAAM - Personality webinar
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PAAM - Introduction to Psychiatry
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Low prevalence disorders
- Schizophrenia
- Bipolar disorder
- eating disorders
High prevalence disorders
- Depression
- Anxiety disorders
PAAM OSCI
- Establishing rapport - Eliciting the symptoms - Checking for Suicidality and
Dangerousness - Assessing substance abuse - Presenting a good mental state exa
mination - Making a sensible differential diagnosis Suggesting sensible managem
ent strategies for frequently encountered conditions: - Biological, psychologic
al and social
---------------------------------PAAM - Overview of Psychiatric Disorders
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abn -think, feel, behave
psych disorders
- disease state
- abn thinking, feeling, behaving
- 2 components = cause significant distress + impair
. ability to work / play / love
- epi - 40%
. anxiety most common
. then substance and affective disorders
The Sick Role - Talcott Parsons
- exempted from normal social responsibility and for own condition
- price = exclusion from full participation in society
- obligation = try and get well
Sx
- behaviour - change/suicide
- relationships
- emotion - depression, manic, anxiety, irritation
- thinking - content (delusions, obsessions, overvalued ideas), form
- perception - hallucinations, illusions
- cognition
- insight and judgement
Classifications = both categorical based on criterion
- DSM 5 (mental disorders only)
- ICD 10 (europe, physical and mental disorders)
Biopsychosocial model
- genetic vulnerability, environmental, pathophysical interaction
- high expressed emotion (negaive) - contributes to schizophrenia
- mutated 5HTTLPR gene + environmental stress = depression risk
- effect of violence in childhood = MAO-A gene
- trauma stress
. complex = experience of significant ongoing childhood adversit
y eg physical abuse
Comorbidity is common
- grouping of psychiatric disroders
- psych + medical problems
Gender difference
- men - substance
- female - anxiety
Case Formulaton
- explanatory description of why you think they are presenting today - personality, medical, stressor
- plan or effect matrix: predisposing, precipitating, perpetuating, patt
ern, protective prognosis
. Biological
. psychological
. social
Treatments can by medical, biologicall, psychological, social
Recovery
- reintegration into culture and community
- satisfying relationships
- meaningful work and leisure activity
- spiritual dimension
- individual goals
Mental health Act
- care, treatment and control of persons who are mentally ill or mentall
y disordered
- to facilitate the involvement of persons and persons caring for them i
n decisions involving appropriate care, treatment and control
- definition mental illness
. seriously impairs temp/perm functioning - delusions, hallucina
tions, serious disorder of thought form, disturbance of mood, repeated irrationa
l bheaviour indicating symptoms
- Detain a person = section 14
. ground for believing that care, treatment or control of person
is necessary for their own protections from serious harm, or protection of othe
rs
- mentally disordered person s15
. irrational behaviour - justifies on R grounds that temporary c
are, treatment or control is necessary for their own protection or for others
- involuntary admissions s12-13
.medical officer (RMO or registrar or consultant) .person is mentally ill or disordered + not other less restricti
ve is safe/effective, appropriate or reasonably available
Flow chart of detaining a person
- detaining + inform primary carer within 24 hours
- initial exam by authorised MO, 2nd exam by another MO if the first is
not a psychiatrist + complete form 1 within 12 hours
- can detain
Mental health review tribunal
Psychiatry and autonomy
---------------------------------PAAM - History of Psychiatry
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no content
---------------------------------PAAM - Introduction to Addiction Medicine
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What range of disorders does it cover?
What is the nature of the disorders?
What diagnoses are made? is it different from general medicine? How does it rel
ate to psychiatry?
Addiction medicine - deals with addictive disorders - substance abuse/ psychotropics
- electronic/gambling
substance abuse/ psychotropics
- aims
. prevention of hazardous use, addictive behaviours and harms, d
ependence
. behaviours
. recognition of disorder
. management
- spectrum of disorder
. non user -> hazardous use -> dependence syndrome/addiction/com
pulsion
. substance abuse = harmful use + addiction
Development of dependence
- repeated consumption of substance with psychodependence activity (alco
hol, tobacco, drugs)
- repeated use of one or multiple causes profound changes in meso-limbic
system (ventral tegmental of mid brain AND nucleus accumbens of forebrain)
- develops enduring biological changes
- continue to use, abuse, addiction
Resetting of neurocircuitry
- 4 neurocicurits are reset in an enduring and difficult to reverse ways
of reward, stress, inhibitory control systems of the meso limbic systems
. changes result in
- under activity of the reward systems
- over activity of stress system responsises to psychoac
tive substances and triggers
- an internal (subconscious) driving force directing fur
ther substance use
- decr influence of voluntary control due to impaired in
hibitory system
- 1. reward system
. pyscho active substance initially activate reward pathways of
. main ones are dopaminergic systems (esp for psychostimualnts a
nd nictoine) + opioid system (alcohol + opioids)
- repeated used suppresses the systems, tolerance develops and more subs
tance required to maintain normal state
. normal activities with reward effects become blunted or ineffe
ctive
. negative mood and motivational state ensures
- 2. alertness or excitatory system
. with repeated activation there is activation of stress pathway
s (glutaminergic transmission) and CRF
. suppression + uncoupling of anti-stress systems (GABA and neur
opeptide Y)
. results in heightened activation from exposure to triggers
- 3. salience pathways (prioritisation)
. reset in favour of continued substance use = higher priority f
or thinking, anction over other tasks and responsibility
- 4. frontal inhibitory (behavioural) control pathways
. precentral gyrus of frontal lobe down to centers incl N accumb
ens and ventral tegmental
. impariemnt of behavioural control
. less control over the other neurocircuits then would normally
control
. assoc with def in executive functioning and frontal lobe impai
rment
COre syndroms with diagnostic criterion: lesat to most severe (separate harms/cl
assifications from physiological complications eg hepatitis, cirrhosis etc)
Hazardous use (WHO, NHMRC)
. repeated use of substance with risk of harmful consequences
Harmful use (ICD 10)
. actual harm (physical, psychological)
Substance abuse (DSM-IV)
Substance
.
Substance
.
.
Neuropsychiatric complications
.Delirium
.Wernickes encephalopathy
.Memory impairment (amnestic syndrome)
.Frontal lobe and other brain damage
.Cerebellar disease
.Stroke
.Brain contusion
.Intracranial haematoma
.Peripheral neuropathy
.Rarer conditions
Social complications
- Domestic and Allied Problems
.Loss of friends
.Domestic arguments
.Domestic violence
.Neglect of children
.Separation
.Divorce
Occupational
.Absenteeism (especially Mondays)
.Poor work performance
.Unexplained absence during working day
.Failure to gain promotion
.Demotion
.Dismissal
.Unemployment
Financial Problems
.Loss of regular income from employment
.Hardship from money spent on alcohol
.Gambling debts
.Victim of fraud
Legal Problems
.Drink-driving offences
.Loss of motor vehicle licence
.Property crime
.Assault
.Homicide
Miscellaneous
. Prostitution
Substance
-
Substance
-
Alcohol epi
- 90% adults
- ~20% hazardously + har,
- ~6% have dependence
- highest consumption in english world
- declining since 1977
- 4500 related deaths/yr
- 5% of all deaths
- 10% premature years of life lost
- $6000 million per year
- 40% of inpatients have underlyuing alcohol problem
- 20% of GP practice have underlyuing alcohol problme
Benzos/sedative-hypnotics epi
- 7% adults regularly (decr 13% in 1977)
- 350 deaths/yr (overdose)
Cannabis
- most widely used illicit drug
- prevalence varies with age
- 20-40 yrs
. 50% have tried > 1
. 20% used in last month
. 5% are dependent
Opioids
- varies with age
- decr in heroin since 2000 due to difficulty in obtaining
- heroin
. 1.6% ever tried
. 75000 dependent in australia
- use has incr
- 10000/yr in 1998 but now decr
Amphetamines / psychostimulants
- 15% have tried>1
- crystal meth/ ICE is most common
- causes - agression, violence, psychotic phenomena
- 1/3 regular users experience psychosis
20% adults
decr prevalence
19000 related deaths/yr
$6500 million per annum cost
1/3 inpatients are current smokers
1/3 inpatients are exsmokers
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
OE - General appearance
. flush, erythematous face
. thin, gaunt malnourished
- Signs of intoxication
- Features of withdrawal
. tremor, sweating
- Evidence of tolerance evident when little or no impairment despite rec
ent high use of sedatives or elevated BAC
- Mental state
. Anxiety and agitation
. flat, distresed
- Cutaneous stigmata (alcohol)
. facial telangiectasis
. partoid gland enlargement
. overgrowht of skin - rosacea
. dupuytrens contractures
- Evidence of injecting use
. ante-cubital fossa
. forearms, hands
. femoral vein
- Complications occur in every system look for unexpected combinations e
.g. hepatomegaly and hypertension
Complications of IV route of admnistration
- scarring, obstruction
Corroborative info
- spouse, accompanying person
- GP, previous hospital record
Screening tools
- AUDIT for alcohol
1. how coften do you have a drink containing alcohol
2. how many SDs do you have on a typical day when u r drinking
3. how often do you have 6 or more drinks in one occassion?
4. How often during the last year have you found that you were n
ot able to stop drinking once you had started
5. How often during the last year have you failed to do what was
normally expected from you because of drinking?
6. How often during the last year have you needed a first drink
in the morning to get yourself going after a heavy
7. How often during the last year have you had a feeling of guil
t or remorse after drinking
8. How often during the last year have you been unable to rememb
er what happened the night before because you had been drinking
9. Have you or someone else been injured as a result of your dri
nking
10. Has a relative, a friend, a doctor or another health worker
been concerned about your drinking or suggested you cut down?
- 0 - abstainer
- up to 7 - non hazardous safe drinker
- up to 12 - hazardus or harmful alcohol use
. feedback + brief intervention
- > 13 - alcohol dependence
. feedback
. referr to specialist
. ? need for detox
. pharmacotherapy
Lab markers of alcohol dependence
- incr GGT
- incr AST more then ALT
- incr uric acid
- incr HDL cholesterol
- CDT carbohydrate deficient transferrin
- etoh metabolites - ethyl glucuronide (urine), ethyl sulfate
- acetaldehyde-protein adducts (blood)
Negative sx
Cognition
Duration of Undiagnosed Psychosis
?adherence
Assessment
- goals
. what is the dx
. why this person and
. why now in their life
- can the consent to the treatment
- which tx is best
- what location/site is best o tx pt (eg involuntary)
Detailed hx from pt + family
- duration of sx (duration of undiagnosed) psychosis
- individuals response to sx - aggression ?
- developmentla hx - functioning
- mental state examination
risk assessment
- danger - suicide, homicide
- tx adherence
- absconding
- vulnerability to exploitation, risk taking, to further deterioration
physical examination - neuro - bmi
Comorbidities
- assume coexistence of following until proven wrong
. substance abuse
. mood disorder
. anxiety
. developmental
Ix after 1st episode - broad
- FBC, EUC, Ca++, LFT, TFT
- Fasting BSL, lipids
- Urine drug screen
- Immunological screen
- ECG (varies with medication, age)
- Neuroimaging (CT, MRI)
- EEG (if suggesting of epilepsy)
5 domaines of sx (pos, neg, cog, anx, disorg)
- positive
. hallucinations (auditory most common ~80%)
. delusions
- negative
. loss of function
. affective blunting (emotion, charm, modulation+expression of a
ffect)
. anhedonia (cannot experience pleasure)
. amotivation
. alogia (poverty of thougt and content, concrete thinking, slow
ness of thought and movement)
. asociality (apathetic in pursuing social life, loss of meaning
of social connections)
- cognitive
. deficits present at 1st episode
. consistent profile of deficits
Case manaement
- brokerage model - not best...hi case loads
- extended hours team
- assertive community care - better...lower case loads, direct intervent
ion, shared load
Psychoeducation
- educate pt + families about the illness and treatment
- improvements in rates of relapse, readmission, medication compliance
Supportve psychotherpay
- regular visits, time to vent, reflection
- support rxn to illness 0 denial, engulfment, acceptance
Family therapy
- decr relapse OR 0.6, NTT 6.5
- impro social fn, sx, employment
Interventions for anxiety and depression
- hi rates of anxiety 40%, depression 60%
- pharmacotherapy SSRIs
Problem solving
- rational approach to problem
- prioritise, brain storm solution, step by step, review and return to s
tage 1
Coping techniques
- relxation
- activity scheduling
social skills
self instruction
desensitisation
distraction
remediation
use of cognitive tasks best run using computer softward
self paced
enjoyable
- melancholic
. marked insomnia, esp early morning wakening
. apetite and wt loss
. flat affect
. psychomotor change
. pervasive anhedonia
- non-melancholic
. depression w/o melancholic sx
. non-mood
. 5HT dysfunction (tx with 5HT antidepressants)
. mostly motor sx
Things to tell the pt pre-tx
- antidepressants take upt to 4 weeks to work
- SE being straight away
- non-addictive
- BUT don t stop suddenlty bc of withdrawal syndrome
- you can drink with them (except for MAO-Is)
- relapse is 100% when you stop the antidepressant
- must completely treat the episode to stop the relapse
Response vs remission = IN THE EXAM
- HAMD17 score of > 20+ = depressed
- response to treatment by HAMD17 score
. decr in HAMD by 50% = a response to the treatment
. (eg if score = 20, then response score = 10)
. around 2/3 people get a response with 1st agent
- remission definition on HAMD17 score
. decr of HAMD < 7 = remission
. about 1/2 people get a remission after 1st agent, 2/3 with 2-3
trials
- message = have to be prepared to try multiple agents.
The problem with the HAMD17 evidence
- the evidence is skewed by psychiatrists would not put their melancholi
c patients on placebo
- people who are answering the advertisement will have less serious depr
ession, possibly where antidepressants wouldn t work anyway.
How long to reat
- 6 mo AFTER recovery from 1st breif episode
- 2 yr AFTER recovery from 1st LONG episode
- lifelong - if 3 previous episodes
- lifelong - if psychotic depression (hi recurrence rate, risk of suicid
e, homicide)
Can I stop antidepressant ?
- recurrence rate is hi
- it is a chronic illness
- risk of recurrence after 1st episode incr with subsequent episodes = 2
nd (50%), 3rd (75%), 4th (100%)
Maintenance antidepressants - NO - what gets you well, keeps you wel
Ceasing
- slowly
- withdrawal effects
- reduce over 7 several months to avoid relapse
MOA
- monoamine neurotransmitter system (5HT, NorEPI, DA)
- block depletion of this OR inhibitory receptors
- blocking of MAO enzyme (the enzyme usually degrades the neurotransmitt
ers)
Why does more monoamines help
- post synaptic cell
- monoamine binds receptor
weak antidepressants
good for anxiety disorders
harmless in overdose
SE - lost libido, slows down orgasm, fuzzy headedness
fluoxetine, sertraline, citalopram, escitalopram, fluvoamine
SNRIs
- venlafaxine (>225mg = also get NorEPI with this level) and duloxetine
. good antiedepressant but SE of sweaty
- slow release venlafaxine (effexor) has prolonged cardiotoxicity in ove
rdose.
- withdrawal syndrome
Tricyclic antidepressants
- most effective for AD
- SE - anticholinergic effects, weight gain, sedation, hpotension, dry m
outh, dental caries
- decr reuptake of norEPI nd serotonin
- cardiotoxic in overdose
Monoamine oxidase inhibitors
- very effective
- inhibit MAO in synapse and the gut (where MAO breaks down tyramine)
. the excess tyramine (bc the MAO is blocked) then displaces nor
epi and epi -> results in intracranial hypertension -> intracranial hemorrhage
. sources of tyramie
- matured cheeses
- salami
- yeasty beers
- chianti
- chocolate
- coffee
- liver
- pickled herring
- vegemit
- sauerkraut
ECT
- most effective anti-depressant therapy
- indicated for
. melanchholic and psychotic depression
. unable to eat or drink
. highly suicidal or tormented
. bipolar depression and mania
- regimen
. 6-18 treatments requireed
. 2-3 times per week
. 5 min GA + muscle relaxant
. 30 - 1100 mC
. aim for current thru R frontal/temporal lobe
. avoid L hippocampus where many memories are stored (major SE =
memory loss)
- MOA
. generalised seixzure
. neurotransmitter + neutrophin incr
- SE
. memory,
. antero-grade memory impairment
. scattered retrograde losses
. post-ictal headache and confusion
. blood pressure instability
. post ictal bradcardia
- post ECT Mx
. requires maintenance ADs, lithium, maintenance ECT
What is the ADs are ineffective after 1 mo? - hierarchy of approach
- higher dose
- use more potent class
- consider whether it is a biological depression or some other cause
- Augmentaiton
. lithium
. 2nd gen antipsychotics (eg olanzepine)
- ECT
Types of non-drug therapies
- individual and group psychotherapies
- exercise
- meditation
- r/ship
- social interventions
Psychotherapy
- psychoeducation
- CBT
- interpersonal therpay IPT
- longer term psychodynamic therpay (for longer term depressin)
Psycho-education
- should be doen for all pt
- gives then control and rapport
- 1-2 sessions
. cover eti
. natural hx
. tx effects and SE
. make them aware of their early warning signs (for when they ar
e better ) - as a red flag for representation
- early waking
- not talking as much
CBT
- change thoughts - theway they behave
Interpersonal psychotherapy
- 12-20 session
- r/ships influence onset of and or recovery from depression
- 4 interpersonal problem areas
1. grif
2. dispute
3. role transition
4. lack of r/ships
Psychodynamic psychotherapy (freudian type)
- explores childhood isses
- poor short term outcomes for depression
- good for chronic childhood trauma
- aim for deep changes to personality
For depression: CBT = IPT = ADs
but therapy + Pill works better
Exercise
-
lifts mood
reduces anxiety
30 min 3-5 times a week improve depression
best for NON-melancholic depression
effect thry
. serotonin changes
. corticotrophin releaseing hormon CRH and cortisol
. endorphins
. neurotrophins
R?ship interventions
- couples therapy
- family therapy - must check whether kids are safe
Bipolar disorder (manic depression)
- both manic and depressive episodes
- some recovery bw episodes
- a primary mood disorder
- epi
. 2% life prevalence,
. M =F
. 90% recurrence
. avg onset 17-21 yr
. genetic ie 1/6 of a persons children will get it - risk 15% in
1st degree relative
. delayed diagnosis common ~8 yr
Mania
- at least 1 week of
. mood
- euphoric, angry
- affect - labile, intense, ecstatic
. activity and behaviour
- increased - purposeful and non-purposeful
- agitated - pacing
- poor judgement - risk taking
- pressure of speech
. thought
- racing thoughts, flight of ideas (mood congruent - del
usions of grandeur, special ability or talents, special artistry/creativity)
- little insight
- psychosis
Hypomania
- no psychotic symptoms
- not severe enough to cause significant impairment in functioning
NB mood incongruet = more persecution or paranoid
Depressive episodes of bipolar
- mj depression
- anergia, hypersomnia (sleeping 12 hour plus) or insominia
- chronic
- hi suicide risk
Dx bipolar disorder
- time lag to dx - 8 yr
- poor recall of highs
- typical pc
. young peolple with bipolar type depressoin
. pschotic depression
. postpartum psychosis
. severe postpartum depression
- Bipolar 1 = depressions + manias
- bipolar 2 = depression + hypomania
- bipolar 3 = depression but then if tx with ADs then go hi, but if not
tx with AD then never go hi
- bipolar 4 = depression + mixed
- bipolar 8 = mod instability of borderline personality disorder
Bipolar spectrum
- less powerful classes SSRI may not work -> ongoing disability and suic
ide.
---------------------------------PAAM - Sleep wake cycle
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sleep histroy
- time to bed, sleep
- bed time rituals (contributing to anxiety)
- beliefs about sleeping/not sleeping (eg being depressed, losing jobs etc that raise the stakes of not sleeping)
- use of stimulants, alcohol
- exercise
- eating habits
- sleep environment
- time of arising
sleep hygiene
- winding down time
- avoid stimulants or blue light (tv screens, computer screens)
- cool, dark, quiet
- time of rising sets body clock -same time everyday, including weekends
- exercise enhances quality of sleep
- control of nocturnal worry
Strategies
- lifestyle factors - factors, diet, alcohol, caffein
- underlying medical, psychiatric conditions (depression for early, midd
le and late insomnia; medications)
- sleep hygiene
- stimulus control - associating bed with sleep; exlcuding music, device
s; if they are not asleep within 15 minutes getting out of bed to wait for sleep
wave to come again.
- sleep restriction - keep a sleep diary for a week or two to chart the
time asleep. The sleep chart helps to get an idea of lseep efficiency.
---------------------------------PAAM - Cognitive Behavioural Therapy
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COgnitive therapy = change unhelpful thinking
behavioural therpay = changing unhelpful behaviour and acheiving desired behavio
ur
The premise is that how we feel emotionally is more determined y how we think ab
out ourselves, our environment and situations we encouter, rather than by what a
ctually happens to us
When is CBT helpful
- ups and downs of life - ordinary human suffering
- acute psychological distress (losses, disappointments)
- mental disorders
. primary therapy in - moderate depression, anxiety, eating diso
rder, presonality, susbtance use
- adjunct therapy in severe depression, schizophrenia, bipolar,
personality disorder
Targets of CBT
- enhanced problem solving VS dorsolateral prefrontal cortex
. executive funtion,
. working memory
. cognitive flexibility
- moediying persectives on self and relationships VS anterior cingulate
We have a biological tendency to create and subscribe to beliefs about self, oth
ers and world around -> these can influecne emotions and behaviours and thought
processes; these beliefs may be inaccurate or not helpful
- eg I never succeed at things like this so that theres no point trying
. immediate failure cost: so they never try = fail = confirm own
opinion as incompetent and don t attempt in future
. reinforces/perpetuates the belief into behaviour back to reinf
orce the belief
. opportunity cost: also miss the opportunity for success, learn
ing and possible incr in skill and confidence
- eg I must never disagree with anyone or they will not like me
It is posible to identify and modify unhelpful beleifs
- reduces unpelasant psych symtpoms and 2nd physical
- help change undesired behaviour
- reduces vulnerability
- help improve mood and function
Core properties of CBT (difference from psychoanalytic therapy bc the therapist
is more active, there is more of a r/ship / collaboration to understand problems
and identify strategies; problem focused rather then symptom focused; rely on E
BM to match strategies to problems; pt has say in goals and mode of tx; time lim
ited and structured; should ahve a plan for every session and how many sessions
will be required)
Problem-focused
Here-and-now
Collaborative therapeutic relationship E
ducative focus P
atient-initiated goals
Guided discovery to gain insight into basic underlying beliefs (schemas)
Skills-based
Time-limited
Structured based on individualised formulation
"Homework" outside session considered essential - to practice the new sk
ills
Key cognitive strategies
Psychoeducalion
Socratic dialogue/guided discovery (to elicit in fo for greater understa
nding, involves asking questions to get pt to unearth greater understanding of t
hemselves)
Cognitive challenging
Worry control
Structured problem solving
Motivation enhancement therapy
Schema-focused work
Key behaviour strategies
Progressive muscular relaxation
Hyperventilation control
Exercise
Graded exposure
Exposure and response prevention
Behavioural experiments
Activity scheduling
Interoceptive exposure
Social skills training
Sleep-wake cycle management
Meditation
Stages of CBT in practice - focuses on the here and now - however you can to thi
s point, lets develop strategies to move forward.
1. Assessment of the problems (physical. emotional, psychological, behav
ioural, interpersonal )
2. Fonnulation: descriptive and explanatory statement about why have the
se problems developed and persisted; protective factors
3. Diagnosis
4. Psychoeducation regarding the causes. treatments and prevention of re
currence of the illness
5. Evidence-based Strategies selected to target the troublesome symptoms
6. The strategies are practiced by the patient
7. Outcome is measured (baseline measurment)
8. Relapse prevention strategies are planned
Cognitions
- automatic thoughts
Automatic thoughts
- premise - humans are constantly evaluating internal and external stimu
li
. influenced by underlying beliefs, previous exp, culutre and pe
rsonal factors
. they occurr rapidly, often outside of consc awareness
. represent repeated patterns of reacting to particular triggers
(situations, thoughts, feelings)
. cause emotional distress when they are unhelpful or unrealisti
c
. drive our emotional reactions and behaviour
- may be unhelpful, unrealistic, excessive, unreasonable
. it is not necessarily irrational to have negative reactions to
ambiguous situations, disappointments, losses, unfair tx
Changing automatic thoughts - STEPS
- 1st step is to identify the thoughts and patterns - become more aware
of the thoughts
- need to become more aware of the thoughts
- need to identify the emotional and behavoural consequences
- use the SUDS approach
- 2nd step is the challenge the thoughts
. whether they meet the aims of being helpful and realistic to l
ife
- 3rd step is replace them with more helpful and realistic way of thinki
ng
- 4th step is to base their behaviour on the more helpful and realistic
way of thinking (behaviour helps change thinking)
SUDS
- subjective units of distress
- a unit to try and estimate how upsetting a thought is
- typically somwether bw 0-100 or upward / downward arrows
- try to get to the hot thought that is a core schema or core belief
about themselves
Typical examples of an exercise for a person
A. activating event or situation
. eg having to start work on a project
B. beliefs, interpreation
. it will be rubbish
. I can t do it
C. consequences, emotions
. anxiety 70
. sadness 80
. confusion 75
There is no clear link bw the statements and the emotions
Use socratic method to identify why eg tell me what went thru your mind.
what are the consequences of doing somethig ?
Try to identify the connection bw the thinking and the consequences.
Cannot use technique of cognitive challenging (how do you know it would
be rubbish...)
Downward arrow technique:
It will be rubbiish -> I can t concentration -> I feel confused
-> I m incompetent -> I m worthless = hot thought = hi levels of emtional distre
ss
Cognitive challenging
- do the thoughts help us meet the aims of being helpful and realistic t
o life
- good questions for this
. What is the evidence?
. What alternative views are there? how else could i look at thi
s situation, how would my support person think of it
. How likely is it? has it ever happened
. How much would it really matter? (relative assessment)
. What do I gain by thinking this way?
. What do I lose by thinking this way?
Cognitivie error concept
- patterns in the way we habitually respond
. catastrophising - immediately jump to worst consequence
. black and white thinking - good or bad, closely related to per
fectionism; related to appraisal of r.ships (assoc with generalising)
. personalisation (everything taken personally)
. generalisation (based on one example)
. perfectionism
. mindreading (I know they thought I was an idiot; they didn t l
ike me)
. fortune telling (will never be able to do it..)
Case formulation
- developing hypotheses to explain why symptoms have arisen and why they
have persisted for this person. Knowledge of common risk and maintaining facto
rs assists in developing hypotheses Hypotheses are then used to guide individua
lly tailored treatment Useful to represent these hypotheses graphically. but no
set way to do this
- develop cognitive model and FEEDBACK LOOPS
- FEEDBACK LOOPS ARE THE POINTS OF INTERENTION
Cognitive model
1. antecedents, risf factors
2. triggers
3. symtpoms and persistence
4. beliefs
5. coping strategies
6. feedback loops = PIONTS OF INTERVENTION
Treatment planning
- based on case formulation
change model
peopple vary in their state of readiness to change
typically < 20% of people are ready to take action
an individual may go forward or back in their state of readiness to ch
ange
- transtheoretical model
. precontemplation
. contemplation
. preparation
. action
. maintenance
- readiness to change relies on the importance they place on the change
+ their confidence in being able to change
. eg smoking cessation - they know it is important, but they are
worried about being able to cope (ie the modern quit campaigns are on maintenan
ce)
. ie have to convince them it is do-able as well
Resistance
- resistance to change = roll with resistance
- eg these tablets are the only thing that has worked for me
---------------------------------PAAM - Prescription Drug Misuse
__________________________________
Obj
What is prescription drug misuse
Substances Extent of problem
Recognising the problem
Managing the problem
Prescription drug misuse = use other then how indicated
Aberrant drug behaviours - behaiours suggesting substance abuse or addition ie t
hat the behavious are pathological (selling, sharing etc)
Spectrum = ingeston, diversion, injection, dependence
Medications commonly misused
- sedating, stimulant, performance enhancing
- sedating
. Opioids-prescribed and OVER THE COUNTER
. Benzodiazepines
. Non-benzodiazepine hypnotics
. Antipsychotics
. Gabapentinoids
. Propofol
. Ketamine
. Antihistamines-prescribed and over the counter
. Barbiturates (rarely)
- stimulant
. methyphenidate
. dexamphetamine
- performance enhancing
. Diuretics
. Anabolic Androgenic Steroids
. Hormones EPO, hGH, Insulin, glucocorticoids
. B Agonistsl B blockers
. Steroid antagonists
. Stimulants Opioids
Extent of
-
the problem
lifetime misuse of pharm ~10%
in the last 12 mo ~5%
in the last week ~1.2%
misuse
14% Injecting drug user have misused in last 6 mo
peak age 16-19
prevalence of non-prescribed stimulant use is 35%
eti
- alcohol is a GABA agonist + causes release of endogenous opoids which
are depressors -> reward pathway linked
- GABA activity decr = less inhibitory
- glutaminergic activiy incr = more excitatory
PC
- autonomic
. sweating, tachycardia, tremor, anxiety, fevers
- GIT
. nausea, vomiting, diarrhoea
- insomnia
- seizures
Serious PC
- seizures - within 2 days
. in 10% of alcohol dependent
. recurrence in 25% within 12 hr
- delirium tremens DTs - from 36h to 5 days
. in 5% of alcoholic dependents
Predictors of severity
- past severe withdrawal
- past seizures
- amount of alcohol consumed
- needing a mornign eye opener (how early in the day they will drink) ie a drink needed to alleviate the withdrawal
Why do we
-
stinent
. AA attendance
Relapse figures from 2007, USA
- after withdrawal, abstinence is the most stable state
- advise 1 yr of abstinence post withdrawal to allow control centeres to
recoer
Acute mx
- long acting benzos
. regular dose
. or PRN (symptomatic)
. front end loading (hi dose early)
. combination (most common - depedning on severity
- review is needed
- inpatient vs outpatient
. depends on patient selection
. only outpatient if no unstable medical/psych problems, no othe
r drug use and stable, supportive home environment
Thiamine deficiency vit B1
- def
. decr diet intake
. alcohol decr gut absorption
. decr ability to use thiamine in metabolic pathways
. thiamine requirements go up during withdrawal
- outocmes
. wernikes encephalopathy
- confusion
- ataxia
- nystagmus
- ophthalmoplegia
. korsakoff syndrome
- amneais (anterograde, retrograde)
- confabulation
- apathy
- tx
. 3 d of IV thiamine
. 100 mg 3/d for 3 days then switch to tablet
. if wernickle - then 500 mg 3/d continued for a week
Monitoring
- clincial institute withdrawal assessment OR acute withdrawal scales
- medical exam and assessment
Mx - acute
- long term (after hospital)
. comorbidities (med, psych)
- liver/psych - reconsider use of benzos
Relapse prevention
- requires planning
- meds
PBS
. naltrexone
. acamprosate
non PBS
. disulfiram
. baclofen
. topiramate
Naltrexone (rivia)
- 50 mg daily
- opioid antagonist
- moa
. etoh causes release of endogenous opioids which act via GABA-e
rgic interneuron to incr DA availability in nucleus accumbens
. by blocking the opioids we block the effect of DA
- indicated for
. reward drinkers (for feeling of buzz, or feel good)
. family history with OPRM1 mutation of mu-opioid receptor
. adherence, only need once daily use
- best if started before or after withdrawal period
. good bc if not ready for withdrawal, then can still use it
- main effect to reduce heavy drinking days
- in those that are already abstinent, it helps them to keep off it.
- contraindicatinos
. if pt LFTs (transaminases) are > 5 x normal
. hepatic metabolised
. it can cause idiopathic hepatitis
. if pt taking opiates
. naltrexone will trigger opioid withdrawal
Acamprosate (campral)
- 666 mg TDS
- bc TDS, adherence is an issue
- MOA
. modulates GABA
. NMDA blocker
- effective if started after withdrawal period
- not effective if still drinking
- main use/effect is to helps maintain abstinence
- indications
. withdrawal avoidant drinkers (people who drink to avoid the ef
fects of withdrawal)
- contraindications
. LFT abn, liver diseaes, varices
. unstable cardiac and respiratory dz
Disulfiram
- 200 mg/d
- not on PBS
- MOA
. inhiits acetaldehyde dehydrogenase and B-hydroxylase
- buildup of acetaldehyde
- acetaldehyde toxicity causes
. facial flushing, sweating, N/V, diarrhoea, pain
. aversion therapy
- inhibiting b-hydroxylase inhibits the conversion of DA to nor-
epinephrine
. incr DA concentration in brain = helps those with crav
ings
- only effective if you have superivision to make sure you take it bc no
n-adherence is high
- don t start it until ~4days after last drink
- has long half life = have to wait ~2 weeks after taking it to start dr
inking again
- indicated for
. motivated people with low risk of nonadherence
. thsoe who can be supervised
- contraindications
. severe liver dz, varices
. unstable cardiac/respiratory dz
pyschosocial tx to prevent relapse
- individual counselling - public clinics or GP arranged
- family counselling
- group therapy
. alcoholics anonymous
- 12 step program
. SMART self management and recovery therapy
- cognitive behaviour therapy
- new wave
. mindfulness based
- eg acceptance and commitment therapy
Motivational interviewing to prevent relapse
- a directed (guided), client centered (the client comes up with the rea
sons for change themselves) counseling stype to elecit behaviour change to help
them explore and resolve ambivalence
- aim is to strengthen the part of them that wants to change
which therapy is best ? Project MATCH 1998
- all had similar outcomes
- highly dependen on r/ship bw pt and counsellor rather then the mdoalit
y
- more angry people had better outcomes with motivational therpay
- social drinkers/lonely had better outcome with AA
recovery
- ~60% wil achieve lifelong abstinence
Recovery phase
- phase 1 - withdrawal/stabilisation (weeks)
- phase 2 - early remission (up to 1 yr)
- phase 3 - sustained remission (1-5 yr)
Recovery - what is needed = CHIME
- C - connectedness (to counter boredom and loniliness) - men s sheds
- H - hope
- I - identity
- M - meanng - why they are doing so
- E - empowerment - how motivated they are to make changes
---------------------------------PAAM - Alcohol: Brief Intervention
__________________________________
- 3rd most reversible cause of disease and disability
- effects fetal and home environment
- use any opportunity
Risks of OST
Death during induction onto methadone
Death in the month after leaving treatment (by overdose)
. due to decr in tolerance and then subsequent relapse
Diversion and misuse of unsupervised doses
.(most methadone related deaths occur in people not in treatment
) ie diversion = methadone going to people with low tolerance can result in deat
h
Persisting misuse of heroin, stimulants, sedatives and alcohol
Outcomes of OST
- People cycle in and out of treatment, with relapses between episodes a
nd little sustained change
- (12 month retention methadone 50%, bup 35%)
- With long-term treatment 50-75% cease heroin use
even faster
- slow metabolisers
. smoke less
. less addicted
. asians, japanese esp, african americans
Smoking anything
- polycyclic aromatic hydrocarbons eg burnt steak, cigarettes
. these induce other liver enzymes CYP1A2
. CYP1A2 metabolises caffeine
. smokers drink a lot of coffee
. caffeins toxicity seen in withdrawals
. alcohol intake is double in smokers
. tolerance to alcohol drops in withdrawal
- smokers need more of the following bc of induction of CYP1A2
. insulin, pain relievers, anti-psychotics, anti coag, caffeine,
alcohol
. quitters need less of those things
- ie on hospitalisation, the effective dosage of things
doubles
Nicotine withdrawal - maybe confused with sx of drug toxicity
- craving, urges
- anxiety
- tension
- aggression
- incr in appetite
- inability to concentrate
- sleepinesss/sleeplessnes
- depression
- hunger
- mouth ulcers
- constipation
- worst in1st week
- sx diminish over time
- 62% relapse due to withdrawal within 2 wk
Smoking is negatively correlated with ulcerative colitis and parkinsons, alzheim
ers
- potential treatment in aggression, anxiety
Toxicity from nictoine toxicity is vanishingly rare.
NRT
-
v low dose
patches take hours to peak
no eivdence that you need to wean people off patches
no benefit to start on lower dose
they downregulate subtype reecptors
best to use NRT (patches, gum, inhalers) and smoke at the same time
vaping/electric cigarettes are very addictive - delivery of nicotine
to help them wean of cigarettes
. advise they take gum, then patch, and use cigarettes at the en
d
. apply 24 hr 21 mg patches last thing at night so that it peaks
in the morning
Varenicline (campix)
- more then one type of nACh receptor responds to nicotine
- women do better on varenicline
occurs of
anti-spastic
neuropathic pain in MS
antiemetic
appetite stimulant
analgesia
dependencies (obesity, tobacco, alcohol)
antagonists cause depression
Myths
- harmless, safer. no addiction, gateway drug, icnr potency, schizophren
ia
THC content incr ?
- YES - incr
- in naive users - hi potency
. greater dysphoria and pscyhotic sx
. gr risk accidental injury
. ptoential for gr discontinuation
- in regular
. allows them to titrate the dose -> less repiratory risk
. greater dependence
Effects of cannabis
- mental - euphoria, appetite, disinhibition
- physical effects - vasodilation, bronchodilation
EPI
-
. schizophrenia
cannabis psychoses
- rare (ie. as a result of heavy cannabis use)
- mild dose dependent paranoia common
Cannabis and schizophrenia
- can precipitate (RR=24) AND exacrbate schizophrenia
- naive schizophrenics have higher levels of anadamide in their CSF and
incr CB1 receptors
Cannabis use questions
- qantity, freq, route (cones v joints)
- gram amount
- $ spent per day/weel = impact
- dependence s?
- predisoposing factors - psychiatric illness, substance misuse
- complications
Features of dependence
- withdrawal syndrome
- compulsion
- tolerance
- prioritisation
- continued use despite evidence of harm
- ussage despite complications - schizophrenia, paranoia
Prevalence of dependence
- 4% population
- 9% of lifetime users are dependent
- 50% of daily users are dependent
withdrawal
- worse in first week
- mild sx
. irritable, anger, restless, anxiety, sleep dist, strange dream
s, craving, weight, depression
Tx for dependence
- self help
- intreventions
- psychotherpay
- for withdrawal
. dizepam 5 mg tds for 5 d
. lithium is ineffective
. cannabis antagonists ineffective
. agonists help (eg sativex)
- psychotherapy
1. How long is his withdrawal syndrome likely to last? 1 wk
2. What complications of his past cannabis use might you check for? Respiratory
complications (airways disease, wheeze); psychiatric complications (e.g. exacerb
ation of schizophrenia if ever present)
3. How might you reduce his risk of relapse? Brief intervention: reinforcing ben
efits of cutting down, identifying at risk periods
---------------------------------PAAM - Psychostimulants
__________________________________
2 groups - synthetic, natural
synthetics - pharmaceuticals, illicit
Pharmaceuticals
Pseudoephedrine
Dexamphetamine
Methylphenidate (Ritalin)
Diethylpropion (Tenuate)
Phentermine (Duromine)
Illicits
Amphetamine sulphate i.e. speed
Methamphetamine e.g. ice, base, speed
Amphetamine analogues
e.g. MDMA (Ecstasy), PMA
Naturals
Tobacco (nicotine)
Adrenaline
Khat
Cocoa (chocolate)
Caffeine
Cocaine
Guarana
Effects
-
MOA amphetamines
- work on monoamine synapse
- monoamines incl DA, 5HT, NA
- incr availability of monoamines in synaptic cleft by 5 ways
- 1. they block reuptake transporter DAT
- 2. direct agonists at post syndaptic membrane
- 3. symport exchange stimulator - pumps more DA, NA, 5HT back i
nto the cleft
- 4. inhibits VMAT (transport into vesicles) so that cytoplasmic
levels of DA is higher
- 5. inhibits MAO
- cuases sharp peak in DA
Addiction
- stimuli - ventral tegmental - trhu nucleus accumbens - hippocampus + a
mygdala - frontal cortex - cingulate cortex
- nucleus accumbens involved in saliency (prioritisation - how important
is the substance to me right now = source of addiction)
- feeding forward, the drive to do something, comes from frontal orbital
cortex - (to take soemtime or not)
- amygdala (emotional memory) + hippocampus = form memory of salience (h
ow important the stuff is too you) = related to how much DA has been released
- how important is it to you
In addicted brain
- big DA release
- big salience (nucleus accumbens)
- strong memory (amygdala, hippocampus)
- strong drive (frontal cortex)
- weakens self control / inhibitory
- becomes automatic
- reduces agency or choice
hydroxy butyrate)
direct agonist at GABA-B receptors and GHB receptors
GHB is metabolised to GABA
at low conc, GHB acts on GHB-receptors as a stimulant
at hi conc, GHB stimulated GABA-neurons and is a depressant
kinetics
. t/12 - 60 min
. interacts with alcohol - causes it to be more of a depressant,
hypoventilation, aspiration
- a prodrug is gamma butyl lacterone
. the converting enzume is inhibited by etoh, prolongs the effec
t
polydrug
- normal for amphetamine users
- co-use of nictoine, benzos, analgesics, etoh is common
- cocaine + etoh common bc cocaethylene has longer half life
Harms of psychostimulants
- amphetamine vs death
. incr since 2011
- amphetamines vs hospital pc
. psychosis 50%
. dependence 25%
stimulant psychosis
- PC
-Tactile hallucinations (formication or cocaine bugs)
-Suspiciousness, paranoid delusions
-Auditory hallucinations (voices)
-Visual (snow lights), gustatory, olfactory
-Repetitive, compulsive behaviour common
-Mood - fearful, agitated, often labile
-Orientated but no insight
-Violent behaviours
- behaviour sensitisation
. become more sensitive to the stimulant effects as you take the
drug
. but become more sensitive to risk of psychosis
- kindling
. if you have one episode of psychosis, your recurrence will inc
r with the more episodes - can lead to constant psyshcosis/schziophrenia
- cross sensitisation - if other stimulants have caused psychosis, then
amphetamines can then cause psychosis as well
Toxic effects
-Generally:
Sympathomimetic Syndrome
Seizures
Hyperthermia
HTN, atherosclerosis and ACS
Cerebrovascular event
Cardiomyopathy (reverse takotsubo = ballooning of basal segment
of heart)
Rhabdomyolysis
Acute liver and kidney injury
-Specifically
Amphetamines smoked, cocaine: Crack lung (looks like ARDS)
MDMA: Hyponatraemia (SIADH + polydipsia/hi temperature/body heat
)
Cocaine: Pneumothorax, pneumomediastinum (snorting), vasoconstri
ction (lost nasal septum)
Risky behaviours
- IVDU/sex
. viruses - HIV, HVC HBV
- injuries - MVA, burns
- child safety issues
Impact on society
- poverty
- domestic violence
- crime
-assaults
absenteeism
- maternal effect on fetus
Tx - amphetamines - withdrawal and relapse management
- EPI
. 5 yr gap bw problme use and seeking help
. more likely to seek tx if risky use/IV, need help for other pr
oblems
ment
- including the infants distance regulation and conformity to care giver
- become maladaptive and then symptomatic
Separation anxiety - manifets as 1.insecure ambivalence or 2. insecure avoidant
attachment
- infant 18 mo - 3 yr
- anxiety when separated from care-giver
- anxious, restless, clingy
- decr after 3 yr
- why do some people experience the anxiety
. when r/ship is not safe enough, child has ambivalence to the c
aregiver and wants them alsways to be present
. ambivalence leads to clinging
- 1. in an adult, separation anxiety comes out in the form of difficulty
in managing bw sessions, bc they are unable to internalise the caregiving role
of the therapist
. results in frequent contacts, or presentaitons to ED for more
care, self-harming for more care
- if this type of behaviour - need to address by incr the number of sess
ions
- 2. Another type is insecure or avoidance = indifferent or ambivalent c
aregiving - results in pseudo-independence, no fear of separation anxiety, self
sufficiency
. manifests in adults as a fear that the theapist will not be ab
le to help them - so they miss sessions, or arrive late to decr the talking time
- Boundaries are rquired to manage this separation anxiety ie locations,
time range, not exploit pt by receiving gifts/friendships/rships
Shame
- avoid provoking shame and humiliation
- reduce # questions
- supplant questions with empathic statements
- note pt affect or changes in it
- facilitate emotional expression
- if pt unable to talk other then in single word or non verbal,
. need to help them feel comfortable
. start with underttanding comments, validating comments then bu
ild to more mature language
Taking notice of trauma
- severely traumatised pt exhibit characteristics of fragility
. fragmentation of sentences
. monosyllabic
. disconnection
. confusion of time frames (past/prestn)
. loss of connection with the other person
. later experiences are interpreted consistently with past exper
iences
- need to start from where the pt is at
. meet monosyllabilic with nonverbal, monoysllabic et
- most pt dissociate - causes mingling of time frames
- loss of sense of self and trust in the world
- best not to ask them direct questons, dwell or dig up past traumatic e
xperiences
Personality disorders
- problems in thinking feeling and behaving in the r.ship bw self and ot
hers
- tailored to suit the pt
- multiple personality disorders may be present in chronic depression, c
hronic anxiety
----------------------------------
. IF YES - describe it
. How long did it take you from the beginning of an episode to t
he moment when you felt the worst (when you felt most anxious)? Was it a matter
of a few minutes? Or even seconds?
- panic attacks can conceal medical conditions t/f need to rule out unde
rlying medical conditions
. Racing heart, chest pain > Heart disease
. Breathlessness > Heart and pulmonary disease
. Dizziness > Vestibular and neurological conditions
. Trembling, numbness and tingling sensations (pins and needles) >
Neurological conditions
. Sweating, hot and cold flushes > Endocrinological (especially t
hyroid) disease
. Nausea, stomach churning, diarrhea > Gastrointestinal conditions
(especially irritable bowel syndrome)
- anticipatory anxiety
. fear of another panic attack = fear of fear, preoccupation of
sx of panic attack (fear of dying, loss of control, embarrassment, shame)
. screen for anticipatory anxiety
- Q: After one or more of these episodes (panic attacks)
, did you become preoccupied with having another one?
- If so, what are you concerned about? Why are you afra
id of panic attacks?
- What do you think could happen as a result of these ep
isodes? Why do you think so?
- epi
. lifetime 2 %
. 30% lifetime panic attack
. F:M = 3:1
. onset mean 25 yr
. hi prevalence 10%, in hospitals due to nature of symptoms
- natural history
. 30% recover
. 50% chronic + fluctuations
- mild, occasional tx req
. 20% chronic w/o fluctuation
- severe, interference with adl/fn, continous tx
- bio eti of panic attack
- resp disturbance
. CO2 inhalation,
. hyperventilation,
. lactate infusion
. hypersenstivity of CO2 brain stem chemoreceptors
. low threshold of suffocation alarm mechanism
- brains
. abn sensitivte anxiety regulating mechnism in amygdala
. hypersensitivity or pre-synaptic alpha-2 receptors (in
hibitory)
. failuyre of GABA systmen to inhibit locus coeruleus
- cognitive factors
. exaggerated perception of threat and danger (common to
ALL ANXIETY DISORDERS)
. Threat is perceived to originate within ones body
. Hypervigilance about physical sensations and bodily fu
nctioning
. Fear of anxiety and its (physical) symptoms because of
beliefs that anxiety and its (physical) symptoms are dangerous
. misinterpret phsyical sensations as sign of impending
catastrphge
AG
- characteristics
. Avoidance of multiple situations: crowded places public transp
ort, shopping centres, cinemas, travelling ar away from home, standing in a queu
e, etc
- avoidance can be:
. panic driven ie to avoid panic attacks
. otherwise eg fear of getting lost, mugged etc
- Fear and avoidance of the cluster of situations
. When alone and/or outside of ones own safety zone, where immedi
ate medicalyor other help might not be available (e.g., travelling far away from
home) .
. Where it might be difficult or impossible to escape immediatel
y (e.g., crowded places, public transport)
. Where it might be awkward or embarrassing to escape immediate
ly (e.g., standing in a queue)
- screening questionws
. Q: Do you avoid several situations, such as crowded places, pu
blic transport, shopping centres, cinemas, travelling far away from home or stan
ding in a queue?
. If so, what exactly do you avoid? Can you ever go into these
situations on your own or do you regularly need someone to accompany you?
. Why do you avoid these situations? What do you think might hap
pen to you in these situations? Does it have something to do with panic?
. If so (related to panic), are you concerned that no one will b
e there to help you in case of a panic attack? Or that you wouldn t be able to g
et out? Why would you need help? Why would you want to escape?
- epi
. 3% lifetime
. F:M = 4:1
. onset mean ~17
. strong association with work disability
- eti
. learning = assoc of unpleasant anxiety sx, panic attacks with
certain situations
. avoidance then reinforces, maintains
GAD
- characterisitics
. Pathological worry
- endless worrying
- live in future (full of potential dangers)
- worry driven by uncertainty
- continuous doubt, no closure (constant anticipation of
possible problems, no solution in sight)
- difficulty in shifting focus of their attention
- fruitless thinking which inhibits problem solving and
decision making
. Symptoms of tension%
. physical symptoms (less prominent than in panic disorder)
. Chronic course, with some fluctuations at times or stress/stre
ssors
- cascade of pathological worrying describes condition
. flu -> what if serious illness (shld check it) -> what if test
results are wrong (even bf check) -> ask for 2nd opinion (what if I can t affor
d it) -> better check finances (what if I run out of sick leave) -> financial di
saster...
- screening questions
. Q: Do you tend to worry a lot about many different things?
. If so, what do you worry about? How often worry most of the t
ime (nearly every day, most of the day)?
. making mistake
. having visible physical sx (blushing, sweating, trembling)
. of performing poorly
- DIFFERENT FROM SHYNESS
. when a shy person enters a social situation, they do feel anxi
ety, but this level goes down when they get positive feedback
. SAD people s level of anxiety remains hi no matter what feedba
ck they get
- screening q
. Q: Are of you afraid of certain social situations, do you feel
discomfort in them and/or do you avoid them? For example, speaking in front of
a group of people?
. If so, what are these situations? Why are you afraid of them?
What do you think would happen if you were in one of these situations?
. When you are inka social situation, does the level of your an
xiety ever go down? Especially when people seem nice to you? (distinguishes fr
om shyness)
Do you think that this fear and/or avoidance have significantly
interfered with your life? How?
- epi
. 3 % lifetime
. F:M = 3:2 in community (but equal in clinic)
. onset ~15 yr
. More likely to be single, unemployed, in the lower socio-econo
mic group, with lower levels of education (= consequence of SAD)
. Higher risk of alohol abuse than in people with other anxiety d
isorders (se|f-medication")
- eti
. genetic
. behavioural inhibition to the unfamiliar
- component of inborn temperament observable in 1st year
of life
Difficulty sleeping in unfamiliar surroundings
Irritability in novel s tuations
Avoidance of contacts with unfamiliar people, pl
aces and objects
. cognitive
- low self esteem + perception of social environment as
hostile => expectation to be evaluated negatively in social situations.
Specific phobias
- group of phobias eg animals etc
1. animal
- danger, disgust driven
2. needle/injection
- disgust
- 2 phases of pathophysiology
. initial tachycardia (fear)
. 2nd phase of vasovagal reaction - bradycardia, hypoten
sion, fainintg
- M:F = 1:1
3. environmental
- heights (acrophobia), water
3. situational
- enclosed places, flying, drying
5. other
- choking, vomiting, dentist
EPI
- 5% lifetime
- F:M = 2.5:1 (except for needle phobia which is equal)
- onset 10 yr overall
avoidance
reassurance seeking
4. mental (cognitive)
covert (metal, cognitive) compulsions
- screen for ocd
. Are you often preoccupied with thoughts, images or impulses th
at are unwanted, unpleasant or make you feel anxious? For example, tormenting th
oughts that you are dirty or contaminated or that you may have left your home un
locked or images of you harming someone even though you don t want to do that? S
omething else similar to this?
. If so, what thoughts, images or impulses do you have?
. How have you been coping with these thoughts, images or impuls
es? Do you have to do something? Perform a certain act, avoid something, ask for
reassurance? Why do you do that?
- epi
. lifetime ~1.5 %
. F:M = 1:1
. onset ~21 yr (earlier in males)
- natural history
. 50% chronic fluctuating or steady
. 20% recovery (minority)
. 15% progressive deteriorating
- eti
. bio
- serotonin neutrotransmitter dysfunction
- incr DA fn
- Implicated brain structures
Limbic system: orbitofrontal cortex, cingulate,
amygdala, thalamus
Basal ganglia: striatum (caudate nuclei)
- Dysfunction in the orbitofrontal (limbic)-basal gangli
a circuits or cortico-striato-thalamo-cortical
- Certain forms of OCD in childhood: autoimmune process
after an infection with group A beta- haemolytic streptococci
MANAGEMENT
Goals of Mx (intensity, frequnecy, behaviours, coping, reoccurrence, functioning
, qol
- decrease in the intensity and frequency of anxiety and its manifestati
ons (especially physical symptoml of anxiety)
- decrease in behaviours (e.g., escape, avoidance, compulsions) that are
related to or are a consequence of anxiety
- Better coping with anxiety
- Decreased vulnerability and prevention of recurrences Prevention of c
omplications
- Improved functioning and quality of life
Most common modalities
- pharmacotherapy
- CBT (psychotherapy)
- combination
Modality options
- pharmacotherapy
- psychotherpay
. behav, congitive, CBT, mindufllness/acceptabnce,
. psychodynamic psychotherapy, marital, supportive
- symptoms control / dearousal technique
. relaxation techniques
. breathing retraining
- combinations
- PD, GAD
. Benzos + venlafaxine
- PD, GAD, SAD
. Classical MAOIs
- SAD
. clomipramine
- PD, OCD
. pregabalin, duloxetine, agomelatine, quetiapine, buspirone, hy
droxyzine
- GAD
- anxiety disorders vs drugs
. PD
- benzo
- venlafaxine
- ssri
- clomipramine
. GAD
- benzo
- venlafazine
- imipramine
- ssri
- pregabalin
- duloxetine
- agomelatine
- quetiapine
- buspirone
- hydroxzine
. SAD
- MAOIs
- benzo
- venlafaxine
- ssri
. OCD
- clomipramine
- ssri
- choice of pharmacotherapy when there is no difference in efficacy (eg
PD)
.
.
.
.
.
- typical SE
. SSRIs/SNRI
Increased anxiety and agitation (jitteriness syndrome) at
the [beginning of treatment
. frequently leads to premature discontinuation
of treatment
Nausea, upset stomach and other GI disturbance, usually
at the beginning of treatment
Dizziness, headache, insomnia
Sexual dysfunction (most common and most troublesome, le
ads to discontination)
withdrawal/ Discontinuation symptoms
. TCAs
Sedation, anticholinergic effects, weight gain, sexual d
ysfunction
. Benzodliazepines
Dependence
- phobia of lifts
- no air -> wont be able to breath - lifts are dangerous
- i will screen -> they ll think i m crazy - lift are da
ngerous
Behaviour therapy
- based on exposure treatments
. Changing and eliminating behaviours (e.g., avoidance, compulsi
ons) which help maintain pathological anxiety bc Pathological anxiety will great
ly diminish or disappear vvith disappearance of these behaviours
. Most effective in those anxiety disorders that are characteris
ed by pathological behaviours (e.g., avoidance in phobias and certain compulsion
s in OCD)
- need to demonstrate to pt how this works
- eg fear of useing public transport -> avoidance -> decr phobic fear on
ly whilst avoidance is possible -> reinforces avoidance + maintains the phobic f
ear
. ie there are 2 loops, t/f importance of targeting avoidance
- gradual, self directed, in vivo
Which types of pschotherapy are good for which disorders
- PD = cognitive therapy + sx control (breathing retraining)
. Correcting misinterpretations of physical sensations and sympt
oms
. Modifying beliefs about body-based threat and the dangerous na
ture of anxiety
. Learning not to be afraid of anxiety/panic and its symptoms
- AG = exposure/behavioural therapy
. Exposure (hierarchy-based, gradual, self- directed, in vivo) t
o phdbic situations
- GAD = sx control (muscle relax) + cognitive therapy
. Imagery exposure to the content of worries
. Identifying specific beliefs about the benefit of worrying + c
hallenging these beliefs
. Improving coping with uncertainty
. Improving decision-making and problem- solving processes
- SAD = CBT
. exposure to social situation
Gradual
First therapist-assisted (with role-play), then self-dir
ected
First imaginal (often in-session), then in vivo
. social retraining if needed bc of deficit in social skills
. cognitive therapy
- modify assumptions, beliefs about self, others, social
situations
- modifying appraisals of social situations as threateni
ng and perception of social environment as hostile
- specific phobias = behavioural/exposure therapy
. usually therapist directed gradual + imagery guided
. flooding is rare
- OCD = behavioural therapy (exposure + response prevention), 2nd line =
cognitive therapies
. Exposure (to the obsession- and compulsion-related cues) and
. Response prevention (abstaining from performing the compulsio
n)
. cognitive
- targets beliefs by the pt that they are responsible fo
r having the obsession
- targets beleifs by the pt that having unacceptable/rep
- chronic
.
.
.
. buspirone
PTSD (Failure of other methods) - STRUCTURED TX is best
sequential approach
education + mx comorbidity
arousal reductio (breathing)
. structured treatments
- confront traumatic memory in controlled and safe envir
onment thru imaginal expsoure
- CBT = identify, challenge and modify distored thoughts
/interpretations
- in-vivo expsoure
- CBT + EMDR
. arousal reduction and exposure based
. long term and supportive
. aim to build up self and affect regulation needed in chronic c
omplex trauma
1. Acute and one-off trauma
The NHMRC-approved Australian guidelines for the treatment of adults with acute
stress disorder and posttraumatic stress disorder are currently rescinded but gu
idelines for the recovery from acute trauma are available at the websites of the
Australian Centre for Posttraumatic Mental Health (http://guidelines.acpmh.unim
elb.edu.au/__data/assets/pdf_file/0008/851489/ACPMH_Full_ASD_PTSD_Guidelines.pdf
)
2. Trauma-informed care for chronic complex trauma
(Adults Surviving Child Abuse) ASCA Practice Guidelines for Treatment of Complex
Trauma and Trauma Informed Care and Service Delivery
http://www.asca.org.au/About/WHATWEDO/ASCAsPracticeGuidelinesforTreatmentofCompl
e.aspx
READ: *Bomyea J, Risbrough V, Lang AJ. A consideration of select pre-trauma fa
ctors as key vulnerabilities in PTSD. A consideration of select pre-trauma facto
rs as key vulnerabilities in PTSD. Clinical Psychology Review 32 (2012): 630-64
1
Forneris CA. Gartlehner G. Brownley KA. Gaynes BN. Sonis J. Coker-Schwimmer E. J
onas DE. Greenblatt A. Wilkins TM. Woodell CL. Lohr KN. Interventions to prevent
post-traumatic stress disorder: a systematic review. Am J Prev Med 2013;44(6):6
35 650
Rothbaum BO, Kearns MC, Price M et al. (2012) Early intervention may prevent the
development of posttraumatic stress disorder: a randomized pilot civilian study
with modified prolonged exposure. Biological Psychiatry 72: 95763
Jonas DE, Cusack K, Forneris CA et al. (2013) Psychological and pharmacological
treatments for adults with posttraumatic stress disorder (PTSD). Rockville, MD,
USA: Agency for Healthcare Research and Quality. Comparative Effectiveness Revie
w: 92
*Watts BV, Schnurr PP, Mayo L et al. (2013) Meta-analysis of the efficacy of tre
atments for posttraumatic stress disorder. Journal of Clinical Psychiatry 74: e5
4150
Summary
- PTSD is reasonably common with a 12-month prevalence of 1.3%
Women are affected more commonly than men
The risk of PTSD is greater after some types of traumatic events
Premorbid factors increase the risk of PTSD
Psychological treatments are first-line; antidepressants may be used as
adjunctive treatment
Chronic complex trauma an important factor in mental health
Trauma an important factor in psychiatric and related stress system diso
rders
---------------------------------PAAM - Trauma and its effects on development
__________________________________
General effect of trauma is to create a state of disconnection
1. Trauma has primary effects not only on the psychological structure of
self, but also on the systems of attachment and meaning that link individuals a
nd community.
2. Trauma destroys the person s fundamental assumptions about safety in
the home and in the outside world.
3. Trauma calls into question basic human relationships it breaches atta
chment it undermines the belief system trust - that gives meaning to human exper
iences.
types of trauma
1. emotional neglect/abuse
2. physical abuse
3. sexual abuse
4. combination
Effects of trauma
- disrupts sense of self
- in development
- if already formed
- interrupts stream of consciousness => causes fragmentation of time - t
hey live in the present as if the trauma has just occurred
- overthrows self reflectivity (which normally develops by age 5yr) - ca
nnot reflect on the effect they have on selves and on others
- alienates from other
- introduces feelings of self loathing, shame
Sense of self
- develops early
- affects other relationships and attachment
attachment
- intimate attachments to other humans are the hub around which a person
s life revolves, throughout life
- secure attachment is protective against fragmentation, maintainng equi
librium and continuity of self (stream of consciousness).
pathological attachment
- if there are no attachments to carfe-giver in early months of life - p
roper nurture impeded
- later in infancy - early childhoodthis trauma is often in the form of
devaluation of a repeated nature
Disorganised attachment
- traumatic in itself
- common in severe borderline states
- attachment to a fragile, depressed caregiver who rapidly shift from an
gry to hostile and back again
- causes rapid shifts in representation of self and other
- bc infants representation is fragmented and dissociated and they still
don t have a theory of mind (capacity of self-reflection which doesn t develop
until 5 yr) - they cannot attirbute what frightens them.
Effects of trauma at different leels
- somatic (straddle physical and psych)
somatisation
psychogenic non-epileptic seizures
chronic abdominal pain
chronic migraines
hyperchondriasis
- emotional
personality problems (they develop in early adolescent)
- cognitive
. shake hand
. close to door, not obstructed
- engagement
. explain role
. simple lang
. empathise
. let them rant, lesten to why angry , thoughts of violenc
. don t interrupt
. open questions
. explain actions, delays
. offer blanket, food, drink
. USE MEDICAL PROBLEMS AS A WAY IN (pain, sleep problems, rash,
flu sx)
.
.
.
.
- pmhx
. comorbidities
. rule out ;hysiological causes
. contraindications of sedation
. mental health act
- document
Rx sedation
- 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
Rapid sedation
- ORAL
. dizepam
. olanzapine
. haloperiodol + bentropine
- IM
.
.
.
.
larozepam
midazolam
haloperidol
olazapine
- IV
. GA
. benzo
. antipscyh
Suicidality - key assessment/management
- physical assessment
- engagement w pt to get real picture of whats going on
- immediate risk to selves
- mental state
- post assessment planning egspecialist review, D/C planning, admission
indication
Initial assessment
- do thoroughly to avoid need to repeat
demographics
pmhx
fhx
mental illness
physical illness
mental state
intox
mood
psychosis
hopelessnes
acutive suicidal thought
insight
access to harm
supports
no change to circs that created trigger/stressor
Approach to suicide
- General opener ( your doing it tough at the moment huh?", life not wor
th living, better off dead, dark thoughts)
- Duration, intensity, frequency, distress
- Thoughts of how would harm self/kill self
- Speci c plans, access Preparations (wills, belongings, notes)
- What stopping, consequences
- previous suicide attempt
. how help was found or was it sought
. what did you think was going to happen ? eg vomit, never wake
up
. how do you feel now (shame, regret, anger, disappointment)
. potential for change
ILLICIT SUBSTANCE EMERGENCIES
- epi of deaths
. 72% tobacco
. 25% alcohol
. 3% illicit drugs
- methamphetamine adverse effects at high dose
. htn
. arrhythmias
. MI
. aortic dissection
. hemorrhagic/non hemorrhagic stroke
- amphetamine effects
. euphoria, alertness, energy, confidence, stamina
. sleeplessness, reduced appetite, dry mouth
. sucidial, headache, teeth grinding, anxiety
. psychosis, incoherence, incr T, dehydration, thought disorder,
. affective disorder
. resistant depression
- sx toxicity
. Impaired consciousness
. Dysarthria
. Ataxia
. Course tremor
. Muscle twitches
. vomiting
. Increased tone, re exes Myocionus
. Seizures
. Arrhythmias, prolonged QTc C
- RF = lithium + the following
. Li level > 2
. hypovolaemic (low intake, vomiting, diarhoea, sweating, diuret
ics)
Neuroleptic malignant syndrome
- mortality in 20% of cases
- incidence ~3%
- assoc with ligactole and haloperiodol
- sx
- usually develop in 1st 2 wk of neuroleptic (antipsychotic) the
rapy
- but can occur after 1 dose
- RF
. switch to higher dose
. rapid dose escalation
. switching antipsychotics
. parenteral admin
. extreme agitation
. acute catatonia
. dehydration, lithium, depot, acute men
- TETRAD of sx = rigidity, mental state change, hyperthermia, autonomic
instability
1. muscle rigidity
. lead pipe rigidity
. superimposed tremor + cogwheel rigidity
. opisthotonus
. trismus
. chorea
. sialorrhea
. dysarthria
. dysphagia
2. mental state change
. 1st sx in majority of pt
. usually agitation, delerium + confusion
. other = catatonia, mutism
. if severe can progress to encephalopathy and coma
3. hyperthermia
. > 38C
4. autonomic instability
. tachycardia
. htn
. tachypnoea
. dysthymia
. diaphoresis
- Dx
. CK > 1000 (can be up to 100,000) - degree of elevation related
to severity
.
.
.
.
.
.
- Mx
. stop agent
. supportive
- fluid replacement
- euc replacement
- cardiac support
- DIC consider
. control agitation - benzos
- Prognosis
. resolve by 2 wk
. mortality when comorbid D+A, renal impairment,, organic brain
disease
Serotonin syndrome
- RF
. antidepressants
., antimigrain meds
. stimulants
. opiates
. psychedelics
. combination of SSRI + cheese/wine
- TRIAD = cognitive, autonomic, somatic
. cognitive effects
- headache
- agitation
- hypomania
- mental confusion
- hallucination
- coma
. autonomic
- shivering
- sweating
- hyperthermia
- htn
- tachycardia
- nausea
- diarrhoea
. somatic
- myoclonus (mm twitch)
- hyper-reflexia (+clonus)
- tremor
Clozapine
- indcations = schizophrenia
- death due to
. neutropenia (monthly blood levels)
. cardiac - myocarditis, arrhythmias
. respiratory depression
Acute dystonia (movement disorders)
- DA blockers (ie anti-psychotics IV/IM)
. esp 1st gen antipsychotic
- face, neck, trunk\
- prothombotic, inflammatory
- stress releiving strategies
- dysregulated social behaviour
Therapeutic goals
- aim for secure attachment state of mind
- robust sense of self with reflective capacity
- interpersonal sills and organisation
- autonomy
- flexible and spontaeenous
- symptoms reduction, relief from disorders and promotion of resilience
- interpersonal connectidness
READ
Hesse E. (2008).The Adult Attachment Interview: Protocol, Method of Analysis and
Empirical Studies. Handbook of Attachment: Theory, Research and Clinical Applicat
ions, 2" ed, edited by Jude Cassidy and Phillip Shaver, 552-598. New York: The Gu
ildford Press, 2008.
---------------------------------PAAM - Personality Disorders
__________________________________
personality types
personality disorder
categorical vs dimensonal diagnosis
axis 2 vs 1
borderline personality disorder (most common)
separate from axis 1 disorder bc they are patterns of behaviour rather then a on
e off ilnnes
personality disorder . pattern of pervasive and inflexible behaviour and thought that deviate
s from culture acceptance
. early onset - adolescence, early adulthood
. stable over time
. causes distress and impairment
Essential features - DMS 5
- impairments in personality (self and interpersonal) functioning and
- presence of pathological personality traits.
- for Dx the following criteria must be met:
. Impairments in self and interpersonal functioning
. One or more pathological personality trait domains
. Stable across time and situations (ie workplace and home)
. Not normative to the individual s developmental stage or cultur
al environments
. Not due to a substance or general medical condition
- need long term functioning
- take into account ethnic, cultural social background
Personlity - total pattern of feeligs, thoughts, behavuiours, reactions, interac
tions
3 clusters of personality disorders
. odd eccentric
. emotional, dramatic
. anxious
CLuster A = "odd and eccentric" = paranoid, schizoid, schizotypical
cluster B = "dramatic" = antisocial, histrionic, narcissistic, borderline
Cluster C = "anxious" = avoidant, dependent, obs essional
personality
excessive sensitivity to negative evaluatin
feelings of inadequacy
social inhibition
avoid decisions, doing things
Dependant
-
(Monk detective)
- axis 1 disorder (different to obsessional personality)
- obsessions
- compulsions
Axis 1 vs 2
axis 1
- state based or episodic
- feel wrong for the person = ego dystonic
axis 2
- trait based or present enduringly
- feel right for the person = ego syntonic
Narcissistic personality (paris hilton)
- grandiosity
exhibitionistic
lacking empathy
will want to see the top doctor, won;t want to see a GP
consider themselves to be better then everyone else
needing approval
superficial relationships
constitutional defects
genetic
environemntal (negative environemnt of development
organic brain dg
cerebral infection
prenatal and birth trauma
psych factors - culture, family in which they grew
social processes
psychoanalytic factors - defence mechanisms
cognitive, perceptual orgs
affective instability
degree of impulsivity, aggression
neurobiology
- Individual differences in the regulation and organization of cognitive
processes. affective reactivity, impulse/action patterns, and anxiety may in th
e extreme provide susceptibilities to personality disorders such as borderline a
nd schizotypal personality disorder.
- A low threshold for impulsive aggression, as observed in borderline an
d antisocial personality disorders, may be related to excessive amygdala reactiv
ity, reduced prefrontal inhibition, and diminished serotonergic facilitation of
prefrontal controls.
- Affective instability may be mediated by excessive Iimbic reactivity i
n gabaminergic/glutaminergiclcholinergic circuits. resulting in an increased sen
sitivity or reactivity to environmental emotional stimuli as in borderline perso
nality disorder and other cluster B personality disorders.
- Disturbances in cognitive organization and information processing may
contribute to the detachment, desynchrony with the environment, and cognitive/pe
rceptual distortions of cluster A or schizophrenia spectrum personality disorder
s.
- A low threshold for anxiety may contribute to the avoidant, dependent,
and compulsive behaviours observed in cluster C personality disorders.
temperament and geentics vs downsyndrome (very happy people)
Dx
- poor agreement DSM 4
- lack of clear boundaries
- comorbidity
epi
- 15% community prevalence
- M>F
- more women with borderline
- more men with antisocial
- decrease prevalence with age as people develop r/ships and learn how t
o interact with world
- more in urban community (more isolated)
- 20-70% prison (antesocial and borderline)
ddx
- Axis one disorder
Psychotic disorders
Mood disorder
Anxiety disorder
Post-traumatic stress disorder
Substance related disorder
Personality changed due to general medical condition
Personality traits
Mx
- 1st line = drugs (not for personality itself but for con-comittant axi
s 1 disorder eg hi rates of depression tf tx depression)
- psychotheraopy is main stay
- in patient discouraged esp borderline, bc they become dependent on inp
atient involveemtn
- self hlep, psychosurgery, (not in western places),
- day care
- comorbidity
Prognosis
-
Prenatal
- genetic, tri21**
- exogenoous
. infections
. toxins / medicaitons/ drugs/ alcohol
. maternal hypothyroidism
. placental insufficiency
Perinatal
- infections
- birth complications
- newborn issues
. hypoglycemia, hyperbilirubinemia
Postnatal
-
infections
trauma
malnutrition
toxins
vs ID
3% prevalence
unknown r.ship to level of ID
esp catatonic
Anxiety disorder vs ID
- more common in ID
- compulsive behaviours more common and worse in severe ID
Autistic spectrum disorder
- triad of impairment
. Impairments in social development
Problems in developing reciprocal relationships,
- impaired empathy,
- unusual eye to eye contact and facial expression
. Impairments in language and communication
- 50% no useful speech, delayed language development,
- repetition, echolalia,
- lack of reciprocal conversation,
- literal understanding,
- neologisms, pronoun reversal
. Impairments in thought and behaviour
- stereotyped and repetitive play,
- fascination with parts of objects/toys rather then who
le toy,
- preoccupation with topics,
- resistance to change,
- need for routine,
- stereotyped movements eg hand flapping
- comorbid ID and ASD = higher levels of emotional/behavioural disorder
. marker for poorer outcome
. higher levels of carer stress
- 80% autistic have an ID
- 10% mild ID have ASD
Personality disorder
- don t know what a normal personality is in a person with ID
Why are they an at risk population for mental health problems ?
- predisposing biological factor
- limited psychological coping mechanism
- incr exposure to risk factors for mental health problems
. stigma
. isolation
. unemployment
. povery
. abuse
ID at higher health risk
- lower life expectancy
- higher risk of health problems: obesity (poor health choices, group ho
ming,) malnutirtion, sensory (hearing, highlight), dental (esp non verbal popula
tion pain), epilepsy, dermatalogical, endocrine, htn, hpylori infection, constip
ation
- ageing carers
- additional health needs eg tri21 - alzheimers
How is assessment different for mental helath in ID group
- Diagnostic over-shadowing
. attribution of problem to ID rather then considering MH
. there is actually no behaviour consistent with ID
- Communication problems; - difficulty participating interview
- Cognitive capacity to understand symptoms
- Difficulty applying diagnostic criteria
. how do you do the DSM criterion tests on a non-verbal person
- Developmental level Eg self talk, imaginary friends are things that ar
e normal as a means of normal processing
- Unusual symptom profiles Restricted range of experiences
. psychoses sx may become childlike rather then sophisticated pa
ranoia states eg. someone is spitting in my tea, rather then I am being monitore
d by satellite
- Reliance on corroborative information
- Need to be holistic in diagnostic formulation and assessment
Overcoming these difficulties
- appropriately safe place, and enough time + need to talk to a lot of p
ep
- language appropriate to their developmental level and clearly + time t
o answer
- start with simple question - who have you brought with you today
- remember that it is easier to understand a language then express in it
- allow time for response
- use body language as well
- admit you don t understand
- let those who know the pt well help you
- establish rapport
- reassure
- identify times by locate time to an event eg birthday
- check comprehension
- don t suggest the answer you expect so to minimise acquiescence AND ch
eck answers later
If non verbal
- their receptive / understood language may still be ok
- other forms of communication
- is the interpreter ok
- make eye contact
- they may respond with eye movements etc
Psych hx in ID
- a history of change is important - when did the person change, how di
d they change, what is their baseline
- assessment has to be bio, psycho, social
- the only thing normal for a person with ID is the cognitive impairme
nt, there is no normal MH condition
Mental state exam in ID
- appearance and behaviour
. well dressed = level of care
. age appropriate dress
. dymorphology
. eye contact
. social appropriatenes
. stereotypic/self stimulating behaviours
. abn movement (neuroleptics)
. mobility/vision
. support peron
- mood
. difficult to explain it
- affect
. may be confused by their facial expression eg grimacing
. medication effects eg sedation
. check with someone who knows them well
- speech
. articulation problems are common
. check how long they have had the problem to check whether it i
s a medication issue
. assess receptive and expressive communication separately
- Thought
. Form
- perseveration is common
- illogicality is common
. content
- persecution ideation common
- delusions : consistency over time, out of keeping with
developmental level and normal fn
- suicidal/homicidal ideation - pt understandng of letha
lity
- perception
. voices vs thoughts
- don t suffest - get them to describe
- assoc sx
- content of their voices
- self talk is common
- insigh
. maximise ability to consent
- congition
. validitiy of mmse
- risks
. risks to self, repettive self injurious, compulsive self injur
ious,
. D+A
. misadventure/absconding
. from others - exploitation, abuse, neglect
- loss of accommodation of support, community access
Who can conset = GUARDIANSHIP ACT
- cannot give consent if cannot understand nature and effects of tx or c
annot communicate their consent
- treatment classes = urgent, non urgent, special
- Special treatment requires consent of Guardianship Tribunal; this is e
xperimental or highly unusual or aversive treatment
- Urgent treatment (ie needed to save someones life, prevent significant
harm to the person s health or distress) does not require consent
- People under the MHA do not need consent regardless of whether or not
they have a Guardian
- People who have capacity to do so have the right to refuse treatment
- IF pt CANNOT CONSENT and NOT UNDER MHA
. if they don t object (ie they give assent)
- non urgent tx = public guardian, responsible person, t
ribunal
- urgent = no consent req
. if they object (ie do not give assent)
- require tribunal or guardian with specific powers
Responsible person - hierarchy
1. guardian
. 10%
. any time
. sx
- Symptoms of major depression, Low mood fatigue worry
. course
- variable
. cause
- relapse of pre-exisiting or denovo due to psychosocial
(stress, sleep disturbance, interrelational disturbance)
- postnatal depression
. 15%
. post partum gradual onset over 6 mo
. types
- most common = non psychotic non-melancholic major depr
ession
. gradual onset 3 mo
. psycho social in origin
- less common = post partum melancholia
. within 4 wk
. clinical picture of melancholia
- early morning waking
- agitation
- psycho motor change
- loss of apetite
- diuranl mood variation
. biological form of depression
. related to decr estrogen after birth
. tx with antedepression or medication or ECT
. probably related to biopolar disorder and is a
RF for later biopolar
. sx = identical to depression as at other time of life cycle
- major depression, anxiety
. course
- gradual onset, possible chronicity
. causes
- mostly psychosocial (r./ship, support)
- dysfunctional personality
. RF for non-psychotic, nonn-melancholic major depression
- early life (genetics, trauma, their own parenting = ne
glect, abuse)
- sociodemographic (young < 16 yr, low SES, marital stat
us)
- social environment (dysfunctional intimate relationshi
p, poor instrumental and emtional support from partner, poor social support)
- internal environment (estrogen sensitivity, personalit
y style, previous depression or anxiety)
. Impact of postnatal depression on the infant
- lower IQ
- lower interpersonal skills
- cognitive and r/ship problems later
Types of social support required
- cultural 40 day rule
- knowledge support from other females
- practical, instrumental support - help with looking after baby and hou
sehold chores; inverse relatinship bw PND and partner baby care
- emotional support
SCREENING = Edinburgh postnatal depression scale EPDS
Tx of postnatal depression
- recognise it thru screening
- clarify risk factors and causation - take a history
- psychoeducation - explain to them about PND
- help them to prioritise eg
- necessary = feeding/bathing baby
- unnecessary = ironing
- they want to do = going to hair dresser, talking to friend
- non directive counseling
- CBT, IPT, antidepressant medications (cf breastfeeding)
- antidepressants
. indicated for
- moderate to severe depression
- comorbid panic disorder
- bipolar depression (+mood stabiliser)
- patient preference
. BUT little evdence wrt efficacy
. ? breastmilk effect
Implications of depression during pregnancy
- obstetric outcomes - preterm delivery, low birth weight, small for ges
tational age, gestational hypertension, placental function (steroid metabolism a
ffected in fetus ~CRF incr), developmental delays
Assessment of depression in pregnancy
- somatic sx: fatigue, appetite, wt change, sleep disturbance, change in
libido.
- cognition: poor concentration, worthless or guilt.
Risk vs benefits of antidepressants vs no antidepressants in pregnancy
- no antidepressants = doesn t help mum + fetal impact of depression (iq
, cognitive, social) vs no risk of antideprssant exposure
- antidepressants = helps mum BUT risk of infant exposure
Mx - depression in pregnancy
- New onset depression - Determine type and severity of depression >
- Mild-moderate depression
. Psychoeducation . Supportive counseling . CBT or other focused psychological treatment
. Moderate to severe depression
. SSR|s - Lower dose at 36-38 weeks - Liaise with GP / obstetric
team . TCAs for severe, melancholic depression
SSRIs vs pregnancy
- congenital heart defect RR = 2 (balance against background risk of def
ect = 2%)
- persistent pulmonary hypertension + getational htn/pre-eclampsia when
SSRIs after 20 wks gestation (1/1000)
- neonatal abstinence (= poor neonatal adaptation syndrome)(esp paroxeti
ne, venlafaxine)
. insomnia/somnolence
. agitated, jittery, shivering.
. poor feeding
on mother
low matrenal weight gain
preterm delivery
low birth weight
gestational htn
- benzo
. physical defect
. neonatal death
Categories of medicines in pregnancy
D, X - fetal dg/deformity - should not be used in pregnancy
Ebsteins anomaly and lithium
- b/g risk = 1/20,000
- w lithium = 1/1000 (RR = 20)
- anomaly
. atrial septal defect
. displaced tricuspid valve allowing blood back into RA
Lithium carbonate - prophylaxis
- avoid in 1st tri
- restart in last 2nd
- reduce dose to 1/3 in late 3rd
. serum 0.2-0.6 mmol/L
- full therapeutic dose 1 d post partum
- no breastfeeding
Drugs with incr risk of neural tube defects
- carbamazepine, valproate
Drugs with incr risk of epsteins anomaly
- lithium
Drugs with incr risk of cleft palate
- lamotrigine
Valproate fetal/infant effects
- neural tube defects (spina bifida)
- lower IQ in fetus
- should not be used in pregnancy women
Metabolic
idone)
-
Incr r
---------------------------------PAAM - Internalising Disorders in Childhood and Adolescence
__________________________________
Anxiety disorders in children and adolescents
- F > M
- overall risk = 20% by time of 18 yr
- hi rates of comorbidity
- anxiety can be causal, or associated with, or resulted from other cond
itions eg substance use disorder
Anxiety disorders
- characterised by feelings of anxiety and fear, out of keeping with act
ual threat; worry about future events; phsyical sx of racing heart and shakiness
- subtypes
. Generalised anxiety disorder GAD
. social anxiety disorder SAD
. specific phobias (eg spiders)
. separation anxiety (esp in children)
. panic disorder
. agoraphobia
.
- PTSD is
- ETI
.
.
.
.
s
. social adversity/financial impacting on parents capacityto hel
p with child fears and worries
Assessment
- i/v child, as well as family
- devl + pediatric hx
Tx
- guided by formulation + comorbidities
- tx underlying medical disorders (refer to pediatrician, GP)
- address family dynamics, school concerns
- psycholigcal therapies
. CBT
. behavioural approach
. graded appr for specific phobias
. family therapies
- pharmacological
. as part of the holistic approach
. SSRIs at low dose (fluoxetine, fluvoxamine, sertraline)
. OCD (SSRI)
. some anti-d may WORSEN anxiety eg venlafaxine, other worsening
meds eg steroids, ventolin
. short term anxiolytics NOT RECOMMENDED eg BZPs
. quietiapine as adjunct
. Olanzapine and Risperidone NOT RECOMMENDED due to poor effect
and SE
Depression in adolescents + children
- epi
. 10% by yr 18
. F > M
- different presentation to adult depresion
. DSM-5: depressed or sad or irritable
. depending on age
- primary school - less verbal in expressing sx of low m
ood; mostly a behvaioural assessment
- adolescent - less common to have sustained or consiste
nt low mood; more common to have alternating with mood changes
- Sx
. low mood
. irritable, aggreession,
. insomnia, low appetite, lethargy
. anhedonia, social withdrawal
. reduced motivation
. poor concentration, memory issues
. deliberate self harm
- suicide in children and adolescent
. 25% of all deaths 15-19 yr
. unlike adult suicides, F>M
- assessment
. wholistic approach
. i/v with child - cntributing factors
ou appraise the tx plan if the condition did not improve, or began to worsen?
- first thing to do is go back to re-assess situation, looking for addit
ional things you should be doing, more thorough assessment of familya nd child,
re-interview child/family, reconsider formulation - for factors/triggers identif
ied - the idea taht you have developed; determine how shared the formulation is
with the child or family
- vs tx - reconsider domains - therapy, family, school, medication based
- most likely CBT, how the rapport is with the therapist (typical proble
m in teenagers t/f change clinician)
- family work - what factors not addressed - family therapy
- meds - try a second antidepressant or change class
- biological ix eg cytochrome metabolism
beyong blue webiste
blackdog website
reachout.org
---------------------------------PAAM - Externalising Disorders in Childhood and Adolescence
__________________________________
Common externalising disorders
- Attention de cit hyperactivity disorder (ADHD) - 5% of childrehn
- Oppositional de ant disorder (ODD) - 4%
- Conduct disorder (CD) - 4%
- more common is males then female
Do they grow out of it?
- not always
- many adults manifest ODD
- CD morphs into antisocial personality disorder
ADHD
- main features
. Inattention
. Problems regulating activity
. Impulsive behaviour
- sx are clinically significant IF
. Age inappropriate
. Maladaptive
. Commence before age 12 years
. Lead to signi cant impairment in two or more settings
- subtype
. combined
. predominant inattentive
. predominant hyperactive/impulsive
- WHY DO THESE CHILDREN PRESENT TO CLINIC ie - common problems associate
d with ADHD in children and why they present
. Non-compliant behaviour
. Sleep disturbance
. Aggression
. Temper tantrums
. Literacy and other learning problems
. Motor tics
. Mood swings
. Unpopularily with peers
. Clunulsincss
. Immature language
- Typical comorbid disorders
. ODD (MAJOR ONE)
. CD
ODD
-
pattern
agry/irritable mood
argumentative/defiant behavior, or
vindictiveness
lasting at lease 6 mo and not just directed to siblings
sx
. Lose temper. touchy. angrylresenlful
. Argue with adults
. Non-compliant
. Annoy others
. Blame others for their misdemeanours
. Spitefull / vindictive
- pattern varies w age
. < 5 yr = every day
. > 5 yr = at least once per week
- ETI
. genetic - MOA transporter gene (deficiency in MOA transporter)
. perinatal
. toxins - lead through cognitive impairment causing the problem
later
. psychosocial
- parenting sytle / maltreatment
- social adversity
- modelled behavoir
. best evidence pointing to combination of MOA transporter gene
mutation + maltreatment being required to produce the disorder, neither one alon
e sufficient.
. amygdala damage - (callous unemotional traits)
What is the difference bw these and normal child behaviours
- they cause significant impairment in function
- repeititve, reoccurent
- causes problmes at home or school
Conduct disorder = more malignant probelm
- persistent pattern of behaviour in which rights or other or age approp
riate sociatetal norms are violated
- onset in childhood or adolescent
- typically precededed by ODD
- Sx
. aggressive to peopoe and animals
. destruction of property
. deceitful
. theft
. abscond
- subtype
. childhood onset
. adolescent onset
- ETI - same as for ODD
ADHD Eti
-
deficit of ATTENTION
FLUCTUATING level of arousal and severity
REVERSAL of sleep wake cycle (awake in night, asleep during day)
HALLUCINATION, DELUSIONS (paranoid esp)
onset = hours/days
labile affect
Attention
- 4 components
ppressing
Epi
-
1% people
25% acute hospital admission
50% post operative elderly
90% ICU elderly pt
- nature of psychotic sx
How do I tell if someone has a comorbid psychotic illness
- SUDDEN deviation from baseline
- fluctuating arousal
- psychosis has deficit in frontal lobe and executive fn
- delerium has deficit in attention
Why is delerium such a big deal
- incr length of stay and institutionalisation
- twice as high costs of care
- reduced subsequent functional status (not easily reversible; change is
sudden vs dementia which has protracted decline)
- 62 % chance of dying in next year
Tx derlium
0. 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
1. treat medical causs
2. non pharm = best tx and prevention
- reduce environmental stimulation (single room, low light, redu
ce staff changes)
- tx pain
- reorientate - repeat what day and why in hospital
- avoid restraints
- frequent turning to avoid bed sores, active physio for mobilis
int, DVT prophylaxis
- Chart sleep, behaviour, food, fluid
3. NEVER use benzodiazepines
- only for etoh r benzo withdrawal
4. AVOID antipsychotics
- until behavoural disturbance impacting on treatment or recover
y
5. Haloperidol
- most often used bc many admin routes
6. Quetiapine
- BEST bc can titrate dose (low potency)
- less extrapyramidal SE, so better for those with Parkinsons
- other = olanzapine, risperidone
Nb - med
Prevention
- avoid polypharmacy
- hydration, nutrition
- pain relief
- correct sensory def
- early mobilisation
. IHN
. arrhthmyias
. mitral valve prolapse
. myocarditis
respiratory
. chronic airflow limitation
. Pulm embolism
neuro
. tia
. essential tremor
. myasthenia gravis
endocrine
.phaeo
. thyrotoxicosis
. decr BSL
. adreno-cortical insuff
intoxications
. caffein, amphetamines, sympathomimetics
etoh, benzo, barbituate withdrawal
secrecy
hasty trips to bathroom
chewing gum
laxative packets
diet coke
vegetariansim
avoidance of meals
academic success then problems
mood swings
tantrums
blocked drains
hoarding
Complications
- Sudden death, hypoK, hypothermia, dehydration, hypoglycemia, hypothyro
idism (do not treat with thyroxine)
- Cardiac failure, arrhythmias (altered HRV)
- Pancytopenia (bone marrow suppression - reversible - infection can be
missed bc of overlying hypothermia)
- Brain/cognitive changes, peripheral neuropathy (eg foot drop)
- Immune suppression, major infection
- Osteoporosis and infertility
- Dental decay (bulimia, parotid swelling), sialadenosis
- Upper GIT, constipation (low intake), rectal prolapse
- Renal failure, secondary diabetes insipidus, hyperaldosteronism
- Skin, hair, eyes. ENT, body odour (laxatives, ketotic breath), oedema
Psychatric complications
- psychosis
- depression
anxiety ocd
autistic spectrum
personality derailment
substance abuse
dsh somatisation suicide
duty of care
compulsory treatment
things to note
rapiditiy of weight loss
duration of semi-starvation
extent of starvation
highest weight they were, Lowest weight they were
onset
purging behaviuor
fluid intake incl caffein and alcohol
chewing and then spitting rather then swallowing
syndrome
Can be lethal
CCF, chest pain, MVP, QTC > 470ms
Delirium ?Wernickes encephalopathy
Beri beri (wet and dry) ie B1 de ciency
Peripheral oedema (insulin, sodium, protein)
Putative cause = hypophosphatemia
Adaptation to uid depletion and low intake
HRV (heart rate variability), arrhythmias
wt restoration
therapeutic age appropriate millieu
PT and psychotherapy
social integraiton
dischrage planning
future tx
Medications FLX OLZ quetiapine topirimate
Heating Jackets
Mandometer W
Opioid antagonists
Endocannabinoids
Oxytocin
EBM tx
- CBT
- family based counselling
---------------------------------PAAM - Psychiatry of Old Age
__________________________________
Epi
- > 65 yr: 2012-61 - 14%->24% (11 mil)
- > 85 yr: 2007-61 - 2-6% (3 mil)
- median age: 2012-61 - 38-46 yr
- # people working age: 2002-42 - 5->2.5
Prevalence of mental disorders in old age
- organic
. dementia 10%
. delerium 2%
- major depression 2.5%
- mania 0.5%
- schizo 2%
- anxiety 4%
- alcoholism 3%
- personality disorders
Higher rates of mental disorder in residential care or hospital: dementia, depre
ssion, delirium
Elderly people have lower prevalence of mental disorders
Location of assessmnet
- home, residence, outpt, inpt
- carers will be present
- home: look at medications, compliance issues
Outpt
- functional illness, memory clinics
Risk assessment
- wandering, judgement, gas/taps off, driving, neglect, abuse?, suicidal
- murder, aggression, disinhibited, poor driving, gas
Cognitive fn on 1st interview
- screening tests: MMSE or RUDAD, clock drawing test
- MMSE
. impacted by age, educational, lanuage
. doesn t test frontal lobe/executive fn
. change meds
. compliance
- use dosette box
- supervision if cognitively impaired
- allergies
Functional assessment
- ADLs - how much assistance, hygiene, continence, dressing, eating
- necessities - finance, home appliances, drive, organise medicines
Environmentla assessment
- house - safety ?
- neighborhood
- financial
- services/transport
- home support
Social
-
spouse/support/family/neighbors
carer stress
formal services
culture
Elder abuse
- repeated acts against or failure to act for older person causing distr
ess, dg
- 4 % older people
Pharm
- drug interactions
- SE
. tardive dyskinesia with anti-psychotics (irreversible mvoement
disorder)
. deliriium with anticholinergics
. postural hypotension
. icnr risk of cerebrovascular accident in those prescribed anti
psychotic medications
- start low and go slow
Pharmacokinetics
- absorption
. decr oral absorption
- distribution
. incr in fat mass
. plasma binding
- metabolism
. induction or inhibition of CYP450
- excretion
. renal impairment - lithium, aim for lower serum lithium levels
Psychological treatments
- indications
. 1st line tx for disorder
. their preference
. to help distressed care giver
. releive psychological problems assoc with ageing
Mwhat causes behaviour problems in people with dementia
- deliirum
substance abuse
executive impairment/frontal lobes
psychotic disorders
depression
hypomania
personality disorder
Dementia
- progressive neuro degeneration
. cognitive, psych, behavioural, personality factors
- depression common
Cognitive impairment in dementia
- affects higher cortical fn eg emmory, planning
Psych sx in dementia
- depression (commonest and earlist)
- anxiety, paranoia, hallucinations, delusions, disinhibitio, theft, apa
thy
BPSD Behavioural and psychological symptoms of dementia
- sx of disturbed perception, thought content, mood or behaviour frequen
tly occuring in pt with dementia
- 3 sx clusters: agitation, psychosis, mood disturbance
BPSD - agitation
- wandering
- purposeless activity (hoarding, rummaging thru possessions, restlessne
ss, pacing)
- verbal aggression or persistent screaming
- physical aggression (scratching, biting, pushing, spitting)
- sexual disinhibition
BPSD - psychosis
- delusions (persecutory, spousal infidelity, abandoned by family, posse
ssion being stolen, intruders, decesased relatives still alive)
- hallucinations (usually visual, people on TV are real, reflection in m
irror not real)
BPSD - mood disturbance
- apathy (loss of initiative and motivation - change to frontal lobe/exe
cutive fn)
- depression
- fear and anxiety of upcoming events - esp with change in routine
- mood lability
Epi of BPSD
- alzheimer, vascualr dementia, FTD: up to 85% show BPSD
- higher in dementia with lewy bodies
- ~50% pt in residential care have BPSD
BPSD - natural history
- sx usually persist but may fluctate
- worse at evening (sundowning), meal times, dressing, undressing, toile
ting, when things are being done to the person
- depression and hallucinations may resolve
- agigation more likely to persist
Triggers of BPSD
1. Biological
sx in elderly
delusion
female predominance
social isolation
sensory impairment
many comorbid with dementia
hallucinations
dementia
delirium (meds, infection, withdrawal, exacerbation of illness)
depression
drugs - meds, abuse (etoh, benzos)
primary pscyhotic disorder: depresson, bipolar, delusion, schizophreni
a
- primary medical disorder: myxedema, hyperPTH, CVA, metabolic
Delirium
-
delusions
delusions of people, animals, objects or radiation
things that can pass thru impermeable barrier
up to 70% in late schizoprehnia
. encourage them to talk to mental health team and not their nei
ghbours
- re housing doesn t work
- antipsychotics DO WORK esp as DEPOT in low dose, to ensure compliance
Late life
ic)
-
depression
melancholic depression common
psychotic features more likely esp delusios (hypochondriacal, nihilist
assoc with cerebrovascular disease
>
>
>
>
>
Psychosocial stressors
> Interpersonal disputes
> Losses
> Role changes
> Disruption or lack of support
ssessment of suicidality
> Previous self-harm or suicide attempts
> Losses and lack of social resources
> Role of alcohol or other disinhibiting factors
> Mental state features - hopelessness, distress in response to psychosi
s, command hallucinations
ssessment of Dangerousness
> Pre-existing vulnerabilities e.g. perinatal period (FAS), personality
variables
> Mental illness
> Drugs or alcohol
> Current symptoms/state of mind e.g. paranoid psychosis
involvin
g a specific individual or group
> Long-term social factors and stressors
> Current social situation and triggers
Summarise and check as you go
MENTAL STATE EXAMINATION - distinct part of psychiatric assessment - objective a
ssessment
(reflect pt mental status at tiem of interview, not in the past)
includes verbala nd non verbal communication
- Appearance
> Contextual
> Level of self care
> Appropriateness of attire
> Evidence of physical injury
> Tattoos, body art, piercing
> Stigmata of physical disease
- Behaviour
> Quality of rapport and examiners countertransference
> Movements
> Interpersonal behaviours
- Hostile or menacing
- Avoidant or tentative
- Charming
- Coy or seductive
- Overfamiliar
- Expansive
- Abnormal movements
- Neurological signs
- Medication induced e.g. akathisia
- Mannerisms
- Stereotypies
- Compulsions
- Catatonic phenomena
- Psychomotor change: agitation, retardation or acceleration
about suicide
- fatuous
- perplexed, confused
- suspicious, guarded
- THought
-
form
capacity to process info
normal = logical, sequential
blocked
poverty of speech
derailment
flight of ideas
circumstantiality
tangentiality
Content
. ideas/concepts in their mind
. bizaree, delusional
. poverty of thought content
. in context of depression, cognitive disorders
- Delusions
- unshakeable beliefs, incosistent with persons cultureal and so
cial background
- metabolic syndrome
- dietician education
- help meal planning and budgeting
- rehab for exercise
- statins, metformin
- avoid changing to different antipsychotic due to risk of relapse ie ol
anzapine is effective for him
CASE 2.4 - 34M, married, sad, teary, trouble sleeping, feeling exhausted. Lost a
petitie, cared for by wife. Feels worthless and guilty. Considering suicide
- major depression
- melancholic features = guilt, psychomtor retardation, diurnal mood var
iation
- start antidepressant
. SNRI (dual acting on more then one neurotransmitter)
- malncholic features are assoc with greater likelihood of response to a
ntidepressant
- investigate his suicidal ideation
CASE 2.5 - 83M - sad, teary, other same as 2.4
- older = consider other medical conditions and risk of medications and
doses
- risk of hyponatremia for antidepressants and elderly - monitor electro
lytes
- SNRI still appropriate
CASE 2.6 - Josiah is an 83 year old married man whose wife says that he has been
terribly sad and teary over the last couple of months. He is often awake in th
e early hours of the night. He has stopped doing things he used to enjoy, like w
alking the dog and seeing friends. He doesnt want to get up in the morning. He ea
ts a little when his wife pushes him to, but isnt eating as much as usual and has
lost 8 kg over the past 3 months. Several times his wife has returned from outi
ngs to find him sitting in the dark exactly where she left him he gets agitated
about having lights on or using the air conditioner, saying that they have no mo
ney (this is not true) and he doesnt deserve to be comfortable. He has recently b
een saying that his wife would be better off if he wasnt alive.
- melancholic features (psychomotor retardation, inanition, complete anh
edonia, diurnal mood variation (worse in mronig)
- psychotic features - beleif they have no money, underlying delusions o
f guilt
- these delusions are mood congruent ie gloomy, negative and in keeping
with depressed mood and outlook
- he need admission to mental helalth unit
- ECT or pharmacotherapy
- ECT for distressed, depressed pt in whom pharmacotherapy is ineffectiv
e or pt who are at imminent risk of serious harm eg not eating or drinking
- in this case, not yet so severe, so SNRI + antipsychotic
CASE 2.7 - Jed is a 16 year old high school student brought in by his mother who
says that he has been very irritable and withdrawn over the last couple of mont
hs. He says hes been having trouble sleeping, and feeling exhausted during the d
ay. He says that hes lost interest in seeing friends, and even just getting up i
n the morning is an effort. His grades have dropped because he cant concentrate o
n his schoolwork. He says hes lost his appetite and lost some weight also. Hes f
eeling worthless and guilty about the effect it is having on his family. He has
been wondering whether things would be better if he wasnt alive, though he hasnt
had any specific thoughts about killing himself.
- major depression
- exclude - home (parents fighting etc), school (bullying)
- psychotherapy should be first line
c
---------------------------------PAAM - Behaviour management
__________________________________
---------------------------------PAAM - Interviewing the difficult adolescent
__________________________________
---------------------------------PAAM - Family interviewing
__________________________________
---------------------------------PAAM - Cardio-metabolic health and general adverse effects
__________________________________
---------------------------------PAAM - Personality webinar