Mental health - complete from notes/lectures Flashcards
Common conditions
What are the learning objectives of MH term?
- do a comprehensive pyschiatric asssessment including a case formulation
- understand basic psychopharmocology (e.g Lithium- indications, effects, side effects)
- understand basic pyshcological interventions
- Develop rapport
- Recognise pyschiatric disorders in these settings
- Risk assessment and risk management
What are important screening questions needed to cover for every patient in MH - when taking history (MSE etc)
Outline a complete psychiatric history?
what is an acronym to remember this?
1) ENGAGING THE PATIENT
A person sharing their life story, frequently involving trauma, to a person they have never met, who requires a lot of detail in a restricted amount of time, is a privilege.
• Be mindful of:
o Consent
o Confidentiality
▪ Not discussing details outside of health staff involved in the persons care
• Environment
o Privacy – bedside curtains are not sound proof
o Safe
o Comfortable
• Language – there is a lot of inherent judgement in choice of language (mad, crazy, dangerous). Be respectful.
INTRODUCTION
• Introduce yourself, your role, and the purpose of the assessment
• Discuss confidentiality
• To explore the presentation further, begin with an open question to invite the patient to tell you, in their own words, what has happened for them to be here today
• Use this time to observe the patient – this will make up a large part of the MSE
DEMOGRAPHICS
• Name, age, sex, ethnicity
• Mental health act status and method of arrival to facility
• Established dx
• Current rx
• Admission length
• Living situation/arrangements
• Relationship status/children——-> o Must be aware of dependent children
• Education level, Employment status/income or benefit if unemployed
PRESENTING COMPLAINT:
- → Brief summary of how and why the patient has presented for review at this point in time
- It is useful to have a brief look at the chart or referral to gather this information prior to seeing the patient
- Eg: Mr R was brought into hospital by QAS on and Emergency Examination Order following a concerned phone call from Mr R’s ex-wife that Mr R was suicidal
- Chief complaint in own words
- Reason for seeking help
- Current symptoms: does the patient appear manic, depressed, physical health, psychotic, anxious, substance user
- Timeframe
- Premorbid baseline
- Precipitants: 7D’s - death, drugs, didn’t take meds, debt, divorce, disease and developmental
HISTORY OF PRESENTING COMPLAINT
• This is the patient’s story of what they are experiencing and what has led to this presentation.
o Need to get a lot more of the details of what has happened
• This is also where we need to ask very specific questions about symptoms of mental illness.
WHAT DO WE NEED TO ESTABLISH HERE?
• Establish presence and absence of symptoms
• Establish a time frame
• Establish the severity of the symptoms
o ‘How does it affect your life?’
• Establish precipitating factors
• Establish perpetuating factors Eg: financial hardship, chronic pain
o What made it worse/better
• Establish the effect on the person Eg: suicidal thoughts, poor self-care, difficulty studying or attending work
• Establish supports/protective factors
PSYCHIATRIC HISTORY
• Diagnosis: timing, length, reasons
• Hospitalisation
• Prior admissions/contact with mental health
• Prior symptoms when unwell
• Treatment
• Medication history and compliance, side effects and source
• Prior psychological treatments (other than medication)
• Past suicide attempts/deliberate self-harm
• Need to consider
o What has this individual experienced in the past?
o Is there a pattern?
o What has been tried in the past?
o What has, and has not, worked?
DEVELOPMENTAL HISTORY:
• → A developmental history gives us clues as to risk factors for developing mental illness, any evidence of a prodromal state, and personality factors.
• Birth-
o History of maternal health (including illnesses such as influenza)/substance use during pregnancy
o Birth complications (?hypoxic damage)
• Childhood-
o Milestones-
o Childhood illnesses
o Relationship with siblings
o History of trauma
• Education-
o Academic performance ?to what year ?any deterioration
o Bullying
o Hx of suspension/expulsion ?why
o Post school aspirations
• Employment history-
o If many jobs, why have they changed? Fired?
o Training/qualifications
• Relationship history
o Quality of relationships? Able to form longer attachments?
o Friendship groups ?still in contact
MEDICAL HISTORY:
• Allergies
• Prescription medications
• Any associated legal, financial, social, health problems
• Personal history of:
o Thyroid disease
o Head injuries
o Seizure disorders
o Chronic pain/chronic illness
o Cardiac history
▪ Some conditions have cardiac and mental health associations
FAMILY HISTORY:
• Genogram sometimes helps
• Mental illness, suicide attempts, cardiac disease, diabetes, seizures, substance use, thyroid, psychiatric illnesses
SUBSTANCE USE HISTORY:
• Alcohol
o First use
o Current use (type, amount, frequency)
o Prior attempts to cease
o Hx of tolerance
o Hx of withdrawal symptoms, including of seizures
o Progression of use over time
o Previous history of treatment or abstinence
Marijuana/THC
• Other illicits
• ?IVDU
• Recreational drugs: what, when, how long, amount per week
FORENSIC HISTORY
• Current charges
o Violence
o Drugs
• Prior incarceration – history of lengths of sentences and when last released
• Juvenile history
COLLATERAL HISTORY
• OBTAIN CONSENT
• Often a very significant part of an evaluation for patients who are unable to give a coherent self-account or those who may be concealing information that would change your opinion or management
• Often needed prior to formulating risk/devising a mx approach
• When gathering collateral it is useful to see the patient and collateral provider together and alone
Outline a complete psychiatric history?
what is an acronym to remember this?
1) ENGAGING THE PATIENT
A person sharing their life story, frequently involving trauma, to a person they have never met, who requires a lot of detail in a restricted amount of time, is a privilege.
• Be mindful of:
o Consent
o Confidentiality
▪ Not discussing details outside of health staff involved in the persons care
• Environment
o Privacy – bedside curtains are not sound proof
o Safe
o Comfortable
• Language – there is a lot of inherent judgement in choice of language (mad, crazy, dangerous). Be respectful.
INTRODUCTION
• Introduce yourself, your role, and the purpose of the assessment
• Discuss confidentiality
• To explore the presentation further, begin with an open question to invite the patient to tell you, in their own words, what has happened for them to be here today
• Use this time to observe the patient – this will make up a large part of the MSE
DEMOGRAPHICS
• Name, age, sex, ethnicity
• Mental health act status and method of arrival to facility
• Established dx
• Current rx
• Admission length
• Living situation/arrangements
• Relationship status/children——-> o Must be aware of dependent children
• Education level, Employment status/income or benefit if unemployed
PRESENTING COMPLAINT:
- → Brief summary of how and why the patient has presented for review at this point in time
- It is useful to have a brief look at the chart or referral to gather this information prior to seeing the patient
- Eg: Mr R was brought into hospital by QAS on and Emergency Examination Order following a concerned phone call from Mr R’s ex-wife that Mr R was suicidal
- Chief complaint in own words
- Reason for seeking help
- Current symptoms: does the patient appear manic, depressed, physical health, psychotic, anxious, substance user
- Timeframe
- Premorbid baseline
- Precipitants: 7D’s - death, drugs, didn’t take meds, debt, divorce, disease and developmental
HISTORY OF PRESENTING COMPLAINT
• This is the patient’s story of what they are experiencing and what has led to this presentation.
o Need to get a lot more of the details of what has happened
• This is also where we need to ask very specific questions about symptoms of mental illness.
WHAT DO WE NEED TO ESTABLISH HERE?
• Establish presence and absence of symptoms
• Establish a time frame
• Establish the severity of the symptoms
o ‘How does it affect your life?’
• Establish precipitating factors
• Establish perpetuating factors Eg: financial hardship, chronic pain
o What made it worse/better
• Establish the effect on the person Eg: suicidal thoughts, poor self-care, difficulty studying or attending work
• Establish supports/protective factors
PSYCHIATRIC HISTORY
• Diagnosis: timing, length, reasons
• Hospitalisation
• Prior admissions/contact with mental health
• Prior symptoms when unwell
• Treatment
• Medication history and compliance, side effects and source
• Prior psychological treatments (other than medication)
• Past suicide attempts/deliberate self-harm
• Need to consider
o What has this individual experienced in the past?
o Is there a pattern?
o What has been tried in the past?
o What has, and has not, worked?
DEVELOPMENTAL HISTORY:
• → A developmental history gives us clues as to risk factors for developing mental illness, any evidence of a prodromal state, and personality factors.
• Birth-
o History of maternal health (including illnesses such as influenza)/substance use during pregnancy
o Birth complications (?hypoxic damage)
• Childhood-
o Milestones-
o Childhood illnesses
o Relationship with siblings
o History of trauma
• Education-
o Academic performance ?to what year ?any deterioration
o Bullying
o Hx of suspension/expulsion ?why
o Post school aspirations
• Employment history-
o If many jobs, why have they changed? Fired?
o Training/qualifications
• Relationship history
o Quality of relationships? Able to form longer attachments?
o Friendship groups ?still in contact
MEDICAL HISTORY:
• Allergies
• Prescription medications
• Any associated legal, financial, social, health problems
• Personal history of:
o Thyroid disease
o Head injuries
o Seizure disorders
o Chronic pain/chronic illness
o Cardiac history
▪ Some conditions have cardiac and mental health associations
FAMILY HISTORY:
• Genogram sometimes helps
• Mental illness, suicide attempts, cardiac disease, diabetes, seizures, substance use, thyroid, psychiatric illnesses
SUBSTANCE USE HISTORY:
• Alcohol
o First use
o Current use (type, amount, frequency)
o Prior attempts to cease
o Hx of tolerance
o Hx of withdrawal symptoms, including of seizures
o Progression of use over time
o Previous history of treatment or abstinence
Marijuana/THC
• Other illicits
• ?IVDU
• Recreational drugs: what, when, how long, amount per week
FORENSIC HISTORY
• Current charges
o Violence
o Drugs
• Prior incarceration – history of lengths of sentences and when last released
• Juvenile history
COLLATERAL HISTORY
• OBTAIN CONSENT
• Often a very significant part of an evaluation for patients who are unable to give a coherent self-account or those who may be concealing information that would change your opinion or management
• Often needed prior to formulating risk/devising a mx approach
• When gathering collateral it is useful to see the patient and collateral provider together and alone
Describe key features of psychiatric physical assessment? What systems etc.
• What are potential signs on examination of medical conditions masquerading as a mental illness?
• Are there any conditions that may complicate management?
o E.g. pregnancy, renal failure, hepatic failure, Parkinson’s disease
• Is there evidence of side effects from prescribed medication? Is there evidence of drug intoxication?
TARGETED PHYSICAL EXAMINATION:
• Vital signs
• Height, weight and waist circumference
• General physical
• Cardiac: Especially if commencing an antidepressant or antipsychotic that can affect heart
• Neurological: Extra-pyramidal side effects
• Thyroid examination
Outline what is a psychiatric formulation? Bio/pyscho/social
Outline basic pyshcotic disorders
What is pyschosis/ pyschotic disroders? What are the different types, and how do we diagnose them?
Describe mood disorders?
1) Depressive disorders
2) Mania/Hypomaina/depressive episodes - bipolar disorder
3) substance induced
Outline major anxiety disorders, and how they are diagnosed?
1) Specific phobias
2) scoial anxiety disorders (social anxiety( fear of negative apprasiakl in social setting
2) panic disorders
4) agoraphobia- fear associated with being in a places wher escape is difficult (frequently shops )
5) generalized anxiety disorders - worrrying zabout a variety of a events or situations
also - two other chapters related to anxiety-
somatic symptoms relatred to phyiscal disroders.
OCD and related disorders
OUtline trauma and stres related disorders? PTSD , acute stress disorder etc.
Post traumatic stress disorder:
1) stressors,
2) intrusive symptoms,
3) avoidance
4) negative alterations in cognitios and mood
5) alterations in arousal and reactivity
Duration- symptoms last for more than 1 month
Acute stress disorder- Less than a month
adjustment disorder- Prolonged responses to difficult events
Describe Eating disorders? Types and features.
Anorexia nervosa:
1) restriction of intake
2) below expected body weight
3) cognitive symptoms- belief of being overweight, fear of being fat
Bullmisa nervosa:
1) Binge- compensation cycle
2) compensation- vommitting, laxatives, diuretics, restriction, excercise
Binge eating disorder:
1)
Describe substance related and addicitve disorders - Substance,
Alcohol, caffiene, hallucingenic, ihlanet, opiod, stimulant
- Increased use, craviongs, feeling of loss of control
- tolerance, and possible withdrawl symptoms.
- Interference with functions including work and relationships
- Use despite knowledge of being harmful/a problem
- Excessive amount of time, spent, obtaining and or recovering from substance use
Gambling disorber
Internet Gaming disorder
Outline the 3 subtypes of personality disorders
Cluser A personality disorder
Cluster B personality disorders
Cluster C personality Disorders
What is a personality disorder?
Personally describe ways of thinking, feeling and behaving.
- Personality traits are inherited and or develop in response to early experiecnes and environment
- personality are usually stable across time
- We all have personality traits that can be unhelpful at time- Perfectionism (not good for you all the time)
- Personality disorder is describved when these pervasicve ways of thinking, feeling and behaving Cause distress or problems in your functioning, relationships and goal functioning
Describe borderline personality disorder?
Stigmatized diagnosis
Very strong association with early adverse experience, high incidence of childhood sexual abuse
Repsonses to early trauama influences BPD
Outline delirum vs dementia - What diagnositic features are needed for both (onset, precipitating factors)
What is the Mental health act 2016? Key points?
- Provide for the involuntary assessment and treatement
- Safeguarding patients right and their freedoms
- Balancing their rights and freedoms of others persons
MHA legislation is designed to protect and provide checks and balnces to the powers of detention (rather than greater focus on the legal power to date)
QLD MHA 2016
- Patients must lack capacity to consent to treatement (if they have capacity you cannot detain under MHA)
- Emphasises commmunity treatment
- Emphasises the patient outcome
What decides capacity and descision making regarding a pts capacity? How to test capacity? Insight?
Always presume an adult has capacity.
Capacity is descision and time specific.
General test for capacity: adult must be capable of:
- Understanding the nature of effect of descisions about the matter -> Understand and weigh the consequences of different options
- Freeling and voluntarily making descisions about the matter
- communicating the descision in some way (communication may need to supported or optimised)
What are the different types of authroities?
What are the treamtent criteria? for MH act (authority)
What do you need to do when someone does not have capacity?
Legal requirements! All adults are assumed to have capacity - the onus is on the clinicans
Supported descison making: Presence of support person
Outline exmaination types examination under the mental health act e.g Examination authority etc.
Examination Authority
An application may be made to the Mental Health Review Tribunal for an Examination Authority where all reasonable efforts have been made to engage a person in a voluntary examination of their mental health and there is, or may be, serious risk of harm or worsening health.
An application to the Tribunal may be made by: an authorised person at an authorised mental health service (AMHS), or a concerned person family member friend colleague, or other member of the community who has concerns about the person. If made by a concerned person, a written statement by a doctor (e.g. general practitioner) or authorised mental health practitioner (of an AMHS) is required with the application.
The Examination Authority authorises a doctor or authorised mental health practitioner to examine the person to determine whether a Recommendation for Assessment should be made.
The Examination Authority is valid for seven days for the examination to occur.
The examination may occur in the person’s home or the person may be transferred to an authorised mental health service.
Outline Emergencyexamination authority (MHA)? Reasons, when, who?
Examination The involuntary process usually commences with a Recommendation for Assessment however, in some circumstances, the Recommendation for Assessment is preceded by an examination authorised under another process such as an:
Examination Authority or an Emergency Examination Authority.
Examination Authority An application may be made to the Mental Health Review Tribunal for an Examination Authority where all reasonable efforts have been made to engage a person in a voluntary examination of their mental health and there is, or may be, serious risk of harm or worsening health. A
An application to the Tribunal may be made by: an authorised person at an authorised mental health service (AMHS), or a concerned person family member friend colleague, or other member of the community who has concerns about the person. If made by a concerned person, a written statement by a doctor (e.g. general practitioner) or authorised mental health practitioner (of an AMHS) is required with the application. The Examination Authority authorises a doctor or authorised mental health practitioner to examine the person to determine whether a Recommendation for Assessment should be made. The Examination Authority is valid for seven days for the examination to occur. The examination may occur in the person’s home or the person may be transferred to an authorised mental health service. Policy: Examination authorities Fact sheet: Examination authorities Form: Application for Examination Authority - Available from the MHRT website Form: Outcome of Examination Under an Examination
Emergency Examination Authority In emergency circumstances, a police or ambulance officer can make an Emergency Examination Authority (EEA) if the officer believes a person is at immediate risk of serious harm, such as threatening suicide, and the risk appears to be the result of a major disturbance in the person’s mental capacity.
This could be caused by an illness, disability, an injury, intoxication or any other reason. There is no presumption that the person subject to the EEA has an underlying mental illness.
For this reason, an EEA is made under the Public Health Act 2005. This ensures that the Mental Health Act captures only those persons within its intended scope and that appropriate treatment and care is provided following an examination.
What is the point of the assessment under and examination authority? What is the purpose of this? What is a RA? TA?
Assessment :
When considering involuntary mental health treatment for a person, the clinician must be satisfied that all treatment criteria are met and there is no less restrictive way for the person to receive treatment for their mental illness, for example, there is no Advance Health Directive or substitute decision maker available.
In this case a Recommendation for Assessment can be made by the doctor or authorised mental health practitioner who completed the initial mental health examination.
Recommendation for Assessment
The purpose of the assessment is to decide whether a Treatment Authority should be made so that the necessary treatment and care can be provided to the person during the period when they do not have capacity to consent to the treatment. Wherever possible, mental health assessments and treatment are provided in the community and preferably in the person’s home.
When is an EEA (emergency examination assessment) used? What for? What is the aim of this?
Allows up to 6 hours,
Must have the treatment criteria for MH act
Behaviour indicates the person is at immediate risk of serious harm
Major distrubances in persons mental capacity caused by illness
The persons appears to require urgent examination, treatment or care
In emergency circumstances, a police or ambulance officer can make an Emergency Examination Authority under the person to a Public Health Act 2005 public sector health service facility ,to detain and transport a if the officer believes a person is at immediate risk of serious harm and the risk appears to be the result of a major disturbance in the person’s mental capacity.
When can an emergency examination authority be made? The emergency examination authority provisions apply if a police officer or ambulance officer reasonably believes that: • • • a person’s behaviour indicates the person is at immediate risk of serious harm (e.g. by threatening to end their life ), and the risk appears to be the result of major disturbance in the person’s mental capacity caused by illness, disability, injury, intoxication or other reason, and the person appears to require urgent examination, treatment or care.
If all these criteria are established, an officer may detain and transport a person to a ‘treatment or care place’
. A treatment or care place means a public sector health service facility (including an authorised mental health service) or another place such as a person’s home, whe re the person may receive appropriate treatment and care. A watch house is not a ‘treatment or care place’.
Why are the provisions located in the Public Health Act 2005?
A disturbance in a person’s mental capacity may be caused by illness, disability, inj ury, intoxication or another reason. Including the provisions in the Public Health Act 2005 the aims to ensure that Mental Health Act 2016 captures only those persons that are within its intended scope and that appropriate treatment and care is provided after a person is examined.
What does an emergency examination authority allow?
An emergency examination authority allows a person to be det ained and transported by a police officer or ambulance officer without their consent, with the help and using the force that is necessary and reasonable in the circumstances.
What must be explained to a person? A police officer or ambulance officer must ex plain to a person that the person is being detained and transported to a treatment or care place, such as a hospital. The officer must take reasonable steps to ensure the person understands this information, including by having regard to the person’s culture, mental impairment and communication ability. at
What is an RA?
What is a treament authority?
What is the treatment criteria again?
Treatment authority:
- Possible outcome of an RA
- Cannot be made by same dr who made RA -except rural
- An Authrorized dr can make a treatment authority if
- the treatment criteria apply and
- there is no lesss restrictive way for the person to recieve treatement
- Must be confirmed by a pysch within 72 hours
- Regular assessment must be carried out every 3 months
- independently considered at a mental health review tribunal (within 28 days, monthly yearly)
What are the catergories of treatment authority
1) community
2) inpatient
Community: Must be treated in the commmunity unless safely and welfare need cannot be met this way
Inpatient: With or without limited community treatment (LCT) up to 7 days
–> often a graduated programs, takes time, with increased lvl of leave etc.
What is a forensic order?
Who is it made by?
What are the catergories?
What is a MHRT? Why do these oocur every 6 months
Made by the mental health court:
- focusedd on community safety
- FO (mental health)
- FO (disability)
Inpatient and community catergories:
- Court/MHRT decides conditions for periods of leave
- court can impose non-revocation period up to 10 years for the most serious charges
- FO are otherwise indefinite
MHRT reviews every 6 months:
- confirm or revoke FO
- COnsider conditions e.g leave
What is an advance health directives and how do they apply to MH?
What are key investigations to be completed when admitting a MH patient?
• Decisions must be justified. Always have a reason for ordering a test!
• Have a list of medical conditions in mind that you need to “rule out” in a psychiatric presentation.
o Full blood count, urea and electrolytes, liver function – think elderly, eating disorders, catatonia, substance use, possible delirium
o Fasting glucose and lipids (pre-commencing an anti-psychotic)
o Thyroid (depression, psychosis and some meds eg: lithium)
o Vit B12 and iron studies
o Infectious screen – syphilis, HIV, Hep B, Hep C
o Medication monitoring: Eg: lithium levels, clozapine levels
o Prolactin level
o Urine drug screen/ MSU if infection suspected
o Pregnancy test
o ECG
o CTB or MRI, EEG
What is a risk asssement in terms of MH patients? How to do this? Importance?
Clinical risk assessments are undertaken to identify risk and inform the clinical management strategies to minimise the risk(s) to consumers
- Involves gathering information and analysis of potential outcomes of identifies behaviours, including identifying specific risk factors relevant to an individual, understanding the context in which they may occur and linking history information to current, anticipated and possible future outcomes
- Based on clinical interview, MSE, collateral information, review of medical records and use of clinical risk screening
- All patients need to be screened for risk of
o Suicide/self harm
o Vulnerability
o AWOP
▪ Breach of community conditions
▪ Treatment refusal
▪ Frustration regarding hospitalisation/ involuntary treatment
o Child protection
o Aggression
o Sexual predatory behaviour
What type of risks need to be identified in the risk assessment? To the person/to the public
• To patient
o Suicide
o Self harm
o Misadventure
o Vulnerability
o Reputation
o Physical harm e.g. falls
• To others
o Violence
o Driving
o Absconding
o Children: neglect, abuse
What are the differences between, static, dynamic risks? Why are protective factors important to acknowledge?
DYNAMIC
• Now, modifiable present
• More amenable to change by intervention, treatment or control over the situation
• Factors are useful for identifying increased risk of imminent or short term risks
STATIC
• Risk factors not subjected to change by intervention
• Past, non-modifiable, baseline
• Generally history factors e.g. childhood abuse, previous violence
• Factors are useful for identifying ongoing/longer term risk
PROTECTIVE FACTORS
• These reduce the likelihood of negative outcomes
• Can reduce risk or enhance rapport and ability to work with a consumer and provide opportunities for intervention
• May include individual strengths e.g. insight, desire for change, supports including family
When do you need to undertake risk assessments?
- On admission
- Daily for first 3 days of a new admission, PICU
- Change in observation category
- On a shift bases for all consumers on constant observations
- Anticipation or experience of a significant interpersonal loss or psychosocial stressor
What are protective factors against violence?
What tests can we undertake to determine violence risk?
PROTECTIVE FACTORS AGAINST
• Strong social support
• Engagement with service
• Good relationships
• Stable employment
• Stable accommodation
• Prolonged abstinence from substance
• Adherence to treatment
• Older age
TOOLS TO ASSESS VIOLENCE
• Historical Clinical Risk Management-20 (HCR-20)
• Static-99: Male Sexual Offenders
• Hare’s Psychopathy Checklist – Revised (PCL-R)
Outline what an MSE is? acronmyn - ABS MAT PCIJ
appearance, Behavuiour, Speech
Mood, Affect, Thought form/content
Perception, Cognition, Insight, Judgement
Outline what to look for in Appearance on MSE?
• Age, sex, ethnicity, posture/ physique, clothes, cleanliness, odours, hair, make up, autonomic function, appropriateness
• Mania- bright clothes, dishevelled
• Impressions:
o Wells vs unwell
o Acute vs chronic
o Perplexed/ confused/ distracted
Outline what to look for in Behaviour in MSE? (CAPER)
Behaviour in Delirum?
BEHAVIOUR (RESPONSE TO ENVIRONMENT) AND ATTITUDE (TOWARDS YOU)- CAPER:
• CAPER
o C- Cooperation (apathetic, reticent, hostile, expansive)
o A- Appropriateness (attitude, alertness, abnormal movements- gait, posture, stance)
o P- Physical activity (motionless/ retardation/ poverty/ normal/ agitation/ frenzy), spontaneity, autonomic activity
14
o E- Eye contact
o R- Rapport (ingratiating, passive, compliant, trusting, engaging, cool, distant, aloof, disdainful, defensive, suspicious, sexually or aggressively provocative, demanding, obstinate)
• Irritability/ agitation/ calm
• Consciousness (Associated with attention- ability to focus in delirium = awareness of self and the environment)
o Response to stimulation? Frequency/ intensity
o Reaction time
o Attention
o Quality of verbal responses
o Motor activity
• Concentration is the ability to maintain attention
• Inattention can be selective (agnosia) or global (delirium) or distractibility
• Environment
o Quantitative change = Hypervigilant, fully alert, clouding, somnolent/ drowsy, stupor, coma
o Qualitative: = akinetic mutism, delirium, automatism, stupor, dreamlike
• Self
o Dissociation = continuity of identity over time
o Depersonalisation, derealisation = ability to experience self + surroundings as real (congruity)
o Passivity = unity of will and action
o Ego boundaries = ability to experience distinction of self from surroundings
DELIRIUM PATIENTS:
• Patients will either be loud (rambling incoherently struggling against efforts to settle) or quiet (little awareness of you and doesn’t attempt to connect)
• Unable to coherently answer “what brings you into the hospital?”
Outline what to Q and look for when evaluating Speech in MSE?
SPEECH:
• General: Thoughtful, articulate, staccato, rambling (dementia), continuous, halting
• Rate: Rapid/slow, pressure (flight of ideas), retardation, mutism
• Volume: Soft/ loud
• Phonation: Aphonia, dysphonia (hoarse, CN IX, thyroid)
• Pitch: High (falsetto)- pseudobulbar palsy, low (bass)
• Articulation: Dysarthria, stutter, lisp, accent (dyslalia)
• Intelligibility
• Tone: Monotone, prosody vs dysprosody
• Spontaneity: Alogia (poverty of thought), poverty (brief, concrete), poverty of content (fails to convey information)
• Latency of response: Normal, increased (depression, psychosis), decreased (manic)
• Fluency: Dysphasia (Abnormal transmission of language), echolalia (reply to question by repeating in different words, catatonia), coprolalia (compulsively uttering obscenities), glossolalia (unintelligible revelatory message), perseveration (meaningless repetition of sentences or phrases), neologism (newly coined words)
- Ability to articulate and phonate sounds and words
- Language- dysarthria/ dysprosody, aphasia (impaired fluency and/or comprehension, alexia, agraphia)
- How does speech match up to: Facial/ body expression, emotion/ thoughts, level of education, cultural background
Outline what to look for when evaluating Mood and Affect (emotions) in MSE?
EMOTION (MOOD AND AFFECT):
MOOD:
• Mood: Pervasive sustained emotional disposition
• Emotion- physiological and psychosomatic expression of mood
• Anhedonia: Inability to gain pleasure from normally enjoyable
• How do you feel right now?
• How has your mood been over the last few days?
- Depressed: Sad, gloomy, miserable, hopeless
- Anxious: Tense, worried, apprehensive, fearful
- Dysphoric: Uneasy/ unpleasant, generalised dissatisfaction (sulky, angry, ill-humour)
- Euthymic: Normal, expansive decreased, restraint
- Angry: Annoyed, sarcastic, irritable, enraged
- Elevated: Cheerful, high, elated
- Euphoric: Excessive, unreasonable cheerfulness
Affect:
- Stability- smooth/ awkward/ mobile/ stable/ labile
- Appropriateness- congruent/ incongruent (discordance between speech and affect)
- Range- breadth of spectrum (normal/ increased/ decreased
- Reactivity- responsive, non-responsive
- Intensity- depth and quality, intense (manic, histrionic) or flat, blunted (severe depression, negative symptoms), full/ restricted/ constricted (usually in depression)
- Dissociation of affect = depersonalisation/ derealisation/ denial/ la belle indifference/ alexithymia (decreased consciousness of emotions and affect)
- Flat- severe depression (no expression- apathy)
- Blunting- psychotic (reduced emotion)
What are six main clusters used to describe mood at affect?
Appropriateness of congruency
Describe thought 1) Stream 2) form 3) content?
- THOUGHT STREAM:
• Rate/ tempo:
o Hypomanic- Accelerated but coherent, pressured (rapid but ordered)
o Manic- Flight of ideas (rapid and coherent- can be associated with clanging, punning)
o Abnormal velocity- test by asking open-ended questions:
▪ Mute- will not speak
▪ Poverty of thought/ speech- little spontaneity, minimum number of words in responses
▪ Poverty of content- produces copious amounts of speech, but communicates little as too abstract>> perseveration if about single idea
▪ Slowed
▪ Thought blocking- inhibited, begins to say something then stops or forgets in mid-thought
▪ Increased
▪ Racing thoughts- subjective sense that thoughts are so fast person can’t keep up (observed as pressured speech that is difficult to interrupt, loud and intense (mania))
▪ Flight of ideas- both speed and loose associations (jumping between ideas)
▪ Clangs- sounds similar to the first word- mania
• Continuity/ train- to be understandable it should be consistent and goal directed
o Circumstantial (slow, detailed but reaches goal), normal longwinded, anxious demented
o Tangential (side-tracked, doesn’t reach goal, needs frequent redirection)
o Thought blocking (sudden stop, can’t resume)
o Perseveration (repeats words/ phrases/ themes)
2) Thought form:
THOUGHT FORM (ORGANISING CONCEPT):
• Positive formal thought disorder- disturbance in coherence and/or association
o Coherence must be intact to reliably assess association
• Logical linear- does it lead to a conclusion
• Abstractability- ability to conceptualise in meaningful ways vs concrete/ literal
• Coherence- internal relevance, woolly, incoherent due to disturbed syntax of thought or disturbance within the clause
• Relatedness or quality of association- choice of words/ idiom. If continuity intact, may be due to intrusion in
3) thought content: incoming sensation of thought:
• True belief
• Phobia
• Rumination (mood congruent concerns)
• Obsession (unwanted, repeatedly intrusive idea or image)
o Erroneous belief (False judgement)
o Overvalued idea
• Primary delusion
• Secondary delusion
• Preoccupation- centring thought on 1 idea
• Overvalued idea- quantity increased compared to normal belief solitary, preoccupying, abnormal belief strongly toned by affect i.e. not fixed
• Delusion- Abnormal belief compared to normal belief; usually false judgement or false belief; usually false judgement or false beliefs that are out of keeping with social and cultural background
How can we classify delusions .g primary, secondary, systemization, ALWAYS ASK what in thought/form/content?
CLASSIFICATION:
• Primary- not deduced from other phenomena (not understandable)
• Secondary- based on delusional evidence (understandable)
• Systemization- secondary elaboration
• Patient’s response do they act on them
o Congruence
When assessing patient always ask assess risk!!!! ask about suicide, homicidal ideation, intent, means, previous attempts
o Risk/ safety: Suicidal, homicidal, litigious, ideation, intent, immediacy
How do we describe and determine a patients perception on MSE?
• Normal: Imagery (fantasy, day dream, dreams and imagination)
• Distortion:
o Colour (xanthopsia- yellow, chloropsia- green, erythropsia-red)
o Intensity (hyperaesthesia/ hypoaesthesia)
o Spatial form (micropsia, macropsia)
• Deception:
o Illusions
o Hallucinations (see, hear, taste, smell, tactile)
18
o Somatic, cynaesthetic, autoscopy (phantom mirror image)
o Pseudohallucination- vividly experienced but patient aware that it isn’t real
o Re-experiencing- Flashbacks, nightmares, deja vu, deja pensee
Describe Insight and judgement? And examples
- “Why do you think you’ve been having these problems? What needs to happen for your life to improve”
- What does the patient think is wrong?
- Does the patient think they have an illness?/ Is this illness psychological or physical?/ What does the person think will help them? Willingness to take medication and attend for appointments/ future goals
- Denial vs slight awareness but doesn’t admit vs aware problem but blames external factors/ others vs something wrong but doesn’t know what vs intellectual insight = can see own role but not apply vs True emotional insight leading to adaptive change
JUDGEMENT:
• If the patient understands the likely outcome does this influence them?
• How have recent decisions been made, what does the future look like to you?
How do we describe and work out a patients level of cognition on MSE? What are the key areas to cover when assessing cognition?
• Consider LOC (sedated, intoxicated), hearing impairment, level of education, cultural factors
o Judgement
o Insight
o Intelligence
o Attitude + memory
o Specific tests
- Orientation: Registration and short term recall- ball, flag, tree, rainbow
- Attention (can focus) and concentration (ability to maintain attention) = months of the year backward/ world/ digit span
- Intention can be selective (agnosia) or global (delirium) or distractibility
- Clock drawing/ Luria
- Current events in news and PMs
• Memory:
o Short-term- recall at 5 mins
o Long-term- how well can they remember and tell history
Learning objectives for psychiatric emergencies
What is the difference between normal responses and emotions vs distrubances in emotions? E.g Acute beahvioural distrubances? Intoxications? Delirum? Acute mental illness?
And how are these recognized ?
How does personality affect this?
Acute behavioural distrubance: Situatinal crisis, etc
How do we break bad news? SPIKES model
SPIKESS
Setting up the consultation
Perception- what is the patients perception of the situation?
I: Invitation- obtaining the patients knowledge
How do we non-pharmologically calm and destress and acutely distressed patients (EMERGENCY)??? DONTESCALATE
DEESCALATION
D- dont withdrawn privelges
E: ensure safety of others
E: Escape - avoid cornering patient
S: stance= protective and ready
C- Calm and non threatening manner
A- Allow for ventilation
How do we support problem solving in MH patients?
What do we mean by safety in terms of MH patients?
Danger can be to self - suicide, misadventure, etc
Danger to others: Public, family, kids
If person refuses treatment, Involuntary treatment considered under MHA act
When and how do we review patient risk?
examples
- Transition from prodromal to psychosis
- early phase of recovery and relapse
- During rapid fluctuations in mental state
- Prior to granting hospital leave or being admitted
- On discharge, from service (IN THE first month)
- following any deliberate self harm
What screening test can we undertake to assess risk???
SADPERSONS (screening test)
Sex - male
Age less than 19, or older than 45
Depression
Previous suicide attempts
Excessive alcohol or drug use
Rational thinking loss - pyshcosis, organic brain syndrome
Separated, divorced, or widowed
Organized plan or serious attempt
No social support
Sickness chronic disease
Score 1-2 =low risk
3-4 mod
4 = high
What risks should we consider with patient with pyschosis????
- Suicide - impact of illness, command hallucinations, derogatoiry halluncinations
- Violence - comman
- Vulnerability
- Refusal and frustration
- Self neglect
What is an suicide risk assessment? static/dynamic factors?
How do we plan and manage risk?
The C’s of patient risk’s
Clock- is there anytime when patient is high risk? e.g
How do we manage an acute behavioural disturbances? Medical management.
mild-
moderate
severe:
How do we manage a patient holistically with an acute behavioural distrubance?
What are the S’s for Risk management?
Suicide
setting
Status (mental health status)
Specific intructuctions
Symptom releief
What are practical prescribing tips when needing to acutely sedate a patient?
Benzo vs antipsych? why?
Benzodiazepines are preferred over antipyshcotics! Why?
Lower risk of additive side effects, no EPSE
What are common mistakes, when dealing with an acutely unwell MH patient?
Describe types of delusions you may find on MSE?
Grandiose/ persecutory/ nihilistic
• Love (Erotomania- delusional disorder where the affected person believes that another person is in love with them)
• Jealousy/ guilt/ religious
• Somatic or hypochondriacal
• Poverty (Cotard’s delusion- the affected person holds the delusional belief that they are already dead/ putrefying or have lose their blood or internal organs)
• Ekbom’s syndrome (Delusional parasitosis): Delusional disorder where individuals believe they are infested with parasites
• Bizarre (impossible or implausible)/ bizarre
• Special types:
o Delusional misidentification includes:
o Capgras= someone close is an impostor
o Fregoli = stranger is someone else
o Intermetamorphosis = someone close/ stranger identical
o Subjective doubles- another person changed into me
• Shared psychotic disorder (folie a deux):
o Impose
o Communique
o Induite
o Simultanee
What is serotonin syndrome and what is its triad???
- Mental status changes - agitation, anxiety, disorinetation, restlessness,
- Neuromuscular hyperactivity - trremor, sustained clonus, hyperreflexia, muscle rigidity, bilateral babinsky
- Autonomic hyperactivity: Hypertension, Hot> 38c,
How do we treat serotonin syndrome? Also what are usual reasons to cause SS?
tx
- cool, benzos
What is NMS? neuroleptic malignant syndrome?
- Life threatening neurological emergency associated with antipyschotics
- 1-3% of ppl using neuroleptics
- common with “typical” - e.g Haloperidol
What is the DSM 5 for NMS syndrome???
NMS investigations???
Special investigations???
CK,
What are risk factors for NMS?
1) dehydration
- elevated temp
- rapid loading
3.
What is the management plan for pt with NMS???
What are Anticholinergic effects????????? How to look out for them?
What is anticholinergic toxcity syndrome?
How do we distinguish- Serotonin syndrome? NMS? Anticholinergic toxicity?
need to know how to distinguish
Outline basics of MSE? Scoring? What does it assess? What disease does it screen for?
Mild, mod, severe scores?
• MMSE - <24 indicates cognitive impairment
• Total out of 30
• Assesses cognitive function
• Used as a screening tool for cognitive impairment in the elderly, institutionalized adults
• Screening test for dementia
• A score of 25 or higher is normal
o Mild: 21-24
o Moderate: 10-20
o Severe: <10
• The questions are grouped into 7 categories (each representing a different cognitive domain or function):
o Orientation to time- 5
o Orientation to place- 5
o Registration of 3 words- 3
o Recall of 3 words- 3
19
o Language- 8
o Attention and calculation- 5
o Visual construction- 1
DEMENTIA:
• MMSE (needs to be above 10) and need to show a 2 point increase in score and you need to be continually assessed>> for anticholinesterase
What is a frontal assessment battery? what does it try assess? what does it try differentiate?
- Cut off for normal performance in first 6 questions = 15
- Cut off for clock drawing task: 8-10 (normal), 1-7 (abnormal)
- Assesses frontal lobe function- Abstraction, fluency, impulsivity and primitive reflexes
- Differentiates Frontotemporal dementia from Alzheimer’s disease
What is the DSM? What are the underlying principles of it? What are its uses? How is it similair/different to ICD-10?
UNDERLYING PRINCIPLES:
• Diagnoses mental disorders from specific symptoms
• Thoughts, feelings and behaviour can be organised into categories representing disorders
• Categorical- patient has the disease or doesn’t
• Ensures reliability between practitioners and applicability across settings/ countries
USES:
• Guides clinicians to make diagnosis
• Improves reliability in communication
• Inform service delivery by guiding political health care decision makers and funders to budget for health care expenses
• Standardize diagnosis internationally for comparable research
SIMILARITIES WITH ICD-10:
CLASSIFICATION OF MENTAL HEALTH DISORDERS:
• DSM-V and ICD-10 are categorical
• Diagnostic and Statistical Manual of Mental Health Disorders- American Psychiatry Association
• International Classification of Diseases- WHO
DIFFERENCES BETWEEN DSM AND ICD-10:
• ICD
o Hierarchical in nature, which discourages multiple diagnoses
o Categorical by description of condition
o Internationally based
o Descriptive when there is no identifiable etiology
• DSM
o Not hierarchical and encourages multiple diagnoses
o Categorical utilising operationalised criteria
o American-based
o Atheroretical- avoids theoretical explanations when no etiology identifiable
What are the principles of the MHA? Who is excluded from this? What is involuntary assessment? Who can make one and why?
PRINCIPLES:
• Least restrictive alternative
• Effect on liberty and rights is minimum necessary
• Mental illness: A condition characterised by a clinically significant disturbance of thought, perception, mood, memory
EXCLUSIONS:
• Intellectual disability alone
• Drug or alcohol use
• Religious/ cultural/ philosophical or political beliefs or opinions
• Race
• Antisocial or illegal behaviour
• Immoral or indecent conduct
• Family conflict
INVOLUNTARY ASSESSMENT:
• Persuade the patient to attend a medical consultation
• If they don’t want to be examined then trigger an Involuntary assessment
• Assessment can occur in the community, in an in-patient facility or public hospital
REQUEST FOR ASSESSMENT:
• Made by any adult
• Must reasonably believe the person has a mental illness of a nature or extent that involuntary assessment is necessary
• Must be made within 3 days of seeing the person and within 7 days before/ or after the recommendation for assessment
• Can be made by any doctor or an authorised mental health practitioner
• Must be made within 3 days of examining the patient
• Valid for 7 days
What is the assessment criteria under the MHA? (very important) 6 points
- The person appears to have a mental illness
- The person requires immediate assessment
- The assessment can properly be made at an authorised mental health service
- There is a risk that the person may:
a. Cause harm to themselves or someone else OR
b. Suffer serious mental or physical deterioration - There is no less restrictive way of ensuring the person is assessed
- Lacking the capacity to consent to be assessed; or having unreasonably refused to be assessed
What is an emergency examination order?Who can apply for one?
• Police, ambulance or psychiatrist must reasonably believe:
o Person has a mental illness
o There is an imminent risk of significant physical harm being sustained by the person or someone else
o Applying for a JEO would cause dangerous delay and increase the risk of harm
How does the assessment process work? What are the conditions of this e.g eea assessment?
- Assessment period starts when the person is received at the health service
- Authorised doctor to examine the person as practicable but within 24 hours to decide if the patient needs involuntary treatment
- May be detained for up to 24 hours
- Patient must not be detained for longer than 72 hours
- A person can’t be treated involuntarily under assessment documents
What are the treatment criteria for a person for a person to be under a TREATMENT AUTHORITY??
TREATMENT CRITERIA FOR A PERSON ARE ALL OF THE FOLLOWING:
- •The person has a mental illness
- •The person doesn’t have the capacity to consent to be treated for the illness
- • Because of the person’s illness and the absence of involuntary treatment:
- • There is an imminent risk that the person may cause harm to themselves or others; or
- • The person is likely to suffer serious mental or physical deterioration
- • There is no less restrictive way of ensuring the person receives treatment and care for the illness
- • The person continues to be an involuntary patient as long as the treatment criteria are still met, but must be reviewed by a psychiatrist
- • However, there is a need for regular assessment by authorised psychiatrist and review by Mental Health Review Tribunal
• Mental illness: Clinically significant disturbance of thought, mood, memory or perception
• TA require all criteria to be met
What is the basic ethical principle of the mental health act?
- Being least restrictive of the rights and liberties of a person means restricting the rights and liberties only to the extent that is required to protect the person’s safety and the safety of others
- The same basic human rights must be recognised including the right to respect and dignity
What are the 3 main purposes of the Mental health act?
What does he act try to achieve?
- To improve and maintain the health of people with a mental illness who lack the capacity to consent to be treated
- To divert people from the criminal justice system if found to have been of unsound mind at the time of committing an unlawful act or to be unfit for trial.
- To protect the community if persons diverted from the criminal justice system may be at risk of harming others.
THE ACT TRIES TO:
• Safeguard the rights of persons
• Is the least restrictive of the rights and liberties of a person with a mental illness and
• Promotes the recovery of a person who has a mental illness, and the person’s ability to live in the community without the need for involuntary treatment and care
What is required for an individual to have capacity to consent?
E.g what does the consent criteria require?
• Capacity: The ability of a person to give informed consent to a particular treatment at a particular time.
• The clinician must assume the patient has capacity to give informed consent, but can be rebutted.
• Clinicians must support persons in making treatment decisions- translators, visual aids
• A high risk patient can still receive treatment as a voluntary patient if they are able to demonstrate capacity
• A person has capacity to consent to be treated if the person is capable of understanding in general terms:
- The person has an illness or symptoms of an illness that affects their mental health and wellbeing
- The nature and purpose of treatment
- The benefits and risks of treatment and alternatives to treatment
- The consequences of not receiving treatment
- The person must also be capable of making a decision about treatment and communicating the decision
• The ACT recognises the importance of supported decision making- the person may have the capacity with the support of another person.
What principle of Autonomy does the MHA try to enable?
PRINCIPLES OF AUTONOMY AND THE MHA:
- As far as possible, a person must take part in making decisions about their life especially in relation to treatment and care
- The person’s views, wishes and preferences must be taken into account
- A person is presumed to have capacity to make decisions about their treatment and care
- The involvement of family, carers and other supports is encouraged subject to the person’s right to privacy
- The MHA promotes treatment of people with a mental illness in the least restrictive of their rights and liberties by requiring involuntary treatment only to the extent of protecting the safety of the person and others
What are some problems around consent and treatment?
• Mental illness robs you of the capacity to understand the need for treatment
Capacity: The ability of a person to give informed consent to a particular treatment at a particular time.
- The clinician must assume the patient has capacity to give informed consent, but can be rebutted.
- Clinicians must support persons in making treatment decisions- translators, visual aids
- A high risk patient can still receive treatment as a voluntary patient if they are able to demonstrate capacity
- A person has capacity to consent to be treated if the person is capable of understanding in general terms:
o The person has an illness or symptoms of an illness that affects their mental health and wellbeing
o The nature and purpose of treatment
o The benefits and risks of treatment and alternatives to treatment
o The consequences of not receiving treatment
o The person must also be capable of making a decision about treatment and communicating the decision
What are the 3 basic elements of informed consent?
• Threshold element
o Competence
• Information elements
o Disclosure of information- Professional standard, reasonable standard and subjective patient
o Understanding of information
• Consent elements
o Voluntariness
o Authorisation
What are the common types of Abuse? Who are most comon perpetrators? Adults who were abused are at increased risk of developing what type of mental health conditions?
• Types of abuse: Physical, sexual, emotional/ psychological (threats, yelling, constant criticism, educational deprivation)
o Most child abuse cases are from neglect
• Commonly the perpetrators are the child’s own parents
• Adults who were abused as children have an increased risk of developing:
o Anxiety disorders
o Depressive disorders
o Dissociative disorders
o Self-destructive behaviours
o Substance abuse disorders
o PTSD
• They also have an increased risk of abusing their children
What types of things show evidence of sexual abuse in children? How can this affect the child?
Evidence of sexual abuse in a child:
o STDs
o Anal or genital trauma
o Knowledge about specific sexual acts (inappropriate for age)
o Initiation of sexual activity with others
o Sexual play with dolls (inappropriate for age)
• Isolated traumatic incidents → produce discrete conditioned behavioural and biological responses to reminders of the trauma.
• Chronic maltreatment or trauma: Pervasive effects on development
What are ways trauma affects ones psychological developement?
What can trauma affect in neurodevelopment?
PSYCHOLOGICAL EFFECTS OF TRAUMA:
• Self-concept
• Concept of the world
• Concept of people and relationships
NEURODEVELOPMENTAL EFFECTS OF TRAUMA:
• Physical/ Gross development
• HPA axis
• Memory circuits
• Language circuits
What is the stress-vulnerability concept?
STRESS-VULNERABILITY CONCEPT
• Problems with emotion and behaviour are considered to be the consequence of an emotionally/ behaviourally vulnerable person being exposed to a significantly invalidating environment
• Vulnerability:
o Temperament- biological
o Intelligence
o Speech and language functioning/ deficits
o More gross physical deficits
• Stress
o Insecure attachment
o Abuse or neglect
o Lack of experience or learning
o Peer problems
o Inconsistent family or school environment
What is Attachment? What is secure Attachment?
What causes interrupted attachmemt?
What are the implications of interrupted attachment?
ATTACHMENT
• Attachment: The biologically driven strong emotional bond that develops from the infant to the mother.
• This provides emotional and psychological safety to the child
• The primary caregiver provides a secure base, which allows the growing child to explore the outside world
• The attached child is strongly disposed to seek proximity to and contact with a specific figure and to do so in certain situations, especially when they are frightened, tired or ill.
• Attachment provides:
o Safety and security for the child
o Secure base for exploration
• Problems can be from the child (temperament, autism) or in the parent (poor parenting)
• Secure attachment is required to feel safe enough to calm the hypervigilance and to feel safe when emotions are aroused
• Attachment leads to the development of an internalised template for relationships
• Internalisation of the caregiver’s behaviour are gradually constructed from everyday interactions with the attachment figures → influences perceptions of self and others, and guiding behaviours (conscious or unconscious)
CAUSES OF INTERRUPTED ATTACHMENT:
• Absence of an attachment figure (privation) e.g. orphanages
• Significant separations or loss of attachment figure (deprivation) e.g. maternal deprivation
• Abuse and neglect by attachment figures
IMPLICATIONS OF INTERRUPTED ATTACHMENT (E.G. MATERNAL DEPRIVATION):
• Failure of secure base → leads to persistent fear of abandonment
• Neglect, abuse or abandonment will lead to neurodevelopmental changes
• Internalised fear of abandonment: Reactive attachment disorder- angry and clingy
• Externalised fear: Conduct disorder- anger
• Poor attachment disrupts emotional development
• Poor attachment → fear of abandonment with early neglect, abuse, major losses and changes
o Lack of a secure base → poor attachment
o BAD personalities
• Abandonment deficits from attachment issues → individuals who have severe disruption to their personality with persisting abandonment fears
o Borderline PD: When relationships start to breakdown there are threats of self-harm. Idealisation leads to denigration
o Antisocial PD: Perpetrate threats of violence to their partner recurrently
• Persisting abandonment fears will impair self-esteem development
How does trauma affect neurobiological development?
NEUROBIOLOGY
• Brain structure is determined by genetics, but also by the neuronal activity that occurs after birth in the context of experiences.
• Synapses are established through the electrical firing of neurons in response to repeated sensory experiences
• The brain’s rate of growth is highest and its malleability greatest in the first few years of life
• Sensitive and responsive care giving → the adult acts as a regulator of the infant’s state, which provides opportunities for positive affect, minimises negative states (e.g. distress and/or underarousal)
• Prolonged experience to negative states, deprivation or repeated exposure to threat can interfere with normal brain development
o Physical abuse early in life can cause an abnormal stress response
o Emotional neglect can cause atypical patterns of neural activity that affect areas of the brain responsible for empathy, humour, attachment and affect
• Experiences in the 1st year provide the foundation for later development and functioning
What is attachment theory? When does it begin? Why does a child need attachment?
ATTACHMENT THEORY:
• Bonding, attachment, secure base
• Begins from 6 months
26
• Object constancy: Cognitive development of holding onto a constant image
• Attachment theory: Child remains close to parent (child becomes cognitively mature to recognise the object)
o Attachment behaviour and caregiving are instinctive behaviours that ensure survival
• Significant impact on personality development
• The child needs attachment:
o To feel safe enough to calm hypervigilance
o To feel safe when emotions are aroused
What are the 4 types of reactions (attachment- Mary ainsworth) - to attachment?
- Secure attachment- caregiver is a secure base from which to explore; responds well to being picked up by others; settles on reunion
- Insecure ambivalent (clingy and angry): Clingy and then oppositional; cries on separation; acts resentful on reunion
- Insecure avoidant- Engages little with caregiver, cries on separation, but doesn’t re-establish contact on reunion
- Insecure disorganised: No clear behavioural strategy- the baby appears dazed, confused, fearful; show patterns of avoidance, reluctance or extreme fear
What are the types of interventions to gain secure attachement? e.g management/support
- Psychoeducation to parents
- Stable home placement of institutionalised children
- PPP parenting course
- Circle of security
How is the adult identity formed? (factors needed)
What occurs from poor attachment in development?
What is meant by ‘Strange reactions/situations’, in terms of attachment?
• Adult identity (self-concept):
- Neurodevelopment- Intrinsic factors (genetics) + Extrinsic factors (infection, trauma, etc.)
- Secure base
- Self-esteem
- Self-image
• Attachment: Process of connection to provide emotional and psychological safety along with the physiological needs
- Child and parents both contribute → problems child (autism), parent (poor parenting)
• Personality development is strongly influenced by a child’s experiences within the family
- If we feel connected to others → safe and secure
- Unconnected to others → less safe and insecure
• Strange situation:
- Infants explored the playroom and toys more when in the presence of their mother (secure base) than alone or with a stranger.
What factors contribute to development, throughout the ages of childhood/adolescence?
Birth- 6 months?
6 months- 2 years?
2-5 years?
School years?
Adolescence?
Adulthood?
BIRTH- 6 MONTHS:
- A challenge is for the mother and child to develop ways of being together
- Regulation of internal states and sharing of affective experiences are important including forming an attachment bond
- The infant contributes to attachment through instinctive and later learned behaviours that become more organised and preferential e.g. crying, smiling
- Infants differ considerably in their capacities due to genetics, experiences prenatally and at birth
- Mothers differ in what they bring in the relationship with their infant and the care they provide
——————–Past history of receiving inadequate parental –care or unresolved trauma; current stresses (violent partner, recent loss or trauma); immaturity, lack of support or physical or mental illness can affect the parent-child relationship———
- The mother’s ability to respond sensitively to the infant’s needs determines the quality of attachment
6 MONTHS- 2 YEARS
- In the latter half of the first year, the attachment bond grows stronger and attachment behaviour in the infant becomes more organised and obvious.
- The infant seeks proximity to the attachment figure, protests at separation and demonstrates fear to strange people/ objects or to clues of danger or threat
- The mother’s responsiveness to the infant are important
- With increased mobility and the capacity to read their mother’s cues from a distance, the infant is able to move away and encounter more challenging and dangerous situations.
- The mother’s availability as a secure base is necessary for security, emotional regulation and protection from external threat.
- Internalisation of the mother’s support, reliability and responsiveness continues along with her encouragement for exploration
- By this stage, the infant has more than 1 person to whom they are attached
2- 5 YEARS
- Pre-schoolers begin to picture others as having separate goals and they develop the capacity for perspective-taking to understand other people’s motivations and plans
- With increased capacity for representation and to think in terms of time and space, the pre-schooler is able to tolerate separation from an attachment figure and can be comforted by explanations
- Fears and phobias intensify and concerns about safety develop for themselves and others
- Parents need to be emotionally responsive to their child’s needs, and provide guidance and instruction
SCHOOL YEARs
- Children are able to relate more with adults who may serve as additional attachment figures from their parents
- The way that children perceive and respond to these adults is influenced by their expectations of the way adults can act as caregivers
- Children’s attention and participation in class, security and academic competence, and their tendency to report about their feelings and on coping strategies are linked to their attachment representations.
- By 6 years, children have the capacity to monitor their own thinking, memory and action, and to recognise the privacy of thought, which is related to security in attachment and is important in self-awareness and relating with others.
- Peer relationships are important, and the ability to manage conflict with peers and to develop satisfying friendships is influenced by the quality of attachment to parents.
ADOLESCENCE
- Adolescence begins the process of relinquishing the primary attachment to parents
- This can make the adolescent to feel alone, especially if other attachment relationships haven’t formed
- A parallel process where relationships with peers becomes more important for sharing interests, but also in providing support, understanding and contributing to the adolescent’s sense of security.
- Close friendships occur and these friends serve as attachment figures
- The quality of attachment to both parents and peers is related to self-esteem and life satisfaction
ADULTHOOD
- Relationships typically involve couple relationships, but adults often have more than 1 attachment relationship in their life
- Numerous attachment bonds can be formed and severed through one’s adult years
- Secure attachment is a protective factor in psychological health
- When adults become parents, they become the caregiver in the attachment relationshipand their internal representations of being cared for is important to the infant’s development
What are common features of youth depression?
- Difficulty concentrating and making decisions
- Being self-critical and self-blaming
- Negative body image and low self-esteem
- Having thoughts of suicide
- Antidepressants aren’t very effective for adolescent depression
What does adolescent self harm look like? and what are the underlying causes?
SELF-HARM
- Different condition to suicide unless the self-harm was a suicide attempt
- Can be attention seeking for distress, anger, rejection of self, wanting the observer self to be angry with the self-image and stress release
- Self-harm reflects ongoing dysphoria
Outline how important factors and all key areas of History taking in adolescent patients? What history do we take from the Parent?
What areas do we cover in a risk Assessment?
What are static risk factors (risk assessment)? (e.g what has happened in the past)
What are the dynamic risk factors? (e.g what is the patient doing right now)
HISTORY TAKING
- Assess the adolescent’s feelings to ascertain if there are any self-image or self-esteem issues
- Establish rapport, ambitions, hobbies and preferred activities
- Explore FSF- Friends, School and Family
- Family- relationship with siblings and parents
- School- favourite subjects
- Peers- relationships, quality of interactions and friendships, any bullying
- Ask projective questions- wishes for the future, ideal future and fears
- What the main problem is?
- Help- what could be of most help to them
GENERAL HISTORY FROM PARENT:
- Past psychiatric history
- Past medical history
- Drugs and alcohol (including levels of use)
- Family Psychiatric history
- Forensic history
- Neurodevelopmental
- Premorbid personality
RISK ASSESSMENT OF PATIENTS:
- Suicide
- Violence/ aggression
- Vulnerability
- Risk of disengagement
- Drugs and alcohol
- Child protection risk issues————>If the consumer has custody or care responsibilities over a child then they must complete the Mental Health Child Protection form (SW188)
STATIC RISK FACTORS- WHAT HAS HAPPENED IN THE PAST:
- Previous suicide attempt
- History of self-harm
- Family history of suicide
- Long-standing problems- unemployment, physical illness, pain
DYNAMIC RISK FACTORS- WHAT THE PATIENT IS DOING NOW?
- Intent/ plan/ thoughts
- Current suicide attempt
- Distress/ anger
- Isolated/ lonely
- Psychotic symptoms (command hallucinations
- Carries firearms
- Intoxication
What does the doctor investigating self-harm and suicide have to ask and assess?
What are the types of ways these young patients can be identified as ‘vulnerable’?
What is and absence without approval? (Absence without leave)
DOCTOR (INVESTIGATING SELF-HARM AND SUICIDE):
- Thoughts of self-harm: Duration, types of thoughts, ignoring thoughts
- Why is the patient getting the thoughts (triggers): Anxiety, depression
- Plans: Loss of hope, don’t want to live, suicide
- Access to means: You tube, access to lethal means
- Attempts in the past
- FHx of suicide
- Self-harm → managed in the community e.g. BPD>> working on psychotherapy to increase coping mechanisms
VULNERABILITY
- At risk of being sexually abused
- At risk of domestic/ family violence
- At risk of being financially abused by others
- At risk of self-neglect (Basic ADLs, complex living skills)
- Cognitive impairment/ intellectual disability
ABSENCE WITHOUT APPROVAL (AWOL- ABSENCE WITHOUT LEAVE)
- History of absconding
- Treatment refusal
- Frustration regarding hospitalisation/ involuntary treatment
What is anxiety? What does its roles serve physiologically?
What are mainfestiation of anxiety?
When does anxiety become pathological?
What disorders are encompassed as ‘anxiety’ disorders?
What is the difference between fear and anxiety?
What are you differential diagnosis when seeing a patient with ‘anxiety’ like symptoms?
ANXIETY DISORDERS:
- Anxiety is a universal human characteristic involving tension, apprehension, or even terror
- Serves as an adaptive mechanism to warn about an external threat by activating the sympathetic nervous system (fight or flight)
- Manifestations of anxiety can be described through
- Physiology: main brain structure involved is the amygdala (fear conditioning); neurotransmitters involved include 5-HT, cholecystokinin, epinephrine, norepinephrine, DA
- Psychology: one’s perception of a given situation is distorted which causes one to believe it is threatening in some way
- Behaviour: once feeling threatened, one responds by escaping or facing the situation, thereby causing a disruption in daily functioning
• Anxiety becomes pathological when
- Fear is greatly out of proportion to risk/severity of threat
- Response continues beyond existence of threat or becomes generalized to other similar or dissimilar situations
- Social or occupational functioning is impaired
- Often comorbid with substance use and depression
- Anxiety disorders include disorders that share features of excessive fear and related behavioural disturbances
- Fear is the emotional response to real or perceived imminent threat whereas anxiety is anticipation of future threat.
- Anxiety is associated with muscle tension and vigilance in preparation for future danger and cautious or avoidant behaviours.
DIFFERENTIAL DIAGNOSIS
- CVS: Post-MI, arrhythmia, CHF, pulmonary embolism, MV prolapse
- Respiratory: asthma, COPD, pneumonia, hyperventilation
- Endocrine: Hyperthyroidism, Phaeochromocytoma, hypoglycemia, hypoadrenalism
- Metabolic: Vitamin b12 deficiency, porphyria
- Neurologic: Neoplasm, encephalitis
- Substance induced: intoxication, withdrawal
- Other psychiatric disorders: Psychosis, mood disorders, personality disorders, somatoform disorders
What is PSTD?
What are the major DSM V criteria for diagnosis? (hint 8 major criteria need to be met)
(e.g 1) exposure to death/inury/serious violence) 2) Presence of 1> intrusive symptoms (dreams/flashbacks/physiological reactions to internal/external cues resemblin event) 3) persistence of avoidance of stimuli associated with the truamtic event)
What are the major treatment/management options?
What are some complications associated with PTSD?
DSM CRITERIA:
A. Exposure to death, injury or sexual violence in >1 of the following ways
- Directly experiencing the traumatic event
- Witnessing the event to others
- Learning that the traumatic event occurred to a close family member or close friend. In cases of actual or threatened death of a family or friend, the event must have been violent or accidental
- Experiencing repeated or extreme exposure to aversive details of the traumatic event (e.g. first responders collecting human remains; police officers repeatedly exposed to details of child abuse)
- this doesn’t include to exposure through electronic media, TV, movies, unless the exposure is work-related.
B. Presence of >1 of the following intrusive symptoms associated with the traumatic event beginning after the traumatic event:
- Recurrent distressing memories of the traumatic event
- Recurrent distressing dreams where the content and/or affect of the dream are related to traumatic event
- Dissociative reactions (e.g. flashbacks) where the individual feels or acts as if the traumatic event was recurring
- Intense or prolonged psychological distress at exposure to internal or external cues that resemble the traumatic event
- Marked physiological reactions to internal or external cues resembling the traumatic event
C. Persistent avoidance of stimuli associated with the traumatic event, beginning after the traumatic event with >1 of
- Avoidance of distressing memories, thoughts or feelings closely related to the traumatic event
- Avoidance of or efforts to avoid external reminders (e.g. people, places) that arouse distressing memories/ thoughts/ feelings about the traumatic event
D. Negative alterations in cognitions and mood associated with the traumatic event, beginning or worsening after the traumatic event with >2 of the following:
- Inability to remember an important part of the traumatic event
- Persistent and exaggerated negative beliefs or expectations about oneself, others or the world
- Persistent distorted cognitions about the cause or consequence of the traumatic event that leads the individual to blame themselves or others
- Persistent negative emotional state (e.g. fear, horror, anger, guilt or shame)
- Markedly diminished interest or participation in significant activities
- Feelings of detachment or estrangement from others
- Persistent inability to experience positive emotions
E. Marked alterations in arousal and reactivity associated with the traumatic event beginning or worsening after the traumatic event occurred with >2
- Irritable behaviour and angry outbursts with little or no provocation often expressed as verbal or physical aggression towards people or objects
- Reckless or self-destructive behaviour
- Hypervigilance
- Exaggerated startle response
- Problems with concentration
- Sleep disturbance (e.g. difficulty falling or staying asleep or restless sleep)
F. Duration of the disturbance (B, C, D and E) is >1 month
G. The disturbance causes clinically significant distress or impairment of social, occupational or other areas of functioning
H. The disturbance is not attributable to the physiological effects of a substance or other medical condition.
- In children >6 years, repetitive play may occur where themes or aspects of the traumatic event are expressed
- Children may have nightmares without recognizable content
- Trauma-specific re-enactment may occur in play in children
• Patients may have dissociative symptoms- in response to the stressor, the individual experiences persistent or recurrent symptoms of either:
- Depersonalization: Persistent or recurrent experiences of feeling detached from as if the patient was an observer of their own mental processes or body (e.g. feeling as though one were in a dream; feeling a sense of unreality of self or body or of time moving slowly)
- Derealization: Persistent or recurrent experiences of unreality of surroundings (e.g. the world around the individual is experienced as unreal, dreamlike, distant)
- The dissociative symptoms must not be attributable to the physiological effects of a substance
TREATMENT
- Psychotherapy, CBT
- Ensure safety and stabilize- emotional regulation techniques (e.g. breathing, relaxation)
- Establish coping mechanisms
- Explore/ mourn trauma- challenge dysfunctional beliefs
- Exposure therapy- Reconnect and integrate
- SSRIs (e.g. sertraline, paroxetine)
- Prazosin (treats disturbing dreams and nightmares)
- Benzodiazepines (acute anxiety)
- Adjunctive atypical antipsychotics (risperidone, olanzapine)
- Eye movement desensitization and reprocessing (EDR)
COMPLICATIONS:
- Substance abuse
- Relationship difficulties
- Depression
- Social and occupational functioning disorders
- Personality disorders
What is an Acute stress disorder?
What is the DSM V criteria for this? ( 5 major criteria)
What is the typical clinical presentation?
What is the management?
ACUTE STRESS DISORDER:
- Acute stress disorder is distinguished from PTSD because the symptom pattern in Acute Stress Disorder is restricted to 3 days- 1 month following exposure to a traumatic event.
- Acute Stress Disorder
- Acute Stress disorder may be a precursor to PTSD
- Similar symptoms to PTSD
- Symptoms persist >3 days- 1 month after the exposure
DSM:
A. Exposure to death, injury or sexual violation in >1 of the following:
- Directly experiencing traumatic event
- Witnessing
- Learning that the event occurred to a close family member or friend (must be violent or accidental)
- Repeated or extreme exposure to aversive details of the traumatic event (e.g. first responders collecting human remains, police officers repeatedly exposed to details of child abuse). This doesn’t include exposure through electronic media, TV, movies, unless the exposure is work-related.
B. Presence of >9 of the following symptoms from any of the following 5 categories: Intrusion, negative mood, dissociation, avoidance and arousal (beginning or worsening after the traumatic event):
• Intrusion symptoms:
- Recurrent, intrusive, involuntary memories (children-repetitive play)
- Recurrent distressing dreams where the content and/or affect of the dream is related to the event. Children- nightmares)
- Dissociative reactions (e.g. flashbacks) where the individual feels or acts as if the traumatic event is recurring.(Patients may have a complete loss of awareness of present surroundings)
- Intense distress or increased reactions to internal or external cues that symbolize or resemble an aspect of the traumatic event.
• Negative mood
- Persistent inability to experience positive emotions (e.g. happiness, satisfaction, love)
Dissociative symptoms:
- An altered sense of the reality of one’s surroundings or oneself (e.g. seeing oneself from another’s perspective, time slowing)
- Avoiding external reminders (people, places) that cause distressing memories, thoughts or feelings about the event
• Arousal symptoms
- Sleep disturbance (e.g. difficulty falling asleep/ staying asleep/ restless sleep)
- Irritable behaviour and angry outbursts (verbal or physical aggression towards people or objects)
- Hypervigilance
- Concentration problems
- Startled
C. Duration of the disturbance (Criterion B) persists for 3 days-1 month after the trauma
D. Disturbance causes distress or impairment in social/ occupational/ functioning
E. The disturbance is not attributable to physiological effects of a substance (medication, alcohol), medical condition and is not better explained by a psychotic disorder.
CLINICAL PRESENTATION:
- Typically involves an anxiety response that involves a form of re-experiencing or reactivity to the traumatic event
- Dissociative or detached presentation
- Anger response where reactivity is characterised by irritability or aggression
TREATMENT:
- CBT (pharmacotherapy is usually not indicated)
What is an ‘Adjustment disorder’?
What are the 5 major DSM V criteria to diagnose this condition?
What is the typical clinical presentation?
What is the treatment/management?
Adjustment disorder (AjD) is a mental and behavioral disorder, which is a maladaptive response to a psychosocial stressor that occurs when an individual has significant difficulty adjusting to or coping with a stressful psychosocial event. The maladaptive response usually involves otherwise normal emotional and behavioral reactions that manifest more intensely than usual (considering contextual and cultural factors), causing marked distress, preoccupation with the stressor and its consequences, and functional impairment
ADJUSTMENT DISORDER:
DSM:
A. Development of emotional or behavioural symptoms from an identifiable stressor within 3 months of the onset of the stressor.
B. These symptoms or behaviours are clinically significant with at least 1 of:
- Marked distress out of proportion to the severity or intensity of the stressor
- Significant impairment in social, occupational or other areas of functioning
C. The stress-related disturbance doesn’t meet criteria for another mental disorder and is not merely an exacerbation of a pre-existing mental disorder
D. The symptoms don’t represent normal bereavement
E. Once the stressor or its consequences have terminated, the symptoms don’t persist for more than an additional 6 months.
• Specify type!!!
- With depressed mood: Low mood, tearfulness or feelings of hopelessness
- With anxiety: Nervousness, worry, jitteriness or separation nxiety
- With mixed anxiety and depressed mood: A combination of depression and anxiety is predominant
- With disturbance of conduct
- With mixed disturbance of emotions and conduct: Both emotional symptoms (e.g. depression, anxiety) and a disturbance of conduct are predominant
- Acute: Disturbance lasts <6 months
- Persistent (chronic): If the disturbance lasts >6 months
CLINICAL PRESENTATION
- The identifiable stressor can be a single event or there may be multiple stressors
- Some stressors can accompany specific developmental events e.g. going to school, leaving a parental home, getting married
- Adjustment disorders can be diagnosed following the death of a loved one when the intensity, quality or persistence of grief exceeds what is normally expected
- The subjective distress or impairment in functioning associated with adjustment disorders is often manifested as decreased performance at work or school
TREATMENT
- Brief psychotherapy- Individual or group
- Crisis intervention
- Benzodiazepines (significant anxiety symptoms>> short-term, low dose)
What is OCD?
What is the 4 major DSM V criteria for diagnosis?
What is the management of OCD?
What is the prognosis of OCD look like?
What is the differential diagnosis for OCD?
OCD:
DSM-5 CRITERIA
A. Presence of obsessions, compulsions or both
- Obsessions: recurrent and persistent thoughts, urges or images that are experienced at some time during the disturbance, as intrusive and unwanted, and cause marked anxiety or distress in most individuals. The individual attempts to ignore or suppress such thoughts, urges or images or to neutralise them with some other thought or action
- Compulsions: repetitive behaviours or mental acts, that the individual feels driven to perform in response to an obsession or according to rules that must be applied rigidly. Behaviours/mental acts are aimed at preventing or reducing anxiety or distress, or preventing some dreaded event or situation, however these behaviours or mental acts are not connected in a realistic way with what they are designed to neutralise or prevent or are clearly excessive
B. The obsessions and compulsions are time consuming (>1hr a day) or cause clinically significant distress or impairment in social, occupational, or other important areas of functioning
C. The obsessive compulsive symptoms are not better attributable to the physiological effects of a drug
D. The disturbance is not better explained by the symptoms of another mental disorder
• Rate of OCD in first-degree relatives is higher than in general populations and females are effected at slightly higher rates than males.
MANAGEMENT
- CBT: exposure to the feared situations with prevention of compulsive behaviours and cognitive strategies such as challenging the underlying belief
- SSRI/SNRI used in higher doses than in depression
- Clomipramine: TCA or risperidone
PROGNOSIS
• Refractory and chronic
DIFFERENTIAL DIAGNOSIS
- Anxiety disorder
- MDD
- Eating disorder
- Tics and stereotyped movements
- Psychotic disorder
- Obsessive compulsive personality disorder
- PD not characterised by intrusive thoughts, images or urgers or by repetitive behaviours
- Instead it involves an enduring and maladaptive pattern of excessive perfectionism and rigid control
What is a ‘panic disorder?
What is the DSM V criteria for the diagnosis of a panic disordeer?
What is the acronymn to recall the “STUDENTS FEAR the 3CS”. ?
What is the management?
PANIC DISORDER:
- A person has panic attacks, which are intense, overwhelming and often uncontrollable feelings of anxiety combined with a range of physical symptoms (SOB, chest pain, dizziness, sweating)
- The person experiences recurrent unexpected panic attacks and is persistently worried about having more panic attacks or changes their behaviour in maladaptive ways because of the panic attacks
- Panic attacks are abrupt surges of intense fear or discomfort that reach a peak within minutes and are accompanied by physical and/or cognitive symptoms.
DSM-5 CRITERIA
A. Recurrent unexpected panic attacks - a panic attack is an abrupt surge of intense fear or intense discomfort that reaches a peak within minutes, and during which 4+ of the following symptoms occur: → STUDENTS FEAR the 3Cs
1. Sweating
2. Trembling
3. Unsteadiness and dizziness
4. Depersonalisation or derealisation
5. Excessive heart rate, palpitations
6. Nausea
7. Tingling
8. SOB
9. Fear of dying, losing control and going crazy
10. Chest pain
11. Chills
12. Choking
B. 1 month (or more) of “anxiety about panic attacks” - at least one of the attacks has been followed by one or both of the following:
- Persistent concern or worry about additional panic attacks or their consequences
- A significant maladaptive change in behaviour related to the attacks
C. The disturbance is not attributable to the physiological effects of a substance or another medical condition
D. The disturbance is not better explained by another mental disorder
TREATMENT
• CBT: interoceptive exposure (eliciting symptoms of a panic attack and learning to tolerate the symptoms without coping strategies); cognitive restructuring (addressing underlying beliefs regarding the panic attacks), relaxation techniques (visualization, box-breathing)
• Pharmacological
- SSRIs: fluoxetine, ecitalopram, paroxetine, fluvoxamine, sertraline
- SNRI: venlafaxine
- With SSRI/SNRIs start with low doses, titrate up slowly
- Anxiety disorders often require treatment at higher doses for a longer period of time than depression (i.e. full response may take up to 12 wk)
- Treat for up to 1 year after symptoms resolve to avoid relapse
- To prevent non-compliance due to physical side effects, explain symptoms to expect prior to initiation of therapy
- Other antidepressants (mirtazapine, MAOIs)
- Consider avoiding bupropion or TCAs due to stimulating effects (exacerbate anxious symptoms)
• Benzodiazepines (short-term, low dose, regular schedule, long half-life, avoid prn usage)
What is Generalised anxiety disorder?
What is the DSM V crtiteria (6 major) for the diagnosis of Generalised anxiety disorder?
What is the acronym ‘FIRST C’ for symptoms? (needing 3 or more for diagnosis.
What is the management?
What is the management for childhood anxiety disorders?
What are the differential diagnsois for GAD?
GENERALISED ANXIETY DISORDER:
- A person feels anxious on most days, worries about multiple things
- Persistent and excessive anxiety and worry about many events or activities including work and school performance, which the individual finds difficult to control
- The person feels restlessness or feeling keyed up on the edge; easy fatigue; difficulty concentrating or mind going blank; irritability; muscle tension and sleep disturbance
- Adults with GAD often worry about routine life circumstances e.g. job responsibilities, health and finances, health of family members, misfortune to their children or minor matters (e.g. housework or being late for appointments)
- Associated with muscle tension (trembling, twitching, feeling shaky and muscle aches)
- Many patients experience somatic symptoms (e.g. sweating, nausea, diarrhoea)
DSM-5 CRITERIA
A. Excessive anxiety and worry (apprehensive expectation), occurring more days than not for at least 6 months, about a number of events or activities (such as work or school performance)
B. The individual finds it difficult to control the worry
C. The anxiety and worry are associated with three or more (1 or more in children) of the following:
→ FIRST C
1. Fatigue
2. Irritability
3. Restlessness
4. Sleep disturbance
5. Tension
6. Concentration issues
D. The anxiety, worry, or physical symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning
E. The disturbance is not attributable to the physiological effects of a substance or another medical condition
F. The disturbance is not better explained by another mental disorder
MANAGEMENT
- Lifestyle changes: decrease caffeine and alcohol, sleep hygiene
- Medical work-up: FBC, TFT, U&E, urinalysis and urine drug screen.
- Psychological strategies such as cognitive behavioural therapy and mindfulness
- SSRI and SNRIs: sertraline, escitalopram, venlaflaxine
- May use benzodiazepines PRN
CHILDHOOD ANXIETY DISORDERS
- Family psychotherapy in a predictive and supportive environment
- CBT with child and parental education, relaxation techniques, exposure or desensitisation and recognising and correcting anxious thoughts.
- Pharmacotherapy: SSRI (fluoxetine) or benzodiazepines. However, should be used with caution due to addictive potential and possible neurodevelopmental delay
DIFFERENTIAL DIAGNOSIS
- Anxiety disorder due to another medication condition
- Substance/medication induced anxiety disorder Social anxiety disorder
- OCD
- PTSD
What is Separation anxiety disorder? Who does it affect?
What is the DSM V criteria for the diagnosis of separation anxeity disorder?
What is selective mutism? Who does if effect (children and adults - e.g whats time for diganosis w symptoms)? What is the DSM V criteria for diagnosis?
SEPARATION ANXIETY DISORDER
DSM
A. Developmentally inappropriate and excessive fear or anxiety concerning separation from those to whom the individual is attached with at least 3 of the following:
- Recurrent excessive distress when anticipating or experiencing separation from home or from major attachment figure
- Persistent and excessive worry about losing major attachment figures or about possible harm to them (illness, injury, disasters, death)
- Persistent and excessive worry about experiencing an untoward event (e.g. getting lost, kidnapped, having an accident) that causes separation from a major attachment figure
- Persistent reluctance or refusal to go away from home because of the fear of separation
- Persistent and excessive fear of or reluctance about being alone or without major attachment figures at home or elsewhere
- Persistent reluctance or refusal to sleep away from home or to go to sleep without being near a major attachment figure
- Repeated nightmares involving separation
- Repeated complaints of physical symptoms (e.g. headaches, stomach aches, nausea, vomiting) when separation from major attachment figures occurs or is anticipated
B. The fear, anxiety or avoidance is persistent and lasts 4 weeks in children and adolescents and often 6 months or more in adults
C. The disturbance causes clinically significant distress or impairment in social, occupational or other areas of functioning
D. The disturbance is not better explained by another mental disorder (e.g. refusing to leave home because of excessive resistance to change in Autism Spectrum Disorder)
- Individuals with separation anxiety disorder have excessive fear or anxiety about separation from attachment figures to a degree that is developmentally inappropriate
- There is persistent fear or anxiety about harm coming to attachment figures and events that could lead to loss or separation from attachment figures
- Adults with separation anxiety disorder are often overconcerned about their children and spouses and experience marked discomfort when separated from them
- They may experience significant disruption in work or social experiences because of needing to continuously check on the whereabouts of a significant other.
SELECTIVE MUTISM
DSM
A. Consistent failure to speak in specific social situations in which there is an expectation for speaking (e.g. at school) despite speaking in other situations
B. The disturbance interferes with educational or occupational achievement or with social communication
C. The duration of the disturbance is at least 1 month
D. The failure to speak is not attributable to a lack of knowledge with the spoken language required in the social situation
E. The disturbance is not better explained by a communication disorder and doesn’t occur exclusively during the course of Autism spectrum disorder, schizophrenia
- Characterised by a consistent failure to speak in social situations where there is an expectation to speak (e.g. school) even though the individual speaks in other situations
- This causes social, occupational or academic impairment
- Children with selective mutism don’t initiate speech or reciprocally respond when spoken to by others
What is Social anxiety disorder? What is the DSM V criteria for the diagnosis of it?
What is Agoraphobia?
What is the DSM V criteria for diagnosis?
SOCIAL ANXIETY DISORDER (SOCIAL PHOBIA)
- A person has an intense fear of being criticized, humiliated or embarrassed even in everyday situations such speaking in public, eating in public being assertive at work, etc.
- The individual is anxious or avoidant of social interactions and situations that involve the possibility of being scrutinized.
- This includes meeting unfamiliar people, situations where the individual may be observed eating and situations where the individual performs in front of others.
- The cognitive ideation is being negatively evaluated by others, being embarrassed, humiliated or rejected.
DSM
A. Marked fear or anxiety about 1 or more social situations where the individual is exposed to possible scrutiny by others.
B. The individual fears that they will act in a way or show anxiety that will be negatively evaluated
C. The social situations almost always provoke fear or anxiety
D. The social situations are avoided or endured with intense fear or anxiety
E. The fear of anxiety is out of proportion to the actual threat posed by the social situation and to the sociocultural context.
F. The fear, anxiety or avoidance is persistent, typically lasting for 6 months or more
G. The fear, anxiety or avoidance causes clinically significant distress or impairment in social, occupational or other areas of functioning
H. The fear, anxiety or avoidance is not attributable to the physiological effects of a substance or another medical condition
I. The fear, anxiety or avoidance is not better explained by the symptoms of another mental disorder (e.g. panic disorder, autism spectrum disorder)
AGORAPHOBIA
- The individual fears these situations because of thoughts that escape might be difficult or help might not be available in the event of developing panic-like symptoms or other incapacitating or embarrassing symptoms.
- It can cause individuals to become completely homebound in severe forms
- The majority of people with agoraphobia develop this as a response to the onset of recurrent panic attacks
DSM:
A. Marked fear or anxiety about 2 or more of the following 5 situations:
- Using public transport (e.g. automobiles, buses, trains, ships, planes)
- Being in open spaces (e.g. parking lots, marketplaces, bridges)
- Being in enclosed spaces (e.g.. shops, theatres)
- Standing in line or being in a crowd
- Being outside of the home alone
B. The person avoids these situations because escape might be difficult or help might not be available if they develop panic-like symptoms or embarrassing symptoms (e.g. fear of falling in the elderly; fear of incontinence)
C. The agoraphobic situations almost always provoke fear or anxiety
D. The agoraphobic situations are actively avoided, require the presence of a companion or are endured with intense fear or anxiety
E. The fear or anxiety is out of proportion to the actual danger posed by the situation and to the sociocultural context
F. The fear, anxiety or avoidance is persistent, typically lasting for 6 months or more
G. The fear, anxiety or avoidance causes clinically significant distress or impairment in social, occupational or other areas of functioning
H. If another medical condition is present, the fear, anxiety or avoidance is clearly excessive
I. The fear, anxiety or avoidance is not better explained by the symptoms of another mental disorder (e.g. don’t involve only social situations- social anxiety disorder) (GAD)
What are the 4 important psychological variables that predict a persons vulnerability to anxiety?
What other factors contribute to anxiety disorders?
PSYCHOLOGICAL FACTORS CONTRIBUTING TO ANXIETY DISORDERS:
• There are 4 important psychological variables that predict a psychological vulnerability to anxiety:
- Perceived control e.g. lack of perceived control over stressful life circumstances
- Cognitive appraisals
- Cognitive beliefs
- Cognitive distortions
- Personality factors- perfectionism, shy, low self-estee
- Ongoing stress
- Poor coping strategies
- Temperament e.g. neuroticism or anxiety sensitivity
- Other causes:
- Genetics
- Traumatic events that cause significant distress
What is basic process to determine management of Anxiety disorder?
GAD management principles?
Panic attacks/ disorder?
OCD?
Phobic disorders (inc agorphobia, social anxiety disorder)
PTSD?
MANAGEMENT OF ANXIETY DISORDERS:
- Anxiety can be primary or secondary to psychiatric (e.g. depression) or medical illnesses (e.g. hyperthyroidism)
Management
- The first step is to define the type of anxiety disorder
- Identify and address any psychological factors that may cause or exacerbate the disorder e.g. financial, relationship difficulties
- Address lifestyle factors: alcohol, excess caffeine, drugs, excessive work and inadequate sleep
- Firstline treatment for mild-to-moderate disorder: eTherapy and CBT
- Severe or persistent anxiety- medications
GAD
- GAD has a fluctuating course, but tends to be a long-term disorder
- Hyperthyroidism, caffeine intoxication, stimulant use, alcohol/drug discontinuation syndrome must be excluded
- Exclude depression or dementia in middle-aged or older patients first presenting with anxiety symptoms
TREATMENT PRINCIPLES:
- Firstline therapy: Psychological interventions
- Provide information about the anxiety disorder and education on relaxation techniques and coping skills
- Stress management approaches includes activity scheduling, modifying lifestyle factors, problem-focused counselling and structured problem solving
- CBT
• Second-line therapy: SSRIs
- SNRIs can be used
- Buspirone is another alternative (no potential for tolerance or dependence and no discontinuation syndrome)
- Trial reduction and cessation of medication after the patient has been symptom free for at least 6 month
- Benzodiazepines may be used for the treatment of GAD as a short-term measure during crises when anxiety is severe and disabling or causing the patient unacceptable distress
- Benzodiazepines are associated with dependence, cognitive impairment, psychomotor effects- falls
- Treatment with benzodiazepines should be up to 2 weeks followed by gradual reduction of dose to 0 within 6 weeks
- Avoid using short-acting drugs as they are the most highly addictive
PANIC ATTACK
- Treat isolated panic attacks with psychological interventions
- Explanation, support and stress management advice are effective
- People should be told of breathing techniques (slow and deeply) or rebreathing in a bag placed over the mouth
PANIC DISORDER
- Characterised by recurrent panic attacks where the onset of the attack is not associated with a situational trigger.
- Associated symptoms:
- Anticipatory anxiety (persistent concern of having additional attacks)
- Increased generalised anxiety or tension
- Somatic preoccupation
- Phobic avoidance
FIRSTLINE TREATMENTS: PSYCHOLOGICAL INTERVENTIONS
- Education about the disorder (explain how the panic attack produces physical symptoms)
- Breathing control and relaxation strategies
- CBT- exposure to deliberately induced symptoms with techniques for controlling symptoms
SECOND-LINE THERAPIES (IF CBT IS NOT AVAILABLE/ INEFFECTIVE): SSRIS AND VENLAFAXINE
- Medications for panic disorder may need to be continued for 6-12 months. The dose should then be slowly reduced and eventually stopped.
- Always use psychological interventions to minimise the need for prolonged medications
- Use CBT concurrently with medications
- SSRIs/ venlafaxine- On initiation of treatment, there may be a transient increase in anxiety, which usually resolves after several days (It is lessened with lower initial doses or if the patient’s distress is problematic, with short-term use of a benzodiazepine)
- Response to antidepressants takes several weeks
OBSESSIVE COMPULSIVE DISORDER
- Obsessions are recurrent and persistent intrusive ideas, thoughts, impulses that are usually resisted by the person
- Compulsions are repetitive, stereotyped behaviours in response to an obsession to prevent discomfort
MANAGEMENT
- Education and support for family and close friends
- CBT (exposure to the triggers with prevention of rituals)
- SSRIs- responses may not be seen for 6-12 weeks and normally needs to be continued for 6-12 months
PHOBIC DISORDERS INCLUDING AGORAPHOBIA, SOCIAL ANXIETY DISORDER:
- CBT
AGORAPHOBIA
- Control the panic attacks
- Behavioural therapy
SOCIAL ANXIETY DISORDER
- Generalised social anxiety: Fear of numerous social situations including both performance and interactional situations
- Non-generalised social anxiety- fear of 1 or just a few situations of performance type.
GENERALISED SOCIAL ANXIETY DISORDER:
- CBT (incorporating exposure-based therapy, social skills training and cognitive therapy)
- SSRIs (firstline), venlafaxine and irreversible, non-selective MAOIs>> medications need to be continued for 6-12 months
NON-GENERALISED SOCIAL ANXIETY DISORDER:
- Control of hyperventilation
- Cognitive strategies
- Medications are given to reduce physiological symptoms of sympathetic overactivity (e.g. tremor, palpitations and sweating) —-> Beta blockers)
PTSD
- Re-experience, increased arousal, avoidance and dissociative symptoms (e.g. detachment and depersonalisation)
- Re-experiencing symptoms: Intrusive thoughts, dreams, nightmares, flashbacks
- Hyperarousal- increased startle response, irritability, anger, sleep disturbance, poor concentration and memory
- Avoidance and numbing- deliberate attempts to keep the traumatic event out of mind, anhedonia, detachment or estrangement from others, restricted emotional responses
TREATMENT
- Trauma-focussed psychological therapy (either trauma-focussed CBT or eye movement desensitisation and reprocessing)
- Teach emotional regulation skills
- Anger and anxiety management, stress reduction, relaxation therapy and advice on good sleep practices
- Treat co-morbidities especially depression and alcohol use
- SSRIs
ELICIT SIGNS AND SYMPTOMS OF ANXIETY DISORDERS
- Over-generalization and/or deficits in extinction of conditioned fear
- Overactivity in limbic areas (amygdala and insula) during processing of emotional stimuli
SYMPTOMS:
- Palpitations, pounding heart, accelerated heart rate
- Sweating
- Trembling/ shaking
- SOB or smothering sensation
- Feelings of choking
- Chest pain
- Nausea or abdominal distress
- Dizziness, unsteadiness, life-headedness
- Insomnia
- Irritability
- Muscle tension
SIGNS
- Irritable
- Sinus tachycardia
- Tachypnoea
- Diaphoresis
- Nervousness and trembling
How do we explain a “Anxeity disorder”, diagnosis to the patient? (e.g eitology/ explain symptoms), what likely causes? Pathogenesis?
EXPLAIN THE ETIOLOGY OF ANXIETY SYMPTOMS TO A PATIENT
- Genetic factors, family environment, critical life stressors and underlying temperament interact to enhance or trigger cerebral fear networks.
ETIOLOGY FOR ANXIETY SYMPTOMS:
- Medical conditions
- Substance-induced anxiety disorders
- Genetics
- Psychological: Conflict between the id and ego; intrapsychic conflicts; psychiatric co-morbidities
- Environmental factors: Early childhood trauma; traumatic experiences or recurring negative experiences
MEDSCAPE:
- Anxiety disorders are caused by genetic vulnerability that interacts with situations, stress and trauma to cause clinically significant anxiety.
GAD
- Genetics
- History of physical or emotional trauma, low socioeconomic status, internalizing problems, stressful life events (e.g. child abuse)\
- Neurobiological brain changes
- HPA axis: Stress stimulates CRF → ACTH (anterior pituitary)
- Abnormal functioning of serotonin and cortisol
- Increased noradrenaline
PATHOGENESIS
- The amygdala is involved in fear and anxiety
- Anxiety disorders have heightened amygdala responses to anxiety cues
- The amygdala and other limbic system structures are connected to the prefrontal cortex
- Prefrontal-limbic activation abnormalities may underlie anxiety with hyperresponsiveness of the amygdala relating to reduced activation threshold when responding to perceived threats
- Hyperactive amygdala (due to apprehensive expectations) stimulates the SNS and increased cortisol secretion (becomes chronic due to disrupted emotional regulation
- Increased SNS → increased vision, hearing becomes more acute, muscles tense, blood flow to the brain increases, heart and RR increase, redirection of blood.
- Liver releases glucose for the muscles
- Saliva and mucus dries up to increase the size of air passages to the lungs
BRAIN CIRCUITRY AND ANXIETY
- Amygdala: Detecting, coordinating and maintaining fear
- Prefrontal cortex: Governs amygdala function, limits fear response
- Hippocampus: Supplies amygdala with information about the context. Retrieves information from memory.
MEDSCAPE:
- The main mediators for anxiety symptoms in the CNS are: NA, DA, 5-HT and GABA
- The SNS mediates most of the symptoms peripherally
SEPARATION ANXIETY DISORDER
- Genetics
- Develops after a stressful life event (death, illness of an individual, divorce, etc)
- Parental overprotection and intrusiveness
SPECIFIC PHOBIAS
- Temperament: Neuroticism or behavioural inhibition
- Environment: Parental overprotectedness, parental loss and separation; physical and sexual abuse
- SNS arousal
NATURE OF ANXIETY
- The normal fear response to threatening stimuli includes: Defensive behaviours, autonomic reflexes, cortisol, negative emotions, and arousal and alertness
- In anxiety, these reactions occur in an anticipatory manner
What are medications used in 1) acute anxiety 2) chronic anxiety? What are the classes of these drugs?
What are the side effects of these medications?
What are some precautions when prescribing benzodiazpines? What does withdrawl from benzos look like Signs/symptoms?
What is buspirone? What is its MOA?
SSRIS?
Anti-epileptics?
ANTI-ANXIETY MEDICATIONS:
- Anxiety:
- Acute administration: Benzodiazepines and β-adrenergic antagonists
- Chronic administration: Buspirone and antidepressants
- Drugs in the treatment of anxiety disorders:
- Decrease central anxiogenic neural activity (excitability)- Benzodiazepines, Antiepileptic drugs
- Altering central anxiogenic neurotransmission: Buspirone (serotonin), antidepressants (serotonin and noradrenaline), atypical antipsychotics (serotonin, noradrenaline and dopamine)
- Altering peripheral anxiogenic neurotransmission- Beta-adrenoreceptor antagonists
- Antidepressants are the main drugs used to treat anxiety especially when it is associated with depression
Classes of anxiety drugs:
- Antidepressants (SSRIs and SNRIs): Effective in the treatment of GAD, phobias, social anxiety disorder and PTSD
- Also treats concomitant depression
- Benzodiazepines: Treats acute anxiety—> They can be co-administered during stabilisation of a patient on an SSRI
- Useful in panic disorder ——> Buspirone: 5-HT1A receptor agonist
- Useful in GAD—-> Gabapentin, pregabalin, tiagabine, valproate and levetiracetam- effective in treating GAD
- Some atypical antipsychotics: Olanzapine, risperidone, quetiapine – GAD and PTSD
- β-adrenoreceptor antagonists (e.g. propranolol)- treats physical symptoms of anxiety (e.g. sweating, tremor, tachycardia)
BENZODIAZEPINES
- Diazepam, lorazepam and oxazepam are used in anxiety
- Indications: Effective in the treatment of GAD, panic disorder and situational anxiety.
- Anxiolytic effects- Positive allosteric modulator by binding to booster sites on the GABAA receptor complex → enhances the affinity of GABA to GABAA receptors → increases the frequency of channel opening, which increases Cl(-) conductance → hyperpolarisation and inhibition of the neurone
- α2 mediates anxiolytic effects
- α1 mediates sedative effect
• Note: Benzodiazepines increase inhibition of GABA neurons → disinhibits DA neurons in the mesolimbic pathway to cause dependence
SIDE EFFECTS: SEDATIVE, HYPNOTIC, ANTICONVULSANT, MUSCLE RELAXANT
- Impairs cognitive performance and memory
- Affects motor control
- Tolerance to the anxiolytic effects develops with chronic administration
- Should be used for short periods and in conjunction with other medications (e.g. SSRIs) or psychotherapies (e.g. CBT)
Common side effects:
- Drowsiness, oversedation, ataxia, slurred speech, hypersalivation
Withdrawal symptoms:
- Tachycardia, hypertension, sweating, tremors, seizures
- Anxiety, irritability, insomnia, nightmares
- Short-acting benzodiazepines may cause withdrawal symptoms within a few hours
- Long-acting benzodiazepines may take days or weeks and can last for several weeks or longer
PRECAUTIONS
- Respiratory depression: Compromised respiratory drive in respiratory disease or sleep apnoea can cause hypoventilation and hypoxaemia
- Dependence: Benzodiazepines can cause physical and psychological dependence, tolerance and misuse
- Drug-seeking behaviour, craving and disturbed work
- Renal: Use a lower dose in renal impairment as it causes increased sensitivity to CNS effects
- Hepatic: Contraindicated in severe hepatic impairment especially in hepatic encephalopathy. Use low doses to reduce the risk of precipitating coma.
- Elderly: Increase risk of oversedation, ataxia, confusion
PHARMACOKINETICS:
- Midazolam- <6 hours duration of action (ultrashort)
- Lorazepam, oxazepam, temazepam- 12-18 hours duration of action (short)
- Diazepam, chlordiazepoxide- Long (24-48 hours) duration of action
- Clonazepam- Long duration of action
- Benzodiazepines show anxiolytic effects (reduces anxiety and aggression)
PHARMACOLOGY
REDUCTION IN MUSCLE TONE
- Benzodiazepines reduce muscle tone by a central action on GABAA receptors, mainly in the spinal cord
- Increased muscle tone is a common feature of anxiety in humans and can cause aches and pains including headache that often affect anxious patients.
- IV administration of benzodiazepines and in overdose, airway obstruction can occur
ANTICONVULSANT EFFECT
- All benzodiazepines have anticonvulsant effects
- Clonazepam, lorazepam and diazepam are used to treat epilepsy
- They can be IV to control life-threatening seizures in status epilepticus
- Tolerance develops to the anticonvulsant effects of benzodiazepines
ANTEROGRADE AMNESIA
- Benzodiazepines prevent memory of events experienced while under their influence
- Flunitrazepam (Rohypnol)
- Amnesia is due to benzodiazepines binding to GABAA receptors containing the α5 subunit
ACUTE TOXICITY
- In overdose, benzodiazepines cause prolonged sleep without serious respiratory or cardiovascular depression
- However, in the presence of other CNS depressants especially alcohol, benzodiazepines can cause severe, life-threatening respiratory depression.
SIDE EFFECTS
- Drowsiness, confusion, amnesia and impaired coordination, which impairs manual skills (e.g. driving)
- Benzodiazepines increase the depressant effect of other drugs including alcohol in a more than additive way.
- Tolerance and dose dependence occurs with all benzodiazepines
- Withdrawals of benzodiazepines can cause a rebound heightened anxiety with tremor, dizziness, tinnitus, weight loss and disturbed sleep.
- Withdrawal after chronic administration causes nervousness, tremor, loss of appetite and sometimes convulsions
BUSPIRONE
- Effective following chronic treatment for GAD only
- Patients with a panic disorder often have increased anxiety following initiation of Buspirone (Buspirone increases firing of the Locus coeruleus)
- High affinity for serotonin 5-HT1A and 5-HT2 receptors
- Buspirone is a full agonist at presynaptic 5-HT1A receptors (soma and dendrites) → inhibition of neuron firing (inhibitory autoreceptors)
- Buspirone is a partial agonist at postsynaptic 5-HT1A receptors
- Chronic effect: Downregulation of inhibitory autoreceptor → more active 5-HT neuron
- Response may take 2-4 weeks, but an initial response may be apparent within 7-10 days
RANG AND DALE:
- Buspirone is a partial agonist at 5-HT1A receptors
- 5-HT1A receptors are expressed on the soma and dendrites of 5-HT containing neurons where they function as inhibitory autoreceptors
- Chronic use of buspirone induces desensitisation of somatodendritic 5-HT1A autoreceptors, which results in increased excitation of serotonergic neurons and enhanced 5-HT release.
- Initial treatment of buspirone can worsen anxiety due to the initial activation of 5-HT1A autoreceptors and inhibition of 5-HT release.
- Buspirone inhibits the activity of noradrenergic Locus coeruleus neurons → interferes with arousal reactions
- Takes days to weeks to produce its effects
SIDE EFFECTS:
- Nausea, dizziness, headache and restlessness
NOTE:
- Buspirone doesn’t prevent benzodiazepine withdrawal symptoms so if changing from benzodiazepine to buspirone, withdraw benzodiazepine gradually
- Less potential for dependence so it may be preferable to benzodiazepines in managing anxiety for patients with a history of drug dependence
SSRIS/ SNRIS
- SSRIs/ SNRIs are first line treatments for most types of anxiety disorders (except for acute effects)
- Fluvoxamine (SSRI) is approved only for OCD
- The anxiolytic effects of these drugs become manifest following chronic treatment
- There may be some increases in anxiety in the short-term that reduce over time
ANTI-EPILEPTIC DRUGS:
- Gabapentin, pregabalin, Tiagabine and valproate are effective in treating GAD
How do we prevent and manage adverse effects of anti-anxiety medications?
e.g 1) counselling 2) important points to explain to patients
PREVENTION AND MANAGEMENT OF ADVERSE EFFECTS OF ANTI-ANXIETY MEDICATIONS
- Avoid use of benzodiazepine or reduce dose and monitor for use with opioids and other drugs that cause CNS and respiratory depression
- Suddenly stopping benzodiazepines can cause withdrawal symptoms.
- Use low doses of benzodiazepines in renal and hepatic impairment
- Use short-term and in low doses due to increased risk of oversedation, ataxia, confusion, memory impairment.
COUNSELLING:
- Counsel patient that they may feel drowsy; drowsiness may persist the following day and to avoid driving or operating heavy equipment
- Avoid alcohol and other depressants
- If this medication is used for more than 2-4 weeks advise about tolerance and the need for higher doses. Advise of rebound effects (return of original symptoms with greater severity) if the medicine is stopped suddenly.
- Prevent or alleviate by gradual dose reduction
PRACTICE POINTS
- Use for short-term (2-4 weeks) or intermittent use only and shouldn’t be used as sole treatment
- Can be used short-term (up to 2 weeks) to manage agitation when starting antidepressants (e.g. panic disorder)
BUSPIRONE
- Counsel patient that drug may cause dizziness and not to drivemachinery if they’re affected
- Avoid grapejuice as it can increase the risk of side effects
List and explain the spectrum of eating disorders?
What is the epidemiology of them? Aetiology?
SPECTRUM OF EATING DISORDERS
- Anorexia nervosa: Determined wt. loss, abnormal cognitions of and morbid preoccupation with weight or shape
- Bulimia nervosa: Recurrent binges/purges, lack of control, morbid preoccupation with weight or shape
- Disordered eating (Third most common chronic illness amount adolescent girls after obesity and asthma)
- Unhealthy dieting
- Binge eating disorder
- Obesity
EPIDEMIOLOGY
- Age of onset: bimodal 14 and 18 years
- Sex: F:M = 10:1
- Lifetime prevalence
- Anorexia nervosa: 0.9% females, 0.3% males
- Bulimia nervosa: 1-3% females
- Eating disorders NOS: 3-5%
- Familial pattern: More common in sisters and mothers of those with disorder
- Complications: Mortality rates between 5 and 15%
AETIOLOGY
- Multifactorial: psychological, sociological, and biological associations
- Biopsychosocial disorder
- Vulnerabilities in three spheres
- Individual/personal
- Family
- Socio-environmental
- Longitudinal studies looking at eating behaviours in early childhood.
- History of food refusal in early childhood → Higher incidence of eating problems in later childhood
- Early childhood feeding problems → Higher incidence of disordered eating 8 -10 year later
- Sets the stage for later problems
• Weight and body image concerns develop prior to puberty
- Puberty is critical period for development of disordered eating in girls -→ precipitant?
- Individual: perfectionism, lack of control in other life areas, history of sexual abuse
- Personality: obsessive-compulsive, histrionic, borderline
- Familial: maintenance of weight equilibrium and control in dysfunctional family
- Cultural factors: prevalent in industrialized societies, idealization of thinness in the media
- Genetic factors
What are the common presenting symptoms of patients with eating disorder? What are the common presenting physical signs?
What do we need to do when making a diagnosis of an eating disorder? What investigations/nutritional assessment is required?
PRESENTING SYMPTOMS
• Physical symptoms reflect degree of malnutrition
- Weight Loss or inability to maintain normal weight
- Amenorrhea - virtually 100%
- Constipation
- Abdominal pain
- Fatigue
- Cold intolerance
- Light-headedness
- Signs of cognitive blunting
• Presenting physical signs
- Cachexia, muscle wasting
- Hypotension, hypothermia, bradycardia
- Acrocyanosis
- Dry skin, or lanugo-type hair
- Oedema
- Systolic murmur
- Short stature
- Breast atrophy
- Lack of signs indicating other causes to wt. loss
- Enamel loss and salivary gland enlargement with frequent purging
DIAGNOSIS
- Comprehensive history and PE will guide
- Limit laboratory studies on basis of history and examination
Consider differential diagnoses:
- Medical Conditions
- Psychiatric
- Utilize DMS-IV Criteria when appropriate
- Consider alternate classifications
- Laboratory Assessment
- FBC, ESR, U&E, LFTs, Ca, phosphate, Mg, albumin, T4, TSH, ECG
- Consider bone mineral density if amenorrhoeic for > 1 year
• Nutritional Assessment -
- 24 hour recall,
- %IBW – utilize BMI 50%ile for age (~BMI <16)
- Recent losses or gains –> Can determine degree of malnutrition
When should we suspect and eating disorder in primary care setting?
What are aypical presentations in children and adolescents?
ASSESSMENT IN PRIMARY CARE SETTING
When to suspect an eating disorder
- Unexplained weight loss-> Any weight loss or failure to gain expected weight in a child is concerning
- Change in eating patterns —> Progressive change from high caloric density foods to lower caloric
- Vegetarianism/veganism
- Desire to eat healthier”
- Frank restriction
- Change in eating behaviors, focus on food, ritua
- Change in activity patterns, exercise
- Lack of concern by teen/child about emaciation
Atypical presentation in children and adolescents - More often males
- Appears in context of stressful family or life events
- More likely to have co-morbid psychiatric diagnoses (Anxiety, OCD, depression)
- Less likely to have body image disturbances– If they agree that they are thin
- Weight loss is unexpected: “eating healthy” –> Leads to confusion about why parents are concerned
- Can often lead to delay in diagnosis –> Seen as a “passing phase”
- May not have lost amount of weight to meet strict criteria (Any weight loss should be concerning given normal expectations for weight gain and growth)
- Interruption of normal pubertal processes may lead to irreversible stunting
- Changes in brain volumes (MRI); bone accretion
What are the common presenting symptoms of eating disorder? (e.g reflect malnutrition)
What the presenting physical signs? (reflect malnutrition)
PRESENTING SYMPTOMS
Physical symptoms reflect degree of malnutrition
- Weight Loss or inability to maintain normal weight
- Amenorrhea - virtually 100%
- Constipation
- Abdominal pain
- Fatigue
- Cold intolerance
- Light-headedness
- Signs of cognitive blunting
Presenting physical signs
- Cachexia, muscle wasting
- Hypotension, hypothermia, bradycardia
- Acrocyanosis
- Dry skin, or lanugo-type hair
- Oedema
- Systolic murmur
- Short stature
- Breast atrophy
- Lack of signs indicating other causes to wt. loss
- Enamel loss and salivary gland enlargement with frequent purging
How is diagnosis of an eating disorder made? (e.g work-up, laboratory assessment, nutritional assessment)
- Comprehensive history and PE will guide
- Limit laboratory studies on basis of history and examination
- Consider differential diagnoses:
- Medical Conditions
- Psychiatric
- Utilize DMS-IV Criteria when appropriate
- Consider alternate classifications
- Laboratory Assessment
- FBC, ESR, U&E, LFTs, Ca, phosphate, Mg, albumin, T4, TSH, ECG
- Consider bone mineral density if amenorrhoeic for > 1 year
- Nutritional Assessment -
- 24 hour recall,
- %IBW – utilize BMI 50%ile for age (~BMI <16)
- Recent losses or gains——Can determine degree of malnutrition
What is body dysmorphic disorder? What is the DSV V critera (4 major)?
What must you specify when diagnosing this condition?
Clinical presentation of body dysmorphic disorder? What are common co-morbidities associated with this condition?
What are risks associated with this condition?
What is the treatment of this conditon?
BODY DYSMORPHIC DISORDER:
A. Preoccupation with 1 or more perceived flaws in physical appearance that are not observable to others
B. The individual has performed repetitive behaviours (e.g. mirror checking, excessive grooming, etc.) or mental acts (e.g. comparing their appearance to others) in response to appearance concerns.
C. The preoccupation causes clinically significant distress in social, occupational or other areas of functioning
D. The appearance is not better explained by concerns with body fat or weight in an individual whose symptoms meet diagnostic criteria for an eating disorder.
SPECIFY:
• Muscle dysmorphia: The individual is preoccupied with the idea that their build is too small or insufficiently muscular.
• Other specifiers:
- Good or fair insight: The individual recognizes that the body dysmorphic disorder beliefs are not true or that they may/ may not be true
- Poor insight: The individual thinks that the body dysmorphic disorder beliefs are probably true
- Absent insight/ delusional beliefs: The individual is completely convinced that the body dysmorphic disorder beliefs are true.
CLINICAL PRESENTATION
- It is related to OCD
- USMLE: Body dysmorphic disorder is a preoccupation with minor or imagined defects in appearance → causes significant emotional distress or impaired functioning; patients often seek cosmetic treatment
- Patients are preoccupied with 1 or more perceived flaws in their physical appearance, which they believe look unattractive or deformed
- The preoccupations are intrusive and can last 3-8 hours/ day
- Many individuals with body dysmorphic disorder have Delusions of Reference and believe that other people take special notice of them or mock them because of how they look
- It is associated with high levels of anxiety, social anxiety, social avoidance, depressed mood
- Average age (Body Dysmorphic Disorder): 16-17 years
- Muscle dysmorphia is a type of body dysmorphia that occurs almost exclusively in males, which consists of the preoccupation that one’s body is too small or insufficiently lean
NOTE:
- Body dysmorphic disorder is characterized by excessive appearance-related preoccupations and repetitive behaviours that are time-consuming and are difficult to resist or control and cause clinically significant distress or impairment in functioning
CO-MORBIDITIES:
- Major depressive disorder (commonest co-morbidity)
- Social anxiety disorder (social phobia)
- OCD
- Substance-related disorders
RISKS:
- Suicide
TREATMENT:
- CBT
What is anorexia nervosa? What are 3 major features of this condition?
What the two major subtypes of this condition?
What is bullmia nervosa? What are the 3 essential features of this conditon?
What is the DSM V criteria for diagnosis of bullimia nervosa? (5 major) ?
How can we classify severity? (e.g how many compensatory behaviours per week)
What is the prognosis of this condition?
What are major complications to screen for on History and examination? What examination(s) are needed to followign up these complications?
What is your differential diagnosis for a patient presenting with symptoms of bullimia nervosa?
What is the major managment principles for the treatment of this condition? (require multidiscplinary team approach) What mental health specific treatment do they require?
What are the indications for hospitalisation?
What does inpatient treatment focus on?
What advice do you give to families of patients?
ANOREXIA NERVOSA:
• Anorexia nervosa- 3 essential features:
- Persistent energy intake restriction
- Intense fear of gaining weight or becoming fat, or a persistent behaviour that interferes with weight gain
- A disturbance in self-perceived weight or shape
2 TYPES:
- Restricting type: Weight loss is mostly accomplished through dieting, fasting and/or excessive exercise
* No episodes of binge eating or purging over the past 3 months
• Binge-eating/ purging type: Recurrent episodes of binge eating or purging (vomiting, misusing laxatives, diuretics) over the past 3 months
BULLIMIA NERVOSA-
• 3 essential features:
- Recurrent episodes of binge eating
- Recurrent inappropriate compensatory behaviours to prevent weight gain
- Self-evaluation that is unduly influenced by body shape and weight
DSM-5 CRITERIA
A. Recurrent episodes of binge-eating; an episode of binge-eating is characterized by both of the following
- Eating, in a discrete period of time, an amount of food that is definitely larger than what most individuals would eat during a similar period of time and under similar circumstances
- A sense of lack of control over eating during the episode
B. Recurrent inappropriate compensatory behaviour in order to prevent weight gain, such as self-induced vomiting, misuse of laxatives, diuretics, enemas, or other medications, fasting, or excessive exercise
C. The binge-eating and inappropriate compensatory behaviours both occur, on average, at least once a week for 3 months
D. Self-evaluation is unduly influenced by body shape and weight
E. The disturbance does not occur exclusively during episodes of AN
SEVERITY
• Mild: 1-3 inappropriate compensatory behaviours a week
• Moderate: 4-7 inappropriate compensatory behaviours a week
• Severe: 8-13 inappropriate compensatory behaviours a week
• Extreme: 14+ inappropriate compensatory behaviours a week
PROGNOSIS
- Relapsing/remitting disease
- Good prognostic factors: onset before age 15, achieving a healthy weight within 2 yr of
- Poor prognostic factors: later age of onset, previous hospitalizations, individual and familial disturbance
COMPLICATIONS
History and Examination:
- Russell’s sign: knuckle callus due to vomiting
- Parotid gland enlargement
- Perioral skin irritation
- Loss of dental enamel and caries
- Aspiration pneumonia
- Renal failure
- GORD
- Mallory-Weis tear
- Acute gastric rupture or tear
- Muscle wasting
- Pedal oedema
- Trouble concentrating
- Weight fluctuating over time
DIFFERENTIAL DIAGNOSIS
Medical Conditions
- GI - Inflammatory bowel disease, malabsorption
- Endocrine
- DM, Addison’s, thyroid disease
- Malignancies-CNS lesions—- Tumors, intracranial infections, increased ICP,
- Miscellaneous - early pregnancy, sarcoidosis, cystic fibrosis Chronic infections (TB, HIV)
- Psychiatric Disorders e.g next point
- Mood disorders, OCD, Body dysmorphic disorder, Substance use disorders, Psychosis
MANAGEMENT
REQUIRES A MULTIDISCIPLINARY TEAM APPROACH
- Medical - manage medical concerns, monitor wt., coordinate team
- Nutritional - education, nutrition/dietary plans and options, caloric requirements
- Mental health – individual and family needs, focus on affective issues, medication management
- School personnel – assist with reintegrating into more normal functioning
MENTAL HEALTH TREATMENT
Individual therapy
- Cognitive behavioural therapy has best outcomes
- Limited data on efficacy
- Tries to teach relation between thoughts and feelings and behaviour; recognize how related to disordered eating
Key role of family therapy, particularly younger teens most effective
- Explicit family involvement in day-to-day treatment
- No evidence for adding psychotropics in absence of co-morbid mental health conditions
INDICATIONS FOR HOSPITALISATION
- Hypovolemia/ hypotension
- Severe malnutrition - <75% IBW
- Cardiac dysfunction, arrhythmias, prolonged QT interval
- Bradycardia <45 beats/minute
- Electrolyte disturbance – hypokalemia, hypoglycemia
- Rapid weight loss despite interventions
- Intractable binge-purge episodes
- Suicidal thoughts or gestures
- Highly dysfunctional or abusive family Failure of outpatient therapy
PROTOCOL-BASED INPATIENT TREATMENT
Areas of focus for management
- Weight gain expectations
- Supervised eating
- Activity restriction
- Limitation on family/peer interactions
- Include all social networks
- Psychiatric consultation
- Parent education
ADVICE FOR FAMILIES
- Have patience with the process of treatment/recovery Prepare for a marathon, not a 50 yd. dash
- Avoid blaming
- Avoid power struggles over food
- Avoid comments about weight and appearance
- Avoid unreasonable preparations to purchase or prepare special foods
- Get support – individual or couples therapy, support groups
- Get rid of the scale!
- Pay attention to siblings
What is the eitology/ risk factors of Anorexia nervosa?
What is its clinical presentation?
How is the diagnosis made? What Investigations need to be undertaken? (many)
What is a diagnositic test for anorexia?
What are clinical signs associated with anorexia nervosa?
What is the management of anorexia nervosa?
What is the major complication associated with the treatment of anorexia nervosa?
ETIOLOGY, CLINICAL PRESENTATION, DIAGNOSIS AND MANAGEMENT OF EATING DISORDERS
- Bulimia nervosa (0.5-1%) is more common than anorexia nervosa
- Binge eating disorder (2-3%)
- Eating disorder not otherwise specified (EDNOS): Refers to any eating disorder that doesn’t meet criteria for anorexia nervosa or bulimia nervosa>> 5%
- Treatment for all eating disorders- CBT
ANOREXIA NERVOSA
1. Occurs in adolescence or early adulthood
ETIOLOGY (3 MAIN- BIOLOGICAL, PSYCHOLOGICAL AND ENVIRONMENTAL):
- Genetics: Predisposing to anorexia, perfectionism, high sensitivity and perseverance
- Psychological factors: Obsessive-compulsive personality traits,, perfectionism, high parental demands and low self-esteem
- Environmental: Peer pressure, social media, occupations that that encourage thinness
- Temperament: Anxiety disorders or obsessional traits in childhood
- The onset is often associated with a stressful life event such as leaving home for uni
- Occupations that encourage thinness: Modelling and elite athletics
- Adverse experiences during developmental transition stages:
- Early attachment and developmental difficulties
- Feeding and sleeping difficulties in infancy
- Emotional or sexual child abuse
- Adverse experiences during puberty
- Biological risk factors: Early menarche, premorbid obesity
DIAGNOSIS
- FBC: Leukopenia (common); anaemia, thrombocytopenia
- EUC: Dehydration can cause increased blood urea nitrogen; impaired renal function
- Lipid profile: Hypercholesterolemia
- LFTs: Increased
- Hypomagnesemia, hypocalcaemia, hypophosphatemia, hypochloremia and hypokalaemia
- ABG: Metabolic alkalosis (increased serum bicarbonate)- self-induced vomiting
- Endocrine: Low T3/T4; low estrogen (females) and low testosterone (males)
- ECG: Sinus bradycardia, prolongation of the QTc interval
- Bone mass: Low bone mineral density (areas of osteopenia or osteoporosis)
- EEG: Metabolic encephalopathy from fluid and electrolyte disturbances
DIAGNOSTIC TESTING:
- Eating Disorder Examination or Eating Disorder Examination Questionnaire
CLINICAL PRESENTATION:
- Amenorrhoea
- Constipation and abdominal pain
- Cold intolerance
- Lethargy
- Insomnia
- Fainting
- SOB, chest pain and palpitations
SIGNS
- Emaciation
- Hypotension
- Hypothermia
- Bradycardia
- Petechiae and ecchymosis- bleeding diathesis
- Lanugo
- Dry skin
- Peripheral edema
- Yellow skin- hypercarotenemia
MANAGEMENT
- Outpatient therapy is preferred, but if weight gain is the highest priority or if the patient is at high risk of medical complications, inpatient admission to a specialist eating disorder unit may be indicated.
- Supervised refeeding with significantly low weight and malnourishment or evidence of electrolyte imbalances.
- Refer to dietitian and utilize oral nutrition
- To prevent refeeding syndrome, initiate refeeding at less than full energy intake and increase energy intake gradually over 5-7 days
- During the first 2 weeks, regularly monitor and adjust levels of phosphate, K(+) and Mg(+2)
- Counselling and psychoeducation
- Family therapy and CBT
Treat in the least restrictive environment possible- many patients can be treated with outpatient care
- Admit to hospital with high risks of life-threatening medical complications, low weight
- For patients with substantially low weight and malnourishment- admit to inpatient or day patient unit
- Psychological treatment and parenting for self-image disorder- self-image and identity building and desensitization to fear of being judged
- Note: Unlike anorexia nervosa, patients with bullimia nervosa maintain body weight at or above a minimally normal level
COMPLICATIONS: REFEEDING SYNDROME
- This occurs with aggressive refeeding in patients who have had prolonged malnourishment
- Involves hypokalaemia, hypophosphatemia and hypomagnesemia
- Due to rapid intracellular uptake of phosphate, magnesium and potassium triggered by a switch from gluconeogenesis to carbohydrate-induced insulin release
- Insulin-triggered rebound hypoglycaemia exacerbated by low glycogen stores may occur with refeeding.
- Can cause cardiac arrhythmias, heart failure, rhabdomyolysis
- CVS: Pericardial effusions, myocardial atrophy, valvular prolapse, QT prolongation, hypotension
- Endocrine: Hypoglycaemia, amenorrhoea, infertility, hypothyroidism
- Seizures, headache, peripheral neuropathy
- Osteoporosis
What is PICA? What is the DSM V criteria for diagnosis? 4 major?
What is rumination disorder?
PICA
A. Persistent eating of non-nutritive, non-food substances over at least 1 month
B. The eating of non-nutritive, non-food substances is inappropriate to the developmental level of the individual
C. The eating behaviour is not part of a culturally supported or socially normative pattern
D. If the eating behaviour occurs in the context of another mental disorder or medical condition, it is sufficiently severe to warrant additional clinical attention.
RUMINATION DISORDER
A. Repeated regurgitation of food over a period of at least 1 month.
B. The repeated regurgitation is not attributable to an associated GIT or other medical condition (e.g. GERD, pyloric stenosis)
C. The eating disturbance doesn’t occur exclusively during the course of anorexia nervosa, bulimia nervosa, binge-eating disorder or avoidant/ restrictive food intake disorder
D. If the symptoms occur in the context of another mental disorder they are sufficiently severe to warrant additional clinical attention
What is the eitology of bullimia nervosa? What are some key features of this condition?
What are the symptoms of this condition? What are the signs of this condition?
What are complications/risks associated with this condition?
What investigations need to be undertaken when working up this condition?
What are the major management principles for bullimia nervosa?
What screening questionaire can be used for this condition?
BULIMIA NERVOSA
- Individuals with bulimia nervosa are often within the normal weight or overweight range
- Bulimia nervosa is characterized by recurrent episodes of excessive eating followed by compensatory behaviours to prevent weight gain.
- Bulimia nervosa commonly begins in adolescence or early adulthood
ETIOLOGY:
- Biological: Genetics, abnormal dopamine or serotonin levels
- Psychological: Low self-esteem, perfectionism, obsessive personality; Stressful transitions, history of abuse or trauma, negative body image and professions or activities that focus on appearance.
- Environmental: Societal idealizations (media); Internalization of a thin body ideal; childhood sexual or physical abuse; occupations (athletes and models)
- Temperament: Low self-esteem, weight concerns, depressive symptoms, social anxiety disorder
- Personality disorders- especially borderline personality and avoidant personality disorders
SYMPTOMS
- Fluctuations in body weight
- Insomnia
- Muscle weakness
- Fatigue
- Dizziness
- Cold intolerance
- Amenorrhoea
- Bloating
SIGNS
- Hypertrophy of the salivary glands (especially the parotid glands)
- Dental enamel erosion and caries
- Calluses or scars on the dorsal surface of the hand from induced vomiting (Russell’s sign)
- Peripheral edema
- Cardiac arrhythmias
- Rectal prolapse and haemorrhoids due to laxative abuse
- Tachycardia, orthostatic hypotension, low BP may occur with dehydration
COMPLICATIONS
- Dental erosions. caries
- Esophagitis
- Oesophageal tears
- Gastric rupture
- Constipation
- Rectal prolapse
- Cardiac arrhythmias
- Metabolic alkalosis/ Metabolic acidosis
- Hypokalaemia, hyponatremia, hypochloraemia, hypocalcaemia, hypophosphatemia, hypomagnesemia
- Dehydration
INVESTIGATIONS:
- FBC
- EUC: Hypokalaemia, hypocalcaemia, hypophosphatemia, hypomagnesemia, hyponatremia, hypochloraemia
- ECG: Cardiac arrhythmias (e.g. hypokalaemia)
- Random glucose level
- ABG: Metabolic alkalosis (loss of gastric acid through vomiting); Metabolic acidosis (frequent diarrhoea or dehydration through laxative and diuretic abuse)
- TFTs
- Urinalysis- assess dehydration, ketonuria, kidney damage
MANAGEMENT
- CBT (firstline)
- Interpersonal psychotherapy, family therapy, psychodynamic therapy
- Assess nutritional intake
- Consider SSRIs if psychological therapy isn’t available or as an adjunct to psychological therapy.
- Refer to a dietitian for nutritional counselling
- Assess nutritional intake
- Refer patients with vomiting to dentist- monitoring, treatment and prevention of dental erosion
- After vomiting, rinse mouth with water and sodium bicarbonate to neutralize acid
- Most patients should be treated as outpatients
SCREENING:
- SCOFF questionnaire
What is the management plans for those with eating disorders?
- anorexia (what are indiciations for inpatient treatment?)
- Bullimisa nervosa
- Binge eating disorder
MANAGEMENT PLANS FOR THOSE WITH EATING DISORDERS
ANOREXIA NERVOSA
Guiding principles of treatment:
- Restoration to a normal weight range
- Identification and management of any contributing family and personal problems
- Co-morbid anxiety and depression are common
- CBT and family therapy
- Dietitian- dietary counselling
- Assess and treat physical complications- hypokalaemia or dehydration
- Short to medium-term hospital admissions for supervised weight restoration followed by more intensive outpatient programs with hospital backup
- Outpatient treatments are preferred
INPATIENT TREATMENT INDICATIONS:
- Patients who fail to make progress or at physical risk (including young patients where it is essential to gain weight for normal physical development)
- Patients who are at risk of suicide
- Drugs are not of benefit for primary anorexia, but antidepressants can be prescribed if there is a comorbid major depressive illness (not related to nutritional deficiencies)
- Vitamin D and Ca(+2) supplements are recommended
- Iron, B-group vitamins and zinc may be prescribed
- K(+) replacement (lost in purging/ vomiting)
- Patients with anorexia nervosa can have prolonged QTc
- Some antidepressants and all antipsychotics can prolong the QTc interval
REFEEDING:
- Hypophosphatemia can occur with commencing refeeding- PO4(-3) supplementation is required along with Mg(+2), Ca(+2) and B-group vitamins prophylactically
- Provide sufficient fat and protein
BULIMIA NERVOSA
- CBT
- DBT- for patients with severe personality disturbances or other problems and bulimia nervosa
- SSRIs- used in the short-term for some patients (reduces binge eating frequency and/or as an adjunct to psychotherapy)
- Patients are rarely admitted to hospital, but this should be considered if they are at risk of suicide, medically unwell or in the 1st trimester of pregnancy or if the symptoms are refractory to outpatient care
BINGE EATING DISORDER
- CBT and IPT
- Behavioural weight loss treatments
- SSRIs: Adjunctive treatment to psychotherapy especially in those with depressive comorbidities
What is psychosis?
What are key features defining psychotic disorders?
What is a delusion? What is a strongly held idea? What is a hallucination?
What are grossly diosorganised/ abnormal motor behavior? (what terms associated with schizophrenia)
What is meant by’negative’, symptoms of schizophrenia?
What is disorganized thinking? (types -thought form)
What is a thought disorder?
PSYCHOSIS:
- Psychosis: Distorted perception of reality characterized by delusions, hallucinations and/or disorganized thought/speech.
- Can occur in patients with medical illnesses, psychiatric illnesses or both
- Psychosis can be a symptom of schizophrenia, mania and severe depression, and it can be substance-induced.
- Hallucinations and delusions are frequently seen in delirium and dementias
Note: Psychosis as a sign of a psychiatric disorder is a diagnosis of exclusion
- Psychotic disorder: Characterized by significant impairment in reality testing
- Delusions or hallucinations behaving in a disorganised way
KEY FEATURES DEFINING THE PSYCHOTIC DISORDERS:
DELUSIONS:
Delusions: Fixed beliefs not able to be changed despite conflicting evidence
- Persecutory delusions: Belief of being harmed/ harassed
- Referential delusions: Belief that certain gestures, comments, environmental cues are directed at them
- Grandiose delusions: When an individual believes that they have exceptional abilities, wealth or fame.
- Erotomanic delusions: When an individual falsely believes that another person is in love with them.
- Nihilistic delusions: The belief that a major catastrophe will occur
- Somatic delusions: Focus on preoccupations regarding health and organ function
- Bizarre delusions: Delusions that are implausible and not understandable to same-culture peers and don’t derive from ordinary life experiences.
- Thought withdrawal: Thoughts are removed by an outside force
- Thought insertion: Alien thoughts have been put into one’s mind
- Delusions of control: One’s body or actions are being acted on or manipulated by an outside force.
• Non-bizarre delusions: The belief that one is under surveillance by the police despite lacking of convincing evidence.
Note: it’s hard to distinguish a delusion from a strongly held idea
HALLUCINATIONS:
- Hallucinations: Perception-like experiences that occur without an external stimulus
- Auditory hallucinations in schizophrenia
- Hallucinations must occur in the context of a clear sensorium
DISORGANISED THINKING:
• Disorganized thinking (speech):
- Derailment or loose associations: The individual may switch from 1 topic to another (it derails like a train)>> there is a change from 1 answer to another
- e.g. why did you go to the hospital? I went to the hospital because I was brought in by the ambulance and then when a squirrel swims in swimming pool
- Tangential thinking: Completely random answers (to the patient it appears linked)
- Word salad: Severely disorganised speech (incomprehensible) and resembles receptive aphasia
GROSSLY DISORGANISED OR ABNORMAL MOTOR BEHAVIOUR:
- Grossly disorganized or abnormal motor behaviour (includes catatonia): Problems may occur in any form of goal-directed behaviour leading to difficulties in performing ADLs
- Catatonic behaviour: Marked decrease in reactivity to the environment. Includes resistance to instructions (negativism), maintaining a rigid, inappropriate or bizarre posture
- Catatonic (Mutism and stupor): Complete lack of verbal and motor responses (mutism and stupor)
- Catatonic excitement: Includes purposeless and excessive motor activity without obvious cause
- Other features: Staring, grimacing, mutism, echoing speech
NEGATIVE SYMPTOMS:
Negative symptoms: Schizophrenia has diminished emotional expression and avolition
- Diminished emotional expression: Reductions in the expression of emotion in the face, eye contact, prosody (intonation of speech) and gestures
- Avolition: Decrease in motivated self-initiated purposeful activities. The person can sit for long periods of time and show little interest in participating in work or social activities.
- Alogia: Manifested by diminished speech output
- Anhedonia: Decreased ability to experience pleasure or reduced recollection of pleasure previously experienced.
- Asociality: The apparent lack of interest in social interactions
EXPLANATION OF TERMS:
- Delusion: A fixed false belief that persists despite facts and are not typical of a person’s culture or religion.
- Types: Erotomanic, grandiose, jealous, persecutory, somatic, mixed
Hallucination: Perception without an external stimulus
- Visual: Commonly a feature of medical illness (e.g. drug intoxication) than psychiatric illness
- Auditory: Commonly a feature of psychiatric illness (e.g. schizophrenia) than medical illness
- Olfactory: Often occurs as an aura of temporal lobe epilepsy and in brain tumours
- Gustatory: Epilepsy
- Tactile: Common in alcohol withdrawal and stimulant use (e.g. cocaine, amphetamines), delusional parisitosis
- Hypnagogic- occurs while going to sleep
- Hypnopompic- occurs while waking from sleep
Insight: The person’s level of awareness and understanding of their problem.
- Full, partial/ limited, none
Thought disorder: Thought disorder refers to disorganized thinking as evidenced by disorganized speech.
- Thought disorders- derailment, poverty of speech, tangentiality, perseveration, thought blocking
- Alogia (poverty of speech): Lack of speech caused by disruption in the thought process (general lack of additional, unprompted content). Patients will reply sparsely and their answers to questions will lack spontaneous content.
- Blocking: An immediate stop in the middle of a train of thought
Formal thought disorder: Refers to an impaired capacity to sustain coherent discourse, and occurs in the patient’s written or spoken language.
- Formal thought disorders indicate a disturbance of the organization and expression of thought
Delusions reflect abnormal thought content
- The 2 types of disordered thinking includes: Thought disorder (thought form) and delusions (thought content)
What is the role of neurotransmitters in the eitology of psychosis? (dopamine) (what part of the brain) (serotonin/NMDA)
Prevention and Management of violence and agression in acutely disturbed psychotic patient
1) What steps need to be under taken when managing a patient with Acute behavioural disturbance?
2) What is the main objective to achieve when managing acute psychiatric behavioural emergencies?
3) What are important things to do and consider when interacting with these patients? (investigations/safety etc)
ROLE OF NEUROTRANSMITTERS IN ETIOLOGY OF PSYCHOSIS:
- Increased dopamine levels in the mesolimbic pathway
- Increased serotonin with activation of 5-HT2A receptors
- Decreased NMDA glutamate receptors (correlates with positive, negative and cognitive deficit symptoms seen with NMDA antagonists e.g. ketamine)
- Decreased GABA
- Increased noradrenaline
PREVENTION AND MANAGEMENT OF VIOLENCE AND AGGRESSION IN ACUTELY DISTURBED PSYCHOTIC PATIENT:
STEPS IN MANAGING ACUTE BEHAVIOURAL DISTURBANCES
- Recognise warning signs before escalation occurs
- Attend to these patients as a priority as delay exacerbates the situation
- Ensure the safety of self, staff, others and of the patient
- Call support (e.g. security staff) early if the situation is deteriorating
- Use the least invasive method necessary to gain control:
- Verbal de-escalation and early negotiation (including offering oral diazepam or olanzapine>> olanzapine is preferred in acute psychosis)- allow the patient to state their concerns
- Show of force- having a sufficient number of staff visibly backing up the clinicia
- Physical restraint by a trained team
- Chemical restraint- IV diazepam, midazolam, droperidol and olanzapine
THE MAIN OBJECTIVE IN ACUTE PSYCHIATRIC BEHAVIOURAL EMERGENCIES IS TO ACHIEVE TRANQUILLISATION
- Benzodiazepines are preferred over antipsychotics for tranquillisation
- Use the oral route whenever possible and use liquid or wafers compared to tablets to ensure that the dose has been consumed
- Closely monitor vital signs and mental state during and after administration of medication
OTHER SUGGESTIONS (ETG)
- If the situation is too dangerous then request for security and/or police to disarm and restrain the patient
- Assess the patient’s mental state including cognitive function and attempt to reduce the tension of the situation (e.g. offering water)
- If a physical examination is required- the minimum requirements include visual inspection and assessment of vital signs
- Perform a toxicology risk assessment
- Patients with a behavioural emergency require an increased level of observation
- Calm, confident, empathic approach to the patient
- Avoiding sudden movements, intrusion onto the patient’s personal space, prolonged eye contact and confronting behaviours
- Room with 2 exits and furniture that can’t be thrown
- Security and/or police who are nearby, but unobtrusive Duress alarm
- Removal of any personal belongings that could be used as a weapon
- Maintaining a safe distance between the patient and an exit
- Keep the patient in your field of vision at all times, be aware of hidden weapons and spend the minimum time necessar to gather an outline of the history
What is the cause of ‘Positive symptoms’, of psychotic disorder? What neural pathway is it associated with positive symptoms?
What is the cause of negative symptoms’, of psychotic disorders? What neural pathway is it associated with?
“Positive’ symptoms are changes in thoughts and feelings that are “added on” to a person’s experiences (e.g., paranoia or hearing voices). –>
Occur at mesolimbic dopamine pathway, where there is increased inhibition of GABA neurons through D2 stimulus, which causes no GABA-ergeic inhibition of glutamine neurons —> causing symptoms of psychosis
“Negative” symptoms are things that are “taken away” or reduced (e.g., reduced motivation or reduced intensity of emotion).
Negative symtpoms occur in mesocortical pathway, it is caused by decreased dopamine activity through D1 receptors, causing decreased excitation of Glutamine neurons —> leading to Negative and cognitive symptoms of psychosis
What is substance/medication induced psychotic disorders? What is the DSM V criteria?
What is the typical clinical presentation?
What do you need to specify in terms of intoxication and symptoms?
What is a psychotic disorder due to another medical condition? Wht is the DSM V criteria for diagnosis?
What is a typical presentation of this condition?
SUBSTANCE/ MEDICATION-INDUCED PSYCHOTIC DISORDER:
A. Presence of 1 or both of the following symptoms:
- . Delusions
- Hallucinations
B. There is evidence of both:
- The symptoms of Criteria A developing during or soon after substance intoxication or withdrawal or after exposure to a medication
- The involved substance/ medication is capable of producing the symptoms in Criteria A
C. The disturbance is not better explained by a psychotic disorder that is not substance-induced
D. The disturbance doesn’t occur exclusively during the course of a delirium
E. The disturbance causes clinically significant distress or impairment in social, occupational or other areas of functioning.
SPECIFIERS:
- With onset during intoxication: Symptoms occur during intoxication
- With onset during withdrawal: Symptoms develop during or shortly after withdrawal
- Note: This diagnosis should be made instead of substance intoxication or substance withdrawal only when the symptoms in Criteria A predominate
CLINICAL PRESENTATION
- The essential features of substance/medication-induced psychotic disorder are prominent delusions and/or hallucinations that are due to a substance/medication.
- Substance/medication-induced psychotic disorders arise during or soon after exposure to a medication or after substance intoxication or withdrawal but can persist for weeks
- Psychoses can occur with alcohol, cannabis, hallucinogens
- Persecutory delusions may develop after use of amphetamines
- Formication can lead to scratching
- Note: If an individual recognizes that the perception is caused by the drug and neither believes in or accts on the disturbance, t_hen the diagnosis is not substance/medication-induced psychotic disorder, but is substance intoxication or substance withdrawal with perceptual disturbances_
PSYCHOTIC DISORDER DUE TO ANOTHER MEDICAL CONDITION:
A. Prominent hallucinations or delusions
B. There is evidence that the disturbance is due to the direct consequence of another medical condition
C. The disturbance is not better explained by another mental disorder
D. The disturbance doesn’t occur exclusively during the course of a delirium
E. The disturbance causes clinically significant distress or impairment in social, occupational or other areas of functioning
CLINICAL PRESENTATION:
- There are prominent delusions or hallucinations judged to be attributable to the effects of another medical condition, which are not better explained by another mental disorder
- The temporal association of the onset, exacerbation or remission of the medical condition and the psychotic disturbance
What is schizophrenia? What is the DSM V criteria for diagnosis?
What are specifiers used to classify the diagnosis ( 1 year after all criteria was first met)?
What do you need to specify when making a current diagnosis? (specify 4 major symptoms of psychosis)?
What is the typical clinical presentation of schizophrenia? (positive, negative, cognitive, dopmaine)
What is the typical clinical course of schizophrenia?
What is the eitology?
What are major risks associated with patients with schizophrenia?
What are the prognostic factors w this condition?
What are complications commonly seen with patients with schizophrenia?
What are risk factor for development of schizophrenia?
What is the management of schizophrenia?
What is your differential diagnosis when a patient is presenting with symptoms of psychosis?
What are the 5’as of schizophrenia (negative symptoms)?
SCHIZOPHRENIA:
A. >2 of the following present for the majority of 1 month. >1 must be (1), (2) or (3)
- Delusions
- Hallucinations
- Disorganized speech (e.g. frequent derailment or incoherence)
- Grossly disorganized or catatonic behaviour
- Negative symptoms (diminished emotional expression or avolition)
B. Loss of function in work, interpersonal relations or self-care Children/ adolescents: Loss of interpersonal, academic or occupational functioning
C. Continuous disturbance persisting for >6 months (including at least 1 month of symptoms from criterion A. (Prodromal or residual periods may manifest only by negative symptoms or by >2 of the symptoms in Criterion A present in an attenuated form (e.g. odd beliefs, unusual perceptual experiences)
D. Schizoaffective disorder and depressive or bipolar disorder with psychotic features have been ruled out because either (1) no major depressive or manic episodes have occurred concurrently with the acute-phase symptoms or (2) If mood episodes have occurred during active-phase symptoms for a minority of the total duration of the active and residual periods.
E. The disturbance is not attributable to the physiological effects of a substance or medical condition
F. If there is a history of Autism Spectrum Disorder or childhood communication disorder, schizophrenia can only be diagnosed if prominent delusions or hallucinations occur along with the other symptoms of schizophrenia for at least 1 month.
THE FOLLOWING COURSE SPECIFIERS ARE USED AFTER 1 YEAR OF THE DISORDER:
- First episode, currently in acute episode: First manifestation of the disorder meeting the diagnostic symptoms and time criteria. An acute episode is a time period where the symptom criteria are fulfilled.
- First episode, currently in partial remission: Partial remission is a period of time during which an improvement after a previous episode is maintained and where the defining criteria of the disorder are only partially fulfilled.
- First episode currently full remission: Full remission occurs after a previous episode where no disorder-specific symptoms are present.
- Multiple episodes, currently in acute episode: Multiple episodes is >2 episodes
- Multiple episodes, currently in partial remission
- Multiple episodes, currently in full remission
- Continuous: Symptoms fulfilling the symptom criteria remain for the majority of the illness course with subthreshold symptoms being very brief relative to the overall course.
SPECIFY CURRENT SEVERITY:
- Rated by a quantitative assessment of the primary symptoms of psychosis including: Delusions, hallucinations, disorganized speech, abnormal behaviour and negative symptoms.
- Severity is rated from 0 (not present) to 4 (present and severe)
CLINICAL PRESENTATION
- Prodromal symptoms often precede the active phase and residual symptoms may follow it
- Residual symptoms may follow the active phase- characterised by subthreshold forms of hallucination or delusions
- Positive symptoms
- Hallucinations
- Delusions (paranoid)
- Abnormal disorganised behaviour: Stereotyped movements, disorientation and occasionally aggressive behaviours
- Thought disorder
• Negative symptoms
- Withdrawal from social contact
- Flattening of emotional responses
- Anhedonia (inability to experience pleasure)
- Reluctance to perform everyday tasks
Cognitive and other symptoms
- Deficits in cognitive function (prefrontal cortex):
- Selective attention
- Executive memory
- Anxiety
- Guilt, depression and self-punishment
Dopamine in schizophrenia
- Positive symptoms are due to overactivity in the mesolimbic dopaminergic pathway activating D2 receptors
- Negative symptoms: Results from decreased activity in the mesocortical dopaminergic projections where D1 receptors predominate
THE 5 A’S OF SCHIZOPHRENIA (NEGATIVE SYMPTOMS):
- Anhedonia
- Affect (flat)
- Alogia (poverty of speech)
- Avolition (apathy)
- Attention (poor)
CLINICAL COURSE
- The psychotic features of schizophrenia often emerge between the late teens and mid-30s (peak age of onset is 20s)
- Psychotic symptoms tend to diminish with age
ETIOLOGY
- Emotional-behavioural disturbances and psychopathology, intellectual and language alterations, and subtle motor delays.
- Environmental: Season of birth
- Genetics
- Pregnancy and birth complications with hypoxia and greater paternal age are associated with a higher risk of schizophrenia for the developing fetus.
- Other prenatal and perinatal adversities including: Stress, viruses, toxoplasma, malnutrition, maternal diabetes and other medical conditions are linked with schizophrenia.
RISKS
- Many patients attempt suicide (due to command hallucinations to harm oneself or others)
- Social and occupational dysfunction to make educational progress and maintaining employment are often impaired by avolition or other disorder manifestations
- High rates of co-morbidity with substance-related disorders (e.g. tobacco)
- Stress (early childhood, adolescence)
- Cannabis use
- Weight gain, diabetes, metabolic syndrome, CV and pulmonary disease are more common in schizophrenia than in the general population.
POOR PROGNOSTIC FACTORS:
- Early onset
- Gradual onset
- Many relapses
- Poor premorbid functioning (social isolation)
- Comorbid substance abuse
- Poor social support
- Negative symptoms
- Family history
- Male sex
COMPLICATIONS:
- Suicide/ suicidal ideation
- Self-harm
- Anxiety and OCD
- Depression
- Substance abuse
- Inability to work or attend school
- Legal and financial problems
- Social isolation
- Decreased life expectancy from associated medical conditions e.g. weight gain, diabetes, metabolic syndrome, CV/ pulmonary disease
RISK FACTORS:
- Inflammation and autoimmune diseases- increased immune activation
- Older paternal age
- Pregnancy and birth complications- malnutrition, exposure to toxins or viruses
- Taking psychoactive drugs in the teen years and young adulthood
MANAGEMENT
- Acute treatment and maintenance: Antipsychotics (haloperidol, risperidone, olanzapine, paliperidone; clozapine f refractory)
- Adjunctive +/- mood stabilizers (for aggression/ impulsiveness- lithium, valproate, carbamazepine) +/- anxiolytics +/- ECT
- Psychosocial
- Psychotherapy: Individual, family (important), group, supportive
- Behaviour therapy and CBT
- Community treatment- helps people with medication adherence, basic living skills, social support, job placements, resources
- Social skills training, employment programs, disability benefits
- Housing- group home, boarding home
- Vocational rehabilitation
- Positive symptoms: Tends to respond well to antipsychotics
- Negative symptoms: Blunted affect, anhedonia, apathy, alogia, etc. These are often treatment resistant
- Cognitive symptoms: Impairments in attention, executive functioning and working memory
DDX:
- Major depressive or bipolar disorder with psychotic or catatonic features
- Schizoaffective disorder
- Schizophreniform disorder and brief psychotic disorder
- Schizotypal personality disorder
- Delusional disorder
- PTSD
What is a schizophreniform disorder? What is the DSM V criteria for diagnosis? (how long do they need symptoms- less than schizophrenia) What do you need to rule out to make this diagnosis?
What is the prognosis of this condition?
What is the management? (treat as first psychotic episode)
SCHIZOPHRENIFORM DISORDER
- Mental disorder diagnosed when symptoms of schizophrenia are present for a significant portion of the time within a one-month period, but signs of disruption are not present for the full six months required for the diagnosis of schizophrenia.
DSM V CRITERIA:
A. Two (or more) of the following, each present for a significant portion of time during a 1-month period (or less if successfully treated). At least one of these must be 1, 2 or 3.
1. Delusions
2. Hallucinations
3. Disorganized speech (e.g. frequent derailment or incoherence)
4. Grossly disorganized or catatonic behaviour
5. Negative symptoms (diminished emotional expression or avolition)
B. Rule out schizoaffective disorder and depressive or bipolar disorder with psychotic features because either
- No major depressive or manic episodes have occurred concurrently with the active-phase symptoms
- If mood episodes have occurred during active-phase symptoms, they have been present for a minority of the total duration of the active and residual periods of the illness.
C. Rule out other causes: GMC, substances (e.g. drug of abuse, medication)
D. Episode lasts less than 6 months. If the symptoms last more than 6 months, this becomes schizophrenia.
- Severity of schizophreniform disorder is based on assessment of primary symptoms of psychosis. Good prognostic factors include acute onset, confusion, good premorbid functioning and an absence of blunting or a flat affect.
MANAGEMENT
- Treat as first psychotic episode.
- Oral second generation anti-psychotic. Start low and go slow until the initial target dose is met.
- If a less sedating second generation anti-psychotic is used, may need to use diazepam for treatment of anxiety, agitation, insomnia or activation syndrome. This should only be used short-term.
PROGNOSIS
- Better than schizophrenia, with good pre and post morbid functioning.
What is Schizoaffective disorder? What is the DSM V criteria for diagnosis?
What are the two major types of schizoaffective disorder?
What is the management of the schizoaffective disorder?
What is your differential diagnosis when considering this diagnosis?
SCHIZOAFFECTIVE DISORDER
- → Features of schizophrenia and a mood disorder (bipolar disorder or depression)
- → Abnormal thought processes and deregulated emotions
DSM 5 CRITERIA
A. Two (or more) of the following, each present for a significant portion of time during a 1-month period (or less if successfully treated). At least one of these must be 1, 2 or 3. With a concurrent major mood episode that is an uninterrupted period of illness.
- Delusions
- Hallucinations
- Disorganized speech (e.g. frequent derailment or incoherence)
- Grossly disorganized or catatonic behaviour
- Negative symptoms (diminished emotional expression or avolition)
B. Delusions or hallucinations for 2 or more weeks in the absence of a major mood episode during the lifetime duration of the illness
C. Major mood episode symptoms are present for the majority of the total duration of the active and residual periods of the illness
D. The disturbance is not attributable to the effects of a substance or another medical condition.
TYPE OF SCHIZOAFFECTIVE DISORDER
- Bipolar type: more common in young adults
- Depressive type: more common in older adults—> Depressive symptoms correlate with a higher suicide risk.
MANAGEMENT
- Depressed: anti-psychotic and anti-depressant
- Manic: anti-psychotic and lithium or sodium valproate
- → Need to take care as there is an increased risk of side effects due to polypharamacy
DIFFERENTIAL DIAGNOSIS
- Delirium
- Major neurocognitive disorder
- Substance/medication induced psychotic disorder
- Neurocognitive disorder
- Major depressive disorder with psychotic features
- Bipolar disorder with psychotic features
- Brief psychotic disorder
- Schizophrenia
What is a brief psychotic disorder? What is the DSM V criteria for diagnosis?
What is the managment of this condition acutely?
What is the prognosis this condition?
What is your differential diagnosis for this condition?
BRIEF PSYCHOTIC DISORDER
DSM V CRITERIA
A. Two (or more) of the following, an episode of the disorder lasts for at least 1 day, but less than 1 month with eventual full return to premorbid level of functioning
- Delusions
- Hallucinations
- Disorganized speech (e.g. frequent derailment or incoherence)
- Grossly disorganized or catatonic behaviour
B. Rule out schizoaffective disorder and depressive or bipolar disorder with psychotic features because either
- No major depressive or manic episodes have occurred concurrently with the active-phase symptoms
- If mood episodes have occurred during active-phase symptoms, they have been present for a minority of the total duration of the active and residual periods of the illness.
C. Rule out other causes: GMC, substances (e.g. drug of abuse, medication)
MANAGEMENT
- Secure environment
- Very rapid and full resolution of symptoms suggests that a brief course of treatment is possible, otherwise treat for first psychotic episode.
- Second generation anti-psychotic + Benzodiazepine
PROGNOSIS
- Good
- Self-limiting
- Should return to premorbid functioning within 1 month
DIFFERENTIAL DIAGNOSIS
- Other medication conditions
- Substance related disorders
- Depressive and bipolar disorders
- Other psychotic disorders
- Schizophreniform disorder
- Delusional disorder
- Depressive disorder with psychotic features
What is a Delusional disorder? What is the DSM V criteria for diagnosis of this condition?
What is a delsuion?
What are the various types of delusions? Give some examples?
What is your differential diagnosis for a patient presenting with symptoms of this condition?
DELUSIONAL DISORDER
DSM-V CRITERIA
A. The presence of one (or more) delusions with a duration of 1 month or longer
B. Criterion A for schizophrenia has never been met
Note: hallucinations, if present, are not prominent and are related to the delusional theme
C. Apart from the impact of the delusion(s) or its ramifications, functioning is not markedly impaired, and behaviour is not obviously bizarre or odd
D. If manic or major depressive episodes have occurred, these have been brief relative to the duration of the delusional periods
E. The disturbance is not attributable to the physiological effects of a substance or another medical condition and is not better explained by another mental disorder
Further specify: bizarre content, type of episode (e.g. first episode, multiple episode), severity
DELUSIONS
Fixed false belief
- Idea based on morbid mental processes
- An incorrigible belief: an idea based on clearly false evidence
- Defined by form (primary/secondary) or content
- Primary: often most severe, for this person it is so real they are willing to rearrange their whole reality to match this concept
- They might be feeling that someone is watching them and then they begin to think about how people are watching them
TYPES
- Persecutory delusions: The patient believes they are being conspired against or persecuted in some way.
- Delusion of reference: Normal things are misinterpreted as being targeted at the patient
- Delusion of control: False belief that another person, group of people, or external force controls one’s general thoughts, feelings, impulses, or behavior
- Cotard delusion: False belief that one does not exist or has died.
- Delusional jealousy: False belief that a spouse or lover is having an affair, with no proof to back up their claim.
- Delusion of thought insertion: Belief that another thinks through the mind of the person.
- Erotomania: False belief that another person is in love with them.
- Grandiose religious delusion: Belief that the affected person is a god or chosen to act as a god.
- Somatic delusion: Delusion whose content pertains to bodily functioning, bodily sensations or physical appearance. Usually the false belief is that the body is somehow diseased, abnormal or changed.
- E.g. Delusional parasitosis: where one feels infected with bugs/animals and may report being repeatedly bitten
- Grandiose delusions: The patient believes they have special powers or abilities.
- Religious delusions: The patient is preoccupied with false beliefs of a religious nature.Delusions of mind reading: The patient feels that people can read his [her] mind or know his [her] thoughts.
- Thought broadcasting: The patient believes that their thoughts are broadcast so that he himself or others can hear them.
- Thought insertion: The patient believes that thoughts that are not his [her] own have been inserted into his [her] mind.
- Thought withdrawal: The patient believes that thoughts have been taken away from his [her] mind.
- Global rating of delusions: This rating should be based on the duration and persistence of the delusions and their effect on the patient’s Iife
DIFFERENTIAL DIAGNOSIS
- Obsessive compulsive disorder
- Person is completely convince their beliefs are true
Medical cause
- Delirium
- Medical condition
- Substance/medication induced
- Schizophrenia and schizophreniform disorder
- Depressive and bipolar disorders and schizoaffective disorder
What are the major mechanisms by which antipsychotic medication work? What neural pathways do they work on?
What are the receptors they work on? what are the is symptomolgy associated with these receptors? What are unwanted side effects through blocking these receptors?
What are some examples of first generation and second generation antipsychotics?
What is the mechanisms of action of antipsychotic drugs?
ANTIPSYCHOTIC MEDICATIONS
- Antipsychotics act through blocking D2 dopamine receptors in the mesolimbic pathway → relieves the positive symptoms
- 5-HT2A antagonism may help alleviate the negative and cognitive impairments in schizophrenia
- Antipsychotic drugs produce unwanted motor effects through blocking D2 receptors in the nigrostriatal pathway, enhancing prolactin secretion (blocking D2 receptors in the tuberoinfundibular pathway), reducing pleasure (block of D2 receptors in the reward component of the mesolimbic pathway), and worsen the negative symptoms of schizophrenia (blocking D2 receptors in the prefrontal cortex)
AMH
All antipsyhotics block D2 receptors
First Generation (typical) antipsychotic
- Haloperidol —–> Disproportionate D2 affinity
SECOND-GENERATION (ATYPICAL) ANTIPSYCHOTICS
- Clozapine, risperidone
- Atypical antipsychotics act on several other receptors beside D2
- There is a decreased tendency for the newer compounds to cause unwanted motor side effects
- Atypical antipsychotics: Aripiprazole, clozapine, olanzapine, quetiapine, paliperidone, risperidone, lurasidone
MECHANISM OF ACTION OF ANTIPSYCHOTIC DRUGS:
- Antipsychotic drugs are antagonists at D2 receptors
- Antipsychotic potency parallels activity on D2 receptors (therapeutic effect requires 80% occupancy of D2 receptors)
- 5-HT2A and muscarinic activity- reduces extrapyramidal side effects
- Muscarinic, Histamine H1 and α-adrenergic activity → causes side effects
Side effects? First generation drugs (high D2 affinity)
Second generation drugs? (mixed effects on receptors)
What are Motor disturbances associated with antipsychotics? Endocrine side effects? Metabolic syndrome? What are Other specific side effects associated with systemuc antipsychotic administration?
SIDE EFFECTS
FIRST-GENERATION DRUGS (HIGH D2 AFFINITY)
- Motor disturbances → Parkinson’s-like features
- Endocrine problems (Prolactin)
- Anticholinergic symptoms
SECOND GENERATION DRUG (MIXED EFFECTS ON DIFFERENT RECEPTORS):
- Metabolic syndrome (weight gain, diabetes)
- Anticholinergic symptoms
MOTOR DISTURBANCES
Acute dystonia: Involuntary movements, tremor and rigidit
- Direct consequence of blocking nigrostriatal dopamine receptors
- Reversible
Tardive dyskinesia: Involuntary movements of the face and limbs
- Occurs due to proliferation of dopamine receptors in the corpus striatum
- Treatment is often unsuccessful → irreversible
Acute dystonia and tardive dyskinesia is less with atypical antipsychotics, and especially low with clozapine, aripiprazole and zotepine.
Long-term block of D2 receptors in the nigrostriatal dopamine pathway → upregulates these receptors, which can lead to hyperkinetic tardive dyskinesia (facial and tongue movements including tongue protrusions, facial grimaces and chewing) as well as jerky limb movements
- This upregulation may be due to the neuron’s attempt to overcome drug-induced block of dopamine receptors
ENDOCRINE
- Dopamine inhibits prolactin release from the anterior pituitary
- Tuberoinfundibular pathway
- Median eminence
- D2 receptors
- Blocking D2 receptors by antipsychotic drugs → increases plasma prolactin concentration → breast swelling, pain and lactation
METABOLIC SYNDROME
- Antipsychotics increase appetite and weight gain
OTHER
- Antihistamine H1 activity → Sedation, weight gain
- α-adrenoreceptor block → Hypotension, dizziness, drowsiness
- Weight gain and increased risk of diabetes → antagonist actions at H1, 5-HT and muscarinic receptors
- Blurring of vision, increased intraocular pressure, dry mouth and eyes, constipation and urinary retention → block of muscarinic receptors
- Clozapine → agranulocytosis
- Phenothiazines → Obstructive jaundice
- Antipsychotic malignant syndrome → muscle rigidity, rapid increase in body temperature and mental confusion
- Usually reversible but death from renal or cardiovascular failure can occur
SYSTEMICALLY ADMINISTERED ANTIPSYCHOTIC:
- Motor effects: Block of D2 receptors in the nigrostriatal pathway
- Endocrine: Enhanced prolactin secretion (block of D2 receptors in the tuberoinfundibular pathway)
- Reduced pleasure (block of D2 receptors in the reward component of the mesolimbic pathway)
- Worsened negative symptoms (cortical D2 receptors)
What is the MOA of antipsychotics on the different neural pathways they work on?
1) Nigrostriatal pathway
2) Mesolimbic pathway
3) Mesocortical pathway
4) Muscarinic ACH receptors?
MECHANISM OF ACTION:
- Antipsychotic drugs: 5-HT2A activation causes neuronal inhibition
NIGROSTRIATAL PATHWAY:
- 5-HT2A receptors control the release of dopamine
- Olanzapine and risperidone are 5-HT2A antagonists → causes dopamine release by reducing the inhibitory effects of 5-HT on 5-HT2A receptors
- Reduction of extrapyramidal side effects
MESOLIMBIC PATHWAY
- D2 and 5-HT2A antagonism counteracts the increased dopamine function that causes the positive symptoms of schizophrenia
MESOCORTICAL PATHWAY
- 5-HT2A receptor antagonism increases both dopamine and glutamate release → improves the negative symptoms
- Quetiapine is a partial agonist at 5-HT1A receptors (somatodendritic autoreceptors that activate to inhibit 5-HT release
- Activation of 5-HT1A somatodendritic autoreceptors → inhibits 5-HT release increases dopamine release in the striatum and prefrontal cortex
MUSCARINIC ACH RECEPTORS
- In the striatum, dopaminergic nerve terminals innervate cholinergic interneurons expressing inhibitory D2 receptors
- Dopamine neuron inhibits cholinergic neuron via D2 receptor → decreased ACh release
- Blocking D2 receptors in the striatum → increases ACh release onto muscarinic receptors → extrapyramidal side effects
- Olanzapine has muscarinic antagonist properties → enables D2 antagonism and decreased muscarinic activity → no extrapyramidal side effects
- Antagonist of muscarinic receptors: Constipation, dry mouth, blurred vision
Whate are the major differences between first generation and second generation ( what is there adverse effects profile) What are particular things you need to monitor?
How do we prevent adverse effects of antipsychotics?
What specific side effects do we need to watch for? What are the specific ways to manage each of these?
What are some serious conditions that cannot be missed when using antipsychotics? (neuroleptic malignant syndrome)
What do you need monitor with all patients on antipsychotics???
What preventive measure should undertake when prescribing antipsychotics?
FIRST GENERATION:
First generation antipsychotics (Chlorpromazine, Haloperidol)
- These are mainly D2 receptor antagonists
- More effective against positive symptoms
- Indications: Schizophrenia (positive symptoms), psychosis, bipolar affective disorder, delirium
- High potency: Haloperidol- extrapyramidal side effects
- Low potency: Chlorpromazine- anticholinergic, anti-histamine and α1-blockade effects
ADVERSE EFFECTS:
Extrapyramidal side effects:
- Hours to days: Acute dystonia
- Days to months: Akathisia (restlessness), Parkinsonism (bradykinesia)
- Months to years: Tardive dyskinesia
Endocrine:
- Dopamine receptor antagonism → hyperprolactinaemia → galactorrhoea, oligomenorrhoea, gynecomastia
- Antimuscarinic: Dry mouth, constipation
- Antihistamine: Sedation α1-blockade: Orthostatic hypotension
- Metabolic: Dyslipidaemia, weight gain, hyperglycaemia
- Cardiac: QT prolongation
- Ophthalmologic: Chlorpromazine (corneal deposits); retinal deposits
SECOND GENERATION:
- Second generation antispsychotics (Risperidone, clozapine, olanzapine, quetiapine, aripiprazole, paliperidone, lurasidone
- These antagonize 5-HT2A receptors and dopamine receptors
- Indications: Schizophrenia (positive and negative symptoms), bipolar disorder, OCD, mania, depression, anxiety
- Lower risk of extrapyramidal side effects, but increase the risk of metabolic syndrome
- Schizophrenic patients being treated with atypical antipsychotics need to be evaluated for metabolic syndrome: Checking waist circumference, BMI, fasting blood glucose, lipid profile and blood pressure
ADVERSE EFFECTS:
- All-prolonged QT interval
- Risperidone- hyperprolactinemia (galactorrhoea, gynaecomastia and amenorrhoea)
PREVENTION OF ADVERSE EFFECTS OF ANTIPSYCHOTICS:
- Extrapyramidal symptoms: Dystonia, Parkinsonism (resting tremor, rigidity, bradykinesia), Akathisia——-> Treatment: Antiparkinsonian agents- Benztropine, diphenhydramine
- Anticholinergic side effects: Dry mouth, constipation, urinary retention, blurred vision, narrow angle glaucoma — tx Eyedrops, stool softeners
- Metabolic syndrome: Increased blood pressure, increased insulin, increased waist circumference
- Consider switching to first generation antipsychotics or a weight-neutral second generation antipsychotic (e.g. aripiprazole)
- Monitor blood lipids and blood glucose measurements
- Referral for primary care for treatment of hyperlipidaemia, diabetes
- Encourage healthy diet, exercise, smoking cessation
- Tardive dyskinesia: Switch to an atypical antipsychotic
Neuroleptic malignant syndrome:
- Changes in mental status, autonomic changes (high fever, HTN, tachycardia), lead pipe rigidity, tremor, sweating, elevated creatinine phosphokinase levels, leukocytosis and metabolic acidosis
- This is a medical emergency that requires withdrawal of all antipsychotics, assessment and treatment
- Can occur in any patient treated with antipsychotics, but is more frequently associated with the initiation of treatment and at higher doses of high-potency antipsychotics
Chlorpromazine can cause orthostatic hypotension, bluish skin discolouration and photosensitivity
Weight gain - Clozapine and olanzapine have the highest risk of cardiometabolic adverse effects followed by quetiapine
MONITORING (ALL PATIENTS ON AN ANTIPSYCHOTIC):
- Weight, BMI and waist circumference
- BP
- Fasting blood glucose
- Full lipid profile (Triglycerides, total cholesterol, HDL-C, LDL-C)
- Monitoring should be done at baseline, 3 monthly for the first year and 6 monthly for the duration of therapy
PREVENTION:
- Assess the propensity for cardiometabolic problems when prescribing and factor this into the choice of antipsychotic
- Cease any drug that is causing rapid weight gain
- Encourage smoking cessation
- Provide dietary and lifestyle advice before starting an antipsychotic and during use- healthy eating, weight reduction, physical activity
- Review of concurrent medications contributing to the weight gain (e.g. mirtazapine, valproate)
Pharmacotherapy: Metformin for the prevention and treatment of weight gain
- Impaired glucose tolerance or fasting glucose
- Dyslipidaemia
- HTN
- Overweight/ obesity
What is Hyperprolactinaemia? What does it cause?
How do we monitor patients for this?
How do we prevent it?
How do we monitor and prevent QTc prolongation when using antipsychs?
Sedation?
Orthostatic hypotension?
Anticholinergic effcts?
First generation antipsychotics?
Acute dystonia?
Parkinsonism?
Akathasia?
PREVENTION OF ADVERSE EFFECTS OF ANTIPSYCHOTICS:
Extrapyramidal symptoms:
- Dystonia, Parkinsonism (resting tremor, rigidity, bradykinesia), Akathisia
- Treatment: Antiparkinsonian agents- Benztropine, diphenhydramine
Anticholinergic side effects:
- Dry mouth, constipation, urinary retention, blurred vision, narrow angle glaucoma
- Eyedrops, stool softeners
Metabolic syndrome:
- Increased blood pressure, increased insulin, increased waist circumference
- Consider switching to first generation antipsychotics or a weight-neutral second generation antipsychotic (e.g. aripiprazole)
- Monitor blood lipids and blood glucose measurements
- Referral for primary care for treatment of hyperlipidaemia, diabetes
- Encourage healthy diet, exercise, smoking cessation
Tardive dyskinesia:
- Switch to an atypical antipsychotic
Neuroleptic malignant syndrome:
- Changes in mental status, autonomic changes (high fever, HTN, tachycardia), lead pipe rigidity, tremor, sweating, elevated creatinine phosphokinase levels, leukocytosis and metabolic acidosis
- This is a medical emergency that requires withdrawal of all antipsychotics, assessment and treatment
- Can occur in any patient treated with antipsychotics, but is more frequently associated with the initiation of treatment and at higher doses of high-potency antipsychotics
Chlorpromazine:
- can cause orthostatic hypotension, bluish skin discolouration and photosensitivity
Weight gain - Clozapine and olanzapine have the highest risk of cardiometabolic adverse effects followed by quetiapine
MONITORING (ALL PATIENTS ON AN ANTIPSYCHOTIC):
- Weight, BMI and waist circumferenc
- BP
- Fasting blood glucose
- Full lipid profile (Triglycerides, total cholesterol, HDL-C, LDL-C)
- Monitoring should be done at baseline, 3 monthly for the first year and 6 monthly for the duration of therapy
PREVENTION:
- Assess the propensity for cardiometabolic problems when prescribing and factor this into the choice of antipsychotic
- Cease any drug that is causing rapid weight gain
- Encourage smoking cessation
- Provide dietary and lifestyle advice before starting an antipsychotic and during use- healthy eating, weight reduction, physical activity
- Review of concurrent medications contributing to the weight gain (e.g. mirtazapine, valproate)
- Pharmacotherapy: Metformin for the prevention and treatment of weight gain
- Impaired glucose tolerance or fasting glucose
- Dyslipidaemia
- HTN
- Overweight/ obesity
HYPERPROLACTINAEMIA
- Gynaecomastia, galactorrhoea, amenorrhoea, impaired spermatogenesis, decreased libido, impotence, impaired sexual arousal
- Hyperprolactinaemia can reduce bone mineral density
- MONITORING (ALL PATIENTS):Routinely ask about menstrual irregularities and sexual function
- Monitor prolactin concentrations
PREVENTION
- Reduce dose of antipsychotic or switch antipsychotics in hyperprolactinaemia
QTC PROLONGATION
- Can lead to arrhythmias (e.g. Torsades de pointes)
- Patients who have hypokalaemia, hypomagnesemia, hypocalcaemia, kidney failure and heart failure or who are on a drug that prolongs the QTc interval are more prone to prolongation of the QTc interval
MONITORING
- ECG: Before and after starting treatment if the patient has a history or family history for susceptibility to QTc prolongation
SEDATION
- May be beneficial in agitated patients
- Warn patients about driving and operating heavy machinery
ORTHOSTATIC HYPOTENSION
- Can especially occur with risperidone and paliperidone
ANTICHOLINERGIC EFFECTS
- All antipsychotics cause some anticholinergic activity
- Anticholinergic effects: Dry mouth, blurred vision, increased intraocular pressure, constipation and urinary retention
- Anticholinergic toxicity: Dilated pupils; hot, dry and flushed skin; tachycardia
FIRST-GENERATION ANTIPSYCHOTICS:
- These are associated with Acute dystonia, akathisia, Parkinsonism and tardive dyskinesia
- Use the lowest effective dose of the antipsychotic or change to another antipsychotic
ACUTE DYSTONIA
- Develops within hours to days affecting the face, neck and trunk
- Management: Benztropine
PARKINSONISM
- Reduce the antipsychotic dose or switch to a second generation antipsychotic
- Treatment (Anticholinergic): Benztropine
AKATHISIA
- Reduce the antipsychotic dose or trial an alternative antipsychotic
- Propanolol or diazepam
How do we recognise and manage side effects and risks of commonly prescribed antipsychotics? e.g just explain major systems which are affected) e.g EPSE, Anticholinergi, anti-histaminic
What are other specific conditios that are associated with antipsychotics?
RECOGNISE AND MANAGE THE SIDE EFFECTS AND RISKS OF COMMONLY USED ANTIPSYCHOTIC MEDICATION
SIDE EFFECTS:
- Sedation: Avoid chlorpromazine. Prescribe high-potency antipsychotics (e.g. haloperidol) or risperidone
- Weight gain: Avoid phenothiazines, Olanzapine and clozapine. Prescribe haloperidol
- Postural hypotension: Avoid phenothiazines and prescribe haloperidol
EXTRAPYRAMIDAL SIDE EFFECTS
- Acute dystonia: Contraction of muscles
- Tardive dyskinesia: Continuous slow-writhing movements and sudden involuntary movements
- Parkinsonism: Tremor, rigidity and bradykinesia
- Akathisia: Restlessness (usually lower limbs) and a drive to move
ANTICHOLINERGIC SIDE EFFECTS
- Dry mouth, blurred vision, urinary retention, constipation
- Rarely: Ileus, glaucoma
ANTI-ADRENERGIC SIDE EFFECTS:
- Postural hypotension, tachycardia, sexual dysfunction (erectile dysfunction)
ANTI-HISTAMINIC SIDE EFFECTS:
- Sedation, weight gain
OTHERS:
- Cholestatic jaundice
- Altered glucose tolerance
- Yellow pigmentation to the skin- chlorpromazine
- Neuroleptic Malignant syndrome (rigidity, fluctuating consciousness and pyrexia)
What is clozapine?
When is it indicated for treatment?
What is its mechanism of action?
Whats unique about tis receptor profile?
What are some interactions that are important to explain to patients and to consider when prescribing clozapine?
What is treatement resistant schizophrenia? How do we try and manage this? What do you need to address?
What specific monitoring requirements are required when prescribing clozapine? What is the frequency for these blood tests? How long do thet have to go on for?
What metabolic monitoring needs to be done when prescribing clozapine?
What are the adverse effects? (associared with clozapine) (list 5 major to monitor for)
What are rare or life threatening
CLOZAPINE:
- Clozapine is indicated in the management of Treatment-resistant schizophrenia where patients are intolerant of at least 2 other neuroleptic agents
- Patients on clozapine must have regular FBC with discontinuation if there is evidence of neutropenia
- All patients on clozapine must be registered with a monitoring service
- A normal leukocyte count must precede treatment initiation
INDICATIONS:
- Treatment-resistant schizophrenia (lack of clinical response despite the use of at least 2 groups of antipsychotics for a reasonable duration or developmental of extrapyramidal side effects e.g. tardive dyskinesia
MECHANISM OF ACTION:
- Clozapine blocks D1 and D4 receptors
- It has lower affinity for D2 receptors, which results in less Extra-pyramidal side effects and hyperprolactinaemia
- The increased efficacy of clozapine in treating resistant schizophrenic patients may be due to its additional blockade of 5-HT2 receptors
UNIQUE RECEPTOR PROFILE:
- Clozapine rapidly dissociates from D2 receptors, which results in less severe extrapyramidal side effects
INTERACTIONS:
- Lithium increases the risk of developing seizures, confusion, dyskinesia and neuroleptic malignant syndrome
- Smoking cigarettes increase the clearance of clozapine and may cause a reduction in clozapine plasma concentrations
TREATMENT-RESISTANT SCHIZOPHRENIA MANAGEMENT:
- Address co-morbidities- co-morbid substance misuse is common in schizophrenia and worsens outcome
- Non-compliance: Consider psychoeducation, compliance therapy or family therapy to improve compliance with prescribed medications
- Medications: Clozapine
- Clozapine resistance: Switching from clozapine to a previously untried second-generation antipsychotic (e.g. olanzapine, risperidone, quetiapine) might be of benefit in partial treatment resistance.
- Rehabilitation
MONITORING REQUIREMENTS:
- WBC and neutrophil counts WEEKLY for at least the first 18 weeks and then at least MONTHLY after the first 18 weeks of therapy.
- Cardiac parameters: Body temperature, pulse, RR, and BP- monitored every 2 days for the 1st month, weekly for the first 18 weeks and then monthly
- Troponins and CRP- measured weekly for the first month; monthly to 6 months and then 6 monthly
- ECG- Prior to starting treatment (baseline), repeat at weeks 1, 2, 3, 4 and every 6 months thereafter
- Echocardiogram: Baseline prior to starting therapy and at 6 months
Metabolic monitoring
- Weight, BMI and waist circumference- monthl
- Fasting glucose- Test at 1 month, 6 months and then 6 monthly
- Lipids- 6 monthly
- LFTs (hepatitis and liver failure)- 6 monthly
If a patient has a blood count result in the amber range, blood counts must be repeated twice a week until a green range result is obtained
- If a patient has a blood count result in the red range, clozapine should be immediately ceased and consultation with a haematologist is required
- If a patient on clozapine develops symptoms of an infection (fever, sore throat, mouth ulcers or flu-like symptoms) a WBC and neutrophil count should be performed immediately and a clinical assessment should occur.
ADVERSE EFFECTS
- Neutropenia and agranulocytosis
- Constipation → bowel obstruction, paralytic ileus and toxic megacolon
- Myocarditis
- Cardiomyopathy
- VTE
- Hypertension
- Hypotension
- Weight gain
- Sedations
- Seizures
- Nocturnal enuresis
- Hypersalivation
- Anticholinergic- Constipation, dry mouth, blurred vision, dysuria
- Anti-adrenergic: Hypotension, sexual dysfunction
- Other: Sedation, weight gain, nausea/ vomiting, headache, hypersalivation
RARE OR LIFE-THREATENING SIDE EFFECTS OF CLOZAPINE
- Impaired temperature regulation, fever, hepatitis, cholestatic jaundice, pancreatitis
- Agranulocytosis
- Thrombocytopenia
- Circulatory collapse, arrhythmias, myocarditis, cardiomyopathy
- PE
- Neuroepileptic malignant syndrome
- Diabetes
- Paralytic ileus
What are major factors contributing to adherence (antipsychotics) ?
What are causes of non-adeherence?
FACTORS CONTRIBUTING TO ADHERENCE:
- Knowledge about mental illness and belief in the efficacy of the antipsychotic
- Side effects
- Cultural belief factors- traditional healers
- Regimen complexity- number of tablets to be taken
- Finances- unemployed, homeless
- Poor social support and access to care
- Lack of patient involvement in treatment choice
- Dissatisfaction with HCW
- Health literacy
- Forgetfulness
CAUSES OF NON-ADHERENCE
- Adverse effects
- Lack of symptom relief
- Not understanding the purpose of medication
- Failure to appreciate the consequences
What are psychosocial therapies for schizophrenia?
What are the following and how do they aim to manage these conditions:
Assertive community treatment?
Psychoeducation?
CBT?
Behavioural therapy?
Family therapy?
Social skills training?
PSYCHOSOCIAL THERAPIES FOR SCHIZOPHRENIA AND DEPRESSION:
- Assertive Community Treatment: Care of the patient in the community by a team of mental health professionals who provide a range of psychosocial treatments.
- This may include assistance with medication concordance, social skills training, welfare support, financial planning, health promotion, housing and counselling
Psychoeducation:
- The provision of information about mental illness (symptoms, etiology and treatment), the mental health care system (roles of mental health professionals) and principles of caring for oneself.
- It is provided to the patient and their family or carers over multiple sessions, often in a group format and also one-to-one.
CBT:
- Can be used to control residual positive symptoms and/or assist the patient to cope more effectively with them.
- The treatment involves the patient examining the evidence for a psychotic belief and use reasoning, coping and problem-solving skills to challenge and decrease the salience and threat of their beliefs
- It can be used for lack of insight, hallucinations, delusions and treatment nonconcordance.
Behavioural therapy:
- Aims to alter dysfunctional habits or behaviours by changing the consequences of those behaviours.
- This involves defining the problem behaviours, measuring them and manipulating aspects of the positive and negative reinforcements that help maladaptive behaviours persist.
- This can be used to structure the day of patients with significant negative symptoms to increase their level of activity and self-care
Family therapy:
- Aims to assist families in understanding and coping with their relative’s illness, decrease the degree of expressed emotion and developed better ways for dealing with the effects of the illness on the family and the person with the disorder.
- Caring for a family with a mental illness can be a sgnificant challenge that can disrupt normal family functioning.
Social skills training:
- Increases psychosocial functioning through goal setting, increased routine in the day, rehearsal activities, role modelling, feedback and positive reinforcement
- This improves self-care, ADLs and interpersonal function
- Supported employment- involves a vocational specialist working with the patient to place help them find employment or education
Always involve therapists to provide the psychotherapeutic intervention
What is a mood disorder? What is a major depressive episode? What is ‘mood’? What is affect? What disorders are considered ‘mood disorders’?
What is a major depressive episode? What is the DSM V criteria for this? What makes it an ‘Episode’? (e.g length of time of symptoms)
What are the major symptoms? (ASADACES) Know acronym!
What is a major depressive disorder? What is the DSM V criteria for diagnosis?
What is the aetiology? (biological, psychosocial)
What are risk factors for development of MDD?
What are symptoms of major depressive disorder in children?
What is the treatment/management of MDD? (break into biological and psychological treatment)
What is the prognosis of MDD?
What is your differential diagnosis with a patient with MDD symptoms?
MOOD DISORDERS:
- Mood: The subjective description of the patient’s internal emotional state. It is the pervasive and sustained emotion over a prolonged period.
- Affect: The objective assessment of how the patient’s emotion is immediately expressed and observed to the examiner including the amount and range of emotional expression
- Mood disorder includes: Major depressive disorder, Bipolar disorder, dysthymic disorder and cyclothymic disorder
MAJOR DEPRESSIVE EPISODE
DSM V CRITERIA
A. Five (or more) of the following symptoms have been present during the same 2-week period nearly every day which represent a change from previous functioning AND
a. At least one of the symptoms is either
- (1) Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad or empty) or observation made by others (e.g., appears tearful). Note: In children and adolescents, can be irritable mood.
- (2) Anhedonia: Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation made by others)
b. Note: Do not include symptoms that are clearly due to a general medical condition. Note: In adolescents can come across as increased moodiness
c. ASADFACES – Anhedonia, sleep disturbance, appetite (change of), dysphoria / depressed mood, fatigue, agitation (psychomotor retardation), concentration (diminished ability), esteem, suicidal ideation
- Significant weight loss / weight gain or decrease or increase in appetite
- e.g., a change of more than 5% of body weight in a month
- Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional, not merely self- reproach or guilt about being sick)
- Insomnia or Hypersomnia
- Psychomotor agitation or retardation
- Observable by others, not merely subjective feelings of restlessness or being slowed down)
- Loss of energy or fatigue
- Diminished ability to think or concentrate, or indecisiveness
- Subjective account or observed by others)
- Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide
B. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
C. The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., hypothyroidism)
- Substance induced
- Secondary to a General Medical Condition: Hypo- or hyperthyroidism, epilepsy, head injury, HIV/syphilis, etc.
- . Alternative Axis I psychiatric diagnosis
D: Could be within normal limits or just an intense response to environmental stressor / situational crisis (Adjustment disorder, bereavement, family relationship problems)
- Note: Responses to a significant loss (e.g., bereavement, financial ruin, losses from a natural disaster, a serious medical illness or disability) may include the feelings of intense sadness, rumination about the loss, insomnia, poor appetite, and weight
- Symptoms may overlap
MAJOR DEPRESSIVE DISORDER
DSM-V CRITERIA
A. Presence of a major depressive episode
B. The MDE is not better accounted for by schizoaffective disorder and is not superimposed on schizophrenia, schizophreniform disorder, delusional disorder, or psychotic disorder NOS
C. There has never been a manic episode or a hypomanic episode
- Note: This exclusion does not apply if all of the manic-like, or hypomanic-like episodes are substance or treatment-induced or are due to the direct physiological effects of another medical condition
- Specifiers: with anxious distress, mixed features, melancholic features, atypical features, mood- congruent psychotic features, mood-incongruent psychotic features, catatonia, peripartum onset, seasonal pattern
AETIOLOGY
Biological:
- Genetic: 65-75% MZ twins; 14-19% DZ twins, 2-4 fold increased risk in first-degree relatives
- Neurotransmitter dysfunction: decreased activity of 5-HT, NE, and DA
- Neuroendocrine dysfunction: excessive HPA axis activity
- Neuroanatomy: decreased hippocampal volume, increased ventricle sizes
- Neurophysiologic: decreased REM latency and slow-wave sleep; increased REM length
- Immunologic: increased pro-inflammatory cytokines IL-6 and TNF
- Secondary to medical condition, medication, substance use disorder
Psychosocial
- Psychodynamic e.g. low self-esteem, unconscious aggression towards self or loved ones
- Cognitive e.g. Beck’s cognitive triad: negative views of the self, the world, and the future)
- Environmental factors e.g. job loss, bereavement, history of abuse or neglect
- Comorbid psychiatric diagnoses e.g. anxiety, substance abuse, developmental disability, dementia, eating disorder
RISK FACTORS
- Female
- Family history of depression, alcohol abuse, suicide
- Childhood loss of parent before 11 years old
- Negative childhood environment
- Personality: neuroticism, insecure, dependent, obsessional
- Recent stressors: illness, financial, legal, relational and academic
- Lack of intimate, confiding relationships
- Social isolation
- Low socio-economic status
- Elderly: affects about 15% of the community residents and up to 50% of those in nursing homes.
- High suicide risk due to isolation, chronic medical illness and decreased independence.
- Often somatic complaints such as changes in weight and sleep, or anxiety symptoms.
MAJOR DEPRESSIVE DISORDER IN CHILDREN
- May have insomnia, hypersomnia, somatic symptoms, substance abuse and decreased hygiene. With irritability, boredom, anhedonia, low self-esteem and deterioration in academic performance and motivation, social withdrawal, and listlessness.
- Adolescent onset predicts chronic mood disorder, and significantly increases the risk of suicide attempt, substance abuse and school failure.
- Majority never seek treatment, however psychotherapy and pharmacotherapy combination is evidence based in severe depression.
- Close follow-up needs to occur in adolescents starting SSRIs (fluoxetine) to monitor for increased suicidal ideation or behaviour.
TREATMENT
Lifestyle: increased aerobic exercise, mindfulness-based stress reduction, zinc supplementation
Biological: SSRIs, SNRIs, other antidepressants, somatic therapies
- 1st line pharmacotherapy: sertraline, escitalopram, venlafaxine, mirtazapine
- For partial or non-response can change class or add augmenting agent: buproprion, quetiapine-XR, aripiprazole, lithium
- Typical response to antidepressant treatment: physical symptoms improve at 2 wk, mood/ cognition by 4 wk, if no improvement after 4 wk at a therapeutic dosage alter regimen
- ECT: currently fastest and most effective treatment for MDD. Consider in severe, psychotic or treatment-resistant cases
- rTMS: early data support efficacy equivalent to ECT with good safety and tolerability
- Phototherapy: especially if seasonal component, shift work, sleep dysregulation
Psychological
- Individual therapy (psychodynamic, interpersonal, CBT), family therapy, group therapy
- Social: vocational rehabilitation, social skills training
- Experimental: magnetic seizure therapy, deep brain stimulation, vagal nerve stimulation, ketamine
PROGNOSIS
- 40% will still have symptoms after 1 year that still meet criteria for major depressive disorder
DIFFERENTIAL DIAGNOSIS
- Manic episodes with irritable mood or mixed episode
- Mood disorder due to another medical condition
- Substance/medication induced depression or bipolar
- ADHD
- Adjustment disorder with depressed mood
- Sadness
What is persistent depressive disorder? (dysthmia)
What is the DSM V criteria for diagnosis?
What is your differential diagnosis when considering this diagnosis?
DSM-5 CRITERIA
A. Depressed mood for most of the day, for more days than not, for ≥2 years
- As indicated either by subjective account or observation by others,
- Note: In children and adolescents, mood can be irritable and duration must be at least 1 yr
B. Presence, while depressed, of ≥2 of the following → I HELLPP
- Insomnia or hypersomnia
- Feelings of hopelessness
- Low energy or fatigue
- Low self-esteem
- Poor appetite or overeating
- Poor concentration or difficulty making decisions
C. During the 2 yr period (1 yr for children or adolescents) of the disturbance, the person has never been without the symptoms in criteria A and B for more than 2 months at a time
D. Criteria for a major depressive disorder may be continuously present for 2 yr
E. There has never been a manic episode or a hypomanic episode, and criteria have never been met for cyclothymic disorder
F. The disturbance is not better explained by a persistent schizoaffective disorder, schizophrenia, delusional disorder, or other specified or unspecified schizophrenia spectrum and other psychotic disorder
G. The symptoms are not due to the direct psychological effects of a substance or another medical condition
H. Symptoms cause clinical significant distress or impairment in social, occupational or other important eras of function
DIFFERENTIAL DIAGNOSIS
- Major depressive disorder
- Psychotic disorder with depressive symptoms
- Depressive disorder due to a medical condition
- Substance/medication induced depressive disorder
- Personality disorder
What is post-partum depression?
What are risk factors for the development of it?
What is the management of it?
What is the prognosis like?
What is postpartum blue?
Major depressive disorder than occurs during pregnancy or in the 4 weeks post-partum.
- This typically lasts 2-6 months, however residue symptoms can last up to a year
- This may present with psychosis, however this is rare and usually associated with mania
- Severe symptoms include extreme disinterest in the baby and suicidal and infanticidal ideation.
- Post-partum depression occurs in 10% of mothers, with a 50% risk of recurrence.
RISK FACTORS
- Previous history of a mood disorder
- Family history of mood disorder
- Psychosocial factors: stressful life events, unemployment, marital conflict, lack of social support, unwanted pregnancy and colicky or sick infant
MANAGEMENT
- Psychotherapy with CBT and mindfulness
- SSRI: short term safety for infant established however long term effects are unknown
- ECT if severe
PROGNOSIS
- Impacts child’s development with increased risk of cognitive delay, insecure attachment and behavioural disorders
- Treatment of mother improves outcomes for child
POSTPARTUM BLUES
- Defined as a transient period of mild depression, mood instability, anxiety, decreased concentration, considered to be normal changes in response to fluctuating hormonal levels, the stress of childbirth, and the increased responsibilities of motherhood
- This occurs in 50-80% of mothers and begins 2-4 days post-partum, and usually lasts a short period of time (may be up to 10 days)
- This does not require psychotropic medication.
How do you define depression in terms of severity? Mild, moderate, severe? And what indicators determine severity?
What is melancholic depression? What are key DSM V criteria for this diagnosis? What are key features of it?
What is atypical depression? What are key features of this condition?
What is psychotic depression?
What is catatonic depression?
What is peripartum Depression?
What are Medical causes of depression? (list 5)
TYPES OF DEPRESSION:
SEVERITY:
- Mild: Few symptoms to make the diagnosis. The intensity of the symptoms is distressing but manageable, and the symptoms result in minor impairment in social or occupational functioning.
- Moderate: The number of symptoms, intensity of symptoms and/or functional impairment are between “mild” and “severe”
- Severe: The number of symptoms is significant, the intensity of the symptoms is distressing and unmanageable, and the symptoms interfere with social and occupational functioning.
MELANCHOLIC:
A. One of the following is present during the most severe period of the current episode:
- nhedonia (loss of pleasure in all or almost all activities)
- . Lack of reactivity to usually pleasurable stimuli
B. 3 or more of the following:
- Depressed mood characterized by profound despondency, despair and/or moroseness
- Depression worse in the morning
- Early morning wakening (at least 2 hours before usual awakening)
- Psychomotor agitation or retardation
- Anorexia or weight loss
- Excessive or inappropriate guilt
ATYPICAL:
A. Mood reactivity (mood brightens in response to positive events)
B. 2 or more of the following:
- Significant weight gain or increase in appetite
- Hypersomnia
- Leaden paralysis
- A long-standing pattern of interpersonal rejection sensitivity that results in significant social or occupational impairment.
C. Criteria are not met for “with melancholic features” or “with catatonia” during the same episode
PSYCHOTIC (DELUSIONS AND/OR HALLUCINATIONS ARE PRESENT):
- With mood congruent psychotic features: The content of all delusions and hallucinations is consistent with personal inadequacy, guilt, disease, death, nihilism or deserved punishment.
- With mood-incongruent psychotic features: The content of the delusions or hallucinations doesn’t involve personal inadequacy, guilt, disease, death, nihilism or deserved punishment.
CATATONIA:
- Catatonia is present during most of the episode
PERIPARTUM:
- Most recent episode of major depression with mood symptoms occurring during pregnancy or in the 4 weeks following delivery.
MEDICAL CAUSES OF DEPRESSION:
- Neuro: Huntington’s disease, Parkinson’s disease, MS, epilepsy, dementia, CVA
- Endo: Hypothyroidism, Cushing’s disease, Addison’s disease, anaemia
- CHF, renal failure, liver failure
- Sleep apnoea
- Pancreatic cancer
Treatment for Depression:
When diagnosing and speaking to a patient about depression, what should you adress? In terms of the diagnosis, the prognosis, lifestyle changes, biological and psychological treatment?
What are the main psychological interventions for depression? What do they address?
What are the major pharmacotherapies used for depression? What do you need to explain to a patient when prescribing them? How long should they be continued?
What are indications for inpatient treatment for patients with depression?
What is ECT? What does it involve? What are indications for its use?
What is the treatment regiment? E.g frequency, timing, relapse?
What are adverse effects from ECt treatement? What is bifrontal ECT?
What medications needed to be tapered or stopped during ECT? What can litium cause?
What are the indications for ECT?
What are the contraindications?
TREATMENT OF DEPRESSION:
- Discussions with the patient and/or family about:
- Acute or chronic stressors
- Nature of the depression, course, treatment options and adverse effects of treatment
PSYCHOLOGICAL TREATMENT FOR DEPRESSION
- Structured problem-solving or stress management
* Addressing specific stressors, encouraging effective coping strategies and using potential supports - CBT, IPT (Interpersonal psychotherapy) and short-term dynamic therapy- good for moderate depression
PHARMACOTHERAPY
- Combinations of antidepressants are not recommended for first-line treatment of major depression
- SSRIs are relatively safer in overdose and preferred for use
- Response may take 2-4 weeks
- Antidepressants should be continued for at least 6 months and preferably up to 12 months after a single episode of major depression as there is a high risk of relapse during this period.
INITIAL PHARMACOLOGICAL THERAPY:
- Antidepressants recommended first-line in the community are SSRIs, SNRIs and mirtazapine
MILD DEPRESSION
- Psychological therapies
MODERATE DEPRESSION
- Psychological therapies and antidepressants
SEVERE DEPRESSION
- Psychological therapies and antidepressants
PSYCHOTIC SYMPTOMS (ADD):
- Antipsychotics and ECT
MELANCHOLIC DEPRESSION
- ECT
INPATIENT TREATMENT (ALLOWS INTENSIVE ASSESSMENT AND TREATMENT OF COMPLICATED AND TREATMENT-RESISTANT DEPRESSION):
- Patient is experiencing depression with psychosis
- Risk of suicide or homicide (e.g. woman suffering perinatal depression → infanticide)
- Poor support at home
- Physically unwell
- Note: Depressed patients may act on their suicidal ideas in the early stages of response to treatment because apathy often remits before depressed mood.
ECT:
- ECT involves the delivery of an electric current to induce a seizure
- ECT is indicated for the treatment of severe depression if any of the following are present:
- Psychotic depression (ECT is more effective than antidepressants combined with antipsychotics)
- Melancholic depression unresponsive to antidepressants
- Depressive stupor, severe psychomotor disturbance leading to severe self-neglect or life-threatening refusal to accept fluid or food
- Severe postnatal depression and psychosis
- Strong suicidal ideation
- Previous good responses to ECT
- ECT can be helpful in treatment-resistant mania and bipolar depression
- It can be effective for schizoaffective psychoses (acute phase) and treatment-resistant acute schizophrenia
TREATMENT
- Treatments are given 3 times per week and reduced to twice weekly if severe cognitive impairment emerges
- A course of ECT is typically 6-14 treatments, but can be up to 24 treatments
- Relapse rates after ECT are high and recovery should be maintained with medication that had previously not been effective.
ADVERSE EFFECTS
- Muscle aches and pains from the muscle relaxant
- Headaches and usually transient confusion for 1 hour after treatment
- Memory loss- especially autobiographical memories (personal experiences) for the period of treatment and to a lesser degree for antecedent events
- Cognitive adverse effects are greater with bilateral than right unilateral treatment
- Bifrontal ECT may have fewer cognitive adverse effects than bitemporal treatment
- Benzodiazepines should be tapered and ceased to reduce the seizure threshold for ECT
- Antidepressants should be ceased as they can increase adverse effects
- Lithium should be ceased, because it can cause severe postictal confusion
- Patients with epilepsy won’t have their antiepileptics withdrawn for ECT due to the high risk of spontaneous seizures
- However, patients taking antiepileptics for bipolar disorder will have them withdrawn before or early in the course of ECT
USE:
- Put the electrodes on the non-dominant hemisphere
- Bitemporal- causes memory impairment, but more effective
- Unilateral- minimises memory impairment
INDICATIONS OF ECT:
- MDD with psychomotor retardation (melancholic depression)
- Paranoid schizophrenia (not responding to antipsychotics)
- Catatonic schizophrenia
CONTRAINDICATIONS:
- SOL or recent MI within 3 months
- Note: ECT can be given to pregnant women
What is mania? What impact can mania have on a patient? Why do manic episodes often relapse after treatment? What drugs are effective in acutely controlling the symptoms of mania?
What are the DSM V Criteria for diagnosis of an “manic episode’? How long must it last? What is an acronym for symptoms of mania?
What is the treatment of acute mania? What are long term psychological biological treatment options?
What is the first line drug treatment of severe acute mania? (what classes of drugs are used)
MANIC EPISODE
- An episode of acute mania is a medical emergency as patients can destroy their reputations, relationships and finances within hours or days.
- Insight and judgements are impaired early
- Manic relapses are often due to poor treatment concordance, substance abuse, use of antidepressants and stressful events
- Many patients with acute mania require hospitalisation for their protection
- Antipsychotics are the most effective drugs in acutely controlling symptoms of mania- olanzapine, risperidone and haloperidol
DSM-5 CRITERIA
A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased goal-directed activity or energy, lasting ≥1 week and present most of the day, nearly every day (or any duration if hospitalization is necessary)
B. During the period of mood disturbance and increased energy or activity, ≥3 of the following symptoms have persisted (4 if the mood is only irritable) and have been present to a significant degree and represent a noticeable change from usual behaviour → GIFTS DP
- Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation
- Inflated self-esteem or grandiosity
- Flight of ideas or subjective experience that thoughts are racing
- More talkative than usual or pressure to keep talking
- Decreased need for sleep (e.g. feels rested after only 3 h of sleep)
- Distractibility (i.e. attention too easily drawn to unimportant or irrelevant external stimuli)
- Excessive involvement in pleasurable activities that have a high potential for painful consequences (e.g. engaging in unrestrained shopping sprees, sexual indiscretions, or foolish business investments)
C. The mood disturbance is sufficiently severe to cause marked impairment in social or occupational functioning or to necessitate hospitalization to prevent harm to self or others, or there are psychotic features present
D. The episode is not attributable to the physiological effects of a substance or another medical condition
- Note: A full manic episode that emerges during antidepressant treatment but persists at a fully syndromal level beyond the physiological effect of that treatment is sufficient evidence for a manic episode, and therefore, a bipolar I diagnosis
- Note: Criteria A-D constitute a manic episode. At least one lifetime manic episode is required for the diagnosis of bipolar I disorder
TREATMENT
Psychological
- Traditionally psychotherapy was the principal treatment for dysthymia; recent evidence suggests some benefit but generally inferior to pharmacological treatment. Combinations of the two may be most efficacious
Biological
- Antidepressant therapy: SSRIs (e.g. sertraline, paroxetine) TCAs (e.g. imipramine) as an outpatient
TREATMENT OF ACUTE MANIA
Treat acute symptoms: antimanic agents
- Lithium or an antipsychotic e.g. risperidone, olanzapine
- Treat behavioural disturbance: short acting benzodiazepine + antipsychotic
Treat cognitive disturbance: antipsychotic
- Olanzapine, Risperidone, Aripiprazole, Paliperidone, Quetiapine, Haloperidol (not recommended for first-line due to side effects), Lithium, sodium valproate or carbamazepine
- Combination therapy with any of the antipsychotics recommended for acute mania plus either lithium or sodium valproate is common, especially for patients with more severe episodes of acute mania or if there is failure to respond to monotherapy.
- Continue treatment for at least 12 months following remission of a first episode of mania to prevent relapse.
- If an antipsychotic is used in combination with lithium or sodium valproate for acute treatment, the antipsychotic should be withdrawn within a few months after remission
AMH
- First-line drug treatment in severe acute mania or mixed episodes is an antipsychotic plus either lithium or valproate
- Initial phase of manic episode: Antipsychotic and benzodiazepines are needed to relieve symptoms before the onset of lithium
- Monotherapy with lithium or valproate may be adequate in less severe episodes
- Antipsychotics can be used in monotherapy
- ECT can be used in patients in patients unresponsive to drug treatment or those with severe symptoms
- ECT is the best treatment for a manic woman in pregnancy
What is a ‘hypomanic episode’?
What is the DSM V criteria for the diagnosis of this?
How long must the manic episode to be considered hypomanic?
HYPOMANIC EPISODE
DSM V CRITERIA:
A. A distinct period of persistently elevated, expansive or irritable mood and increased activity or energy lasting at least 4 consecutive days
B. During the period of mood disturbance and increased energy and activity, >3 of the following symptoms have persisted:
- Inflated self-esteem or grandiosity
- Decreased need for sleep
- More talkative than usual or pressure of speech
- Flight of ideas or racing thoughts
- Distractibility
- Increase in goal-directed activity (socially, work or school or sexually) or psychomotor agitation
- Excessive involvement in activities with painful consequences
C. The episode is associated with a change in functioning out of character of the individual when not symptomatic
D. The disturbance in mood and change in functioning are observable by others
E. The episode is not severe enough to cause marked impairment in social or occupational functioning or to necessitate hospitalization.
F. The episode is not attributable to the physiological effects of a substance or another medical condition.
What is bipolar disorder? What is the eitology of bipolar?
What is DSM V criteria for diagnosis?
What is bipolar 1 and Bipolar 11 and how are they distinguised? What the symptoms associated with each?
What is the treatment of bipolar depression? What is important to consider giving anti-depressants in bipolar? What agents should be used in conjunction?
Describe what maintenance therapy is in the treatment of bipolar disorder? What is the best agent for prophylaxis?
What are key interventions in the management of patients with bipolar?
What are common co-morbidities of bipolar?
What other important inteventions (lifestyle) are to be considered in management?
BIPOLAR:
- Acute mania is a medical emergency as patients can destroy their reputations, relationships and finances within hours or days
- Insight and judgement are usually impaired early
- Patients often require hospitalisation for their protection
- Mania
- Hyperaroused state (euphoria or dysphoria)
- Increased motor activity
- Racing thought
- Impaired judgement
- Decreased sleep
Depressed
- Depressed mood
- Suicidal ideation
- Anhedonia
- Impaired sleep
- Reduced psychomotor activity
- Impaired memory and concentration
ETIOLOGY OF BIPOLAR DISORDER:
- Genetics
- Abnormal neural serotonin
- Environment: The onset of bipolar disorder is linked to a stressful life event, seasonal onset (chance of onset increasing in Spring) and rapid increases in hours of sunshine trigger depression and mania by affecting the pineal gland
- Medications/ stimulants
- Post-natal period can coincide with bipolar disorder
DSM:
• H: Hypomanic
• Y: You rang-increased calls
• P: Pressure of speech
• O: Overactive
• M: Money spending excessively
• A: Affect- infectious euphoria
• N: No sleep
• I: Irritability
• C: Concentration impaired
BIPOLAR I
A. Criteria have been met for at least 1 manic episode
B. The occurrence of the manic and major depressive episode is not better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder or other psychotic disorders
BIPOLAR II
A. At least 1 hypomanic episode and at least 1 major depressive episode
B. There has never been a manic episode
C. The occurrence of the hypomanic episode and major depressive episode is not better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder or other psychotic disorder
D. The symptoms of depression or the unpredictability caused by frequent alternation between periods of depression and hypomania causes clinically significant distress or impairment in social, occupational or other areas of functioning.
SYMPTOMS:
- Involves at least 1 episode of major depression and at least 1 episode of hypomania
It is not a “milder” condition than Bipolar I because of the amount of time individuals with this condition spend in depression and because the instability in mood is typically accompanied by serious impairment in work and social functioning
- A common feature of bipolar II disorder is impulsivity, which can contribute to suicide attempts and substance use
TREATMENT OF BIPOLAR DEPRESSION
- Antidepressants shouldn’t be used as monotherapy as they can induce a switch into mania (acutely) or rapid cycling pattern (long-term continuation (>4 a year)
- SSRIs are best
- It is recommended that all antidepressants are withdrawn as soon as possible (preferably within 1-2 months of bipolar depression resolution)
However, this may not be possible with relapses
- There is strong evidence for the use of quetiapine monotherapy in Bipolar depression
- Antidepressants (e.g. SSRIs, SNRIs) plus a prophylactic drug for bipolar disorder OR quetiapin
Psychotherapies- CBT and psychoeducation techniques
ECT- effective in bipolar depression and should be considered especially if the patient is psychotically depressed or displays significant psychomotor retardation or agitation.
- Treat acute episode of mania with olanzapine or risperidone
DESCRIBE THE MAINTENANCE TREATMENT OF BIPOLAR DISORDER
- Continue pharmacological treatment for at least 12 months following the first episode
- Maintenance treatment following treatment of an acute episode should be considered if the patient has had 2 or more previous episodes of either mania or depression or if the 1st episode was particularly severe.
MAINTENANCE THERAPY:
- Lithium is the best for prophylaxis of bipolar disorder- more effective in preventing panic rather than depressive episodes
- Olanzapine, risperidone depot (oral is not effective), quetiapine or aripiprazole
- Lamotrogine (effective for prophylaxis of depressive), carbamazepine or sodium valproate
KEY INTERVENTIONS:
- Case management services
- Assertive Community Treatment
- CBT (e.g. medication compliance therapy, motivation interviewing for substance abuse, coping strategies enhancement, symptom control interventions)
- Psychoeducation techniques
- Cognitive remediation for cognitive deficits
- Social skills programs
- Supported employment programs
- Accommodation and disability support options
- Education and training assistance
MANAGE CO-MORBIDITIES
- Actively monitor substance use
- Inform patients about the risk of substance dependence or abuse in increasing the risk of relapse, increasing symptoms, increasing the risk of self-harm
- Treat other mental illnesses
MAINTAIN PHYSICAL HEALTH
- Physical exercise
- Healthy eating
- Smoking cessation (may increase the plasma concentrations of some antipsychotics (e.g. clozapine, olanzapine)
- Monitor weight, BMI, waist circumference, BP, serum lipids and blood glucose
- Engage the patient and their family in a psychoeducation program
- Family therapy- focussing on communication
- Carer assistance programs- supports and educates family members, and provides respite care
AMH:
- Lithium and valproate are first-line agents
- Maintenance sessions of ECT may be considered in people who respond to ECT in acute episodes
- Can use Lamotrogine (especially if depressive episodes are a feature) and carbamazepine
- Antipsychotics e.g. Olanzapine are useful
- Antidepressants can provoke mania so antidepressant monotherapy is not recommended for depressive episodes
- Consider Interpersonal behaviour therapies and CBT along with drugs
What is cyclothymia?
What are the symptoms of it?
What is the DSM V criteria for diagnosis?
Symptoms
People with cyclothymia experience both depressive phases and hypomanic phases (which are less severe than a full hypomanic episode).
- The depressive and manic symptoms in cyclothymia last for variable amounts of time due to the unstable and reactive nature of the disorder.
- The depressive phases are similar to major depressive disorder and are characterized by dulled thoughts and sensations and the lack of motivation for intellectual or social activities.
- Most people with cyclothymia are generally fatigued and tend to sleep frequently and for long periods of time. However, other people experience insomnia.
DSM V criteria- cyclothymia
A. For at least 2 years there are numerous periods with hypomanic symptoms that don’t meet criteria for a hypomanic episode and numerous periods with depressive symptoms that don’t meet criteria for a major depressive episode
B. During the 2 year period, the hypomanic and depressive periods have been present for at least half the time and the individual has not been without the symptoms for more than 2 months
C. Criteria for a major depressive, manic or hypomanic episode haven’t been met
D. The symptoms for criteria A are not better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder or other psychotic disorder
E. The symptoms are not attributable to the physiological effects of a substance or another medical condition
F. The symptoms cause clinically significant distress or impairment in social, occupational or other areas of functioning.
SYMPTOMS:
- This is given to adults who experience at least 2 years of both hypomania and depression without fulfilling the criteria for an episode of mania, hypomania or major depression
- The main feature of cyclothymic disorder is a chronic, fluctuating mood disturbance involving periods of hypomanic symptoms and periods of depressive symptoms that are distinct from each other.
What is the general role of neurotransmitters in depression? Mania?
What is the general aitiology of mood disorders? Bipolar affective disorder? Depression? (think in terms of 1) genetics 2) enviormental 3) Neurotransmitters
ROLE OF NEUROTRANSMITTERS IN MOOD DISORDERS:
- Depression results from functional deficits of 5-HT, NA and DA at certain sites in the brain
- Mania results from functional excess of NA and 5-HT at certain sites – DA and glutamate transmission also involved
- CRH hyperfunction may be associated with depression by causing diminished activity, anorexia and increased anxiety.
- Hypothalamic neurons controlling pituitary function receive NA and 5-HT inputs, which control the discharge of these cells → releases CRH → stimulates pituitary cells to secrete ACTH → cortisol
PREVALENCE, AETIOLOGY OF MOOD DISORDERS:
BIPOLAR AFFECTIVE DISORDER:
ETIOLOGY
Bipolar:
- Genetics (80% of the etiology)
- Environmental: Stressful life events- Divorced/ widowed, substance misuse, seasonal factors (increased in Spring), rapid increase in hours of bright sunshine can trigger depression and mania by affecting the pineal gland
- Pregnancy- bipolar disorder can begin during pregnancy or after birth
- Neurotransmitters: Dysregulation in 5-HT, NA and DA
DEPRESSION ETIOLOGY
- Genetics
- Life events: Long-term unemployment, living in an abusive relationship, long-term isolation or loneliness, prolonged work stress
- Neurotransmitters: Decreased 5-HT, NA and DA
- Neuroanatomy changes: Decreased hippocampal volume
- HPA axis hyperactivity
- Neurophysiology: Decreased REM latency and increased REM length
- Immunologic: Increased pro-inflammatory cytokines (IL-6 and TNF)
- Secondary to medical condition, medication, substance use disorder
- Psychodynamic- low-self-esteem, disordered attachment
- Cognitive- distorted schema, Beck’s cognitive triad
- Personality: Neuroticism (negative affectivity), social avoidance, self-criticism
- Environmental: Adverse childhood experiences, co-morbidities (e.g. substance misuse, anxiety and borderline personality disorder), chronic or disabling medical conditions (e.g. diabetes, obesity)
Outline how you would carry out a clinical assessment of a patient with depression. E.g
Evaluate risks, psych history, (psychosocial, pre morbid, psych hx, snap, meds, medical hx, fam hx) etc
What questions would need to ask when assessing suicide risk? How do you ask about a previous attempt?
How do you ask about harm to others?
What are risk factors for suicide? (list 10)
CARRY OUT A CLINICAL ASSESSMENT OF A PATIENT WITH A MOOD DISORDER:
ASSESSING PATIENTS WITH DEPRESSION
- Risk: Assess the risk of suicide, self-harm, children
- Psychosocial aspects: Ask about stressful situations (e.g. relational, occupational, financial or legal problems; domestic violence; gambling problems)
- Pre-morbid personality: Assess the patient’s usual coping styles
- Psychiatric history
- Bipolar disorder- screen for manic/ hypomanic episodes
- Anxiety
- Alcohol and drugs
- Medication: Changes in medications or doses (e.g. corticosteroids, beta blockers, oral contraceptives, Levodopa)
- Medical history- assess and treat (e.g. cerebrovascular disease, hypothyroidism)
- Family history of mental illness
SUICIDE RISK:
- When people are under a lot of stress, they sometimes they think that life is not worth living. Have you ever thought about committing suicide?
- How often do you having these thoughts?
- Have you thought about how you would act on these? (is there a feasible plan, are the methods available)
- Have you thought about when you might act on this plan?
- Are there any things (reasons) that stop you from acting on these thoughts?
- Have you tried to harm yourself in the past and how many times?
- When was the most recent time?
- Do you know anyone who has recently tried to harm themselves?
- Do you feel safe at the moment?
- Query the patient’s thoughts about death and the presence of a desire to actively end their life
- Current mood
IF A SUICIDE ATTEMPT HAS BEEN MADE?
- What were you hoping would happen as a result of your attempt? (Did they want to die or end their pain?)
- Do you regret that you did not succeed?
- Do you still have access to the method used?
- Did you use alcohol or drugs before the attempt?
- Do you have easy access to a weapon?
ASSESSMENT OF HARM TO OTHERS?
- Have you thought of hurting anyone else? Have you acted on these thoughts?
- Have you been involved in any fights recently? Were you using alcohol or drugs at the time?
RISK FACTORS FOR SUICIDE:
- Psychiatric disorder- especially major depression, bipolar, schizophrenia, schizoaffective disorder, substance use disorder, personality disorder
- Current psychosis- hallucinations, delusions (high risk of suicide)
- Family history of suicide
- Access to means of suicide- drugs, firearms, ropes
- Plan for suicide attempt
- History of dangerous behaviour on impulse
- Low likelihood of suicide attempt being detected
- Ambivalence towards survival of a suicide attempt
- Social isolation/ absence of social supports
- Chronic medical illness especially if painful
- Feeling of hopelessness
What are mood stabilisers?
What are the main drugs for bipolar affective disorder? ( list mood stabilisers, antiepileptics, and antipsychotics)
When are these drugs used? How long do they take to be effective? When are antiepileptics and atypical antipsychotics useful in treatment of bipolar? Whats lithiums role in treatment of bipolar? What phase of the illness is it best at treating?
MOOD STABILISING DRUGS:
- Mood stabilisers are drugs that are effective in the acute treatment of mania and/or bipolar depression or are effective in preventing episodes of mania and/or bipolar depression
MAIN DRUGS FOR BIPOLAR AFFECTIVE DISORDER:
- Lithium
- Carbamazepine, valproate, lamotrogine
- Antipsychotics- Olanzapine, risperidone, quetiapine and aripiprazole
- When used to treat bipolar disorder, lithium and antiepileptic agents are often referred to as Mood stabilisers
- Used prophylactically in Bipolar disease, these drugs can prevent mood swings and thus can reduce both the depressive and manic phases of the illness.
- They are given over long periods and their beneficial effects take 3-4 weeks to develop
- When given in an acute attack, these drugs are effective only in reducing mania, but not the depressive phase
- Antiepileptic and atypical antipsychotic drugs are equally effective in treating acute mania; they act more quickly and are safer so the clinical use of lithium is mainly confined to prophylactic control of manic-depressive illness
What is lithium used for? What is prophylactic use?
What is the effective plasma concentration of lithium? When does it become toxic?
What is its MOA? 3 major areas
What are important pharmokinetic charateritics of lithium? What medications should be avoided with lithium? What diseases?
What are symptoms/signs of lithium toxicity? (renal effects? thyroid?
What does acute lithium toxicity present like?
When iniating lithium what are important things to considers ? (e.g explain onset of action to patient)
How do you monitor lithium? How often? Why is it important to monitor? What other investigations are important for patients of lithium treatment?
What can lithium interact with? What medications are important to consider restricting? What organ system is lithium excreted by?
What things can precipitate lithium toxicity? (e.g sweating, reduced fluid intake)
At what level does toxicity occur? What are the features of toxicity? What should you advise patients about lithium toxicity when starting it? (things to look out for)
What are long term adverse effects of lithium?
What effects does lithium have on pregnancy? what do you need to tell women of child bearing age?
LITHIUM
- Used in prophylaxis and treatment of mania, and in the prophylaxis of bipolar or unipolar disorder (manic depression)
- Lithium is a monovalent cation effective at a plasma concentration of 0.5-1mmol/L (toxic >1.5mmol/L)
- Mimics the role of Na(+) in excitable tissues
- Targets voltage-gated Na(+) channels (responsible for action potential production)
- Accumulates inside excitable cells → partial loss of intracellular K(+) → depolarisation of the cell
MECHANISM OF ACTION:
- Inhibition of inositol monophosphatase
- Inhibition of glycogen synthase kinase 3 (GSK3) isoforms
- Inhibits dopamine release and increases 5-HT release
INHIBITION OF INOSITOL MONOPHOSPHATASE
- Lithium blocks the Phosphatidyl inositol (PI) pathway at the point where inositol phosphate is hydrolysed to free inositol → causes depletion of Phosphatidyl inositol
- This prevents agonist-stimulated inositol triphosphate formation
- This blocks many receptor-mediated effects
INHIBITION OF GLYCOGEN SYNTHASE KINASE 3 (GSK-3) ISOFORMS
Lithium inhibits GSK-3:
- Directly: Competes with Mg(+2)
- Indirectly: Stimulates PI signalling → AKT increases → inhibition of GSK3
- GSK3 phosphorylates many key enzymes and is involved in pathways leading to apoptosis and amyloid formation.
Lithium → Inhibition of GSK3 → No inhibitory effects of GSK3 on downstream signalling → activation of neuroplasticity genes → Neuroplastic changes and synaptic remodelling → improved function
PHARMACOKINETICS
- Lithium is given oral and is excreted by the kidneys
- ½ of an oral dose is excreted within 12 hours while lithium taken up by cells is excreted over 1-2 weeks
- Na(+) depletion increases lithium reabsorption by the proximal tubule → increases the likelihood of toxicit
- Diuretics also increase reabsorption of lithium
- Renal disease predisposes to lithium toxicity
LITHIUM TOXIC EFFECTS:
- Nausea/ vomiting, diarrhoea
- Tremor
Renal effects:
- Nephrogenic diabetes insipidus → polyuria
- Na(+) retention is associated with increased aldosterone secretion
- Renal tubular damage occurs with prolonged treatment>> need to monitor renal function in lithium-treated patients
- Thyroid enlargement and hypothyroidism
- Weight gain
- Hair loss
•Acute lithium toxicity → neurological effects that progress from confusion and motor impairment to convulsions, coma, death
INITIATION
- The serum lithium concentration in acute mania is higher than for prophylactic therapy
- Onset of action of lithium may be delayed for 6-10 days so consider adding a benzodiazepine or antipsychotic in severe mania
- When remission is achieved, dosage is reduced stepwise
MONITORING
- Serum lithium concentration should be measured 8-12 hours after the last dose
- Measure concentration 5-7 days after starting treatment and after each dose change until stabilised.
- Measure serum lithium concentration every 3-6 months after a stable therapeutic concentration is achieved
- Monitor lithium concentrations more frequently during illness, manic/ depressive phases, changes in diet, pregnancy, etc
- Monitor renal function (serum creatinine, eGFR and electrolytes) every 3-6 months
- Measure TSH every 6-12 months
- Screen hyperparathyroidism- Ca(+2) concentrations every 1 year
- Assess kidney, thyroid and parathyroid functions before commencing lithium
INTERACTIONS
- Lithium is excreted by the kidneys so impaired renal function reduces lithium elimination
- Intercurrent illness, fluid loss, diuretics (especially thiazides), NSAIDs, ACEIs/ARBs (Angiotensin II receptor blockers) may reduce the renal clearance of lithium and lead to increased tissue concentrations and toxicity
- Reduced fluid intake, severe reductions in sodium chloride intake; fluid loss from vomiting, diarrhoea or excessive sweating and kidney impairment can cause lithium toxicity
- Thiazide diuretics exert a paradoxical ADH effect resulting in water retention and lithium intoxication
- Side effects of antipsychotics especially haloperidol may be potentiated by lithium therapy
- Calcium channel blockers may increase the neurotoxic effects of lithium, and serum lithium concentrations need to be at the lower end of the therapeutic range
- Sodium bicarbonate may lower serum lithium concentrations by increasing urinary lithium excretion
- NSAIDs can increase serum lithium levels through reducing its renal clearance
TOXICITY (OCCURS AT CONCENTRATIONS >1.5MMOL/L)
95
- Impaired consciousness, disorientation, dysarthria, Ataxia
- Muscle twitches, coarse tremor
- Vomiting
- Acute kidney failure
- Convulsions, coma, death
- Advise patients that confusion, unsteadiness, nausea, diarrhoea or worsening tremor may indicate toxicity
ADVERSE EFFECTS (LONG-TERM)
- The commonest adverse effects to tell patients are: Increased thirst, polyuria, nausea/vomiting, tremor, fatigue
- Hypothyroidism
- Hypercalcaemia
- Nephrogenic diabetes insipidus
- Tremor, muscular weakness (rare) and extrapyramidal features (rare)
- Cognitive impairment including memory problems
PREGNANCY
- Lithium is teratogenic (congenital heart defects, neurotoxicity, hypothyroidism)
- Carbamazepine, valproate and lamotrogine can’t be used in pregnancy
- Lithium is also excreted in breast milk so bottle feed infants
What are the 3 most commonly used anticonvulsants for treatment treatment of bipolar?
What is the MOA of
- valporate
- Carbamazepine
- Lamotrogine
What atypical antipsychotics are effective in against mania?
ANTICONVULSANT THERAPY:
- Valproate and carbamazepine are effective in treating acute attacks of mania and in the long-term treatment
- Lamotrogine is effective in preventing the recurrence of both mania and depression
- Gabapentin and pregabalin are used as adjuncts to treat the chronic pain and anxiety
VALPROATE
- Potentiates GABA activity through increasing expression of GAD67 in the brain → increases GABAergic transmission
- Reduces PKC activity in manic patients (increased PKC activity is associated with mania)
- Inhibits GSK
- Weak inhibition of GABA transaminase
- Inhibits Na(+) channels
- Inhibits T-type Ca(+2) channels
CARBAMAZEPINE
- Use-dependent inhibition of Sodium channels
- Side effects: Liver-inducing agent; sedation, ataxia, mental disturbances, water retention
LAMOTROGINE
- Sodium channel blockade
- Calcium channel blockade
- NMDA receptor antagonist
ATYPICAL ANTIPSYCHOTICS (EFFECTIVE AGAINST MANIA)
- Olanzapine
- Risperidone
- Quetiapine
- Aripiprazole
What are the two major neurotransmitters associated with depression? When are anti-depressants indicated?
What are the different classes of antidepressants?
What is their major mechanism of action?
How long does clinical effect require to develop?
ANTIDEPRESSANT DRUGS:
- Depression involves decreased activity of serotonin and noradrenaline neurotransmission
- Principles of treating major depression:
- Mild depression- treated with non-drug measures
- Antidepressants for moderate- severe depression
Classes of Antidepressants:
- SSRIs (Selective Serotonin Reuptake Inhibitors)- Fluoxetine, fluvoxamine, paroxetine, sertraline, citalopram
- SNRIs (Serotonin and Noradrenaline reuptake inhibitors): Venlafaxine, duloxetine
- NARIs (Noradrenaline reuptake inhibitors): Bupropion, reboxetine, atomoxetine
- TCAs- imipramine, amitriptyline, nortriptyline, desipramine
- Monamine receptor antagonists (Mostly α2 adrenergic)- mirtazapine, trazodone, mianserin
- Monamine oxidase (MAO) inhibitors:
- Non-selective MAO-A/B (irreversible, non-competitive inhibitors): phenelzine, tranylcypromine
- Selective MAO-A: Moclobemid
Antidepressants mechanism of action: Antidepressants block the reuptake pump, which causes more neurotransmitter to be in the synapse → Increase in neurotransmitter causes receptors to downregulate
- Clinical effects of antidepressants require at least 2-4 weeks of treatment to develop – Dr. Jamal says 1 week effects start being felt
- The direct neurochemical effects of antidepressants occurs rapidly (minutes to hours) while their antidepressant effects take weeks to develop
What are SSRIs?
What role does serotonin have on the depressed brain? What receptors are targeted and effected? What receptors are downregulated?
Side effects of SSRIs?
What is serotonin syndrome?
What are risks associated with SSRIs?
SSRIS
- Depressed state: Low 5-HT, upregulated receptors, low number of signals in the neuron to release more 5-HT
- SSRIs block 5-HT reuptake both at the dendrites and the axon of the presynaptic neuron
- The increase in 5-HT causes the 5-HT1A autoreceptors to desensitize/ downregulate
- The downregulation of the 5-HT1A autoreceptors causes the neuron to release more 5-HT at the axon
- The increase in 5-HT at the axon causes the postsynaptic receptors to desensitize/ downregulate to reduce side effects
- There is a delay of 2-4 weeks before the therapeutic effect develops
- Paroxetine and fluoxetine must not be used with TCA as they inhibit the CYP2D6 enzyme, which impairs TCA metabolism → causes TCA toxicity
- Note: Acute administration of SSRIs causes an increase in synaptic 5-HT levels causes increased activation of 5-HT1A receptors on the dendrites and soma, which inhibits these neurons and reduces 5-HT release.
SIDE EFFECTS OF SSRIS:
- Nausea, insomnia, decreased libido and failure of orgasm
- The use of SSRIs should not be used for treating depression in children under 18
- Adverse effects: Excitement, insomnia and aggression in the first few weeks of treatment
- Possibility of increased suicidal ideation
- Serotonin syndrome (in combination with MAOIs): Tremor, hyperthermia and cardiovascular collapse
- “Citalopram and escitalopram cause prolongation of the QTc interval”
RISKS:
- Bipolar disorder: All antidepressants may provoke mania in bipolar disease
- People at high risk of bleeding (e.g. NSAIDs, previous upper GI bleeding): Increased risk of serious bleeding
- Precipitation of acute angle-closure glaucoma
- Serotonin toxicity: Treatment with either Moclobemide or a MAOI can cause serotonin toxicity.
- Reduce dose in hepatic impairment
- Children (<18 years): Excitement, aggression, insomnia and suicidal ideation
- Pregnancy: May be safe in pregnancy and safe in breastfeeding
What are SNRIS? What is their MOA?
What conditions are they used to treat?
What are risks associated with this drugs?
What are common side effects?
SNRIS (VENLAFAXINE, DESVENLAFAXINE AND DULOXETINE)
- These are relatively non-selective for 5-HT and NA reuptake inhibitors
- Venlafaxine is a 5-HT reuptake inhibitor but less selective for 5-HT vs noradrenaline —> Metabolised to desvenlafaxine → antidepressant
- Duloxetine inhibits NA and 5-HT uptake
USED TO TREAT OTHER DISORDERS:
- Venlafaxine, desvenlafaxine and duloxetine- anxiety disorders
- Duloxetine and milnacipran- neuropathic pain and fibromyalgia
- Duloxetine- urinary incontinence
RISKS:
- Bipolar disorder: All antidepressants may provoke mania in bipolar disease
- People at high risk of bleeding (e.g. NSAIDs, previous upper GI bleeding): Increased risk of serious bleeding
- Precipitation of acute angle-closure glaucoma
- Serotonin toxicity: Treatment with either Moclobemide or a MAOI can cause serotonin toxicity.
- Cardiac- SNRIs can cause palpitations, tachycardia, HTN and orthostatic hypotension.
- Pregnancy: Safe in pregnancy and breastfeeding
- “Venlafaxine can cause seizures”
SIDE EFFECTS:
- Headache, insomnia, impotence, dry mouth, dizziness, sweating and anorexia
What is NARIS?
NARIS
- Bupropion: Inhibits both noradrenaline and dopamine (but not 5-HT) uptake
- It is metabolised to active metabolites
- Also used to treat nicotine dependence
- Reboxetine and atomoxetine: Highly selective NA reuptake inhibitors but their efficacy in depression is less than TCAs
- Atomoxetine is used to treat ADHD
What are TCAs? What is their MOA?
What are the major side effects associated with TCAs?
What are the major risks associated with TCAs?
What can acute toxicity cause?
What investigations are important when assessing TCA toxicity?
TCAS
- TCAs inhibit the reuptake of NA and 5-HT (less effect on dopamine uptake) by pre-synaptic nerve terminals
- Improvement of emotional symptoms:
- Enhancement of 5-HT transmission
* Relief of biological symptoms - Facilitation of noradrenergic transmission
* Metabolites of TCAs have considerable pharmacological activity (sometimes greater than the parent drug)
TCA SIDE EFFECTS:
- TCAs cause sedation, confusion and motor incoordination (occurs in the first few days of treatment) and wears off in 1-2 weeks
- Anti-cholinergic effects: Dry mouth, blurred vision, constipation and urinary retention
- Postural hypotension
- Sedation- daytime performance is often affected by drowsiness and difficulty in concentrating
- Ventricular dysrhythmias- prolongation of the QT interval
RISKS:
- Bipolar disorder: All antidepressants may provoke mania in bipolar disease
- Seizures: Use cautiously in those with an increased risk of seizures
- Hepatic: Accumulates in hepatic impairment
SIDE EFFECTS
- Headache, dry mouth, agitation, insomnia (nightmares), concentration difficulties
- Sedation, orthostatic hypotension, Anticholinergic effects (dry mouth, constipation, urinary retention, blurred vision), Postural hypotension, seizures, impotence, loss of libido
- TCAs cause Sedation (H1 block), confusion and motor incoordination
- Anticholinergic effects (muscarinic block): Dry mouth, mydriasis, blurred vision, constipation, urinary retention, increased body temperature
- Sodium channel blockade → cardiotoxicity and CNS effects
- Postural hypotension (α-adrenoreceptor block)
- Ventricular dysrhythmias associated with prolongation of the QT interval
- Altered mental status- agitation, confusion, lethargy
RISKS:
- Prostatic hypertrophy- can precipitate urinary retention
- Hyperthyroidism- can have increased response to TCAs
- Epilepsy, history of seizures or other seizure risk factors: TCAs increase the risk of seizures
- Cardiovascular:
- Prolongs the QT interval and increases the risk of arrhythmias
- Tachycardia (anticholinergic effects or reflex tachycardia) can precipitate or exacerbate angina
- Avoid in those with suicidal ideation
ACUTE TOXICITY:
- Excitement and delirium
- Convulsions, coma and respiratory depression
- Dry mouth and skin, mydriasis and inhibition of gut and bladder
TCA MECHANISM OF ACTION
- TCAs block the uptake of amines (NA and 5-HT and less of dopamine) by nerve terminals
- Improvement of emotional symptoms- enhancement of 5-HT-mediated transmission
- Relief of biological symptoms- facilitation of noradrenergic transmission
- Metabolites of TCAs have considerable pharmacological activity (can be greater than the parent drug)
INVESTIGATIONS
- ABG- metabolic acidosis
- ECG
- EUC- renal impairment
What are monamine receptor antagonists?
Give an example? What is their MOA?
What unwanted effects does it try prevent?
Monoamine oxidase inhibitors, what are they? What are their side effects? When are they indicated?
What are their side effects?
What are risks associated with MAOis? What diseases/conditions are important to consider when prescribing them?
What are the management of side effects of each class of antidepressants?
What are general principles when prescribing antidepressants? What adverse effects should you review the patient for?
What do you need to explain to patients when starting them?
5 major side effects and things to watch out for when starting them?
MONAMINE RECEPTOR ANTAGONISTS
MIRTAZAPINE:
- Mirtazapine: Blocks α2 receptors + 5-HT2c receptors
- Blocks α2 receptors → increases NA and 5-HT release
- Blocks 5-HT2A and 5-HT3 receptors → reduces unwanted effects (e.g. sexual dysfunction and nausea)
- Blocks H1 receptors → sedation
- Note: Inhibiting presynaptic α2-adrenoreceptors on noradrenergic nerve terminals within the CNS → reduces negative feedback from released NA → increases further NA release
OTHERS:
- Trazodone: 5-HT2A and 5-HT2c receptor antagonism and 5-HT reuptake inhibition
- Mianserin: α2 receptor antagonism
- Blocks H1, 5-HT2A and α1-adrenoreceptors
- Can cause bone marrow suppression and agranulocytosis
MONAMINE OXIDASE INHIBITORS (MAOIS)
- Indicated for major depression in patients who have not responded to other drugs
- Irreversible, long-acting, non-selective MAOA/B inhibitors- Phenelzine, tranylcypromine
- MAOIs cause a rapid and sustained increase in 5-HT, NA and DA (5-HT is affected most while DA is least) in the synapse
- The main effect of MAOIs is to increase the cytoplasmic concentration of monoamines in nerve terminals without greatly affecting the vesicular stores that are releasable by nerve stimulation.
- The increased cytoplasmic pool results in increased spontaneous leakage of monoamines and release by indirectly acting sympathomimetics (e.g. amphetamine and tyramine)
- Tyramine therefore causes a greater increase in BP in MAOI-treated patients → causes headache and intracranial haemorrhage
* Note: MAO regulates the free intraneuronal concentration of 5-HT and NA
Reversible, short acting, MAO-A selective:
- Moclobemide- Major depression and social phobia
- No cheese reaction and other drug interactions are less severe and shorter lasting than with irreversible MAOIs
SIDE EFFECTS:
- Postural hypotension (sympathetic block)
- Atropine-like effects (as with TCAs)
- Weight gain
- CNS stimulation → restlessness and insomnia → acute overdose
- Hepatoxicity and neurotoxicity
- Cheese reaction: Severe hypertensive response to tyramine-containing foods (e.g. cheese, beer, wine, yeast)
RISKS:
- Catecholamine-secreting tumours (e.g. phaeochromocytoma): MAOIs can provoke hypertensive crisis
- Cerebrovascular or cardiovascular disease: Use with caution due to the risk of orthostatic hypotension and hypertensive crisis.
- Angina: MAOIs can reduce pain associated with myocardial ischaemia
- Diabetes: MAOIs can reduce blood glucose concentration (affects control of diabetes); the doses of antidiabetic drugs may need to be reduced.
- Serotonin toxicity in combination with other drugs e.g. SSRIs
SIDE EFFECTS:
- Cheese reaction to tyramine-containing foods (e.g. cheese, beer, wine)- can occur up to 2 weeks after treatment is discontinued
- Anticholinergic side effects: Dry mouth, blurred vision, urinary retention
- Orthostatic hypotension
- Increased CNS stimulation: Tremors, insomnia and convulsions
- Increased appetite and weight gain
MANAGEMENT OF SIDE EFFECTS AND RISKS FOR EACH CLASS:
- Orthostatic hypotension: Monitor supine and standing before and after treatment and after each dose change
GENERAL PRINCIPLES
- Start at low doses and step up the dose slowly
- For adverse effects: Review the dose, timing of the dose and potential drug interactions
BLEEDING
- SSRIs can increase the risk of bleeding, especially GIT bleeding
- Consider an alternative class of antidepressant or the addition of a gastroprotective drug e.g. PPI
- Use less gastrotoxic NSAIDs e.g. Ibuprofen
HYPONATREMIA
- Can be induced by TCAs, SSRIs, SNRIs and MAOIs
- Consider measuring serum Na(+) in patient at high risk of hyponatremia 4 weeks after initiating treatment.
- If hyponatremia occurs, discontinue the causative drug to normalise serum Na(+) concentration within 2 weeks
- If the causative drug is an SSRI, subsequent rechallenge with the same or different SSRI may be possible without the recurrence of hyponatremia
- Otherwise consider moclobemide
PSYCHOMOTOR IMPAIRMENT AND SEDATION (SSRIS, SNRIS, MIRTAZAPINE)
- Warn patients that sedating antidepressants can impair psychomotor skills (e.g. driving, operating machinery, reaction times as a pedestrian)
- Sedation may persist the following day after night time dosing
- Commence treatment at a lower dose and increase the dose slowly as tolerance develops
- Avoid use of alcohol and benzodiazepines
SEROTONIN TOXICITY
- Can develop within hours
What is “Personality’? What are personality traits? What are personality types?
How can childhood trauma effect ones personality?
What are the major management options for patients with a personality disorder?
What is the DSM V criteria for diagnosis of a personality disorder?
What is the aetiology of personality disorders? (psychological factors, biological factors, social cultural factors)
What is trauma theory? How does it relate to BPD? What about attachment in BPD? What can poor parenting lead to in terms of attachment? What do patients with BPD fail to develop?
What are different types of attachment and what do they lead to in the childs development?
What are common defence mechanism of patients with BPD?
What is ENDURING PERSONALITY CHANGE AFTER CATASTROPHIC EXPERIENCE?
What is the management of patient with BPD?
What is DBT? What does it try to address in patients with BPD?
What role does Psychodynamic psychotherapy have in BPD?
What are contraindications to treatment in BPD?
Outline a management plan for a patient with BPD w the following areas:
- Psychiatric treatment
- adjunct therapies
- Behaviour therapy
- Psychodynamic therapy
- Couple therapy
PERSONALITY DISORDERS:
- Personality disorders are not diagnosed in adolescence because of ongoing development of personality and the stigmatising nature of the diagnosis.
PERSONALITY
- The integrated pattern of an individual’s ways of thinking, behaving, feeling, perceiving and willing, which determine and are modified by attempts to adapt to the ever-changing environment of life.
- Personality traits: Relatively stable patterns over time and across various contexts
- Personality type: Cluster of traits prominent and consistently occurring together
- Personality may also be understood using a trait-based dimensional approach, with traits rated on a continuum of dysfunctional effects:
- Extraversion
- Agreeableness
- Conscientiousness
- Neuroticism
- Openness
SUMMARY
- Childhood trauma causes lasting psychological and neuro-biological abnormalities
- Distorted expectations of interpersonal relationships
- Impaired affect regulation
Management
- There are evidence based treatments available
- Multi-dimensional and flexible
- Empathic and supportive
- Encourage autonomy rather than regression
- Medication has a role
Psychotherapy
- Present-focus: problem solving, interpersonal relationships, self-awareness, affect regulation
- Dialectical behavioural therapy (DBT)
- Psychodynamic therapies
DSM IV: PERSONALITY DISORDER
- Enduring pattern of inner experience and behaviour that deviates markedly from the expectations of the individual’s culture
- Is pervasive and inflexible
- Is stable over time
- Leads to distress or impairment
- Has an onset in adolescence or early adulthood
AETIOLOGY
Psychological factors
- Defenses
- Attachment style
Biological factors
- Genetics
- Childhood trauma
Social and cultural factors
AETIOLOGY: TRAUMA THEORY
- Borderline patients often have histories of severe childhood physical and sexual abuse
- Childhood trauma causes enduring neurological and endocrine abnormalities which affect
- Affect regulation
- Information processing
- Memory
- Lack of parental empathy and atonement; inconsistent and abusive parenting etc. gives rise to:
- Distorted attachment patterns and internal working models
- Attachment figures experienced as unpredictable and dangerous
- Disorganized attachment
- No single attachment strategy: multiple, bizarre and ineffective strategies of engaging with attachment figure
- Attachment does not facilitate self-soothing and affect regulation
- Mood instability, unstable relationships
- Coercive, controlling, manipulative strategies
A failure to develop “reflective capacity” and “mentalization”
- Inability to “mind-read”
- Inability to understand the mental states, emotions and motivations of others
- Lack of awareness of ones own mental states, emotions and motivations
AETIOLOGY: PSYCHODYNAMIC THEORY
- “I love you and I hate you”
- Wish to attack object, co-existing with fear of abandonment: provokes massive anxiety
- Failure of reality testing
- Attribution of internal emotions and motivations to people in the environment
- Treating people as if they really are like that
- Provoking people to behave in keeping with these beliefs
- The internal conflict gets externalised as a conflicted relationship
ATTACHMENT
- Patterns of infant attachments persist into adulthood
- Patterns of insecure attachment may manifest in adult life as unstable, destructive or otherwise inappropriate relationships
- Development of coherent sense of self is affected by person’s attachment pattern (disturbed by pattern of insecure attachment)
DEFENCES:
Immature defences
- Denial
- Projection
- Acting out
- Splitting
- Passive aggression
Neurotic defences
- Isolation of affect
- Displacement
- Dissociation
- Repression
- Reaction formation
Mature defences
- Suppression
- Sublimation
- Altruism
- Humour
ENDURING PERSONALITY CHANGE AFTER CATASTROPHIC EXPERIENCE: ICD10
- Enduring personality change, present for at least two years, following exposure to catastrophic stress.
- The stress must be so extreme that it is not necessary to consider personal vulnerability in order to explain its profound effect on the personality.
- The disorder is characterized by a hostile or distrustful attitude toward the world, social withdrawal, feelings of emptiness or hopelessness, a chronic feeling of “being on edge” as if constantly threatened, and estrangement.
- Post-traumatic stress disorder may precede this type of personality change
- Personality change after e.g. Concentration camp experiences, disastersm, prolonged captivity with an imminent possibility of being killed
MANAGEMENT
DIALECTIAL BEHAVIOURAL THERAPY (DBT)
- Group programs which follow Linehan’s program closely lve training in 4 key areas:
- Mindfulness techniques – techniques designed to increase the ability of clients to stay ‘present focussed’ and to overcome the mental wrestle over unwanted intrusive thoughts, images & emotions.
- ‘Interpersonal Effectiveness Skills’ – skills at negotiating interpersonal challenges, especially confrontation and conflict.
- Emotion Regulation Skills – skills designed to replace unhelpful and/or destructive emotion coping approaches
- ‘Distress Tolerance’ Skills – skills to tackle the extreme emotional pain, often associated with crises.
PSYCHODYNAMIC PSYCHOTHERAPY
- As distinct from supportive, directive, CBT
Original conceptualisations of goals included
- Making the unconscious conscious
- Facilitating insight
- Facilitating the emergence of more mature psychological defences
CONTRAINDICATIONS
- Too ill – psychotic, markedly unstable bipolar disorder
- Current significant substance use
- Too many current stressors
- Suicidality / severe acting out / violence / previous hospitalisations
- Motivation poor / unrealistic expectations (effort, time, difficulty, agency)
- Coerced into treatment against their will / secondary gain from illness or treatment
- Organic brain syndrome
- Multiple previous unsuccessful therapies
MANAGEMENT PLAN:
- Psychiatric treatment goals address symptoms, problems and personality
- Adjunct therapies: The aim of adjunct therapies is to improve self-efficacy from the strengths and abilities already present.
- Psycho-education
- Self-help groups
- Mindfulness
- Family and individual support
- Exercise
- Behaviour therapy/ CBT/ Dialectical Behaviour Therapy
- Psychodynamic therapy- transference based therapy
- Couple therapy or systemic family therapy
What are cluster A, “MAD”, personality disorder?
What are the common features of these conditions?
What is paranoid personality disorder?
What is Schizoid personality disorder?
What is Schizotypal disorder?
CLUSTER A: ‘MAD’ PERSONALITY DISORDERS
- Odd, eccentric, withdrawn
- Familial association with psychotic disorders
- Common defence mechanisms: intellectualization, projection, magical thinking
PARANOID PERSONALITY DISORDER
- Pervasive distrust and suspiciousness of others, interprets others motives as malevolent and blames their problems on others and seems angry and hostile
- Diagnosis requires 4 or more of SUSPECT
- Suspicious that others are exploiting or deceiving them
- Unforgiving
- Spousal infidelity suspected without justification
- Perceive attacks on character, counterattacks quickly
- Enemies or friends? Preoccupied with acquaintance trustworthiness
- Confiding in others is feared
- Threats interpreted in benign remarks
SCHIZOID PERSONALITY DISORDER
- → Neither desires or enjoys close relationships including being a part of a family. Prefers to be alone and has a life-long pattern of social withdrawal. Seen as eccentric and reclusive with a restricted affect.
Diagnosis requires 4 or more of DISTANT
- Detached/flat affect and emotionally cold
- Indifferent to praise to criticism
- Sexual experiences of little interest
- Tasks done alone
- Absence of close friends that are not 1st degree relatives
- Neither desires nor enjoys close relationships
- Takes pleasure in few (if any) activities
SCHIZOTYPAL PERSONALITY DISORDER
- → Pattern of eccentric behaviours and peculiar thought patterns
Diagnosis requires 5 or more of ME PECULIAR
- Magical thinking
- Experiences unusual perception (body illusions)
- Paranoid ideation
- Eccentric behaviour or appearance
- Constricted or inappropriate affect
- Unusual thinking or speech
- Lacks close friends
- Ideas of reference
- Anxiety in social situations
What are cluster B “Bad” personality disorder?
What are the 4 major types?
Explain the moods and behaviours that are common in BPD; Explain in BPD; Affect? Cognition? Behaviour? Interpersonal relationships?
Outline what is needed for the diagnosis? List 5 or more criteria required for diagnosis? What is an acronym to remeber this? (IMPULSIVE)
What are the principles of treatment of BPD? List 5 aspects of treatment to explain to the patient?
What role does medications have in BPD?
How do manage a acute crisis presentation? List 6 things important aspects of management of this?
What is the aeitology of BPD? What are the three maain theories to explain its cause?
What are common defense mechanisms of patients with BPD? List 6
How do you assess suicide? What do you need to screen for? What aspects of the history are important?
What does the term “Transference” and “counter Transference” mean in relation to BPD?
What is antisocial personality disorder? What does te DSM V criteria require for diagnosis? (CORRUPT)
What is narcissitic personality disorder? What is the DSM V criteria needed for dagnosis (GRANDIOSE)
What is histrionic personality disorder?
CLUSTER B: ‘BAD’ PERSONALITY DISORDERS
- → Patients seem dramatic, emotional and inconsistent.
- There is a familial association.
- Common defence mechanisms include denial, acting out, regression, splitting, projective identification and idealisation and devaluation.
BORDERLINE PERSONALITY DISORDER
→ Unstable moods and behaviour, feel alone in the world and have problems with self-image.
- There is often a history of repeated suicide attempts and self-harm behaviours.
- Affect: depression, worthlessness, anger, guilt, anxiety, loneliness, emptiness
- Cognition: non-delusional paranoia, quasi- psychotic symptoms
- Behaviour: substance abuse, sexual deviance, suicidal behaviour, other impulsive behaviour
- Interpersonal relationships: instability, dependency, fear of abandonment, fear of engulfment, devaluation, sado-masochism
Diagnosis requires 5 or more of IMPULSIVE
- Impulsive: at least 2 self-damaging ways (sex, drugs, spending)
- Mood/affect instability
- Paranoia or dissociation under stress
- Unstable self-image
- Labile intense relationships
- Suicidal gestures/self-harm
- Inappropriate anger
- Vulnerability to abandonment
- Emptiness
DSM
- A pervasive pattern of instability of interpersonal relationships, self-image and affects and marked impulsivity beginning early adulthood. >5/9 of the following:
- Frantic efforts to avoid real or imagined abandonment
- A pattern of unstable and intense interpersonal relationships alternating between extremes of idealization and devaluation
- Identity disturbance: Markedly and persistently unstable self-image or sense of self
- Impulsivity in at least 2 areas that are potentially self-damaging (e.g. spending, sex, substance abuse, reckless driving, binge eating)
- Recurrent suicidal behaviour, gestures, threats or self-mutilating behaviour
- Affective instability due to marked reactivity of mood (e.g. intense dysphoria, irritability or anxiety that lasts for a few hours)
- Chronic feelings of emptiness
- Inappropriate, intense anger or difficulty controlling anger (e.g. frequent displays of temper, constant anger, recurrent physical fights)
- Transient, stress-related paranoid ideation or severe dissociative symptoms
PRINCIPLES OF TREATMENT:
- Provide patient education
- Psychotherapy- individual, group and family
- Social support
- Assist patients to develop constructive responses (cognitive reframing, mindfulness, distraction)
- Psychodynamic psychotherapy: Decreases the need for hospital care, improves psychiatric symptoms, reduces the need for medication and improves social adjustment.
- DBT (Dialectal behaviour therapy): Improves general psychiatric symptoms and decreases self-harm and hospital presentations)
- Psychodynamic therapy
- CBT
- Interpersonal therapies
- Transference-focused therapy
- Mentalization-based treatment
PHARMACOTHERAPY (BORDERLINE PERSONALITY DISORDER):
- Medication is not recommended as primary treatment for borderline personality disorder
- Consider medication for co-existing psychiatric disorders after weighing risks of adverse effects and lethality
- Personality disorders need a long-term treatment strategy based in the community where the person can face their stressors and learn to deal with them effectively
- Pharmacotherapy- this should he undertaken in a targeted way using 1 drug at a time. It can be used to treat specific symptoms.
- Patients with BPD may be at increased risk of suicide with overdose of medication
- Note: Pharmacological treatment has limited use in managing personality disorders and is not a primary treatment for Borderline Personality Disorder
- Consider medication for co-existing psychiatric disorders
- Psychological treatments are the mainstay of treatment
ETG (NO MEDICATION, BUT THE FOLLOWING HAVE LIMITED EVIDENCE FOR HELP):
- Lithium, antiepileptics, antipsychotics
- Antidepressants and omega-3 fatty acid supplements
- Antidepressants may only be useful in patients with coexisting anxiety or depression
ACUTE CRISIS PRESENTATION:
- Assess suicide and self-harm risk
- Most people respond to being given support and time to talk about their concerns
- Simple problem-solving strategies to address immediate precipitants
- Involve family and carers
- If these treatments are unsuccessful- use a sedative
- Hospitalization for patients who pose a serious threat of harm to self or others
- Develop crisis management plan for self-harm or threats or sudden overwhelming emotional distress and psychosocial dysfunction
During psychiatric crisis:
- Respond promptly with focus on current issue
- Conduct risk assessment- determine if brief inpatient care should be considered
- Evaluate psychiatric state and rule out co-occurring mental health disorders (e.g. major depression or substance use disorder)
- Empathic interviewing- show support and concern
- Consider brief admission to acute inpatient psychiatric facility
- Refer patient to a specialist or make follow-up appointment
• Emergency presentations include:
- Repeated presentations to the ED following acts of self-injury or self-harm
- Psychiatric crisis with sudden overwhelming emotional distress and psychosocial dysfunction
- Paranoid ideation, severe dissociative symptoms or hallucinations
EITOLOGY OF BPD:
Attachment
- Affect + Behaviour + Cognition forms personality
- Attachment theory leads to the development of an internalised template for relationships
- Biological self + (Temperament + Secure base + Self-esteem + Self-image) = Personality
- Problems with the secure base leads to fear of abandonment and Borderline Personality Disorder
Abandonment deficits → causes attachment issues
- Individuals who have severe disruption to their personality with persisting abandonment fears leads to Borderline personality disorder (idealisation leads to denigration) and Antisocial personality disorder.
- Physical and sexual abuse, neglect, hostile conflict and early parental loss are more common in childhood for those with borderline personality disorder
Trauma
- Early or ongoing exposure to trauma is common in BPD, but not all patients with BPD have a history of trauma
- They have a low self-esteem, insecure identity and/or lack of goals in life
- Childhood abuse (emotional, physical, sexual) and/or neglect may be associated with increased risk, severe symptoms and increased lifetime suicide attempts
- Attachment disorganization in childhood
Maternal factors including:
- Inconsistency in upbringing
- High over-involvement
- Parental stress
- Parental arrest
- Parental alcohol and other drug problems
- Low SES of family of origin
• Borderline personality disorder etiology:
- Genetics
- Childhood trauma and stress
BPD is generally associated with a limited range of coping skills and a lack of capacity to reflect on one’s and others’ mental state or a disturbance in self-identity.
Defence mechanisms
- Enhances or impairs coping
- Largely unconscious or partially conscious
BORDERLINE PERSONALITY DISORDER DEFENCE MECHANISMS (5):
- Projection, splitting, regression
- Self-harm and denial
- Defence mechanisms: Psychological mechanism to shield ego from conflicts. Enhances or impairs coping and is largely unconscious or partially conscious.
- Denial: Denial is the refusal to accept reality or fact acting as if a painful event, thought or feeling didn’t exist while being apparent to others
- Splitting: The individual tends to think in extremes (i.e. an individual’s actions and motivations are all good or all bad with no middle ground)
- Projection: Misattribution of a person’s undesired thoughts, feelings or impulses onto another person who doesn’t have thoughts, feelings or impulses
- Regression: Reversion to an earlier stage of development when faced with unacceptable, fearful, threatening thoughts or impulses
- Self-harm: This is a form of coping by hurting the self; a form of stress relief but also self-punishment and expression of rejection of the self.
- Acting out: Performing an extreme behaviour in order to express thoughts or feelings the person feels incapable of otherwise expressing e.g. self-injury is expression through physical pain of what can’t be stand to feel emotionally.
ASSESSING SUICIDE
- Assess suicidal ideation and threats to commit suicide (including from the past)
- Repeated use of self-harm to regulate emotions
- Impulsive or preconceived suicide attempts
History of suicidal behaviours
- Patterns of self-harm
- Patient’s current or potential psychologic support
- Screen for depression, delusions and suicide thoughts
- Access to lethal and feasible means of suicide and preconceived plan for suicide
- Risk of others to harm including dependent children
- Co-occurring depression or substance use disorder
THE TERMS “TRANSFERENCE” AND “COUNTER-TRANSFERENCE” IN RELATION TO BPD
Transference:
- Refers to the unconscious transfer of previous relationships experiences
- Each person will recreate relationships, transferring these feelings from previous relationships into a current relationship, especially with an authority figure
Transference:
- Unconscious redirection of the feelings a person has about someone else onto another person. It often concerns feelings about an important second-person relationship from childhood and is sometimes considered inappropriate
- Transference: In therapy transference refers to the redirection of a patient’s feelings for a significant person to the therapist.
- Our relationships are influenced by an internal model, which we had built from our previous relationships. This is transferred onto an authority figure e.g. doctor.
Countertransference:
- The doctor’s emotional response to the patient- impacting on the doctor
- Personality disordered patient
- Doctor’s previous experience with patients
- The doctor’s personal crisis impacting on the doctor’s response can impact on the doctor’s treatment of the patient.
- Countertransference: A redirection of a therapist’s feelings towards a patient (therapist’s emotional entanglement with a patient)
- This gives the therapist insight into what the patient is attempting to elicit in them (the therapist must look at how the patient might be eliciting this attraction)
- The emotional response the doctor has to the patient
ANTISOCIAL PERSONALITY DISORDER
→ Lack of remorse for actions, manipulative and deceitful, often violate the law.
- May appear charming on first impression.
- Pattern of disregard for others and violation of others rights must be present before age 15.
- However, for the diagnosis of ASPD patients must be at least 18.
Strong association with conduct disorder, history of trauma and abuse is common.
Diagnosis requires 3 or more of CORRUPT
- Cannot conform to law
- Obligations ignored
- Reckless disregard for safety
- Remorseless
- Underhanded (deceitful)
- Planning insufficient (impulsive)
- Temper (irritable and aggressive)
NARCISSISTIC PERSONALITY DISORDER
→ Sense of superiority, needs constant admiration, lacks empathy but has a fragile sense of self. Consider themselves special and will exploit others for personal gain.
Diagnosis requires 5 or more of GRANDIOSE
- Grandiose
- Requires excessive admiration
- Arrogant
- Needs to be special (associate with other specials
- Dreams of success, power beauty and love
- Interpersonally exploitative
- Others: lacks empathy, unable to recognise feelings and needs of others
- Sense of entitlement
- Envious or believes others are envious
HISTRIONIC PERSONALITY DISORDER
- → Attention-seeking behaviour and excessively emotional. Dramatic, flamboyant and extroverted.
- Cannot form meaningful relationships and are often sexually inappropriate.
Diagnosis requires 5 or more of ACTRESSS
- Appearance used to attract attention
- Centre of attention
- Theatrical
- Relationships are believed to be more intimate than they are
- Easily influenced
- Seductive behaviour
- Shallow expression of emotions which rapidly shift
- Speech is impressionistic and vague
What are the cluster ‘C” personality disorders?
What are their common defence mechanisms?
What is Avoidant personality disorder?
What is dependent personality disorder?
What is obsessive -compulsive personality disordeer?
CLUSTER C: ‘SAD’ PERSONALITY DISORDERS
- → Patient’s seems anxious and fearful.
- Common defence mechanisms include isolation, avoidance and hypochondriasis.
AVOIDANT PERSONALITY DISORDER
→ Timid and socially awkward with a pervasive sense of inadequacy and fear of criticism.
- Fear of embarrassing or humiliating themselves in social situations, so remain withdrawn and socially inhibited.
Diagnosis requires 4 or more of CRINGES
- Criticism or rejection reoccupies thoughts in social situations
- Restraint in relationships due to fear of being shamed
- Inhibited in new relationships due to fear of inadequacy
- Needs to be sure of being liked before engaging socially
- Gets around occupational activities required interpersonal contact
- Embarrassment prevents new activity taking or risks
- Self-viewed as unappealing or inferior
DEPENDENT PERSONALITY DISORDER
→ Pervasive and excessive need to be taken care of, excessive fear of separation, submissive behaviours.
Diagnosis required 5 or more of RELIANCE
- Reassurance required for everyday decisions
- Expressing disagreement difficult
- Life responsibilities assumed by others
- Initiating projects difficult as they have no confidence
- Alone makes them feel helpless or uncomfortable
- Nurturance: goes to excessive lengths to obtain
- Companionship sought urgently
- Exaggerated fears of beings left to care for themselves
OBSESSIVE-COMPULSIVE PERSONALITY DISORDER
- Preoccupation with orderliness, perfectionism and mental and interpersonal control. Is inflexible, closed off and inefficient.
Diagnosis requires 4 or more of SCRIMPER
- Stubborn
- Cannot discard worthless objects
- Rule/detail obsessed to the point of loss of activity
- Miserly
- Perfectionistic
- Excludes leisure due to devotion of work
- Reluctant to delegate to others
What is a Somatic disorder?
What is a somatic symptom?
What are features of somatic disorder?
What is primary gain and secondary gain in terms of a somatic disorder?
What is the DSM V criteria required for the diagnosis of this condition?
What is a conversion disorder?
What is a factitious disorder? How can they be imposed on self and on another?
SOMATIC SYMPTOM DISORDER
DSM-5 CRITERIA
A. one or more somatic symptoms that are distressing or result in significant disruption of daily
B. Excessive thoughts, feelings, or behaviours related to the somatic symptoms or associated health concerns as manifested by at least one of the following
- Disproportionate and persistent thoughts about the seriousness of one’s symptoms
- Persistently high level of anxiety about health or symptoms
- Excessive time and energy devoted to these symptoms or health concerns
C. Although any one somatic symptom may not be continuously present, the state of being symptomatic is persistent (typically >6 months)
- Specifiers: With predominant pain (previously pain disorder) for those whose somatic symptom is primarily pain
- Patients have physical symptoms and believe these symptoms represent the manifestation of a serious illness
- They will persist in this belief despite negative medical investigations and may develop different symptoms over time
- Lifetime prevalence may be around 5-7% in the general adult population
- Females tend to report more somatic symptoms than males do, cultural factors may influence sex ratio
- Complications: anxiety and depression commonly comorbid, unnecessary medications or surgery
- Often a misdiagnosis for an insidious illness so rule out all organic illnesses (e.g. multiple sclerosis)
CONVERSION DISORDER
- One or more symptoms or deficits affecting voluntary motor or sensory function that mimic a neurological or GMC (e.g. impaired coordination, local paralysis, double vision, seizures, or convulsions)
- Does not need to be preceded by a psychological event as per previous DSM criteria, however this is still worth exploring as many patients will present after such an event or related to a medical diagnosis in a first-degree relative
- More common in rural populations and in individuals with little medical knowledge
- Spontaneous remission in 95% of acute cases, 50% of chronic cases (>6 mo)
- Key to diagnosis is specific neurological testing to detect incompatible findings
FACTITIOUS DISORDER:
FACTITIOUS DISORDER IMPOSED ON SELF:
A. Falsification of physical or psychological signs or symptoms or induction of injury or disease associated with identified deception
B. The individual presents themselves to others as ill, impaired or injured
C. The deceptive behaviour is evident even in the absence of obvious external rewards
D. The behaviour is not better explained by another mental disorder such as delusional disorder or another psychotic disorder.
FACTITIOUS DISORDER IMPOSED ON ANOTHER
A. Falsification of physical or psychological signs or symptoms, or induction of injury or disease in another that is associated with identified deception.
B. The individual presents another individual to others as ill, impaired or injured
C. The deceptive behaviour is evident even in the absence of obvious external rewards
D. The behaviour is not better explained by another mental disorder such as delusional disorder or another psychotic disorder
- Note: The perpetrator, not the victim, receives this diagnosis
Define the following terms:
Somatic symptoms disorder
Hypochondriasis
Medically unexplained physical symptoms
Conversion disorder
How do we manage these unexplained illnesses?
DEFINITION OF THE TERMS
These disorders share a common feature of the prominence of somatic symptoms associated with significant distress and impairment
Somatic symptom disorder
- Somatic symptom disorder: Individuals often experience distress that is mainly focused on somatic symptoms and their significance. The individual’s suffering is authentic, whether or not it is medically explained.
- Somatic symptom disorder involves a person having a significant focus on physical symptoms such as pain, weakness or SOB; that results in major distress and/or functional impairment
- The individual has excessive thoughts, feelings and behaviours relating to the physical symptoms
- The physical symptoms may or may not be associated with a diagnosed medical condition, but the person is experiencing symptoms and believes they are sick.
- The emphasis of somatic symptom disorder is the extent to which the thoughts, feelings and behaviours related to the illness are excessive or out of proportion.
- Somatic symptom disorder is any mental disorder that manifests as physical symptoms that suggest illness or injury, but which can’t be explained fully by a general medical condition or by a substance, and is not attributable to another mental disorder.
- The patient must be excessively worried about their symptoms, and this worry must be out of proportion to the severity of the physical complaints themselves.
Hypochondriasis
- Most individuals with hypochondriasis are now classified as having somatic symptom disorder, but some cases involve the diagnosis of illness anxiety disorder
- Illness anxiety disorder entails a preoccupation of having acquired a serious, undiagnosed medical illness
- This refers to the preoccupation with and fear of having or acquiring a serious disorder
- Patients are so preoccupied with the idea that they are or might become ill that their illness anxiety impairs social and occupational functioning or causes significant distress.
- It is confirmed when fears and symptoms persist for >6 months despite reassurance after a thorough medical evaluation.
- The patient’s fears may derive from misinterpreting nonpathologic physical symptoms or normal bodily functions
- llness anxiety disorder is a preoccupation that physical symptoms are signs of a serious illness even when there is no medical evidence to support the presence of an illness
- They have an unrealistic fear of having or developing a serious disease
- Medically unexplained physical symptoms
- These are symptoms for which a treating physician has found no medical cause or whose cause remains contested.
- Strictly, this term means that the cause for the symptoms is unknown or disputed with no scientific consensus.
Conversion disorder
- Conversion disorder is sometimes applied to patients who present with neurological symptoms such as numbness, blindness, paralysis or fits that are not consistent with a well-established organic cause and can be traced back to a psychological trigger
- Symptoms of conversion disorder arise in response to stressful situations affecting a patient’s mental health or an ongoing mental health condition such as depression.
- The symptoms often develop abruptly and onset can often be linked to a stressful event
- Conversion disorder has a psychological stressor and usually begins with a stressor
- Symptoms can affect body movement and function
- The patient usually has blindness, paralysis, weakness, pseudoseizures, tremors or other neurological symptoms that can’t be explained by medical evaluation
- The diagnosis is only made after a comprehensive medical examination and tests to rule out neurologic or general medical disorders that may account for the symptoms.
- An important characteristic is that the symptoms and signs are not consistent with neurologic disease.
- Conversion disorder symptoms may occur because of a psychological conflict
- People who have conversion disorder aren’t making up their symptoms (malingering)
- The physical symptoms are an attempt to resolve the conflict the person feels inside
- Conversion symptoms result from an unconscious process
- Conversion disorder is a condition that presents as an alteration or loss of a physical function suggestive of a physical disorder, but is taken to be the expression of an underlying psychological conflict or need.
MANAGEMENT OF UNEXPLAINED ILLNESSES:
- Psychoeducation
- CBT
- A trustful and supportive therapeutic relationship
- Reassuring the patient
Concepts of normal and abnormal illness behaviour:
What is meant by the “sick role”? What is the concept of this?
What are problems with the sick role?
What are rights to the sick role?
What are obligations of the sick role?
What is illness behaviour? What does it involve?
What is Abnormal illness behaviour? Give examples?
What are Subconcious psychological motivators? What is meant by primary gain? Secondary gain?
CONCEPTS OF NORMAL AND ABNORMAL ILLNESS BEHAVIOUR:
SICK ROLE
- Denotes an individual who has fallen ill and adheres to socially patterned sick role
- Being sick is not simply a “state of fact” or condition, it entails socially conditioned rights and obligations
CONCEPT OF SICK ROLE:
- Being sick means that the person enters a role of sanctioned deviance that disturbs the social function of society.
- From a functional perspective, a sick person is not a productive member of society
- This deviance needs to be policed by the medical profession
PROBLEMS WITH THE SICK ROLE:
- Blaming the sick person e.g. AIDS
- Chronic illness- role prolonged
- Different ways people perceive and act upon symptoms can be due to class, education, wealth
- Social or financial rewards from the sick role
RIGHTS:
- The sick person is exempt from normal social roles
- The sick person is not to be blamed for being sick
OBLIGATIONS:
- The sick person should try to get well
- The sick person should seek technically competent help and cooperate with the medical profession
ILLNESS BEHAVIOUR
- This describes ways people respond to bodily indications and the conditions under which they view them as abnormal
Illness behaviour involves the manner in which people:
- Monitor their bodies
- Interpret their symptoms
- Take remedial action
- Utilize various sources of help
Illness behaviour: Illness behaviour refers to any actions or reactions of an individual who feels unwell for the purpose of defining their state of health and obtaining relief from their perceived illness
- Illness behaviour describes an individuals’ different ways for responding to their own health status
ABNORMAL ILLNESS BEHAVIOUR
- Abnormal illness behaviour is not a diagnosis, but description of social behaviour
- Attempts to explain behaviour not explained by an underlying disease process or disorder
- This is not a diagnosis, but can be used as a pejorative label
Abnormal illness behaviour:
- Illness affirming somatically focussed- conversion disorder
- Illness denying somatically focussed e.g. ignoring chest pain symptoms with heart disease
- Illness affirming psychologically focussed e.g. claiming PTSD for minor MVA
- Illness denying psychologically focussed e.g. denial or grief and depression following major trauma
Abnormal illness behaviour encompasses several clinical conditions characterized by a maladaptive mode for experiencing, perceiving and responding to one’s own health status
SUBCONSCIOUS PSYCHOLOGICAL MOTIVATORS:
- Primary and secondary gain describes the significant subconscious psychological motivators patients have when presenting with symptoms.
- If these motivators are recognised by the patient and especially if they are fabricated or exaggerated for personal gain then this is malingering
Primary gain:
- Produces positive internal motivations. Somatic symptoms represent a symbolic resolution of an unconscious psychological conflict to reduce anxiety and conflict with no external incentive.
- It is most typically demonstrated in conversion disorder (psychiatric disorder where stressors manifest themselves as physical symptoms without organic causes)
Secondary gain:
- This can be a component of any disease, but is an external motivator.
- Secondary gain occurs if a patient’s disease allows them to miss work, avoid military duty, obtain financial compensation, obtain drugs or avoid ail .e.g. an individual having stomach cramps when household chores are completed by the family.
Addiction and substance use disorders:
Define the following terms:
Substance use disorder?
Substance abuse?
Hazaradous use?
Harmful use?
Dependence?
TERMINOLOGY:
- Substance use disorder: The essential feature of a substance use disorder is the cognitive, behavioural and physiological symptoms indicating that the person continues to use substances despite significant substance-related problems (e.g. failure to meet work, family, school obligations).
- Substance use disorders involve the overuse or dependence on a drug leading to effects that are detrimental to the individual’s physical and mental health or the welfare of others.
- Substance abuse: Refers to the harmful or hazardous use of psychoactive substances
- Substance abuse: It is a patterned use of a drug in which the user consumes the substance in amounts or with methods that are harmful to themselves or others.
- Hazardous use: A pattern of substance use that increases the risk of harmful consequences for the user. Compared to harmful use, it refers to patterns of use that are of public health significance despite the absence of any current disorder in the individual user.
- Harmful use: This is a pattern of substance use that increases the risk of harmful consequences to user, but is defined by consequences to physical and mental health.
- Damage may be physical (e.g. hepatitis following IVDU) or mental (e.g. depressive episodes secondary to heavy alcohol intake)
- Dependence: This is an adaptive state the develops from repeated drug administration and which results in withdrawal upon cessation of drug use.
- Psychological dependence refers to impaired control over drug use
- Physical dependence refers to tolerance and withdrawal symptoms
What do you look for when considering “gambling” as a significant addiction?
What is a quick screening tool/ questions to ask on history?
What is the DSM V criteria for the diagnosis a gambling addiction?
What is the severity? Mild/Mod/Severe? How many criteria do they need to meet?
What are associated features of gambling addiction?
Explain what nicotine addiction is?
What is the DSM V criteria for the diagnosis? How long does the nicotine use need to be problematic?
What are associated features of nicotine addiction?
What are the signs/symptoms of tobacco withdrawl?
NICOTINE:
DSM V
A. Problematic use of tobacco leading to clinically significant impairment or distress as manifested by >2 of the following within 12 months:
- Tobacco is taken in larger amounts or over a longer period than was intended
- . There is a persistent desire or failed attempts to cut down or control use
- Time spent in activities for obtaining or using tobacco
- . Craving to use tobacco
- Recurrent tobacco use resulting in a failure to fulfil roles at work, school or home
- Continued tobacco use despite persistent social or interpersonal problems caused by tobacco (e.g. arguments with others about tobacco use)
- Social, occupational or recreational activities are given up or reduced because of tobacco use
- Recurrent tobacco use in situations where it is hazardous (e.g. smoking in bed)
- Tobacco use is continued despite knowledge of having a persistent physical or psychological problem that has been caused or exacerbated by tobacco
- Tolerance (defined by either of):
- A need for increased amounts of tobacco to achieve the desired effect
- A markedly diminished effect with continued use of the same amount of tobacco
- Withdrawal (either of the following):
- The characteristic withdrawal syndrome for tobacco
- Tobacco or nicotine is taken to relieve or avoid withdrawal symptoms
ASSOCIATED FEATURES
- Tolerance to tobacco occurs with the disappearance of nausea and dizziness after repeated intake and with a more intense effect of tobacco the first time it is used during the day.
TOBACCO WITHDRAWAL
A. Daily use of tobacco for at least several weeks
B. Abrupt cessation or reduction in the amount of tobacco used followed within 24 hours by >4 of the following:
- Irritability, anger, frustration
- . Anxiety
- Difficulty concentrating
- Increased appetite
- Restlessness
- Depressed mood
- Insomnia
C. The signs and symptoms cause clinically significant distress or impairment in social, occupational or other areas of functioning
D. The signs of symptoms are not attributed to another medical condition and are
What is opioid use disorder?
What are the DSM V criteria dor diagnosis?
What is the scale of severity of this condition?
What are associated features of this condition?
How do you diagnose it? What tests should be done when suspecting this in patients?
What is the suicide risk in these patients? When is it highest?
What are consequences of opioid use disorder? List 6
What is opioid intoxication? What are DSM V criteria for diagnosis?
What is opiod withdrawl? What are the features of it? What is the DSM V criteria for this? What features of criterion A must they meet?
OPIOID USE DISORDER
A. Problematic use of opioid leading to clinically significant impairment or distress as manifested by >2 of the following within 12 months:
- Opioid is taken in larger amounts or over a longer period than was intended
- There is a persistent desire or failed attempts to cut down or control use
- Time spent in activities for obtaining, using or recovering from opioids
- Craving to use opioid
- Recurrent opioid use resulting in a failure to fulfil roles at work, school or home
- Continued opioid use despite persistent social or interpersonal problems caused by opioids (e.g. arguments with others about opioid use)
- Social, occupational or recreational activities are given up or reduced because of opioid use
- Recurrent opioid use in situations where it is hazardous (e.g. smoking in bed
- Opioid use is continued despite knowledge of having a persistent physical or psychological problem that has been caused or exacerbated by opioids
- Tolerance (defined by either of):
- A need for increased amounts of opioids to achieve the desired effect
- A markedly diminished effect with continued use of the same amount of opioids
k. Withdrawal (either of the following):
- The characteristic withdrawal syndrome for opioid
- Opioids are taken to relieve or avoid withdrawal symptoms
SEVERITY:
Mild: 2-3, moderate: 4-5, Severe: 6+
ASSOCIATED FEATURES
- Daily activities are planned around obtaining and administering opioids
- Associated with a history of drug-related crimes (e.g. burglary)
- Marital difficulties, unemployment are often associated with opioid use disorder
- Develops in the late teens or early 20s commonly
- Relapse following abstinence is common in treated populations
- The risk of opioid use is related to family, peer and social environmental factors
- Impulsivity and novelty seeking are individual temperaments that relate to the risk of developing a substance use disorder
DIAGNOSIS
- Urine Drug Screen
- Hepatitis A, B and C virus; HIV are positive in IVDUs
- LFTs- increased either from hepatitis or from toxic injury due to contaminants that have been mixed with the injected opioid
SUICIDE RISK
- Repeated opioid intoxication or withdrawal may be associated with severe depression that is temporary, but can be intense enough to lead to suicide attempts and completed suicides
CONSEQUENCES OF OPIOID USE DISORDER:
- Lack of mucous membrane secretions causing dry mouth and nose
- Slowing of GIT and constipation
- Pupillary constriction causing impaired visual acuity
- Sclerosed veins and puncture marks
- Cellulitis and circular appearing scars can result from individuals directly injecting into the subcutaneous tissue
- Tetanus and C. botulinum can result from injecting opioids with contaminated needles
- Bacterial endocarditis, hepatitis and HIV
- TB- usually asymptomatic
- Sniffing opioids can cause irritation of the nasal mucosa and perforation of the nasal septum
- Death most often results from overdose, accidents, injuries
- Erectile dysfunction. Females have disturbances in reproductive function and irregular menses
- Low birth weight infants and infants with physiological dependence on opioids
- Patients with opioid use disorder are at risk for developing depression
OPIOID INTOXICATION
A. Recent use of an opioid
B. Problematic behavioural or psychological changes (e.g. initial euphoria followed by apathy, dysphoria, psychomotor agitation or retardation) that develop during or shortly after opioid use
C. Pupillary constriction and >1 of the following signs developing during or shortly after opioid use:
- Drowsiness or coma
- Slurred speech
- Impairment in attention or memory
D. The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder
- Note: Alcohol intoxication and sedative hypnotic intoxication can cause a similar clinical picture. This can be excluded on the absence of pupillary constriction or the lack of response to a naloxone challenge.
OPIOID WITHDRAWAL:
- Opioid withdrawal can occur after administration of an opioid partial agonist (e.g. Buprenorphine) to a person currently using a full opioid agonist
- Classic symptoms of withdrawal: Anxiety, restlessness, muscle aches, irritability and increased sensitivity to pain
- The speed and severity of withdrawal of opioids depends on the half-life of the opioid used
- Short-acting drugs (e.g. heroin) start having withdrawal symptoms within 6-12 hours after the last dose
- Acute withdrawal symptoms for a short-acting opioid peak within 1-3 days and subside over 5-7 days
- Less acute withdrawal symptoms can last weeks to months and can include anxiety, dysphoria, anhedonia and insomnia
- Symptoms take 2-4 days with longer-acting drugs (e.g. methadone, buprenorphine)
DSM:
A. Presence of either:
- Cessation or reduction in opioid use that has been heavy and prolonged (i.e. several weeks)
- Administration of an opioid antagonist (e.g. naloxone or naltrexone) after a period of opioid use
B. >3 of the following developing within mins to several days after Criterion A:
- Dysphoria
- Nausea and vomiting
- Muscle aches
- Lacrimation or rhinorrhoea
- Pupillary dilation, piloerection or sweating
- Diarrhoea
- Yawning
- Fever
- Insomnia
C. The signs or symptoms cause clinically significant distress or impairment in social, occupational or other areas of functioning
D. The symptoms are not attributable to another medical condition and are not better explained by another mental disorder
What is “sedative, hypnotic or anxiolytic use disorder?
Has does it present?
What are the criteria for DSM V covering all substance use disorders? List 6 out of the 12 criteria
What are associated features of this condition?
How do you diagnose this condition?
What is the DSM V criteria for ‘Sedative, hypnotic or anxiolytic intoxication’?
What is the criteria for sedative, hypnotic or anxiolytic withdrawal?
What are associated features of this condition?
SEDATIVE, HYPNOTIC OR ANXIOLYTIC USE DISORDER
- Same criteria as Tobacco and Opioids
- Sedative, hypnotic or anxiolytic substances include: Benzodiazepines, Benzodiazepine-like drugs (e.g. zolpidem, zaleplon), carbamates, barbiturates
- This class of substances include all prescription sleeping medication and almost all prescription anti-anxiety medications (excluding buspirone)
- These substances are brain depressants like alcohol
- If these drugs are prescribed or recommended for appropriate medical purposes and if they are used as prescribed then the resulting tolerance or withdrawal doesn’t meet the criteria for diagnosing a substance use disord
ALL SUBSTANCES
Problematic pattern of use leading to clinically significant impairment or distress manifesting at least 2 of (in 12 months):
- Substance is taken in large amounts or over a longer time than was intended
- There is a persistent desire to unsuccessful efforts to cut down or control use
- A great deal of time is sent in obtaining, using and recovering from the substance
- Craving or a strong desire to use substance
- Recurrent use resulting in a failure to fulfil major obligations
- Continued use despite persistent or recurrent social or interpersonal problems caused or exacerbated by use
- Important social, occupational or recreational activities given up or reduced due to use
- Recurrent use in situations that may be hazardous
- Use is continued despite knowledge of harm
- Tolerance
- Withdrawal syndrome on cessation or reduction
- ?2-3 mild; 4-5 moderate; 6+ severe
ASSOCIATED FEATURES
- Impulsivity and novelty seeking are temperaments that relate to the propensity for developing a substance use disorder
- Sedatives are often used to alleviate the side effects of other substances
- Tolerance to brain stem depressant effects takes a slower period of time so as the person takes more substance to achieve euphoria there may be a sudden onset of respiratory depression and hypotension, which can result in death.
- An initial pattern of intermittent use socially can lead to daily use and high levels of tolerance
- This can cause increased interpersonal difficulties, increased cognitive dysfunction and withdrawal
- The social and interpersonal consequences of this substance use disorder mimics alcohol in terms of disinhibited behaviour
- Benzodiazepines have a wide safety margin, but at higher doses, these substances can be lethal especially when mixed with alcohol
- Acute intoxication can cause accidental injuries, automobile accidents, falls
- Disinhibiting effects of these agents can cause aggressive behaviour
DIAGNOSIS
- Urine Drug Screen
- Blood drug test
SEDATIVE, HYPNOTIC OR ANXIOLYTIC INTOXICATION
A. Recent use of a sedative, hypnotic or anxiolytic
B. Maladaptive behavioural or psychological changes (e.g. inappropriate sexual or aggressive behaviour, mood lability) that developed during or shortly after sedative, hypnotic or anxiolytic use
C. >1 of the following signs or symptoms during or shortly after use:
- Slurred speech
- Incoordination
- Unsteady gait
- Nystagmus
- Impaired cognition (attention, memory)
- Stupor or coma
D. The signs and symptoms are not attributable to another medical condition and are not better explained by another mental disorder
ASSOCIATED FEATURES
- Memory impairment is a prominent feature of sedative, hypnotic or anxiolytic intoxication and is often characterized by an anterograde amnesia
SEDATIVE, HYPNOTIC OR ANXIOLYTIC WITHDRAWAL
A. Cessation or a reduction in sedative, hypnotic or anxiolytic use that has been prolonged
B. >2 of the following developing within several hours to days after the cessation or reduction in sedative, hypnotic or anxiolytic:
- Autonomic hyperactivity (e.g. sweating, tachycardia, tachypnoea, fever)
- Hand tremor
- Insomnia
- Nausea and vomiting
- Transient visual, tactile or auditory hallucinations or illusions
- Psychomotor agitation
- Anxiety
- Grand mal seizures
C. The signs and symptoms cause clinically significant distress or impairment in social, occupational or other areas of functioning
D. The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder including intoxication or withdrawal from another substance.
- Note: When hallucinations occur in the absence of intact reality testing, a diagnosis of substance. medication-induced psychotic disorder should be considered
ASSOCIATED FEATURES
- Relief of withdrawal symptoms with administration of any sedative-hypnotic agent supports a diagnosis of sedative, hypnotic or anxiolytic withdrawal
- Withdrawal from shorter-acting substances that are rapidly absorbed and have no active metabolites can begin within hours after the substance is stopped
- Medications that last <10 hours (e.g. lorazepam, oxazepam, temazepam) produce withdrawal symptoms within 6-8 hours that peak in intensity on Day 2 and improve markedly by Day 4-5.
- Medications that have longer half-lives (e.g. diazepam) may not develop symptoms for more than 1 week, peak in intensity during week 2 and decrease markedly during week 3-4
- Withdrawal from substances with long-acting metabolites (e.g. diazepam) may not begin for 1-2 days or longer
- The withdrawal syndrome produces by substances of this class is often characterized by delirium, which can be life-threatening.
- The longer the substance has been taken and the higher the doses used, the more likely it will cause a severe withdrawal.
- High doses can cause withdrawal seizures or delirium
- The substance withdrawal delirium is characterised by disturbances in consciousness and cognition with visual, tactile or auditory hallucinations
- Seizures and autonomic instability in a history of prolonged exposure to sedative, hypnotic or anxiolytic medications suggests a high likelihood of sedative, hypnotic or anxiolytic withdrawal
- The symptoms of withdrawal can be mimicked by other conditions including hypoglycaemia and DKA
What are the physiological and psychological aspects to substance dependence?
What are the physioogical steps taken to form dependence? Explain.
What are the psychological aspects to dependence?
PHYSIOLOGICAL AND PSYCHOLOGICAL ASPECTS OF THE ETIOLOGY OF SUBSTANCE DEPENDENCE:
DEPENDENCE- PHYSIOLOGICAL STEPS
- Exposure to substance with abuse potential (crosses the BBB and can activate the reward pathway)
- Positive aspects of neurochemical activation outweigh negative aspects in the individual
- Environmental context is conducive to repeated use
- Repeated use results in receptor adaptation (function or number)
- Downstream neurological function alters to adjust for receptor adaptation (homeostasis)
- Same amount of drug produces less physiological response- more drug required for equal outcome- tolerance
- Tolerance fuels desire for more drug to achieve same outcome
- Normal function now requires increased levels of binding (presence of the drug)- dependence
- Removal of substance produces adverse effects- withdrawal
DEPENDENCE- PSYCHOLOGICAL ASPECTS
- Psychological factors involved in the likelihood of trying the drug
- Psychological factors involved in resistance to social forces (e.g. Peer pressure)
- Psychological factors in the resistance to adverse experiences in stopping if desired
- Those with poorer coping strategies are more likely to seek out dissociation from their reality
- Internal- resilience, sense of control, identity
- External- supports, role models, opportunities
What are amphetamines?
What are the acute effects of amphetamine?
What are the immediate effects of amphetamines?
What are the chronic effects of amphetamines?
How do you diagnose usage? What other tests are important and why?
What is the treatment for acute amphetamine intoxication?
AMPHETAMINES
- Dexamphetamine- legal prescription drug
- Methamphetamine
- Speed: Powdered base form
- ICE- crystalline form (usually higher potency)
ACUTE EFFECTS:
- Tachycardia, tachypnoea, fever, hypertension
- Dry mouth
- Increased sweating, pupil dilatation
- Headaches, stomach cramps, nausea
- Dizziness, blurred vision
IMMEDIATE EFFECTS OF AMPHETAMINES:
- Less inhibition, restless, agitation
- Alert
- Increased sense of wellbeing, energy, strength, libido
- Feeling a sense of power and superiority over others
- Paranoia, irritable, hostile and aggressive
- Itching, picking, scratching
- Dizziness, blurred vision, Tremor
- Amphetamine psychosis- paranoid delusions, hallucinations, bizarre or violent behaviour
- Strokes, heart failure, seizures
CHRONIC EFFECTS
- Amphetamine psychosis
- Amphetamine use during pregnancy: Bleeding, premature labour, miscarriage
- Low birth weight, slow growth and development
- Overactive and agitated at birth
- Feed poorly and irritable- breastfeed
ETG
- Amphetamine toxicity is characterised by cardiovascular and autonomic stimulation, delirium, hallucinations and agitation.
- The commonest management problem is delirium and agitation
DIAGNOSIS
- Urine Drug Screen- Urine amphetamine measurement
- Saliva toxicology screening
- ECG- arrhythmias, myocardial ischaemia/ infarction; prolonged administration of amphetamines can cause dilated cardiomyopathy
- RBG- for amphetamine intoxication who present with seizures
- EUC- for amphetamine intoxication who present with seizures; for patients with prolonged hyperthermia (renal function)
- LFTs- for patients with prolonged hyperthermia
- Urine and serum CK- monitor for rhabdomyolysis
- Urine dipstick- Positive for blood in rhabdomyolysis
- Follow up with urinalysis MCS- few or no RBCs
- CXR: Perform in all patients with chest pain to look for aortic dissection, pneumothorax or pneumomediastinum
- Troponins- patients with chest pain or myocardial ischaemia
- Head CT: All patients complaining of a headache or altered LOC- subarachnoid haemorrhage, intracerebral haemorrhage or cerebral edema
TREATMENT
- Sedation (IV benzodiazepines) and observations
- ABC
- All patients need IV fluids
- HTN- treated with IV benzodiazepines, but if hypertension persists then IV GTN
- Treat hyperthermia through active cooling, but if there is no response then intubate and paralyse the patient
- Manage rhabdomyolysis through aggressive IV fluids
CNS STIMULANT WITHDRAWAL (APPROXIMATES DEPRESSANT INTOXICATION)
- Poor concentration, mood instability, hypersomnia
- Lowering of BP/HR/ RR/ temperature
- Withdrawal amphetamines- strong hunger, dyspnoea
AMPHETAMINE WITHDRAWAL:
- Key risks (mainly left over from intoxication): Heart complications, stroke, rhabdomyolysis, renal failure, psychosis, self-harm, treatment-resistant depression
- Withdrawal scale: Amphetamine Withdrawal Scale
- Approach: Symptomatic relief and psychotherapy; can use a slow (controlled gradual reduction) approach
What are the acute effects of Opiate intoxication?
How do you treat overdose?
What tests should be conducted when suspecting opiate intoxication?
How do you manage opiod overdose after the patient has been initially treated with naloxone?
When cold you consider inpatient opioid dextoxification?
What are the signs/symptoms of opioid withdrawl?
What is opiate substitution program? What are the main medications used?
What is the rough time course of opioid withdrawl?
What risks associated with opioid withdrawl?
What are the acute effect of alcohol?
What are the chronic effect of alcohol use? (list effects on each system) ?
What are important initial tests to undertake when managing a patient with Severe Alcoholism? (all blood tests)
What are the signs and symptoms of Alcohol withdrawal? (list 5)
What are the management principles of alcoholism?
When is with drawal likely? (think in terms of consumption and AUDIT score)
What are scoring systems used for alcohol withdrawal? AUDIT/CIWA-AR/AWS
What are the key points to managing a patient with alcholism?
What are important things to address after the withdrawal phase?
What are the Guidelines for alcohol use in Australia?
ACUTE EFFECTS:
- Slurred speech, loss of coordination, vomiting, diarrhoea, disinhibition
- Cognitive impairment, respiratory depression, coma, death
- Some people experience aggression or excitatory effects
- Foetal Alcohol Syndrome
- Alcohol poisoning- respiratory depression, seizures, aspiration
CHRONIC USE:
- Liver failure
- Pancreatitis +/- secondary DM
- Gastritis
- Wernicke’s and Korsokoff’s syndrome
- Nutritional- Protein, vitamin deficiency, obesity
- Muscular- myopathy
- Cardiac- hypertension, arrhythmias, dilated cardiomyopathy
- Pulmonary- increased risk of pneumonia, TB, aspiration
- GIT- fatty liver, alcoholic hepatitis, cirrhosis; acute or chronic pancreatitis; GORD, gastritis; chronic diarrhoea, malabsorption
- Metabolic- High uric acid/ gout, osteoporosis
- Endocrine- DKA, hypo/ hyperglycaemia; low testosterone/ testicular atrophy/ erectile dysfunction; gynaecomastia; irregular menses
- Blood- macrocytosis, anaemia, leukopenia, thrombocytopenia, coagulopathy (secondary to liver disease)
- Insomnia, fatigue, anxiety disorder
- Depression
- Suicide, suicidal ideation
DIAGNOSIS
- Blood alcohol level
- FBC: Anaemia (increased MCV), thrombocytopenia
- RBC folate and serum vitamin B12: Decreased due to malabsorption
- EUC: Hypokalaemia
- CMP: Hypocalcaemia, hypomagnesemia, hypophosphatemia
- LFTs- Increased AST, increased GGT
- Coagulation profile: Increased PT and PTT
- RBG: Hypo= or hyperglycaemia
WITHDRAWAL (APPROXIMATES CNS STIMULANT INTOXICATION)
- Restless, agitation, tremor
- Insomnia, nausea, sweating
- Tachycardia, tachypnoea, hyperpyrexia, hypertensio
- Seizures
- Hallucinations
- Dilated pupils
MANAGEMENT
- Counselling- brief psychological or behavioural interventions
1. Includes motivational interviewing, non-judgemental feedback, recommendations for behaviour change, goal setting - Mutual support groups and 12 step programs (Alcoholics anonymous)
- Medications: Oral naltrexone, acamprosate, disulfiram
- Anticonvulsants may reduce alcohol consumption
- Management of psychiatric comorbidities
- Follow up with GP
PRINCIPLES:
- Withdrawal: Diazepam/ oxazepam + THIAMINE
- Long-term and not stopping: THIAMINE
Dependent and stopped:
- Do not use Diazepam/ ozazepam (apart from withdrawal)
- Thiamine (first 1-3 months or if relapsed)
- Naltrexone- μ opioid receptor antagonist → decreased effects of endogenous opioids → decreases reward with alcohol and cravings. Anti-craving and reduces pleasure in response to drinking. Caution in liver dysfunction (test LFTs prior to commencement and at 1st month), not in pregnancy or if on opiates.
- Acamprosate: Activator of GABAA receptors and weak antagonist of NMDA receptors. Anticraving medication. Decreased protracted abstinence syndromes with decreased feelings of a “need” for alcohol. Caution in renal dysfunction or low body weight (reduce dose).
- Disulfiram: Inhibits acetaldehyde dehydrogenase → increases acetaldehyde after drinking → toxic → flushing, nausea if exposed to ethanol and can cause hepatotoxicity and psychoses. Abstinence is reinforced to avoid the resulting adverse reaction
WITHDRAWAL LIKELY IF:
- Regular alcohol use >8 standards in males, >6 standards in females
- <1 week after last drink
- AUDIT >13
- Raised GGT or MCV
- CIWA-AR
- AWS (Alcohol Withdrawal Scale)
KEY POINTS:
- Can be fatal so requires close monitoring
- Mainstay treatment- Diazepam (use short-acting alternative Oxazepam if liver is impaired)
- Tailor to a withdrawal scale
- Thiamine (prevent Wernicke’s/ Korsokoff’s syndrome)
- Management of electrolytes is vital
- Hydration and nutritional support
- Manage as inpatient if significant seizure history, previous severe/ complicated withdrawal or significant comorbidities
- Outpatient treatment for patients who are not at high risk for delirium tremens or withdrawal seizures
AFTER WITHDRAWAL
- Taper diazepam
- Acamprosate (needs dose reduction in renal disease),
- Naltrexone (not suitable if taking opiate medication or significant liver disease) or disulfiram
- Address reasons why person was drinking
ALCOHOL GUIDELINES:
- To reduce the risk of alcohol related harm over a lifetime of more than 2 standard drinks on any day
- To reduce the risk of harm from alcohol-related injury arising on a single occasion no more than 4 standard drinks on a single occasion
- No alcohol for under 18s
- No alcohol during pregnancy or breastfeeding
- A standard drink contains 10g of pure alcohol
- Number of standard drinks = Volume of container (L) x %alcohol by volume (mL/100mL) x 0.789
List some of the neurpsychiartric consequences of alcohol abuse? (list 5)
What is wernickes Encephalopathy? What is the deficiency that causes it? How do you treat it? What can it progress to if it remains untreated?
How does it present? What is the “triad” of symptoms?
What is the pathogenesis?
What are important things to ask on history?
What is your differential diagnosis when patient presents with these symptoms?
What investigations should be performed?
What is the managemnet of this condition? (list 5 important points of treatment)
What is koraskoffs syndrome?
NEUROPSYCHIATRIC CONSEQUENCES OF ALCOHOL ABUSE
- Alcohol withdrawal syndrome (delirium tremens)- seizures, delirium tremens and psychosis
- Wernicke’s encephalopath
- Korsakoff’s syndrome
- Cerebellar degeneration
- Dementia
- Peripheral neuropathy
- Central pontine myelinolysis
- Traumatic brain injury
WERNICKE’S ENCEPHALOPATHY:
- This is an acute neuropsychiatric syndrome caused by thiamine deficiency (Vitamin B1)
- Triad: Confusion, ataxia, nystagmus and ophthlamoplegia
- Treatment: IV Thiamine (to minimise progression to Korsakoff’s syndrome, which is irreversible neurological damage)
- It presents with an acute onset of mental status changes ranging from confusional state to coma
- Acute thiamine (vitamin B1) deficiency is a direct cause of Wernicke’s encephalopathy that most commonly results from malnourishment in patient’s with alcohol dependence
- Patients with alcohol use disorders are at increased risk for developing thiamine deficiency due to:
- Poor diet with inadequate nutritional intake
- Compromised thiamine absorption from the GIT
- Impaired thiamine storage
- Reduced thiamine phosphorylation
PRESENTATION
- Acute mental status changes in malnourished patients with alcohol abuse
- Triad: Gait ataxia, eye signs (nystagmus and ophthalmoplegia) and confusion
- Cognitive signs of symptoms include: Altered mental status, impaired alertness (coma, stupor, lethargy, drowsiness), disorientation, impaired short-term memory, impaired concentration
PATHOGENESIS
- Wernicke’s encephalopathy can result from chronic alcohol use, which depletes Mg(+2) and thiamine and leads to cell damage in mammillary bodies, thalamus and hippocampal areas.
HISTORY
- Memory disorder characterised by clear sensorium with severe impairment of current and recent memory, confabulations, retrograde amnesia (spanning weeks to months before disorder) and disorientation to time
- Severe anterograde amnesia (patients aren’t able to recall events from previous 30 mins)
- Amnesia doesn’t improve with thiamine treatment
- Emotional changes: Apathy, euphoria, blunted responses
- Note: Persistent nystagmus and ataxia may suggest incomplete recovery from Wernicke’s encephalopathy
DDX
- Alzheimer’s
- Vascular dementia
- Alcohol-related brain damage or dementia
INVESTIGATIONS
- Low blood thiamine level
- MRI brain- cytotoxic edema and vasogenic edema
MANAGEMENT
- Measure total serum thiamine
- IV thiamine
- Nurse one-on-one in dimply lit, quiet room in reassuring and orientating manner
- Maintain fluid and electrolyte balance
- Ensure serum Mg(+2) levels are normal- low levels increase risk of nonresponse to parenteral thiamine replacement.
KORSAKOFF’S SYNDROME
- Irreversible confusional/ amnesic state
- This is a chronic condition of anterograde amnesia, short-term memory loss with confabulation and relative preservation of long-term memory and other cognitive skills) resulting from repeated episodes of thiamine deficiency
- Confabulations, nystagmus, opthalmoplegia, short-term memory loss, disorientation, agitation
- Caused by Thiamine deficiency
- Doesn’t respond to thiamine
- Decreased level of consciousness, coma, death
COGNITIVE AND PSYCHIATRIC COMPLICATIONS INCLUDE:
- Impaired executive function:
- Impulsivit
- Low frustration tolerance
- Cognitive impairment
• Substance-induced disorders of:
- Mood
- Anxiety
- Psychosis
- Personality
- Suicidality
- Increased risk for major depression
What is delirium Tremens?
What are symptoms of delirium tremens and signs? (list 6)
What are risk factors for Delirium tremens?
What investigations need to be completed when treating this patient? (Screening tools e.g CAGE/AUDITS = Blood tests
What are special tools used for assessing alcohol withdrawal?
What is very important when evaluating patients with features presenting as delirium? (think of conditions to rule outm e,g hypoglycemia, head injury etc)
What are indications for inpatient management? List 5
What supportive care should be provided in the management of this condition?
DELIRIUM TREMENS
- Alcohol withdrawal delirium
- Occurs 3-7 days after stopping alcohol, but can occur at any time up to 14 days
DELIRIUM TREMENS SYMPTOMS:
- Hallucinations (usually visual), disorientation, agitation
- Tachycardia, Tachypnoea, hypertension, fever, diaphoresis
- Delirium tremens consists of the following in patients with alcohol withdrawal syndrome:
- Decreased attention or awareness
- Disturbances in memory, orientation, language, visuospatial ability or perception
- The disturbance fluctuates throughout the day
- Delirium tremens is associated with disrupted fluid status, electrolyte abnormalities, hypovolaemia and deficiencies in K(+), Mg(+2) and phosphate
RISK FACTORS FOR DT INCLUDE:
- Sustained heavy drinking
- Age >30 years
- Increasing days since last alcohol use
- Prior episode of DT or seizures
- Presence of withdrawal symptoms with high blood alcohol level
- Concurrent illness
INVESTIGATIONS:
- AUDIT-C: Screen at admission to identify hospital inpatients who will develop alcohol withdrawal syndrome
- CIWA-Ar or Alcohol Withdrawal Scale- important for assessing initial severity and monitoring treatment
- Blood alcohol level- withdrawal symptoms with an elevated blood alcohol level may suggest impending severe withdrawal
- FBC- anaemia, thrombocytopenia (thrombocytopenia is a risk for developing severe withdrawal)
- Homocysteine- hyperhomocysteinaemia increases the risk for developing severe withdrawal
- EUC- hyponatremia or hypokalaemia are associated with severe withdrawal
- CMP- need to monitor Magnesium and Phosphate (magnesium deficiency common in alcohol withdrawal)
- Serum glucose- hypoglycaemia
- LFTs- increased AST and GGT are associated with severe withdrawal
- Coagulation profile- PT and PTT
- Urine and Serum Drug Screen
- Magnesium, thiamine and electrolyte deficiencies are common in alcohol withdrawal
TOOLS:
- CIWA-AR (Clinical Institute Withdrawal Assessment- Alcohol revised) to assess the initial severity of withdrawal and monitor treatment
- Alcohol Withdrawal Scale
KEY EVALUATION TIPS FOR DELIRIUM TREMENS
- Monitor vital signs
- Obtain tests to rule out common causes of delirium including:
- Hypoglycaemia
- Electrolyte imbalance
- Head injury leading to subdural haemorrhage
- Septicaemia
- Kidney or liver failure
MANAGEMENT (ALCOHOL WITHDRAWAL SYNDROME):
- Outpatient treatment for patients with mild-to-moderate symptoms who are not at high risk for delirium tremens or withdrawal seizures
INDICATIONS FOR INPATIENT MANAGEMENT
- Severe withdrawal symptoms or high CIWA
- Signs of withdrawal in presence of high blood alcohol content
- High risk or presence of delirium tremens and/or withdrawal seizure
- UDS positive for other substances
- Serious psychiatric conditions- suicidal ideation, psychosis
- Poorly controlled chronic medical conditions
- Thiamine/ folic acid/ multivitamin
- Supportive care: Hydration, nutritional support and electrolyte replacement
- Correct metabolic abnormalities
- IV Benzodiazepine titrated to CIWA-Ar
- Diazepam, lorazepam/ oxazepam
- Consider adjunctive antihypertensive agent in patients with persistent cardiac adrenergic symptoms despite treatment of dehydration and electrolyte imbalances
- Clonidine or beta blockers along with benzodiazepines
SUPPORTIVE CARE:
- Quiet room, low lighting and minimal stimulation
- Monitoring dehydration and IV fluids
- Sedation and nutrition
- Restrains to prevent injuries
- Treat electrolyte and glucose disturbances
- Thiamine
What can cannabis cause in some individuals?
What are the acute effects of cannabis?
What/how do you diagnose cannabis intoxication?
What is the mainstay to management of cannabis withdrawal?
What is the symptoms and phases of withdrawal?
What scale can use to identify severity of cannabis withdrawal?
CANNABIS
- Can cause psychosis in some individuals
- Can cause acute respiratory problems especially with existing respiratory disease
ACUTE EFFECTS OF CANNABIS
- Quiet euphoria, sedation, increased appetite
- Sensory intensification; illusions or distortions
- Paranoia, anxiety, depression and sedation
- Reduced coordination and reaction time
- Confusion, short-term memory loss
DIAGNOSIS
- Urine Drug Screening
- Blood toxicology test
- Saliva drug testing
TREATMENT
- CBT
WITHDRAWAL
- Most symptoms start on Day 1
- Peaks Day 2-3
- Returns to normal after 1-2 weeks
- Symptoms: Sleep disturbance, anorexia, irritability, anger and aggression
WITHDRAWAL SCALE: CANNABIS WITHDRAWAL SCALE
- Note: Cannabis use may increase the likelihood of a subsequent diagnosis of schizophrenia with heavier consumption and earlier use conferring greater risk.
What is a solvent addiciton?
What is the clinical presentation of solvent intoxication?
What important tests are to be undertaken when investigating this patient?
What are the prinicples of management of solvent intoxication?
What is Kava? What are the effects of it?
SOLVENTS
- Deliberate inhalation of volatile solvents and aerosol
- Includes: Petrol and solvents (glues, paints, correction fluids)
CLINICAL PRESENTATION:
- Euphoria, disinhibition and excitation
- Drowsiness, disorientation, hallucinations
- Blurred vision, slurred speech, Ataxia
- Asphyxia and ventricular fibrillation
- Chronic use: Peripheral neuropathy and encephalopathy
- Sudden sniffing death- cardiac arrhythmia or arrest
DSM:
- Euphoria
- Dizziness, incoordination, slurred speech
- Nystagmus, incoordination, psychomotor retardation
- Generalized muscle weakness
DIAGNOSIS
- Repeated intoxication with negative results in drugs screens (doesn’t detect inhalants)
- FBC: Chronic users may exhibit bone marrow suppression- aplastic anaemia, thrombocytopenia
- EUC: Hypercholaemia, hypokalaemia; Azotaemia occurs with chronic exposure but resolves with abstinence
- CMP: Hypophosphatemia
- LFTs- some volatile substances are toxic to the liver
- ABG: Some inhalants (toluene) cause Renal tubular acidosis with a high anion gap
- Serum or urine toxicology- can help to exclude other chemicals
- βhCG: Risk of embryopathy
- Creatine phosphokinase (CPK): Useful in patients with muscle tenderness or myoglobinuria- rhabdomyolysis
- ECG- many inhalants are proarrhythmic (tachycardia, bradycardia, arrhythmias or even cardiac ischaemia with solvent abuse)
TREATMENT
- ABC- oral fluids;; manage dehydration and acid-base disturbances
- Removal of the causal agent and bed rest
- For acute behavioural disturbances- use sedatives (IM midazolam or IV diazepam)
WITHDRAWAL:
- Lasts 2-5 days in most people and 1 week in heavy users
- Common withdrawal symptoms: Headache, nausea, irritability, trembling, sleep disturbances
MANAGEMENT
- Provide a quiet safe place to recover
- Ensure adequate fluid intake
- Analgesics
- Manage anxiety or agitation with a short-acting benzodiazepine (e.g. lorazepam or oxazepam)
- Paracetamol- fever or headache
- Regular observations
- Counselling
- Note: Antipsychotics can lower the seizure threshold and increase the risk of cardiac arrhythmias
KAVA
• The roots are processed and then taken as a beverage
CLINICAL PRESENTATION:
• Analgesia, muscle relaxation, sedation
• Ataxia, Slurred speech
• Similar effects to alcohol and benzodiazepines, and combining kava with these drugs produces additive effects.
• Hepatotoxic and nephrotoxic
What are the chronic effects of benzodiazepines use?
What are the signs and symptoms of benzo withdrawal?
What is the key risk to manage?
How to manage this risk?
What are basic principles of management of any withdrawal from any drug?
What is the acute management prinicples?
What role does the following have?
- Case management
- Psychotherapy
- Rehabilitation
BENZODIAZEPINES
- Sedative hypnotics that are dissociative e.g. diazepam, alprazolam, oxazepam, temazepam
- Induces a hypnotic state (mimicking sleep), dissociative state, sense of wellbeing and euphoria
- Can cause respiratory depression, which is worsened in the presence of another depressant (alcohol, opiates)
- Some people get paradoxical aggression and seizures on intoxication
CHRONIC EFFECTS
- Memory impairment
- Falls (sedation, hypotension, dizziness)
- Paradoxical excitation, mania on withdrawal
- Ataxia, cognitive impairment, reflex tachycardia
- Seizures
WITHDRAWAL (APPROXIMATES CNS STIMULANT INTOXICATION)
- Restless, agitation, hyperactive
- Anxiety, insomnia, tremors
- Tachycardia, tachypnoea, hyperpyrexia, hypertension
- Seizures
- Dilated pupils
Key features: Similar to alcohol withdrawal, but usually starts later and is more prolonged.
- Key risks: Can be fatal, seizures are common
- Withdrawal scale: CIWA-B
- Approach: Avoid severe withdrawal by tapering the dose
- If taking a short-acting benzodiazepine then swap to a long-acting (at 50% of the equivalent dose) and taper
OTHER:
BASIC WITHDRAWAL MANAGEMENT
- Client: Co-morbidity, severity of dependence, stage of change, safety
CHOICES FOR WITHDRAWAL
- Stop
- Symptomatic relief
- Slow- controlled gradual reduction
- Substitution therapies
MANAGEMENT OF ANY DRUG WITHDRAWAL
SUPPORTIVE CARE
- Regular monitoring of vital signs, mental state and severity of withdrawals
- Provide non-stimulating cool environment
- Encourage the person to maintain their fluid intake
- Rehydration/ nutrition/ thiamine
- Reassure/ orientate/ support
- Prevent the person harming themselves or others
- Encourage supportive friends and relatives to stay
MANAGEMENT OF DRUG PROBLEMS:
ACUTE MANAGEMENT
- ABC
- Bleeding, clottin
- Trauma
- Hypoglycaemia, electrolyte disturbances
- Treat comorbid conditions
CASE MANAGEMENT
- Medium-long term care for addictions
- Motivational interviewing and patient-centred, focused on improving functionality (literacy, job training, access to health care)
PSYCHOTHERAPY
- Helps with adjusting to life without the drug
- Positive psychology models- builds resilience and coping strategies
REHABILITATION
- Needs commitment from the patient
- Can include withdrawal
- Case management in a controlled environment
- Advantages: Protected and supportive environment; peer support, monitoring; stepping stone (less temptations than real world)
- Disadvantages: Expensive, limited places
What are organis disorders?
What is dementia? What is delirum?
What is the difference for the folowing in these two conditions?
Level of attention?
Onset?
Course of illness?
Consciousness?
Hallucinations?
Prognosis?
Treatement?
Psychomotor changes?
Memory?
Thoughts?
What are the 8 signs of delirium? (DELIRIUM)
What is needed for the diagnosis of delirium? (clinically no a lab test)
What is the DSM V criteria for the diagnosis?
What are the common symptoms (list several for each component for MSE)
What is a screening tool for delirum? List 2
What are risk factors for Delirium?
Aetiology of delirum? List many acoording to systems?
What investigations are standard for any patient when suspecting delirum? (or working up a patient for suspected delirum) Standard test, as indicated?
Explain the management of delirium? Explain in terms of, intrinsic, extrinsic, biological?
Assessing severity of delirum?
How do we prevent delirum?
DELIRIUM:
8 SIGNS OF DELIRIUM
- D- Disordered thinking: Slow, irrational, rambling, incoherent ideas
- E- Euphoric, fearful, depressed or angry- labile mood
- L- Language impaired- speech is reduced or repetitive and disruptive
- I- Illusions/ delusions/ hallucinations: Tactile or visual hallucinations (Auditory hallucinations suggests psychoses)
- R- Reversal of sleep-awake cycle: May be drowsy by day and hypervigilant at night
- I- Inattention: Poor focussing, sustaining and shifting attention
- U- Unaware/ disoriented to time/ place/ person
- Memory deficits (often marked)
- Globally impaired cognition and impaired awareness/ consciousness
DIAGNOSIS OF DELIRIUM- CLINICAL (NOT DIAGNOSED WITH A LAB TEST)
- Disorientation, abnormal behaviour and hallucinations
- New onset deterioration in behaviour, cognition and function
- Occurs within hours and involves an acute change in consciousness or difficulty focussing on what was being said during the interview.
- Insomnia, daytime drowsiness or nightmares
- Emotional disturbances- depression, anxiety, fear, irritability
- Delusions
Main symptoms of delirium includes:
- Clouding of consciousness
- Difficulty maintaining or shifting attention
- Disorientation
- Illusions and hallucinations
- Fluctuating level of consciousness
- Dysphasia/ dysarthria/ tremor
- Hyperactive, increased arousal, hypervigilance OR hypoactive, withdrawn and sleepy
→ Atypical onset = delirium until proven otherwise
DSM-5 CRITERIA
A. Attention and awareness: disturbance in attention (i.e. reduced ability to direct, focus, sustain, and shift attention) and awareness (reduced orientation to the environment)
B. Acute and fluctuating: disturbance develops over short period of time (usually hours to days), represents a change from baseline attention and awareness, and tends to fluctuate in severity during the course of a day
C. Cognitive changes: an additional disturbance in cognition (e.g. memory deficit, disorientation, language, visuospatial ability, or perception)
D. Direct physiological cause: evidence that disturbance is a direct physiological consequence of another medical condition, substance intoxication or withdrawal (i.e. due to a drug of abuse or medication), toxin, or is due to multiple aetiologies
- Note: can have HYPERactive, HYPOactive, or MIXED presentation
E. Explanation not due to alternative: disturbances in criteria A and C are not better explained by another neurocognitive disorder (pre-existing, established, or evolving) and do not occur in the context of a severely reduced level of arousal (e.g. coma)
CLINICAL PRESENTATION
Common symptoms
- Distractibility, disorientation: Time, place, rarely person
- Misinterpretations, illusions, hallucinations
- Speech/language disturbances: Dysarthria, dysnomia, dysgraphia
- Affective symptoms: Anxiety, fear, depression, irritability, anger, euphoria, apathy
- Shifts in psychomotor activity: Groping/picking at clothes, attempts to get out of bed when unsafe, sudden movements, sluggishness, lethargy
-Folstein Mini Mental Status Exam is helpful to assess baseline of altered mental state
o i.e. score will improve as symptoms resolve
RISK FACTORS
- Hospitalization
- Previous delirium
- Nursing home residents
- Polypharmacy (e.g. anticholinergic)
- Old age (especially males)
- Severe illness (e.g. cancer, AIDS)
- Recent anaesthesia or surgery
- Substance abuse
- Pre-existing cognitive impairment, brain pathology, psychiatric illness
AETIOLOGY
- Infectious: Encephalitis, meningitis, UTI, pneumonia
- Withdrawal: Alcohol, barbiturates, benzodiazepines
- Acute metabolic disorder: Electrolyte imbalance, hepatic or renal failure)
- Trauma: Head injury, post-operative
- CNS pathology: Stroke, hemorrhage, tumour, seizure disorder, Parkinson’s
- Hypoxia: Anaemia, cardiac failure, pulmonary embolus
- Deficiencies: Vitamin B12, folic acid, thiamine
- Endocrinopathies: Thyroid, glucose, parathyroid, adrenal
- Acute vascular: Shock, vasculitis, hypertensive encephalopathy
- Toxins: substance use, sedatives, opioids (especially morphine), anesthetics, anticholinergics, anticonvulsants, dopaminergic agents, steroids, insulin, glyburide, antibiotics (especially quinolones), NSAIDs
- Heavy metals: Arsenic, lead, mercury
INVESTIGATIONS
- Standard: FBC and differential, electrolytes, Ca , PO4 , Mg , glucose, ESR, LFTs, Cr, BUN, TSH, vitamin B12, folate, albumin, urine MCS, R&M
- As indicated: ECG, CXR, CT head, toxicology/heavy metal screen, VDRL, HIV, LP, blood cultures, EEG (typically abnormal - generalized slowing or fast activity, can also be used to rule out underlying seizures or post-ictal states as etiology)
- Indications for CT head: focal neurological deficit, acute change in status, anticoagulant use, acute incontinence, gait abnormality, history of cancer
MANAGEMENT
• Intrinsic
- Identify and treat underlying cause immediately
- Stop all non-essential medications
- Maintain nutrition, hydration, electrolyte balance and monitor vitals
• Extrinsic
- Environment: quiet, well-lit, near window for cues regarding time of day
- Optimize hearing and vision
- Room near nursing station for closer observation; constant care if patient jumping out of bed, pulling out lines
- Family member present for reassurance and re-orientation
- Frequent orientation - calendar, clock, reminders
• Biological
- Low dose, high potency antipsychotics: haloperidol has the most evidence; reasonable alternatives include risperidone, olanzapine (more sedating, less QT prolongation), quetiapine (if EPS), aripiprazole
- Benzodiazepines only to be used in alcohol withdrawal delirium; otherwise, can worsen delirium
- Try to minimize anticholinergic side effects
• Physical restraints if patient becomes violent
ASSESSING SEVERITY OF DELIRIUM:
- Delirium Index
PREVENTION:
- Adequate hydration and nutrition
- Pain relief
- Promotion of sleep
- Correction of visual and hearing impairments
- Avoidance of restraints
- Clocks and calendars
- Close involvement of family
Define what is dementia?
What are the areas of deficits?
How does it initially present? What are the early symptoms?
What are the symptoms of later presentation?
What are common symptoms of dementia?
What is Alzheimers disease?
What causes dementia?
What is the DSM V criteria for dementia?
What are the subtypes?
What are the management principles of dementia list 5?
What is your differential diagnosis when considering dementia and patient with dementia like symptoms?
What is needed in a Dementia Screen?
Outline an assessment with for a patient with newly diagnosed dementia? What screening tools can be used to assess cognition and mental state?
What are routine blood tests done?
List 4 scoring systems for assessing the overall severity of dementia?
DEMENTIA
- Progressive deficits in several cognitive domains: Impaired new learning, apraxia, agnosia, language and loss of executive functioning.
INITIAL PRESENTATION (EARLY SYMPTOMS)
- Memory loss and impaired ability to learn new information
- Personality or behavioural changes (e.g. disorientation)
- Increased confusion
- Reduced concentration
- Depression, apathy and withdrawal
- Loss of ability to do everyday tasks
- Language (anomia- word-finding problems)
- Executive functioning (planning and organizing)
LATER PRESENTATION:
- Agitation, aggression, apathy
- Impaired communication
- Dependence on others- eating, dressing, washing, toileting
- Bladder and bowel incontinence
- Difficulty speaking and swallowing
- Infections; groaning, moaning and grunting
- Poor judgement
- Confusion and disorientation
- Anorexia and weight loss
- Death usually occurs from aspiration pneumonia, respiratory failure or septicaemia
COMMON SYMPTOMS OF DEMENTIA
- Memory loss
- Difficulty performing familiar tasks
- Language problems- forget simple words or substitute inappropriate words
- Disorientation to time and place
- Poor judgement
- Problems with abstract thinking
- Personality and Behaviour changes
- Loss of initiative
ALZHEIMER’S DISEASE:
- Progressive cognitive impairment: Memory, language, visuo-spatial skills (gets lost) and executive functioning (planning)
- Anosognosia
LATER:
- Irritability and Mood disturbance (depression or euphoria
- Behavioural changes (e.g. aggression, wandering, disinhibition)
- Psychosis (hallucinations or delusions)
- Agnosia (inability to interpret sensations and recognize things e.g. unable to recognize self in the mirror)
END
- Patients become sedentary
OTHER FEATURES:
- Agitation, aggression, wandering
- Hallucinations
- Slow repetitious speech, apathy, mood disturbance
CAUSES OF DEMENTIA:
- Alzheimer’s disease: Beta amyloid plaques, NF tangles; memory loss → aphasia, apraxia, personality changes
- Vascular dementia (multi-infarct or post-stroke dementia): Initial symptoms of impaired judgement or ability to make decisions, plan or organize
- Dementia with Lewy bodies: Patients often initially have memory loss and thinking problems; sleep disturbance, visual hallucinations, slowness, gait imbalance
- Parkinson’s disease dementia: As Parkinson’s disease progresses, it often results in a progressive dementia similar to dementia with Lewy bodies. Many people with Parkinson’s disease eventually develop dementia.
- Frontotemporal dementia: Language, behavioural and personality changes initially. These symptoms precede memory disturbances
- Creutzfeldt-Jakob disease
- Huntington’s disease
- Korsakoff’s syndrome
- AIDS
- Mixed dementia: Combinations of multiple dementias e.g. Alzheimer’s disease, vascular dementia and Lewy body dementia.
- Frontotemporal dementia: Presents with personality changes and alteration in behaviour early. Disinhibition and insightless, word finding problems that progresses to nonfluent dysphasia (semantic dementia)
- Lewy body dementia: Visual hallucinations, motor parkinsonism, fluctuations in mental state
DSM-5 CRITERIA
A. Evidence of significant cognitive decline from a previous level of performance in one or more cognitive domains (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition) based on
- Concern of the individual, a knowledgeable informant, or the clinician that there has been a significant decline in cognitive function and
- Substantial impairment in cognitive performance, preferably documented by standardized neuropsychological testing or, in its absence, another quantified clinical assessment
B. Cognitive deficits interfere with independence in everyday activities (i.e. at a minimum, requiring assistance with complex instrumental activities of daily living such as paying bills or managing medications)
- Note: if do not interfere in B, and impairments are mild-moderate in A, considered “mild neurocognitive disorder”
C. Cognitive deficits do not occur exclusively in the context of a delirium cognitive deficits are not better explained by another mental disorder (e.g. major depressive disorder, schizophrenia)
SUBTYPES
- With or without behavioural disturbance (e.g. wandering, agitation)
- Early-onset: age of onset <65 yr
- Late-onset: age of onset >65 yr
MANAGEMENT
- Treat underlying medical problems and prevent others
- Provide orientation cues for patient- e.g. clock, calendar
- Provide education and support for patient and family (e.g. day programs, respite care, support groups, home care)
- Consider long-term care plan (nursing home) and power of attorney/living will
- Consider pharmacological therapy
- Cholinesterase inhibitors (e.g. donepezil [Aricept®], rivastigmine, galantamine) for mild to severe disease
- NMDA receptor antagonist (e.g. memantine) for moderate to severe disease
- Low-dose neuroleptics (e.g. risperidone, quetiapine), antidepressants or trazodone if behavioural or emotional symptoms prominent – start low and go slow
- Reassess pharmacological therapy every 3 months
DDX
- Hypothyroidism
- Anaemia
- Sleep apnoea
- Neurosyphilis
- Normal pressure hydrocephalus
- Vitamin B1/ B6/ B12 deficiency
- Subdural haematoma
- Poisonings- heavy metals e.g. lead
- Brain tumours
DEMENTIA SCREEN:
- FBC- anaemia and infection
- ESR/CRP
- EUC
- Ca(+2)
- RBG
- Homocysteine- fasting
- LFT
- TFTs
- Serum B12/ RBC folate (treat low-normal)
- Autoantibodies
- Syphilis serology
- HIV antibodies
- MSU
- ECG
- Non-contrast CT brain>> cortical atrophy, infarcts and tumours
- EEG
- LP-CSF
- Medication review
- MSE and MMSE
ASSESSING SEVERITY FOR DEMENTIA:
OVERALL DEMENTIA SEVERITY:
- Clinical Dementia Rating (CDR)
- Global deterioration scale (GDS)
- GPCOG (General Practitioner Assessment of Cognition)
- MMSE
- FAB- assesses frontal lobe function
- Kimberly Indigenous Cognitive Assessment (KICA)
What is your differential diagnosis for dementias?
What is and acquired brain injury?
What are causes of this?
How do we distinguish organic syndromes from psychoses? ( Dementia, Delirum, Depression)
Think:
1) Onset
2) Duration
3) Natural history
4) Level of consciousness
5) Attention
6) orientation
7) Behavior
8) Psychomotor
9) Sleep wake cycle
10) Mood and affect
11) Cognition
12) Memory loss
13) language
ABI
- This referes to any brain damage that occurs after birth
- The specific symptoms or losses of function depend on the brain area affected
- Memory deficits are the most common symptom
- Slowness in processing information, planning and solving problems (Behaviour and personality changes
Causes of ABI
- Traumatic brain injury
- Stoke
- Tumor
- Alcohol or drugs
- Degenerative brain conditions (AIDS, Alzheimers or Parkinsons disease)
- Encephalopathy
- Anoxic brain injury (drowning)
- MS
What is frontal lobe syndrome?
What are common features of this condition?
What are the signs and symptoms (movement, emotional, cognitive, behavioural)
What tests can be used for Frontal lobe syndromes (screening)? (remember MMSE is not specific for frontal lobe syndrome)
- Frontal lobe disorder, also frontal lobe syndrome, is an impairment of the frontal lobe that occurs due to disease or frontal lobe injury. The frontal lobe of the brain plays a key role in executive functions such as motivation, planning, social behaviour, and speech production.
- Frontal lobe syndrome can be caused by a range of conditions including head trauma, tumours, neurodegenerative diseases, Neurodevelopmental disorders, neurosurgery and cerebrovascular disease.
- Frontal lobe impairment can be detected by recognition of typical signs and symptoms, use of simple screening tests, and specialist neurological testing
- The specific symptoms or losses of function depend on the brain area affected
- Memory deficits are the commonest symptom
- Slowness in processing information, planning and solving problems; behaviour and personality changes
CAUSES:
• Traumatic brain injury (e.g. physical trauma from assaults, accidents, neurosurgery)
• Stroke
• Tumour
• Alcohol or drugs
• Degenerative brain conditions: AIDS, Alzheimer’s disease, or Parkinson’s disease
• Encephalopathy
• Anoxic brain injury (e.g. drowning)
• MS
FRONTAL LOBE SYNDROME:
- Changes in personality, behaviour, impulsivity, apathy
- Changes in work performance
- Impairment in organizing, planning and executing difficult tasks
- Language problems
- Loss of inhibition
- Changes in a person’s personality may involve: Loss of social awareness, disinhibition, emotional instability, impulsiveness.
- There may be mood changes with depression, anxiety or apathy
- Reduced verbal fluency
- Lacking in insight and judgement
- Decreased spontaneity, attention, abstract thought (can’t understand proverbs)
- Perseveration (continuing with a behaviour when a situation requires a change)
SIGNS AND SYMPTOMS:
Movement
- Tremor, apraxia, dystonia, gait disorder
Emotional
- Disinhibition of emotions, anger, excitement
- Depression
- Lack of empathy
Language
- Expressive aphasia
Cognitive
- Planning and reasoning
- Reduced attention
- Executive dysfunction- poor working memory and short-term memory
Behavioural
- Utilization behaviour (where patients grab objects in view and start the ‘appropriate’ behaviour with it in an ‘inappropriate’ time- signs of impulsiveness.
- Perseveration
- Social inhibition
- Compulsive eating
NOTE: THE MMSE IS INSENSITIVE AND NOT SPECIFIC FOR FRONTAL LOBE DYSFUNCTION
- The Frontal Assessment Battery (FAB) and Montreal Cognitive Assessment (MoCA) are used
- The frontal lobe is involved in motivation, planning, social behaviour and speech production
- Frontal lobe syndrome can be caused by head trauma, tumours, degenerative diseases (e.g. Pick’s disease), neurosurgery, cerebrovascular disease
What are cholinesterase inhibitors? What are they used to treat? When are they subsidised/ what score (on MMSE)?
What are other drugs used to treat organic brain disease?
What are adverse effects of cholinesterase inhibitors?
What role does psychotropic drugs have in treating organic brain disorders? When are they indicated?
What are the major management prinicples for treating a patient with a organic brain injury?
What is the management prinicples of treating a patient with delirium?
PSYCHOPHARMACOLOGY OF ORGANIC BRAIN DISORDERS:
- Cholinesterase inhibitors or memantine can treat cognitive impairment in Alzheimer’s disease
- Cholinesterase inhibitors improve alertness and function and can maintain cognitive scores at or above the baseline for up to 12 months
- They don’t modify the underlying progression of pathology
- Not all patients benefit from cholinesterase inhibitors
- If patients tolerate and appear to benefit from cognitive enhancing drugs then the drug should not be ceased until the patient is in an advanced state of dementia (usually having lost independent mobility)
To be PBS subsidised for Alzheimer’s disease therapy, the patient must:
− Achieve an MMSE >10 for mild to moderately severe Alzheimer’s disease
DRUGS:
- Donepezil
- Galantamine
- Rivastigmine
- Memantine (NMDA receptor antagonist)
ADVERSE EFFECTS OF CHOLINESTERASE INHIBITORS:
- Anorexia
- Nausea and vomiting
- Vivid dreams
PSYCHOTROPIC DRUGS
- Mainstay of mood and behavioural disturbances is non-pharmacological
- Sometimes psychotropic drugs are used
- Weekly review of symptoms and adverse effects (including: sedation, postural hypotension, ESPEs and anticholinergic effects e.g. dry mouth, constipation, urinary hesitancy and delirium)
- There is an increased risk of cerebrovascular side effects in patients treated with risperidone and olanzapine
- This risk is highest in those with poorly controlled vascular risk factors (AF, hypertension or diabetes) or a history of past stroke
- Use of Olanzapine and risperidone should be given to patients with intractable aggression or psychosis
- Behavioural and psychological symptoms in dementia are often temporary
- Psychotropic drugs should be reviewed before 3 months
- Never use 1st generation antipsychotics for dementia with Lewy bodies or for Parkinson’s disease
- Olanzapine- useful in treating aggression and psychosis complicating dementia
- Risperidone- useful in treating aggression and psychosis complicating dementia
- To control hallucinations, delusions or disturbed behaviour: Olanzapine or risperidone
- To relieve symptoms of severe anxiety and agitation: Oxazepam (benzodiazepines shouldn’t be used for >2 weeks as they increase cognitive impairment and the risk of falls)
MANAGEMENT
- Family education and support
- Appropriately stimulating environment with personal belongings and orientation cues
- Glasses and hearing aids
- Refer to Dementia Behaviour Management Advisory Service (DBMAS)
- Alzheimer’s Australia- information, care advice, support groups, counselling
- EPOA/ AHD
- Review driving ability and report to road authority
DELIRIUM MANAGEMENT
- Medications are unnecessary for most delirious patients
- The key principle is to identify and treat the underlying cause
- Review the patient’s medication history as delirium is commonly due to drugs
- Psychopharmacology
- Treats anxiety, agitation, aggression, delusions and/or hallucinations
- Thiamine- delirium can be caused by alcohol withdrawal so give thiamine when the cause of delirium is unknown
- Haloperidol/ olanzapine/ risperidone- hallucinations, delusions or behavioural disturbances
- All these drugs cause orthostatic hypotension, but especially risperidone
- A single dose is usually required, but all antipsychotics have significant adverse effects including aggravating delirium.
- Avoid benzodiazepines except for delirium related to alcohol withdrawal or seizures as long-acting benzodiazepines increase the risk of delirium
What is an altered mental state?
What is the GCS score, how do you score it? What is reflective of certain scores?
OVERVIEW
- The GCS is a neurological scoring system used to assess conscious level after head injury
- It is now usually scored out of 15 and is comprised of 3 categories, best eye response, best vocal response and best motor response (e.g. E4V5M6 = GCS15)
CALCULATION OF GCS
Eye response (E)
- No eye opening
- Eye opening in response to pain stimulus (a peripheral pain stimulus, such as squeezing the lunula area of the patient’s fingernail is more effective than a central stimulus such as a trapezius squeeze, due to a grimacing effect)
- Eye opening to speech (not to be confused with the awakening of a sleeping person; such patients receive a score of 4, not 3)
- Eyes opening spontaneously
Verbal response (V)
- No verbal response
- Incomprehensible sounds (moaning but no words)
- Inappropriate words (random or exclamatory articulated speech, but no conversational exchange)
- Confused (the patient responds to questions coherently but there is some disorientation and confusion)
- Oriented (patient responds coherently and appropriately to questions such as the patient’s name and age, where they are and why, the year, month)
Motor response (M)
- No motor response
- Extension to pain (extensor posturing: abduction of arm, external rotation of shoulder, supination of forearm, extension of wrist, decerebrate response)
- Abnormal flexion to pain (flexor posturing: adduction of arm, internal rotation of shoulder, pronation of forearm, flexion of wrist, decorticate response)
- Flexion/Withdrawal to pain (flexion of elbow, supination of forearm, flexion of wrist when supra-orbital pressure applied ; pulls part of body away when nailbed pinched)
- Localizes to pain (Purposeful movements towards painful stimuli; e.g., hand crosses mid-line and gets above clavicle when supra-orbital pressure applied)
- Obeys commands (the patient does simple things as asked, e.g. stick out tongue or move toes)
USES
- categorises severity of TBI into mild (13-15), moderate (9-12) and severe (8 or less)
- used in BTF guidelines as part of the indications for ICP monitoring (e.g. GCS 8 or less and abnormal CT head)
- used for determining the need for CT head in TBI by validated tools such as the Canadian CT Head Rule
- Traditional ATLS mantra is “GCS 8, intubate”
- used in APACHE II
- originally described for monitoring depth of coma over time in a neurosurgical unit (never validated)
ADVANTAGES
- most widely recognised of all conscious level scoring systems in the world
- has face validity (looks like it should work)
- quick
- reproducible (this is controversial, in one study 38% of the cases the GCS scores were the same and in 33% of cases the scores varied with more than two points)
- skewed towards motor score, which is good since this is the most reliable measure of short-term prognosis in TBI
- the distinction between a motor score of 2, 3 and 4 is a very useful clinical indicator of the severity of TBI, and the area of brain function that has been affected
- correlates with adverse neurological outcomes such as brain injury, neurosurgical intervention, and mortality
DISADVANTAGES
Problems with the use of GCS
- not originally intended to be converted into a single score — the components (E4,V5, M6) are more important than the total score
- does not incorporate brain-stem reflexes
- M score does not factor in unilateral pathology
- unreliable in patients in the middle range of 9-12
- The same GCS score will predict different TBI mortality depending on the components
- — GCS of 4 with the components 1+1+2 (E+V+M) predicts a mortality rate of 48%
- — GCS of 4 with the components 2+1+1 (E+V+M) predicts a mortality rate of 19%
- grossly predictive but cannot accurately predict outcomes in individual patients (on par with weather presenters predicting rain or WBC predicting appendicitis!)
What is an altered mental state?
What is your differential diagnosis for an altered state of mind? (from slight confusion to coma)
What is mnemonic for this? AEIOU TIPS
What are the top 6 most common causes of altered state of consciousness in Australia? (from QH stats)
What investigations should be done?
Outline basic management principles of a patient with altered state of consciousness?
ALTERED MENTAL STATE:
ALTERED MENTAL STATE CAN RANGE FROM SLIGHT CONFUSION TO COMA:
Altered level of consciousness refers to arousability
- Delirium
- Stroke/ TIA
- Concussion/ contusion/ diffuse axonal injury/ laceration
- Subarachnoid haemorrhage/ Subdural haematoma/ extradural haematoma
- Meningitis, Encephalitis
- Bacteraemia or septicaemia due to UTI or URTI- FBC, blood and urine culture + MCS
- Envenomation
- Hepatic encephalopathy
- Uraemic encephalopathy
- Hypoglycaemia (due to insulin errors, insulinoma or adrenal failure)- decreased blood glucose
- Electrolytes: Hyper/ hyponatremia; K(+), Ca(+2), Mg(+2)
- Thiamine deficiency- decreased RBC ketolase activity
- Post-ictal state/Non-convulsive status epilepticus
- Hypoxia- lung or heart disease: ABG
- Heart: CHF, arrhythmia, MI
- PE
- Shock
- Alcohol withdrawal- increased MCV; LFTs (increased AST, increased GGT). Tremor, confusion, visual hallucinations
- Hypothyroidism
- Thyrotoxicosis
- Adrenal failure (Addison’s disease or secondary to ACTH deficiency)
- Drugs- Opiates, anticholinergic toxicity, serotonin syndrome, neuroleptic malignant syndrome, TCAs, anticonvulsants
MNEMONIC:
- A- Alcohol withdrawal syndrome
- E- Epilepsy, electrolytes, hepatic/ uraemic encephalopathy
- I- Insulin (hypoglycaemia)
- O- Opiate
- U- Uraemia
- T- Temperature (Hyperthermia/ hypothermia)
- I- Infections (meningitis, encephalitis, sepsis)
- P- PE
- S- SOL, stroke, shock, seizure
QH COMMONEST CAUSES OF ALTERED CONSCIOUSNESS
- Alcohol and drugs
- Stroke
- Seizures
- Hypoglycaemia
- Sepsis
INVESTIGATIONS
- Capillary glucose
- ECG
- ABG
Blood tests:
- FBC
- EUC
- CMP
- LFTs
- TFTs
Urine:
- Dipstick and Urinalysis- MCS
- Toxicology screen- UDS, blood drug screen; Blood alcohol level, acetaminophen level
- β-hCG: Always do β-hCG in all women of childbearing age
- Infection screen: Blood culture, urine culture, CXR, LP, serum lactate
MANAGEMENT
- ABC
- Look for signs of trauma (primary survey, secondary survey), protect the C-spine
- Empiric reversal agents: Dextrose, Naloxone, thiamine
- Empiric infection management
- Review medication historyMonitor vital signs
- O2
- Ensure adequate hydration, nutrition and pain relief
- Dextrose
- Naloxone
- Thiamine
Assessment of capacity what criteria does the patient have to meet to have capacity to consent? What 6 criteria must the patient be able to convey to you?
What are some other important factors to consider when assessing capacity?
What are key things a patient is able to communicate to you so you know they have capacity for for making the best descision for them?
ASSESSMENT OF CAPACITY:
A PERSON HAS CAPACITY TO CONSENT TO BE TREATED IF THE PERSON IS CAPABLE OF UNDERSTANDING IN
GENERAL TERMS:
- That the patient has an illness or symptoms of an illness that affects the person’s mental health and wellbeing
- The nature and purpose of the treatment
- The benefits and risks of the treatment and alternatives to the treatment
- The consequences of not receiving the treatment
- The person must be capable of making a decision about the treatment and communicating the decision
- The patient can make a decision freely and voluntarily
OTHER:
- Are the patient’s desired outcomes stable or do they vary over time or depending on who is present
- The Act also recognises the importance of supported decision making where a person may have the capacity with the support of another person
- Practitioners have a legal and professional responsibility to get consent before treating any person.
- A person is presumed to have capacity to make decisions about the person’s treatment and care regardless of their age, circumstances, condition, behaviour or legal status
- Capacity involves understanding the nature and effects of the treatment at the time informed consent is required
Patient should be able to retain and briefly be able to explain back to you the following:
Nature of treatment involves:
- What the medical treatment is?
- What the procedure involves
- Why it is proposed and alternative
- Risks and benefits
- What it means if they don’t have the treatment
Patients with fluctuating capacity may remain on a TA until their capacity becomes stable
KEY FACTS:
Capacity for making decisions:
- Can the patient understand the information relevant to the decision
- Use the information to make a decision
- Retain memory of the decision
- Communicate
OUtline an approach to assessing suicide risk: (have questions for the following)
- Ask every patient
- Classify ideation
- Assess risk
- Determine intent
- Risks
- Past attempts
- Assess suicidal ideation (onset+frequency)
What are important risk factors for suicide? (Think SADPERSONS)
What are common warning signs for suicide?
What is static’ suicide risk? What are is meant by a dynamic suicide risk?
What are protective factors against suicide?
How does suicide present clinically? (list 6-8 symptoms a patient may have)
How do you assess a Suicide attempt?! (think setting, isolated, planned vs unplanned, intoxication etc)
What are important things to elicit from history when a patient presents with the following- list questions you should ask?
- POST suicide attempt?
- Sucidal intent
- If patient says that they have considered suicide
APPROACH
- Ask every patient – e.g. “Have you had any thoughts of wanting to kill yourself?”
- Classify ideation
- Passive ideation: would rather not be alive but has no active plan for suicide- e.g. “I’d rather not wake up” or “I would not mind if a car hit me”
- Active ideation e.g. “I think about killing myself”
Assess risk
- Plan: “Do you have a plan as to how you would end your life?”
- Intent: “Do you think you would actually carry out this plan?” “If not, why not?”
- Evidence of planning
- Writing a note, finishing ‘business’
- Site of attempt e.g. secluded
- Efforts could not be found
- Did you think you would die?
- Potential for rescue?
Risk(s)
- Lethal method e.g. hanging, jumping, shooting
- Or perception of lethality
- Alcohol, motor vehicle
Past attempts: highest risk if previous attempt in past year, ask about lethality, outcome, medical intervention
Assess suicidal ideation
- Onset and frequency of thoughts: “When did this start?” or “How often do you have these thoughts?”
- Control over suicidal ideation: “How do you cope when you have these thoughts?” “Could you call someone for help?”
- Intended lethality: “Do you want to end your life?” or “What do you think would happen if you actually took those pills?”
- Access to means: “How will you get a gun?” or “Which bridge do you think you would go to?”
- Time and place: “Have you picked a date and place? Is it in an isolated location?”
- Provocative factors: “What makes you feel worse (e.g. being alone)?”
- Protective factors: “What keeps you alive (e.g. friends, family, pets, faith, therapist)?”
- Final arrangements: “Have you written a suicide note? Made a will? Given away your belongings?”
- Practiced suicide or aborted attempts: “Have you ever put the gun to your head?” “Held the medications in your hand?” “Stood at the bridge?”
- Ambivalence: “I wonder if there is a part of you that wants to live, given that you came here for help?”
RISK FACTORS
SAD PERSONS
- Sex: male
- Age: 15-25 or >60
- Depression or other mental health illness (bipolar highest)
- Previous attempt
- EtOH or substance abuse
- Rational thinking loss:
- Social supports lacking
- Organised plan or serious attempt (intent)
- No spouse
- Sickness: terminal or painful illness
COMMON WARNING SIGNS
- Obsession with death
- Feelings of hopelessness
- Isolating oneself
- Threatening to commit suicide
- Unexpected/sudden changes of behavioural, personality, eating habits, sleeping patterns, social
- Accessing items to use for suicide
- Excess drug and alcohol intake
PROTECTIVE FACTORS
- Strong self esteem
- Life skills
- Connection with culture, family, community
- Empowerment
- Access to healthcare and support systems
CLINICAL PRESENTATION
→ SYMPTOMS ASSOCIATED WITH SUICIDE
- Hopelessness
- Anhedonia: Inability to feel pleasure
- Insomnia
- Severe anxiety
- Impaired concentration
- Psychomotor agitation
- Panic attacks
ASSESSMENT OF SUICIDE ATTEMPT
- Setting (isolated vs. others present/chance of discovery)
- Planned vs. impulsive attempt, triggers/stressors
- Substance use/intoxication
- Medical attention (brought in by another person vs. brought in by self to ED)
- Time lag from suicide attempt to ED arrival
- Expectation of lethality, dying
- Reaction to survival (guilt/remorse vs. disappointment/self-blame)
- Epidemiology
HISTORY
POST-SUICIDE ATTEMPT
- What did they take and when
- Did they want to kill themselves and did they expect what they took to achieve this
- How long have they thought about it and what made them choose today?
- What preparations had they made
- Any precautions against discovery
- Did they inform anyone before or after
- Are they glad to have survived
SUICIDAL INTENT
- Use of general mood questionnaires e.g. Beck’s Suicidal Intent Scale
- How do they view their future
- Have they ever felt that life wasn’t worth living?
- Have they ever wishes that they could go to sleep and never wake up?
- Have they ever thought of wanting to die?
- Have they ever considered suicide
IF THE PATIENT SAYS THE HAVE CONSIDERED SUICIDE, ASK
- What has lead you to these thoughts
- Have you thought how you would do this?
If yes, ask about access to means
- What has stopped you so far?
- How do you usually cope when things get this bad
- What do you think might make you go ahead?
Outline an approach to a suicide risk assessment!
1) Aim to identify and treat risks and protective factors from the patient
What is the procedure regarding a suicide risk assesment e.g what is meant by “patient high risk of suicide’? How is it treated
What do you need to consider when conducting a suicide risk assessment? (e.g current presentation, psychiatric illnesses, history, psychosocial situation, individual stregths, coping skills, personality traits)
SUICIDE RISK ASSESSMENT
AIM TO IDENTIFY MODIFIABLE AND TREATABLE RISK AND PROTECTIVE FACTORS THAT INFORM THE PATIENTS OVERALL TREATMENT AND MANAGEMENT
REQUIREMENTS
Two peaks
- First week of admission
- First week of discharge
Hazards: external factors which increase the likelihood of danger occurring
- Not necessarily ‘predictors’ of suicide
- Factors in the bigger picture e.g. lack of access to a GP
Protective factors: Factors which may counteract risks
- External: presence of supportive network of friends
- Internal: good coping skills
PROCEDURE FOR SUICIDE RISK ASSESSMENT
- If a patient is at high risk of suicide = medical emergency
- Prompt and comprehensive assessment is to be conducted as soon as is practica
- Treatment process is planned and coordinated across all settings
- Includes prompt and effective psychiatric treatment for individuals with mental health and substance abuse problems, social and psychological support for those with psychosocial problems and counselling and support for significant others
- Consultation and clear/concise information to patient and family
- Clear plans for discharge and follow up
NEED TO CONSIDER
Current presentation of suicidality
- Thoughts, plans, behaviours, intent, methods, hopelessness, alcohol, reasons for living
Psychiatric illness
- Mood disorders, schizophrenia, anxiety, substance abuse, personality disorders
History
- Previous attempts, medical diagnoses, family history
Psychosocial situation
- Crises and stressors, loss, abuse, financial problems
Individual strengths/vulnerabilities
- Coping skills, personality traits, problem solving
What is meant by low, medium and high risk of suicide? What are features associated with each?
What is a suicide risk assessment tool used in clinical practise?
Management of Suicial ideation/attempt: outline steps taken in management of a patient presenting post sucide attempt/ high risk ideation:
What is done in Acute management of suicdal risk (immediate)? (ED)?
On Admission?
As an outpatient?
Medium-long term management?
What is meant by a safety plan in this setting?
What are adjuntive therapies for a patient with high risk suicidal intent?
What therapies are used to treat/manage self harm?
MANAGEMENT
- Assessment of risk: high or low
- High risk: place patient in low risk environment and admit patient: voluntary or under treatment authority if required
- Medium to high risk: follow up within 24 hours of discharge
- Low risk: make a safety plan
Follow up within 1 weeks of discharge
- Discharge
- Inform person’s family
- Follow up health care provide to receive a verbal summary at discharge
- Patient given a treatment plan and 24 hour telephone lines
Follow-up
- Full history, MSE, risk assessment
- Acute problems identified and addressed
- Person needs to be no longer suicidal
- Ensure plan on how to seek help if suicidal ideation recurs\
- Follow up arrangements documented and copy given to the patient and their support
- Family/supports agree with follow-up plan
- Person is medically stable and not intoxicated, delirious, demented or psychotic
- Treatment and support must be arranged for any alcohol or substance misuse problems
- Active suicidal ideation: Thoughts of taking action to kill oneself (I want to kill myself)
- Passive suicidal ideation: The wish or hope that death will overtake oneself (I would be better off dead)
- The first month following discharge from a psychiatric inpatient facility is associated with and increased risk of suicide
Suicide risk assessment tool: Beck Hopelessness Scale
ACUTE MANAGEMENT OF SUICIDE (IMMEDIATE)
- Medical stabilization (surgery- trauma, decontamination and antidotes)
- Remove means for suicide
- Ensure the safety of the patient and others
- Treat existing psychiatric disorders
- Bipolar- lithium
- Depression- SSRIs (safe in overdose, but caution in youths) + lithium stabilization and maintenance therapy (UpToDate)
- Substance abuse- detoxification and monitoring
- Review medications
5) Treat physical injuries
6) MHA
7) Monitoring and follow up
8) Address underlying factors- precipitating, perpetuating factors (Later)
ADMISSION:
- Admit to hospital and observation (for patients with recent suicidal behaviour e.g. suicide attempt or high risk of suicide such as those with severe suicidal ideation, a plan and intent)
- Admit patients if the ability of the patient to be safe outside admission of a treatment facility is in doubt
- Admit patients who also present with psychosis or inadequate social support
- Constant observation
- Reassess
OUTPATIENT
- Appropriate for patients with chronic suicidal ideation, but no history of prior suicide attempts
- Requires a Safety plan
- Requires a strong support network and access to outpatient facilities when required
- Monitoring by family and friends
- Provide patients and caregivers with 24 hour access to clinical support
- Instruct family members that if the patient decompensates then they need to return to hospital
- Restrict access to lethal means and avoiding alcohol/ drugs
- Specify coping strategies and healthy activities to manage or distract oneself from suicidal thoughts
- Treating psychiatric disorders aggressively
- Reassess patient
MEDIUM-LONG TERM MANAGEMENT
- Engagement with community, religious and family supports
- CBT
SAFETY PLAN
- Specifies how patients can cope with recurrent suicidal urges in the future
ADJUNCTIVE THERAPIES
- Psychotherapy- important for recovery for most patients with high risk suicidal intent.
- DBT (intensive and long-term intervention)
- CBT- indicated for psychiatric disorders (e.g. depression)
- Psychodynamic interpersonal therapy- including outreach (increase attendance and compliance)
- Social supports and group interventions
- Developing long-term personal goals, identifying positive expectations and broadening perspectives beyond immediate distress
- ECT: Indicated for severely depressed suicidal patients
- Always reassess patients regularly- assess the re-emergence of precipitating events, adverse life events or mental disorders
SELF-HARMING:
- DBT
- Psychodynamic interpersonal therapy
What are some important psychiatric condiions that have high level of suicide?
What are various ways to manage a suicidal patient? (what should be done in the following situations) (e.g Inpatient vs community, contigency plans, coping strategies when distressed, reassessment, treating mental health disorder)
1) Community
2) At discharge
What is a short term suicide risk management plan? What should it include?
What are basic management techniques for immediate intervention? Longer term interventions?
ELEMENTS OF A RISK MANAGEMENT PLAN FOR A SUICIDAL PATIENT
- Inpatient or community management
- Contingency plans
- Strategies for dealing with symptoms and distress
- Reassessment
- Treating mental disorders
COMMUNITY
- Identify appropriate supports
- Re-assessment of risk
- 24/7 access to clinical expertise for patient or carer
- Psychoeducation to family and support people on how to manage a person with suicidal behaviour
- Maintaining supervision
- Knowing where the person is and who will be with them
- How to contact the team for an urgent re-assessment
- Information about the response of the health service if the person needs to access further help because their distress or suicide risk has increased.
- Contingency planning for urgent and rapid re-assessment is in place for high and medium risk
DISCHARGE
- Follow up with GP
- Must have had resolution of precipitating factors or events
- Improving accommodation, employment and financial situation
- Provide contact details to the person and their family for rapid response re-assessment
- Contingency plans for re-assessment
DEVELOP A SHORT TERM SUICIDE RISK MANAGEMENT PLAN
- Managing recurrent suicidality
- Treat all psychiatric co-morbidities (depression, substance abuse)
- Assess and address any childhood abuse history
- Set clear limits including a management plan and guidelines on expected behaviour
- Psychotherapy and medications
- Clarify problems
- Provide psychiatric crisis intervention
- Provide symptom-focused hospitalisations when the ongoing suicidal threat crosses into an active suicidal state
- DBT- people with personality disorders
What is Neuroleptic Malignant syndrome?
What are the symptoms? (what is the tetrad, Neuro)
What are complications?
What is the treatment?
What is Serotonin Syndrome? What causes it?
What the major symptoms of this condition?
What is most common diagnostic feature?
What are complications of this condition?
What is the treatment?
NEUROLEPTIC MALIGNANT SYNDROME AND SEROTONIN SYNDROME
NEUROLEPTIC MALIGNANT SYNDROME:
- This is a potentially lethal adverse effect from treatment with a drug that affects dopaminergic transmission
- Antipsychotics are the commonest cause, but this can occur with antiemetics or abrupt cessation of dopamine agonists
- Patients develop NMS within hours to days after exposure to the causative drug
SYMPTOMS:
- Tetrad: Pyrexia, altered mental state, muscle rigidity and autonomic instability
- Neuro: Confusion, Delirium, stupor
- Autonomic instability: Tachycardia, tachypnoea, labile BP, sweating
- Raised CK
COMPLICATIONS:
- Rhabdomyolysis, Hyperkalaemia, Kidney failure
- Seizures
TREATMENT
- Discontinue the antipsychotic
- Monitor vitals
- Hydration (IV fluids) and cooling
- Cool the patient and give DVT prophylaxis
- Start antipsychotic treatment 2 weeks after NMS episode has resolved
SEROTONIN SYNDROME
- Caused by SSRIs and other serotonergic drugs (SNRIs, MAO-I, TCAs, St John’s wort)- caused by change in dose or initiation of a drug
- It results from increased CNS serotonergic activity
- Onset usually within 24 hours
- Hyperthermia, rigidity and autonomic hyperactivity
- Anxiety and restlessness
- Neuro: Clonus, hyperreflexia, hypertonia/ rigidity
- Confusion, coma, seizures, ataxia
* Autonomic hyperactivity: Tachycardia, hypertension, hyperthermia, sweating and flushing
Clonus is the most indicative feature (inappropriate plantar flexion, repeated contractions)
COMPLICATIONS:
- Rhabdomyolysis, AKI, metabolic acidosis
- Seizures, DIC
TREATMENT:
- Supportive care is important – ABCDE etc.
- Cease the inciting agent
- Patient should be sedated, cooled and paralysed.
- Antidotes have not got enough evidence to support
- Chlorpromazine causes significant postural hypotension – need to weigh out benefits and risks of therapy
What are some medical treatment for serotonin syndrome?
Approach to patient with overdoses of common medications:
What is the antidotes, Clinical presentations, Investigations and management of the following
Paracetomol?
Opioids?
TCAs?
Organophophates? (paraquat)
Benzodiazepines?
APPROACH TO PATIENTS WITH OVERDOSES OF COMMON MEDICATIONS:
ANTIDOTES:
- Paracetamol- N-acetylcysteine
- Opioids- Naloxone
- TCAs- NaHCO3
- Organophosphates (paraquat)- atropine, pralidoxime
- Benzodiazepines- flumazenil
PARACETAMOL
- Liver damage can occur in patients with paracetamol concentrations above the curved Paracetamol treatment nomogram line- give N-acetylcysteine
- For repeated ingestion of supratherapeutic doses- the dose ingested or abnormal LFTs indicates toxicity. The Paracetamol treatment nomogram shouldn’t be used and advice is required from a clinical toxicologist- give acetylcysteine.
CLINICAL PRESENTATION:
- GIT: Nausea, vomiting, anorexia, RUQ pain
- Liver failure: Hypoglycaemia, severe coagulopathy, metabolic acidosis
INVESTIGATIONS:
- Serum paracetamol concentration: Measure 4 hours after an acute overdose (repeat 4 hours after initial concentration for slow-release preparations). Measure 2 hours for liquid preparations
- LFTs
- Blood glucose concentration
- EUC
MANAGEMENT
- Asymptomatic patients with a paracetamol concentration under the nomogram require no further medical treatment
- Delay to treatment with acetylcysteine is associated with worse outcome
- If acetylcysteine is administered within 8 hours of acute overdose, it often prevents toxicity completely.
- Always check if the paracetamol concentration is above the nomogram line, but if the patient presents >8 hours after ingestion and has ingested a toxic dose or where the paracetamol concentration won’t be known then commence on acetylcysteine
- LFTs and INR should be tested before stopping acetylcysteine in patients who have treatment delayed for more than 8 hours after ingestion
- Patients with abnormal LFTs, liver failure or still have detectable paracetamol concentration require an extended duration of therapy
- The risk assessment in patients with repeated ingestion of supratherapeutic doses is difficult and the paracetamol treatment nomogram shouldn’t be used:
- Ingestions >200mg/kg daily for few days
- Repeated ingestion of combined paracetamol-codeine for weeks to months
- For these patients, measure LFTs and paracetamol concentrations and treat with acetylcysteine
- Repeat LFTs after 8 hours with acetylcysteine therapy and discontinue if these remain static or are normalising
Principles:
- Rehydration and IV fluids
- Decontamination- Activated charcoal
- Refer to specialist liver unit for liver failure
OPIOID
- Causes severe respiratory depression
- Toxicity can’t be predicted from the dose ingested or the serum drug concentration due to the tolerance that develops in opioid dependent patients
- Other predictors of toxicity
- Overdose with long-acting opioids (e.g. methadone) and slow-release formulations requires inpatient admission and critical care observation.
CLINICAL FEATURES:
- Miosis, respiratory depression, drowsiness, coma
- Arrhythmias
- Pulmonary edema
- GIT: Nausea and vomiting
COMPLICATIONS:
- Hypoxia: Seizures, arrhythmias, brain injury
INVESTIGATIONS
- ABG- PaCO2 indicates hypoventilation
- CXR- aspiration pneumonitis or non-cardiogenic pulmonary edema
- ECG- continuous ECG monitoring is required to assess for arrhythmias
TREATMENT
- Airway and breathing- O2 and ventilation
- Circulation- cardiac arrest can occur due to prolonged hypoxia
- IV Naloxone and respiratory supportive care
- Short-acting opioids- 1 dose of naloxone is required
- Long-acting opioids or slow-release formulations- naloxone infusion
- Decontamination is rarely indicated in oral opioid overdoses (risk of sedation and aspiration) except for the following:
- Slow-release opioid preparations
- Opioids with a long half-life
- The activated charcoal must be administered within 1 hour of the time of ingestion to a cooperative patient. It can reduce the duration of toxicity for opioids with slow-release or long half-lives.
- Reversal of opioid overdose is best indicated by an increased level of consciousness and normal respiratory drive
- Titration of naloxone is important to avoid acute withdrawal
- Sudden or complete reversal can cause MIs in the elderly or patients with coronary artery disease, or delirium in patients who are opioid-dependent
- Addiction counselling/ psychiatry review
BENZODIAZEPINE
CLINICAL FEATURES
- Neuro: Ataxia, lethargy, slurred speech and coma
- Resp: Respiratory depression
- CVS: Bradycardia and hypotension (high doses)
- Others: Hypothermia
- Apnoea indicates airway obstruction
MANAGEMENT
ABCDE (intubation and ventilation)
- Patients with poor resp effort shouldn’t have O2 without resp support.
- Hypotension- IV fluids
- Monitor for urinary retention
- Isolated benzodiazepine overdoses usually only causes mild sedation with full recovery expected following supportive care
- Observe for 4 hours after flumazenil
- The addition of other agents including ethanol can complicate management
- Antidote- flumazenil (use with caution)- used infrequently
- Flumazenil is a competitive benzodiazepine antagonis
- Some benzodiazepines have a longer duration of action than flumazenil resedation
- Giving flumazenil means that there is a risk of precipitating a seizure in someone who has ingested proconvulsants (e.g. TCAs), has a history of epilepsy or chronic benzodiazepine use
- If the patient has a seizure then you can’t use benzodiazepines to terminate it
Indications for flumazenil in benzodiazepine overdose:
- Reversal of iatrogenic oversedation
- Elderly patients or patients with respiratory disease (e.g. COPD) because poor respiratory effort may cause atelectasis and poor cough causes respiratory infections
- Accidental pediatric ingestion
- Management of airway and breathing when resources aren’t available to safely intubate and ventilate
What is a ‘Behavioural’, emergency?
What are three most common causes of them?
What is the management of this? What is verbal de-escalation? How do we conduct this? What can we offer the patient?
What role does physical restraints have in these “behavioural emergencies”?
How is this best managed in the following setting (Acute Medical, acute psychiatric setting)
APPROACH TO PATIENTS WITH ACUTE BEHAVIOURAL DISTURBANCE AND SELF-HARM:
BEHAVIOURAL EMERGENCIES
- Behavioural emergencies are situations where patients show behaviour that places them or others at risk of physical harm and that requires immediate targeted intervention.
3 main etiological groups for behavioural emergencies include:
- Medical disorders e.g. delirium
- Substance intoxication or withdrawal
- Psychiatric disorders- schizophrenia, mania, psychotic depression, PTSD and personality disorders
MANAGEMENT
- Recognise warning signs
- Attend to the patient as a priority
- Consult security and police to disarm and restrain the patient where the situation is too dangerous
- Ensure the safety of self, staff and the patient
- Reduce tension through offering water
- Assess mental state, physical examination (visual inspection and vital signs)
- Investigations: O2 sats, blood glucose concentrations and toxicology assessment
- Observation
- Use the least invasive method to gain control:
- Verbal de-escalation and early negotiation (offer oral medication)
- Show of force
- Physical restraint
- Chemical restraint- Diazepam, midazolam, olanzapine, droperidol
VERBAL DE-ESCALATION
- Offer the patient to state their concerns and explain your wish to help them
- Offer support including drinks, assistance (e.g. access to a telephone) and pain
- Offer oral Diazepam or olanzapine
- Diazepam is preferred for drug withdrawal or stimulant intoxication
- Olanzapine is preferred for acute psychosis
PHYSICAL RESTRAINT
- Used for persistent or recurrent evidence of a behavioural emergency
- It should be initiated rapidly if aggression or distress is escalating and violence appears imminent
- Maintain physical restraint until sedation
ACUTE MEDICAL SETTINGS
- Achieve rapid tranquillisation (calmness) to ensure safety of all
- The next priorities are medical examination and investigation to reach a diagnosis
- CPR resources are immediately available and staff are highly trained in their use
- Use physical restraint until the clinical response is apparent
- IV diazepam or midazolam- IV allows titration and an immediate action
- IV Droperidol or olanzapine can be used with diazepam or midazolam or as a single drug in patients who are tolerant to benzodiazepines or if there is a failure of benzodiazepines
- IM midazolam
- IM droperidol or olanzapine in patients tolerant of benzodiazepines
- Use benzodiazepines cautiously in patients with respiratory impairment (e.g. COPD)
- EPSEs (e.g. acute dystonia) can be relieved by an anticholinergic drug
- Note: Diazepam has poor absorption IM
ACUTE PSYCHIATRIC SETTINGS
- Behavioural emergencies vary widely in nature and severity and include many different psychiatric diagnoses especially psychotic illnesses
- Achieve tranquillisation and safety of all
- The next priorities are psychiatric examination and investigation to rule out medical factors, reach a diagnosis and initiate psychiatric management
- Oral tranquillisation is preferred as it encourages patient-staff engagement, allows the patient to feel in control and aids future treatment concordance
- Monitor vital signs and mental state during and after medication administration
- Parenteral medication can only be administered if there is monitoring of vital signs, CPR and appropriate monitoring and resuscitation equipment is immediately available
- Minimum equipment requirements: O2 supply, suction, BP monitor, resuscitation trolley with ECG and pulse oximetry
- Note: IM Onset of effect is less immediate and titration to effect is more difficult
OTHER SETTINGS (E.G. GP)
- Patients may need initial IM Olanzapine or Droperidol before being transported to an appropriate acute setting for further management
- Need to have staff skilled in CPR both at the initial setting and in transport
- In all settings, post-medication monitoring and management should be undertaken
ORAL MEDICATION
- PO diazepam or lorazepam
- PO Olanzapine or risperidone (can cause orthostatic hypotension and EPSEs) or chlorpromazine (can cause orthostatic hypotension) or haloperidol if the effects are not achieved with diazepam or lorazepam alone
IM
- Parenteral should only be administered if monitoring of vital signs is possible, personnel are trained in CPR and monitoring and resuscitation equipment are available.
- IM midazolam or droperidol or olanzapine
What are the main risks associated with the use of medications for behavioural emergencies?
What are the required observations?
POST-MEDICATION MANAGEMENT
The main risks of medication used in the management of behavioural emergencies are:
- Airway obstruction
- Respiratory depression
- Aspiration
- Hypotension
- Laryngospasms (antipsychotics)
- Vigilant monitoring for signs of airway obstruction, respiratory depression and hypotension is essential during the post-medication period.
REQUIRED OBSERVATIONS:
- Airway patency
- Resp rate
- Pulse
- BP
- Skin colour
- O2 sats
- Level of alertness
- Response to medication and evidence of ongoing behavioural disturbances or agitation
How do we manage a patient presenting with self harm? What recommendations/skills can we coordinate with the patient?
Outline 6 skills/techniques you can recommend for management?
What does a comprehensive assessment of self harm ential? What details do you need to elicit from the patient?
What is the overall of treatment for patients presenting with self harm?
What demographics/psychiatric conditions tend to self harm?
What is meant by the mnemonic ‘DEESCALATION”? (for behavioural/self harm behaviours)
SELF-HARM
- A person in crisis engaging in self-harm may not meet criteria for an inpatient admission, but ongoing behaviour could increase the risk of death by accident
- This requires carer/family involvement to ensure the person is safe and to remove potential items of harm
- Treat mental illness
- Improve coping skills
- Prevent suicide- phone numbers
- DBT, CBT, Interpersonal therapy, Problem Solving Therapy, Mindfulness
- Follow up in the community
OTHER RECOMMENDATIONS FOR PATIENTS
- Attend support groups for people with similar problems
- Continue activities that are positive in your life and be hopeful about the future
- Mood diary
- GP- Talk to GP about self-harm
- Lifeline Australia
GUIDELINES (ALL PATIENTS PRESENTING WITH SELF-HARM):
- Patient’s current mood
Detect and treat all mental disorders
- Depression with self-harm- SSRIs
- Depression in BPAD- Lithium + mood stabilizers
- Schizophrenia- atypical antipsychotixc
- Personality traits and disorders- DBT (useful in borderline personality disorder and multiple self-harms)
- Alcohol and drug use
- Personality disorders
- Comprehensive assessment of risk of harm to self and others
- Psychosocial assessment- living arrangements, supports
- Risk assessment
- Teach problem solving and cognitive oriented therapies
- Enhance resilience and promoting adaptive coping strategies
- Safety strategies e.g. if the patient feels like harming themselves, they will seek out a family member
- Create Community Care Plan
Ask whether the patient is having difficulty coping, feelings of frustration/ out of control, or they want to kill themselves
COMPREHENSIVE ASSESSMENT INCLUDES:
- Eliciting thoughts and plans about further self-harm
- Detailed review of current and past episodes of self-harm
- Assessment of the patient’s current social circumstances
- Alternatives to dealing with ongoing stressors
- Assessment of current psychosocial stressors and available support from others
- Contact Mental Health Services
- Ensure safety from further self-harm
- Assess and treat injuries
- Manage suicide risk via psychiatric referral
- Social supports
EXTRA:
- Our main goal is to increase the patient’s resourcefulness and positive coping to prevent repeat episodes, habituation, etc
- For patients with habitual self-harm, we want to prolong the period between episodes of self-harm and reduce injury severity.
- Some patients are admitted to hospital after self-harm to treat mental illnesses
CAUSES OF SELF-HARM:
- People under stress or in crisis and those who have self-harmed before
- Those with mental disorders- anxiety, depression, schizophrenia
- Alcohol and substance abuse
- Childhood trauma or abuse
- Those with a debilitating or chronic illness
MNEMONIC:
• → DEESCALATION
- D Don’t withdraw privileges, seclude or medicate
- E Ensure safety of others
- E Escape – avoid cornering person/being cornered
- S Stance – Protective and read
- C Calm, non-threatening manner
- A Allow for ventilation of anger and feelings
- Leave the area if secure and safe to do so
- A Assistance and enough skilled staff available
- T Time out: offer time in quite room/lounge
- I Invite to sit and verbalise concerns
- O Options/choices = exercise, music, coffee
- N Never turn your back
What is meant by the following terms: (psychiatry)
- ID
- Ego
- Superrgo
- Conscious
- unconscious
How did freud describe this?
TERMINOLOGY:
- id: Comprises 2 kinds of biological drives- Eros and Thanatos. The energy libido and acts upon the mind unconsciously.
- id: Instinctual drives, unconscious
- Ego: The ego develops from the id to satisfy the demands of the id in a safe and socially acceptable way and in contrast to the id, the ego follows the reality principle as it operates in both the conscious and unconscious mind.
- Ego: Sense of self, conscious actions, attempts to satisfy drives of id within confines of reality and demands of superego.
* Supeego: The superego develops during early childhood to ensure moral standards to behave in a socially responsible. - superego: Person’s conscience formed by societal and parental norms
- Conscious: An awareness of an external object or something within oneself. It is the active thinking process. Awareness of and responding to one’s surroundings
- Unconscious: This consists of processes in the mind that occur automatically and are not subject to introspection including: Thought processes, memories, interests and motivations.
- These processes exist under the surface of consciousness, but exert an impact on behaviour.
- Unconscious phenomena include: Repressed feelings, automatic skills, subliminal perceptions, thoughts, habits and automatic reactions and complexes (hidden phobias and desires)
FREUD:
- Freud divided the mind into the conscious mind (ego) and the unconscious mind
- The unconscious mind comprised the id (instinct and rive) and the superego (conscience)
- The unconscious refers to the mental processes of which individuals are unaware
- Psychoanalytically, the unconscious doesn’t include all that isn’t conscious, but rather what is actively repressed from conscious thought
- The unconscious is a repository for socially unacceptable ideas, wishes or desires; traumatic memories, etc
- The unconscious can only be recognized by its effects as expressed in itself in the symptom
- Unconscious thoughts are not directly accessible to introspection, but can be tapped and interpreted through free association and psychoanalysis.
- Slips of the tongue are related to the unconscious in that they often show a person’s true feelings on a subject
- The unconscious is a determinant of personality
What are pscyholgical defence mechanisms as described by Freud? What are they meant to do?
What are primitive defense mechanisms? Who are more likely to use these?
What are less primitive defense mechanisms?
What are mature defence mechanisms?
DEFENCE MECHANISMS:
- Defence mechanisms are psychological mechanisms to shield ego from conflicts
- Enhances or impairs coping and mainly unconscious or partially conscious
PRIMITIVE DEFENCE MECHANISMS
- Denial: Refusal to accept reality or fact, acting as if a painful event, thought or feeling didn’t exist while being apparent to others e.g. alcoholic denying drinking as they function in job, relationships—————– It is characteristic of early childhood development
- Regression: Reversion to an earlier stage of development in the face of unacceptable thoughts or impulses e.g. adults curling up in fetal position when feeling threatened or afraid
- Self-harm: Self-harm is a form of coping by hurting oneself. It is a form of stress-relief but also self-punishment and expression of rejection of the self.
- Splitting: The individual tends to think in extremes (i.e. an individual’s actions and motivations are all good or all bad with no middle ground)
- Acting out: Performing an extreme behaviour in order to express thoughts or feelings the person feels incapable of otherwise expressing e.g. self-injury is expression through physical pain of what can’t be stand to feel emotionally.
- Projection: Misattribution of a person’s undesired thoughts, feelings or impulses onto another person who doesn’t have those thoughts, feelings or impulses e.g. a spouse may be angry at their husband for not listening when in fact it is the angry spouse who doesn’t listen
- Reaction formation: Converting of unwanted or dangerous thoughts, feelings or impulses into their opposites e.g. a woman angry with her boss and would like to quit her job may be overly kind and generous towards her boss.
LESS PRIMITIVE
- Repression: Unconscious blocking of unacceptable thoughts, feelings and impulses e.g. repressed memories (memories that have been unconsciously blocked from access or view)
- Displacement: Redirection of thoughts, feelings and impulses directed at 1 person or object, but taken out upon another person or object e.g. the man who gets angry at his boss but can’t express his anger to his boss for fear of being fired → he comes home and kicks the dog or starts an argument
MATURE DEFENCE MECHANISMS:
- People with more mature defences tend to be more at peace with themselves and those around them
- Humour: Effective way of channelling unacceptable impulses or thoughts into a light-hearted story or joke
- Sublimation: Channelling of unacceptable thoughts, impulses and emotions into more acceptable ones e.g. a person who has sexual impulses they wouldn’t act upon may focus on rigorous exercise
- Suppression: Sometimes we consciously force unwanted information out of our awareness, which is known as suppression. In most cases, the removal of anxiety-provoking memories from our awareness is believed to occur unconsciously.
Roles and different types of therapies in psychiatry:
What is psychotherapy? How is it delivered? What are various types of therapy?
What is behavioural therapy? What are the types and what do they aim to do? When is it indicated?
What is cognitive therapy? What does it aim to achieve? How is this achieved? Who does it work best in? When is it indicated?
What is CBT? What does it aim to achieve? When is it indicated?
What is dialectical behavioural therapy? What does it focus on? When is it indicated?
What is psychoanalytic/pscyhodynamic therapy? What does it aim to do? Who does it work best in?
What is supportive therapy?
What is interpersonal therapy? What does it aim to achieve?
What is motivational interviewing? And motivational enhancement therapy?
What is family therapy? Group therapy?
What is (insight orientated therapy) Psychodynamic therpapy? what does it aim to treat? What patients benefit from this?
ROLE AND TYPES OF THERAPY
- Psychological interventions alone are useful for anxiety disorders, mild to moderate depression and various psychiatric conditions.
- CBT and IPT are the best
PSYCHOTHERAPY
- Treatment in which a person with mental or physical difficulties aims to achieve symptomatic relief through talks with another person
- Delivered by a specially trained social worker, nurse, psychologist, psychiatrist, counsellor or general practitioner
- Various types of therapy exist because of diverse theories of human psychology and mental illness aetiology
- Common factors (30-70% of outcome due to these):
- Warmth: unconditional positive regard
- Accurate empathy
- Genuineness
- Goodness of fit
BEHAVIOURAL THERAPY
TYPES:
- Systematic desensitisation: mastering anxiety provoking situations by approaching them gradually and in a related state that limits anxiety
- Flooding: confronting feared stimulus for prolonged periods until it is no longer frightening
- Positive reinforcement: strengthening behaviour and causing it to occur more frequently by rewarding it
- Negative reinforcement: causing behaviour to occur more frequently by removing noxious stimuli when desired behaviour occurs
- Extinction: causing a behaviour to diminish by not rewarding it
- Punishment/aversion therapy: causing behaviour to diminish by applying noxious stimulus.
INDICATIONS
- Most mental health disorders can benefit from specific application
COGNITIVE THERAPY
- Moods and emotions are influenced by thoughts and psychiatric disorders are often caused by habitual errors in thinking.
- Therapy helps to make explicit their inaccurate automatic thoughts and correct assumptions with a more balanced perspective.
- Uses thought records to help monitor thoughts and the situations that they occur in, and feelings they might provoke due to their underlying cognitive errors.
- Works best in motivated patients who will comply with homework and have an openness to changing their core beliefs
- Indications: depression, anxiety, panic disorder, somatoform disorders
COGNITIVE BEHAVIOURAL THERAPY
- Combines cognitive and behavioural methods to teach patient to change connections between thinking patterns, habitual behaviours and mood and anxiety problems
- Works best when patients have motivation to change.
- Indications: most mental health disorders
DIALECTICAL BEHAVIOURAL THERAPY
- Therapy that combines CBT techniques with Buddhist Zen mindfulness practises and dialectical philosophy.
- Focuses on mindfulness, emotion regulation, interpersonal effectiveness and distress tolerance
- Involves individual therapy, group skills, phone consultations and a consultation team.
- Works best with patients who have severe problems of emotional dysregulation, impulsivity and self-harm.
- Indication: borderline personality disorder
PSYCHOANALYTIC/PSYCHODYNAMIC THERAPY
- Exploration of meaning of early experiences and how they affect emotions and patterns of behaviour.
- Recollection, repetition, working through and gaining insight
- May use free association, dream interpretation and transference analysis
- Works best in people with a high level of functioning who wish to understand selves not just relieve symptoms.
- Indications: anxiety, obsessional thinking, compulsive or conversion disorders, sexual dysfunction and depression
SUPPORTIVE THERAPY
- Behavioural or environmental restructuring to aid adaption and facilitate coping.
- Help patients feel safe, secure and encouraged.
- Works best in individuals in crisis or with severe symptoms.
- Indications: adjustment disorders, psychosomatic disorders, severe psychotic or personality disorders
INTERPERSONAL THERAPY
- Focuses on how interpersonal relationships impact on symptoms.
- Greif and loss, role transitions, conflict and interpersonal deficits are addressed.
- Need to break the interpersonal cycle of depression, self-esteem and social withdrawal
- Indications: bulimia nervosa and mood disorders
MOTIVATIONAL INTERVIEWING AND MOTIVATIONAL ENHANCEMENT THERAPY
- Used for patients with substance abuse disorders
- Understand the client and their reasons for change.
- Listen and empower and convey hope and support.
- Used as brief interventions with many sessions.
GROUP THERAPY
- Aims to promote self-understanding, acceptance and social skills
FAMILY THERAPY
- Family system is considered more influential than individual, especially in children.
- Need to focus on here and now, re-establishing parental authority, strengthening normal boundaries and rearranging alliances.
NARRATIVE THERAPY
- Integrative approach that attempts to understand the patients experience as a whole.
PSYCHODYNAMIC THERAPY (INSIGHT-ORIENTED THERAPY)
- Psychodynamic psychotherapy is effective for anxiety, depression, obsessional thinking, compulsive or conversion disorders, personality disorders, sexual dysfunction
- It focuses on revealing unconscious processes that manifest in a person’s present behaviour in order to alleviate psychic tension.
- The goals include increasing the client’s self-awareness and understanding of the influence of the past on present behaviour through examining unresolved conflicts from past relationships
- Borderline personality disorder: DBT and psychodynamic psychotherapy are the gold standards.
- Psychodynamic psychotherapy may decrease the need for hospital care, improve general psychiatric symptoms, reduce the need for medication and improve social adjustment.
- Psychodynamic psychotherapy is effective for a range of personality disorders including Cluster C (anxious) personality disorders
- Psychodynamic psychotherapy is effective for GAD and postnatal depressio
Extra information to explain to patients!
Cognitive behavioural therapy is a talking therapy that can help you manage your problems by changing the way you feel, think and act. The therapy aims to find practical ways to help you deal with problems in a more positive way by breaking them down into smaller parts.
Behavioural activation - this aims to help you to take positive, manageable steps to meeting specific goals you set with your therapist. These help you to engage with pleasurable activities which in turn can help you move towards enjoying life again.
Interpersonal therapy - this aims to help you identify and manage problems in your relationships.
Mindfulness-based therapy - this helps you learn to focus on the here and now. It can be particularly helpful in keeping depression and anxiety at bay once you have recovered. It may be combined with cognitive therapy.
Psychoanalytic therapy - this looks more at the importance of early relationships and how these templates affect your behaviour in the present
CBT
What does CBT aim to recognize?
What is thought challenging CBT?
What are the techniques required in CBT? - What are you aiming to help the patient do/address?
What role does CBT have in anxiety?
What are firstline treatments of GAD?
What role does CBT have in Panic disorder? Agoraphobia?
What role does CBT in depression? What is its focus? What are the two key principles that CBT has in depression? (cognitions control behaviour and emotion/ Behaviours affect thought patterns and emotions)
What are the key principles of CBT? (e.g what is cognitive restructuring, behavioural acitvation, Specific problems, mood diary, goal orientated)
What patients benefit most from CBT?
What role does CBT have in stress management?
CBT:
- CBT recognises that cognition and behaviour affects emotion
- It addresses negative distortions in the perceptions of ourselves and the world
- Cognitive therapy: Examines how negative thoughts contribute to anxiety
- Behaviour therapy: Examines how you behave and react in situations that trigger anxiety
- CBT suggests that our thoughts (not external events) affect the way we feel
THOUGHT CHALLENGING (CBT):
- The psychologist helps identify unhelpful thoughts and behaviours
- Challenging negative thoughts and beliefs
- Replace negative thoughts with realistic statements that can be used when anticipating or confronting feared situations
- Exposure therapy with strategies to cope with symptoms
TECHNIQUES IN CBT:
- CBT helps people to recognize their fears
- Identifying and replacing cognitive distortions
- Gradual exposure exercises
- Distractions to stop ruminating on thoughts
- Relaxation techniques- breathing techniques, guided imagery, progressive muscle relaxation
- Recognising the difference between productive and unproductive worries
- Teaching the patient to let go of worries and solve problems
- Teaching relaxation and breathing techniques especially muscle relaxation to control anxiety and symptoms of tension.
COGNITIVE BEHAVIOURAL APPROACH TO MANAGEMENT OF ANXIETY
- Psychological interventions including eTherapy and CBT are the most appropriate initial treatment for anxiety
- CBT may be as effective as drugs for those with mild to moderate anxiety
- Severe anxiety requires medications and CBT
- Psychological interventions must be persisted with for sufficient time for the benefits to be seen
- Anxiety disorders are often chronic or relapsing and require ongoing treatment with psychological interventions being most beneficial when patients practice the strategies
- Adjustment disorder with anxious mood: Main interventions are CBT, counselling, relaxation, problem solving and stress management.
- GAD: Firstline treatments are psychological (CBT, stress management, supportive psychotherapy
- Severe GAD requires medications
- Panic attacks- Isolated panic attacks with psychological interventions
- Panic disorder: Psychological interventions are first-line- CBT is the treatment of choice.
- OCD: CBT and medications
- Agoraphobia: CBT
- Social anxiety disorder: Generalised social anxiety: CBT and medications
- Non-generalised social anxiety: Control of panic symptoms, CBT and medications
- PTSD
CBT FOR GENERALISED SOCIAL ANXIETY DISORDER
- CBT incorporating exposure-based therapy, social skills training and cognitive therapy
- Train patients in alternative responses to worry habits
CBT FOR PANIC DISORDER (PANIC CONTROL TREATMENT):
- Involves gradual exposure to deliberately induced symptoms along with techniques (such as controlled slow breathing) for controlling symptoms and reattribution of symptoms to benign causes (e.g. palpitations are not due to cardiac arrest)
CBT FOR OCD:
- CBT involves exposure to the triggers that cause anxiety with prevention of rituals that are performed to reduce the anxiety.
- Many patients, especially those with severe symptoms can’t engage in psychological interventions until they have had medications
CBT FOR AGORAPHOBIA
- Treatment involves behavioural therapy with graduated in vivo exposure to overcome the phobic avoidance.
CBT FOR DEPRESSION:
- CBT assumes that a person’s mood is directly related to their pattern of thought
- Negative thinking affects mood, sense of self, behaviour and physical state
- Thought distortions are involved in the development and maintenance of psychological disorders
- CBT aims to help patients recognise negative thoughts, evaluate their validity and replace them with healthier ways of thinking
- CBT is problem-focused so it is used to treat specific problems related to depression
- The therapist’s role is to assist the patient in finding and practicing effective strategies to address the identified goals and decrease symptoms of the disorder.
PRINCIPLES OF CBT IN DEPRESSION (2 KEY PRINCIPLES):
- Cognitions control behaviour and emotions
- Behaviours affect thought patterns and emotions
- It’s based on the idea that negative actions and feelings are based on current distorted thoughts
- CBT emphasizes the need for a collaborative therapist-patient relationship
- The patient and therapist identify current patterns of thinking or distorted perceptions that lead to depression.
- The patient and therapist replace negative thoughts with constructive ones through learning to control and modify distorted thoughts and reactions
- Learning to accurately assess external situations and reactions or emotional behaviour
- CBT has 12-20 fixed sessions
CBT IS BASED ON:
- Cognitive restructuring: Where the therapist and patient work together to change thinking patterns
- Behavioural activation: Where patients learn to overcome obstacles to participating in enjoyable activities. This decreases avoidance and increases engagement in activities that alleviate depressive symptoms.
- CBT focuses on specific problems: Problem behaviours and thinking are identified, prioritized and addressed. The aim is to recognize how these ideas affect mood, behaviour and physical condition.
- Patients are asked to pay attention to their mood that occurs following automatic thoughts to learn about the relationship between automatic thoughts and their emotions.
- CBT is goal-oriented: Patients working with their therapists are asked to define goals for each session and long-term goals.
- Therapists teach coping skills and problem solving
- CBT uses multiple strategies including role playing, imagery, behavioural experiments, etc
- Scheduling enjoyable experiences often with others to reinforce the enjoyment
DEPRESSION:
- Mild to moderate depression: CBT without medications
- Severe depression: CBT and medications
- Reduces relapses in patients who experience frequent relapses
TYPE OF PERSON MOST LIKELY TO BENEFIT FROM CBT:
- Motivated
- Sees themselves as able to control events that happen around them
- Has capacity for introspection
CBT IN STRESS MANAGEMENT:
- CBT focuses on how people’s thoughts affect their emotions and behaviours
- Understanding this enables people to learn how to combat negative thinking and decrease stress
- Information about the anxiety disorder and education about relaxation techniques and coping skills
- Stress management involves activity scheduling, modifying lifestyle factors, problem-focused counselling and structured problem-solving
- Assess thoughts and rationalise to see if they are logical
- Stress involves an event and a reaction (thinking, feeling or a behaviour) to the event
- Stress are internal thoughts, feelings and reactions to external threatening situations
- Stress occurs when the pressure of life exceeds the ability to cope
What are the cognitive distortions of depresson?
What are some examples of Havibitual negative thoughts?
COGNITIVE DISTORTIONS OF DEPRESSION:
- Automatic thoughts: Patients with depression may have automatic thoughts in response to situations. These are spontaneous, negative and aren’t logic.
- Patients have a dysfunctional assumption that guides the way they view themselves, their situation and the world around them.
- Inertia: A person with depression stops doing things because they think it’s not worth the effort, but this worsens the depression.
EXAMPLES (HABITUAL NEGATIVE THOUGHTS):
- Overgeneralization- everything I do is wrong
- Selective abstraction- I didn’t have a moment’s pleasure today
- Dichotomous thinking- If I can’t get 100% right then no point in trying
- Catastrophic thinking
- Personalization- I did something to offend him
- Arbitrary inference- this won’t work so it’s not worth trying
- Magnification of negatives
- Minimisation of positives
- Labelling and mislabelling: Attributing a person’s actions to their character instead of some accidental attribute. Past errors mean you are always a loser
- Disqualifying the positive: Discounting positive events- rejecting positive experiences by insisting they don’t count for some reason.
- Mental filter: Patients mentally single out only the bad events in their life and overlook the positive.
What is ECT?
What are its indications?
How many treatments usually?
What are its side effects?
What are its contraindications?
How is treatment administered? What prophylactic medication can be given?
What are cardiac side effects (during and after)? What are CNS side effects?
What is Repetitive transcranial magnetic stimulation?
SOMATIC THERAPIES:
ELECTROCONVULSIVE THERAPY (ECT)
- Modern ECT: induction of a generalized seizure using an electrical pulse through scalp electrodes while the patient is under general anaesthesia with a muscle relaxant
- Considerations: unilateral vs. bilateral electrode placement, pulse rate, dose, number and spacing of treatments
- Usual course is 6-12 treatments, 2-3 treatments per wk
INDICATIONS
- Depression refractory to adequate pharmacological trial (MDD or Bipolar I depression)
- Psychotic depression
- Catatonic features
- High suicide risk
- Acute schizophrenia unresponsive to medicatio
- Mania unresponsive to medications
- OCD refractory to conventional treatment
- Medical risk in addition to depression e.g. dehydration, electrolytes, pregnancy
- Previous good response to EC
- Pregnancy
- Medical conditions preventing use of antidepressants
- Familial response to ECT
SIDE EFFECTS
- Risk of anaesthesia
- Memory loss
- May be retrograde and/or anterograde, tends to resolve by 6-9 months, permanent impairment controversial
- Unilateral ECT causes less memory loss than bilateral but may not be as effective
- Headache
- Myalgia
CONTRAINDICATIONS
- Increased intracranial pressure
- Recent (< 2 wk) MI (not absolute but requires special monitoring)
- Unstable or severe CVD
- CHF and valvular disease
- Intracranial SOL with evidence of increased intracranial pressure
- Recent cerebral haemorrhage or stroke
- Bleeding or unstable vascular aneurysm
- Severe pulmonary condition
TREATMENT:
- ECT is administered 2-3 times per week for a total of 6-12 treatments
- The treatment causes a 30-60 second generalized tonic clonic seizure
- Prophylactic beta blockers may be administered before or during ECT to reduce the hypertensive, tachycardia response to the seizure
- Succinylcholine is given to induce skeletal muscle relaxation to minimize the motor seizure and prevent MSK injury –Suxamethonium or Rocuronium
- Anaesthesia: Propofol
CARDIOVASCULAR EVENTS
- A 15-20 second parasympathetic discharge occurs during the procedure as the patient enters the tonic phase of the seizure
- Leads to arrhythmias including bradycardia
- The clonic phase of the seizure leads to a catecholamine urge that causes tachycardia and hypertension
- The duration of the tachycardia usually correlates with the length of the seizure
- These continue into the postictal period and usually resolve within 10-20 mins of the seizure
- The incidence of cardiac complications are rare and almost always occur in older patients and those with underlying CVD
- Patients with pacemakers and implantable defibrillators can undergo ECT
CNS EFFECTS
- ECT causes increased cerebral blood flow and intracranial pressure
- Memory loss, disorientation and delirium
Investigations:
- ECG
- EUC- patients taking diuretics, renal disease or CHF
REPETITIVE TRANSCRANIAL MAGNETIC STIMULATION (RTMS)
- Non-invasive production of focal electrical currents in select brain areas using magnetic induction
- Indication
Strong evidence for
- Treatment-resistant depression
- Pain disorders
Possibly efficacious
- Anxiety disorders
- Eating disorders
- Substance use disorders
Adverse effects
Common
- Transient local discomfort
- Hearing issues
- Cognitive changes
o Rare
- Seizure
- Syncope
- Mania induction
What are barrier for care when dealing with a patient of ATSI descent? What important knowledge/skills facilitate good dr patient relationship?
What are the three branches of cultural psychiatry? What is culture?
- help facilitate the engagement process, it can be helpful for you to:
- try to gain knowledge about the community you will be in
- understand historical knowledge and context of the patient’s community and how this may impact on the patient’s presentation or the manner in which they relate to you
- be aware that you will be observed from the moment you arrive
- be open to recognising that you do not know everything; understand that you have something to contribute but that you have a lot to learn
- not make assumptions about individuals; understand that there is a diverse culture amongst Aboriginal and/or Torres Strait Islander peoples and that everyone is different, with different past experiences and different stories
- be aware of possible patient perceptions of psychiatric services and how these may be a barrier to therapeutic alliance
- be respectful, and openly demonstrate respect
- share a little information about yourself
- be open and non-judgemental
- Try to gain some trust within the community
- speak with, and be guided by, the community liaison, and mental health, workers.
- Cultural psychiatry
- Collective experiences specific to a group
- Requires familiarity with identifying and managing culture-bound syndromes, illness behaviours and sick roles, and language barriers
- Heightened vulnerability to trauma-related conditions, as well as all other mental illnesses due to stress
Legacy of colonisation
- Transgenerational trauma and loss of identity
- Impaired social functioning and prejudiced across all domains of social determinants
- Effective assessment techniques facilitates
- Collection of accurate information
- Interpretation of information accurately
- Accurate understanding by the patient and family
- Interventions including pharmacotherapy, medication adherence and suicide prevention need to be holistic
- Focus equally on clinical assessment and management, social and emotional wellbeing, and social disparities
- There are no quick fixes or short cuts, only commitment to supporting the empowerment and self-determination of indigenous people over time will lead to meaningful generational change
THREE BRANCHES OF CULTURAL PSYCHIATRY
- Indigenous mental health
- Refugee mental health
- Migrant mental health
- Culture
- A set of shared attitudes, beliefs and behaviours that constitute a group’s view of the world and style of life
- Features specific to cultural psychiatry
- Collective experience
- Culture-bound syndrome
- Manifestations of illness and sick role
- Language barrier
- Heightened vulnerability
When conducting an interview, how do we organise it to facilitate strong dr patient relationship (ATSI) ?
e.g ( Aim to optimize) 2) the Setting 3) confidentiality 4) Respect 5) Language 6) Engagement and establishing rapport 7) Cultural safety 8) ATSI Mental health workers
How do we adjust our attitudes, behaviour and communication to promote patient engagement?
How do we develop an indigenous mental health plan?
How do we enhance knowledge of the community?
When considering formulation (what do we need to consider in relation to ATSI)
What is Social Displacement Syndrome?
What is disintergration of Identity?
CONDUCTING THE INTERVIEW
1. AIMS ARE TO OPTIMIZE
- Accuracy of information gathered
- Accuracy of interpretation of information
- Accuracy of patient/family understanding
- SETTING
Presence of others
- Cultural interpreter (not translator)
- Family members or support persons
- Ideally second person should be of gender opposite to yours
Environment
- Clinic office vs outdoors vs home
- Sitting arrangement - personal space
- CONFIDENTIALITY
- Issues of confidentiality require careful consideration, especially if transgressions of traditional law are involved, but should not automatically override the request for others to be present. This will also provide you with a source of collateral information. Do not however assume all issues can be readily discussed with family.
- But in Indigenous settings it’s a very different concept of what is an individual. An individual is part of a family and a network of people. So in fact the family and the network determine the future of that individual, or have a big role, whether we recognise that or not.
- RESPECT
- Respect is shown through a commitment to being aware of and working through Aboriginal and Torres Strait Islander protocol.
- For Aboriginal and Torres Strait Islander peoples past, present and future exist together in the same ‘space’/time. Aboriginal views of time are often described as circular rather than linear, as there are no fixed start and end points.
- LANGUAGE
- be mindful of the fact that English may not be the patient’s first language
- talk in a style that is clear and understandable
- use plain English and/or diagrams to clarify your message and aid understanding
- Choose your words so that you avoid medical terminology, acronyms and jargo
- Speak in gentle tones as high or loud tones are often perceived as patronising
- slow your speech down and be clear with your words
- give the patient time to think, and to answer any questions asked
- recognise and respond sensitively to concerns
- summarise what has been said to confirm validity
- consult with an Aboriginal or Torres Strait Islander work colleague or with local community members to build your knowledge of locally suitable and generally accepted words, and to help minimise misunderstanding.
ENGAGEMENT AND ESTABLISHING RAPPORT
- spending time telling the patient (and others involved), a little bit about yourself
- asking about general matters first and illness-related issues later
- asking the patient whether they are comfortable to talk where they are or whether they would prefer a different location/environment
- asking whether the patient would like family members, elder, health worker or traditional healer or other people to be present or consulted during the interview
- if there are several other parties present, addressing the person nominated as the spokesperson as it may be much later in the consultation when the patient will be responsive
- finding out the patient’s interests and strengths
CULTURAL SAFETY
- Issues such as social injustice, racism and mainstream hostility and ignorance are still causing serious suffering and mental ill health for Aboriginal and Torres Strait Islander peoples.
ATSI MENTAL HEALTH WORKERS
ATTITUDES, BEHAVIOUR AND COMMUNICATION
- adjust your communication style to promote patient engagement:
- be calm, respectful and professional
- avoid being confrontational
- allow the patient to take the lead in the conversation
- allow the patient to dictate the pace and the structure of proceedings
- use mirroring and reflection to verify with the patient
- listen, and be truly present
- do not try to fill silences, it’s OK for things to be quiet
- allow people to express emotion
- keep questions short and straight forward
- allow enough time for questions to be considered
- communicate with empathy and use jargon-free language.
DEVELOPING AN INDIGENOUS MENTAL HEALTH PLAN -
- develop a management plan: o in collaboration with others, including the patient, Aboriginal and Torres Strait Islander mental health workers, family, elders and extended family, who have a central role in the life of the individual. o that is culturally appropriate - understand the importance of working with an
- Aboriginal and Torres Strait Islander mental health worker and/or other members of the Aboriginal and Torres Strait Islander workforce to help facilitate and guide the process - communicate with Aboriginal and Torres Strait Islander patients and their families in jargon-free language to promote understanding of the patient’s condition and ongoing treatment needs. .
- Let people make their own choices about their health. -
Consider the impact of the following factors in developing a successful management plan:
oAccess
- Cost of meds
- Transport to meds and appointments
- Do they understand about waiting times
- Adherence
- Understand quantities of medications
- The timings
- Support
- Do they need family support or reminders by family or local health workers
- Adequate diet?
- Any drug interactions?
- Understanding
- Do they understand that the illness can be given to others?
- Do they comprehend what will happen to them overtime – either their illness, alcohol or drug habit
- What do they think they can do to improve things?
ENHANCING KNOWLEDGE OF THE COMMUNITY
- Utilise resources
- Assess existing knowledge
- Understand the context
- Partake in health service orientation
- Take the time to engage
- Be culturally aware
- Create connections
CONSIDERATIONS FOR FORMULATIONS
- Social disadvantage
- Connection with country
- Background issues
- Getting to know someone
- Not having all the information
- Try and build a picture
UNDERSTAND THE CONTEXT
- get a picture of the individuals’ support network, and their strengths - Probably the other important thing to add is that many Indigenous people, despite adversity and hardship, have a lot of resilience and supports.
- get to know, and work with, the individual, their family and their community to achieve an understanding of their background as well as their current situation
- gain an awareness of the history and context within which we are working
- acknowledge the trauma that has happened over many generations for Aboriginal and Torres Strait Islander peoples and its ongoing impact.
COLLECTING DATA
- community
- cultural identity
- language
- family and kinship
- family history
- any relevant information about grief and loss
- any gender related issues
- cultural/spiritual beliefs
- cultural strengths
SYNTHESIZING DATA INTO A MEANINGFUL AND RELEVANT FORMULATION
- build rapport
- unpacking the layers
- brainstorming
- understanding the story line
- patient centred care
- increasing your knowledge base
SOCIAL DISPLACEMENT SYNDROME
First phase of displacement
- Necessity to leave
- Barbed wire phase
- Time spent in refugee/concentration camps
- Uncertainty about own future and fate of loved ones left behind
- Characterised by suppression or repression of normal emotions in reaction to the situation
Liberation and following year phase
- Life after settling in a country with positive living conditions
- Euphoria
- Cognitive and emotional disorganisation to separation of family members
- Early after-effects phase
- When stable and safe refuge is reached
- Conflict between re-organised patterns of living vs older values and unresolved issues of displacement may result in chronic anxiety, depression, loss of self esteem and recurrent nightmares
- Delayed after-effects phase
- Withdrawal and exacerbation of problems from previous phase
- Family conflict from younger children embracing the newer culture and rejecting the past
- Substance abuse
- Survivor guilt
- Recovery phase
- Assimilation and acceptance
- Coping with discrimination
DISINTEGRATION OF IDENTITY
- Rapid change from strong traditions to legacies of despair through:
- Family and community disconnection
- Geographical dislocation
- Lifestyle change
- Loss of spirituality
- Cultural despair
- Inability to develop stable sense of self
- Reduced capacity for future planning and hope
How does spirituality effect ATSI interaction with healthcare?
What are more hesitant to recieve MH care and services rather than females? What are some ways to manage this? e.g group therapy
What considerations need to be considered when interacting with refugees in MH and health services? What are barriers to care for this group of people?
Therefor how is this situation best managed? (caring for refugees)
SPIRITUALITY
- Sense of wellbeing relies on possessing a strong spirit
- Spirit weakened by poor self-care (physical) and disconnection from land and people
- Spirit can be lost or stolen, commonly by evil spirits or witch doctors
- Weakened spirit or possession by evil spirit can cause physical and emotional symptoms
BACKGROUND AND HESITANCE WITH MENTAL HEALTH
- Many men can show reluctance to admit they aren’t coping or acknowledge PTSD and may present with somatic symptoms
- They may be hesitant to participate in counselling due to stigma associated with mental health problems.
- Group approaches that are activity-based can get men talking to each other about problems they are facing adjusting to Australian life.
REFUGEES:
- Many refugees require an interpreter
- May have physical and psychological sequelae associated with pre-migration trauma and torture
- May have spent extended periods in detention in Australia
- May be struggling with practical tasks of settling in Australia
- May not know where to get assistance
- May require an approach to consultation and management that accommodates the impact of past trauma, prior experience of health care, cultural differences and the stresses of resettlement.
- The process for applying for refugee status can be highly stressful and can exacerbate any pre-existing psychological trauma
- Detention centre experiences, uncertain immigration status, limited access to settlement support and barriers to family reuniting can cause stress
THE PROVISION OF SERVICES TO REFUGEE MEN MAY BE LIMITED BY:
- Lack of knowledge about available services
- Difficulties in developing trust
- Reluctance to seek help or disclose a history of torture or trauma
- Costs of care
- Transport
- Employment commitments
- Distrust for authority figures
- Cultural and religious differences
- Language barriers
- Housing, employment, income and social support
- Schooling for children and child care
MANAGEMENT
- Allow time to establish rapport and trust
- Emphasise doctor-patient confidentiality
- Male patients- male doctors, female patients- female doctors
- Establish if there are any cultural or religious factors that need to be accommodated
- Refer to a psychiatrist, psychologist or a specialist service for survivors of torture and trauma
- Community support agencies
WHat are various self-help groups and consumer support groups avaliable for patients? (and how do these assist patients) (e.g financial support, ATODS, housing, self-help groups)
What is Etherapy? And what benefits does it have? Give examples?
What Adjunct treatments/therapies are avaliable for the treatment of patients with mental health illness? (e.g excercise, yoga, mindfullness, psychoeducation, mood gym)
List psychological support services and what they aim to achieve? List 4 (e.g lifeline, beyond blue, headspace, Moodgym)
SELF-HELP GROUPS AND CONSUMER SUPPORT GROUPS
- Address psychological factors (e.g. financial or relationship difficulties) that can exacerbate anxiety or depression
- Address lifestyle factors (e.g. alcohol use, illicit drug use, excessive work, inadequate sleep) that can exacerbate anxiety and depression
- Provides education and support for patients, families and carers about the disease and its treatment
- Provides practical advice to improve management and achieve goals
- Self-help techniques may assist the patient and their family especially for mild to moderate depression including problem solving or stress management
- Social skills training, supported employment programs, accommodation, disability support options
- Education and training assistance
- Social interventions to prevent isolation
- Carer assistance programs- supports and educates families, and provides respite care
- Engagement of patients helps instil realistic optimism and is important for some mental illnesses that impair insight, motivation and cognitionTelephone counselling support
ETHERAPY
- Multiple self-help programmes for management of psychiatric illnesses are available through interactive websites
- These often provide a CBT-based treatment approach
- They are highly effective in patients who complete the programmes, but dropout rates are high
- Incorporating eTherapy into the primary care management plan has been shown to improve completion rates
SELF-HELP BOOKS FOR PSYCHIATRIC ILLNESS
- Many self-help books are available for treating depression and anxiety
- They are recommended, but have limited efficacy
ADJUNCT THERAPIES:
- Mindfulness
- Psychoeducation
- Exercise
- Self-help groups
- Internet cog-met
- Yoga
- Mindfulness- The aim is to accept what can’t be changed and be at peace with it
PSYCHOLOGICAL DISORDERS RESOURCES AND SUPPORT GROUPS:
- Lifeline
- Beyondblue
- Black Dog Institute
- BluePages
- Headspace
- Mindhealthconnect
- Reconnexion
- SANE Australia
- JobAccess- provides advice on employment for people with a disability including mental illness
- Alcoholics Anonymous Australia- people who share their experience, strength and hope with each other to solve their common problems and help each other to recover from alcoholism
