Psychiatry Flashcards

1
Q

Major Psychiatric Conditions

What is the hierarchy of diagnosis?

A
Organic
Psychosis
Affective (mood)
Neurosis (Anxiety)
Personality
No mental illness
(precedence at top)
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2
Q

Major Psychiatric Conditions

Define psychosis?

A

“loss of connection with reality”
Hallucinations
Delusions

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3
Q

Major Psychiatric Conditions

NO external stimulus + Perception

A

Hallucination

Hallucination is when there is no external stimulus but you feel/ hear something that isn’t there.  Q in history taking; “have you ever seen something that others cant see” “have you ever heard voices when no one else is around”

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4
Q

Major Psychiatric Conditions

External stimulus + distorted perception

A

Illusion

Illusion is a misinterpretation of an actual stimulus.

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5
Q

Major Psychiatric Conditions

What is a delusion?

A

false unshakeable belief,
held in the face of evidence to the contrary
outside of the cultural norms for that individual
nature or content
often bizarre (especially in schizophrenia)
can be negative/nihilistic (in context of depression)
or can be grandiose (in context of mania)

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6
Q

Major Psychiatric Conditions

What is schizophrenia?

A

psychotic disorder with positive and negative symptoms
disorder of thinking, perceiving and motivation
Epidemiology

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7
Q

Major Psychiatric Conditions

Epidemiology of schizophrenia?

A

1% lifetime
M=F
M = 20s
F = ea 30s

Course and prognosis
rule of thirds; 1/3 have 1 episode and get better, 1/3 have relapsing and remitting, 1/3 stay ill.

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8
Q

Major Psychiatric Conditions

+ Positive symptoms of schizophrenia?

A
delusions
hallucinations
thought disorder (insertion, withdrawal, broadcast)
sense of being controlled (passivity)
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9
Q

Major Psychiatric Conditions

- Negative symptoms

A

loss of motivation
loss of affect variation (“blunting”)
paucity of thought
loosening of association

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10
Q

Major Psychiatric Conditions

What is depression?

A

Clinically low in mood with cluster of physical, psychological associated symptoms which distort thinking and reduce motivation

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11
Q

Major Psychiatric Conditions

Epidemiology of depression?

A

lifetime prevalence 15%, point prevalence 5%
female:male 2:1
peak age female-40s; male-60-70s

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12
Q

Major Psychiatric Conditions
Sx depression?

Core / Biological

A

Core symptoms
low mood
low energy
inability to enjoy oneself (anhedonia)

Biological Symptoms
poor sleep
poor appetite
poor concentration
poor motivation
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13
Q

Major Psychiatric Conditions

What is BPAD?

A

manic episodes for the diagnosis
vary between the two
can be once or twice per year but can be much more rapid cycling than that

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14
Q

Major Psychiatric Conditions

Sx of mania?

A

elevated or irritable mood
reduced need for sleep
reduced appetite
increased energy
highly motivated
lots of new interests including religious ideas
poor judgment =>risky activities
 libido promiscuity/risky sexual behaviour
psychotic symptoms -grandiose delusions and hallucinations

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15
Q

Major Psychiatric Conditions

What is somatisation?

A

process of converting psychological into physical symptoms
normal
becomes a disorder when the person attributes pathological meaning to it
eg
atypical cardiac pain
atypical pelvic pain

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16
Q

Major Psychiatric Conditions

What is Conversion Disorder?

A
loss of function as a result of extreme psychological distress
loss of 
memory
power
sensory function
speech
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17
Q

Major Psychiatric Conditions

Impending sense of doom
persistent sense of fear, anxiety, apprehension
motor tension
autonomic hyperactivity

A

Anxiety

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18
Q

Major Psychiatric Conditions
What is a
Personality Disorder?

A

When personality traits cause problems in most spheres of the person’s life
Marked difficulties with interpersonal relationships

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19
Q

Major Psychiatric Conditions

What is dementia?

A

Chronic, progressive cognitive impairment, disturbance of higher cortical functions. No clouding of consciousness

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20
Q

Major Psychiatric Conditions

List primary dementias

A

Alzheimers, LBD, FTD

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21
Q

Major Psychiatric Conditions

List secondary dementias?

A

Vascular (CT head), infective (VDRL), metabolic(B12 and folate), endocrine (TFTs)

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22
Q

Major Psychiatric Conditions

Epidemiology of dementia?

A

50% (commonest of all dementia)
30-40% prevalence at 90 years
Female:male 2:1

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23
Q

Major Psychiatric Conditions

Clinical Sx of LBD?

A

Fluctuates in alertness
Visual hallucinatons
PD
Falls, faints

Life expectancy 6yrs

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24
Q

Major Psychiatric Conditions

What is vascular dementia?

A

One or more thrombotic or embolic infarcts
Can be diffuse and/or focal NB CT head often reported as normal unless you state that you are looking for cerebrovascular disease)

Acute onset, stepwise progression

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25
Q

Major Psychiatric Conditions

RFs for vascular dementia?

A

Male, older age, CVS or cerebrovascular disease, DM, hypertension, cholesterol, smoking, ETOH

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26
Q

Major Psychiatric Conditions

What is delirium?

A

Acute fluctuating confusional state with clouding of consciousness, psychotic symptoms and disturbed behaviour

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27
Q

Major Psychiatric Conditions

Sx of delirium?

A

Can be hypoactive (especially poorly detected as not , hyperactive or mixed
fluctuates
can have paranoid ideas
can have hallucinations esp visual
can be very frightening for patient and staff

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28
Q

Assessing Psychiatric Patients

Thought interference – insertion, withdrawal, broadcasting

Auditory Hallucinations – 3rd person, thought echo, running commentary

Bizarre Delusions often persecutory

Ideas of Reference

Passivity Phenomena – made thoughts, feelings and actions

What condition?

A

Schizophrenia

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29
Q

Assessing Psychiatric Patients
Elation or irritable mood

Inflated self esteem

Increased activity

Increased talkativeness

Poor concentration/distractability

Reduced need for sleep

Overfamiliarity

Increased sexual energy

Irresponsible behaviour

+/- mood congruent psychotic symptoms

What condition?

A

Mania

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30
Q

Assessing Psychiatric Patients

List some Sx of RISK?

A

Pointers to higher risk; sociopathic personality disorder, alcohol and substance misuse, psychosis, and particularly any combination of these
Commanding voices, persecutory delusions, and morbid jealousy.
The best predictor of the risk of future violence is a previous history of violence.

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31
Q

Assessing Psychiatric Patients

Central Sx of depression?

A

Depressed mood

Loss of interest or pleasure

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32
Q

Assessing Psychiatric Patients

Biological Sx of depression?

A

Sleep disturbance

Appetite & weight changes

Reduced energy and concentration

Psychomotor changes

Negative thinking
Loss of confidence / self esteem / worthlessness
Self blame / Guilt
Suicidal thoughts
\+/- mood congruent psychotic symptoms
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33
Q

MHA
How long can Rx under Section 2 last?
Is consent required?
Can it be appealed?

A

28 days.
YES
YES

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34
Q

MHA
How long can Rx under section 3 last?
Is consent required?
Can it be appealed?

A

6 months
YES
YES
Need AMPH/or relative, 2 docs,

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35
Q

MHA
How long can Rx under section 4 last?
Is consent required?
Can it be appealed?

A

72 hours
NO
NO
Need AMPH/or relative, 2 docs,

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36
Q
MHA
How long can Rx under section 5(4) last?
Is consent required?
Can it be appealed?
Who can perform these?
A

6 hours
NO
NO
ONLY NURSE NEEDED

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37
Q
MHA
How long can Rx under section 5(2) last?
Is consent required?
Can it be appealed?
Who can perform these?
A

72 Hours
NO
NO
Only one doctor needed.

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38
Q

Psychodynamic Psychotherapy 1

Define Psychotherapy

A

It is a therapeutic process which helps patients understand and resolve their emotional problems by increasing awareness of their inner world and its influence over relationships both past and present.

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39
Q
Psychodynamic Psychotherapy 1
Describe 5 key concepts explored in psychotherapy?
U
D
T
C
D
A
Key concepts
Unconscious
Developmental perspective
Transference
Counter – transference
Psychological defence mechanisms
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40
Q

Psychodynamic Psychotherapy 1

What is the unconscious?

A

Unconscious: mental state that is totally inaccessible to conscious awareness. It is believed that we repress thoughts that are highly exciting and riddled with guilt or shame e.g. aggressive or sexual thoughts, taboo ideas

Unconscious ideas exert continual pressure upon the mind, finding expression in dreams, irrational actions and moods

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41
Q

Psychodynamic Psychotherapy 1

What is the developmental perspective?

A

All forms of psychoanalytic therapy emphasise the importance of adequate parenting in the development of the personality: earlier years are focussed upon

Hypothesis: A secure early attachment to a “good enough” mother will result in the development of the child’s internalised sense of trust

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42
Q

Psychodynamic Psychotherapy 1

What is Freud’s definition of transference?

A

“a whole series of psychological experiences
(that) are revived, not as belonging to the past,
but as applying to the person of the physician
at the present moment”
(Freud, 1905)

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43
Q

Psychodynamic Psychotherapy 1

List some defence mechanisms?

A
Denial
Projection
Splitting 
Projective identification
Regression
Conversion
Repression
Introjection
Identification 
Undoing
Displacement
Humour
Altruism
Sublimation
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44
Q

Psychodynamic Psychotherapy 1
Carole often experiences hostility towards her in
the street. On a bus one day she is sure she is
being kicked by passengers behind her. So
she follows them off the bus and kicks
them from behind, with a triumphant sense of ‘see
how you like it’. On turning round and, without
them needing to say anything, Carole is horrified
to see that she has attacked two elderly women
who look terrified.

What defence mechanism is this?

A

Projection

  1. Denial of unwanted, usually hated aspects of the personality and experience
  2. Splitting off unwanted parts of the Self
  3. Attributing these characteristics onto ‘bad’ others.
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45
Q

Psychodynamic Psychotherapy 1
James is unable to express his anger to his boss for fear of being fired. He gets angry with his girlfriend when he gets home
Which defence mechanism might be in operation?

A

Displacement

Redirection of thoughts and feelings from on person or object to another that poses less threat.

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46
Q

Psychodynamic Psychotherapy 1

Which types of psychiatric illnesses are suited to psychotherapy?

A
Personality Disorders
Complex Depression
PTSD
Psychosomatic Complaints
Eating Disorders
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47
Q

Psychodynamic Psychotherapy 2

Define transference?

A

Transference: Feelings that the patient has in his/her relationship with the therapist, which gives valuable insight into each individual’s unique way of seeing and relating.

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48
Q

Psychodynamic Psychotherapy 2

Define counter transference?

A

Counter-transference; this is the therapists feelings in his/her relationship towards the patient

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49
Q

Psychodynamic Psychotherapy 2

What is transference interpretation?

A

A transference interpretation concerns the live experience in the room between the therapist and the patient. It has the advantage of addressing the here and now, something that is emotionally “hot” and immediate in the therapist/patient relationship.

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50
Q

History Taking + MSE

MSE main points

A

◊ Appearance & Behaviour

◊ Speech

◊ Mood

◊ Thought

◊ Perceptions

◊ Delusions

◊ Cognition

◊ Insight

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51
Q

History Taking + MSE
CRAMP?
Cognition tool

A
Calculation: Division and Subtraction
Right Hemisphere Function: Intersecting pentagons and Clock-face
Abstraction: Proverbs and Similarities
Memory: STM and Long-term memory
Praxis: Wave good-bye and Comb hair
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52
Q

History Taking + MSE
GOAL
Cognition tool

A
General: Alertness and Co-operation
[STM: Name, Address, Flower to remember]
Orientation: Time and Place
Attention: WORLD backwards and Serial Sevens
Language: Naming and Repetition
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53
Q

History Taking + MSE

RISK Assessment aspects

A

Risk to self: Suicide, DSH, Neglect
Risk to others: Family, carer, general, staff
Risk from others: abuse, Safeguarding
Risk to property
Risk of fire/arson
Risk of falls
Risk of pressure sore , DVT, dehydration, medication

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54
Q

CBT

ABC of CBT?

A

A →B → C

A = Activating Event
B = Beliefs - Thoughts, Attitudes, Assumptions
C = Consequences - Feelings, Emotions,                                                	Behaviors, Actions
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55
Q

CBT

Common thinking distortions seen

A

All or nothing thinking (Dichotomous)
Thinking in absolutes, e.g. good or bad, with no middle ground. Judging people or events using general labels, for example: ‘He’s an idiot., ‘I’m hopeless.

Catastrophizing
Overestimating the chances of disaster; e.g. it’s cancer or if I fail it will be disastrous.

Personalising
Taking responsibility and blame for anything unpleasant even if it has little or nothing to do with you.
e.g. ‘He wouldn’t drink if I was a better wife’

Negative focus
Focusing on the negative and ignoring or misinterpreting positive aspects of a situation. Focus on weaknesses and forgetting strengths. e.g. Anyone could have done that, I missed a bit!

Jumping to conclusions
Making negative interpretations even though there are no definite facts. Predicting the future (fortune telling) and take on the mantle of ‘mind reader’.. e.g. he’s avoiding me, they hate me/It will never work

Living by fixed rules
Having fixed rules and unrealistic expectations. Regularly using the words ‘should’, ‘ought’, ‘must’ and ‘can’t’.

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56
Q

CBT

What is living by fixed rules?

A

Having fixed rules and unrealistic expectations. Regularly using the words ‘should’, ‘ought’, ‘must’ and ‘can’t’.

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57
Q

CBT

Describe what the thought distortion of negative focus refers to

A

Focusing on the negative and ignoring or misinterpreting positive aspects of a situation. Focus on weaknesses and forgetting strengths. e.g. Anyone could have done that, I missed a bit!

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58
Q

CBT

Describe what the thought distortion of dichotomy refers to

A

Thinking in absolutes, e.g. good or bad, with no middle ground. Judging people or events using general labels, for example: ‘He’s an idiot., ‘I’m hopeless.

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59
Q

CBT

Describe what the thought distortion of catastrophizing refers to

A

Overestimating the chances of disaster; e.g. it’s cancer or if I fail it will be disastrous.

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60
Q

CBT

Describe what the thought distortion of personalising refers to

A

Personalising
Taking responsibility and blame for anything unpleasant even if it has little or nothing to do with you. e.g. ‘He wouldn’t drink if I was a better wife’

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61
Q

Biological Management

5 Major drug classes in psychiatry

A

Anxiolytics and Hypnotics

Hypnotics

Antipsychotics

Antidepressants

Mood stabilizers

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62
Q

Biological Management

What is the MoA of benzodiazepines?

A

Anxiolytics &Hypnotics

Act via GABA receptors
GABA is principal inhibitory neurotransmitter
BDZs enhance the effect of GABA
No effect in the absence of GABA or if GABA receptor is blocked
Diazepam is a full agonist at the receptor
Sedative
Anxiolytic
Anticonvulsant

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63
Q

Biological Management

Effects of benzodiazepines?

A

Sedative
Anxiolytic
Anticonvulsant

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64
Q

Biological Management

List clinical uses of benzos

A
Clinical use
Short term use in moderate or severe anxiety
Generalised anxiety disorder
No longer than 4 weeks
Tolerance and dependence
Withdrawal symptoms
Also used in alcohol detoxification
Acute behavioural disturbance.
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65
Q

Biological Management

Beta Blockers drug class

A

Anxiolytics

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66
Q

Biological Management

Contra-indications to B-blockers

A

Asthma / bronchospasm / COPD
Heart failure or heart block
Systolic BP below 90mmHg
Low pulse rate

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67
Q

Biological Management

Hypnotic uses?

A

Short term use
Helps induce sleep
Initial insomnia
Usually effective after ½ - 1 hour

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68
Q

Biological Management

Give examples of hypnotics.

A

Benzodiazepines

Z-drugs; Zopiclone; Zimovane; Zalepon.

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69
Q

Biological Management

MoA of the Z-drugs

A

Zolpidem, Zopiclone, Zalepon
Act via GABA – BDZ receptors
Shorter elimination ½ life
Just as likely to cause rebound insomnia, dependence and neuropsychiatric disturbance
Zopiclone may impair driving performance more than BDZ’s.

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70
Q

Biological Management

BDZ OD Rx?

A

Flumazenil
Competitive antagonist of BDZ’s at the GABA-BDZ receptor
Reverses the CNS depressant effects of benzodiazepine overdose
Intravenous use only
½ life of 1 hour only

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71
Q

Biological Management

How do antipsychotics work?

A

All block DA receptors – D2
Correlation b/w DA receptor binding affinity and clinical potency
Clinical response usually achieved with 60% D2 receptor occupancy
Greater than 80% occupancy predicts likelihood of extrapyramidal side effects (EPSEs)

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72
Q

Biological Management

What are the effects of antipsychotics?

A
Reduce 
hallucinations, 
delusions and 
psychomotor excitement
Also block noradrenergic and cholinergic receptors
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73
Q

Biological Management

What are the risks of 1st generation antipsychotics?

A

Typical or 1st generation
Increased risk of acute EPSE’s, hyperprolactinaemia, tardive dyskinesia.
haloperidol, chlorpromazine

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74
Q

Biological Management

List some 1st generation antipsychotics?

A

haloperidol, chlorpromazine

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75
Q

Biological Management

Why use second generation drugs?

A

Atypical or 2nd generation
Less risk of above
Metabolic side effects
clozapine, olanzapine, risperidone.

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76
Q

Biological Management

List some antipsychotic depot injections?

A
Typical depots (FGA’s) – Clopixol, Depixol
Atypical depots (SGA’s)– Risperdal Consta, Paliperidone
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77
Q

Biological Management

List antidopaminergic effects of antipsychotics?

A

Acute dystonia
Akathisia
Parkinsonian effects
Tardive dyskinesia

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78
Q

Biological Management
What is NMS?
What are the Sx Sx

A
Rare but potentially fatal
All antipsychotics at risk
Sympathetic  overactivity 
Fever, sweating, rigidity, confusion, fluctuating consciousness.
Labile BP, tachycardia
Elevated CPK, Leucocytosis
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79
Q

Biological Management

What are RFs for NMS?

A
High potency typical antipsychotic drugs
Recent or rapid dose increase / reduction
Abrupt withdrawal of anticholinergics
Psychosis 
Organic brain disease
Alcoholism 
Agitation
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80
Q

Biological Management

List common antidepressants?

A
Tricyclic Antidepressants (TCAs)
Selective Serotonin Reuptake Inhibitors (SSRIs)
Monoamine Oxidase Inhibitors (MAOIs)
Others 
NARIs e.g. Reboxetine
SNRIs e.g. Venlafaxine 
NaSSa e.g. Mirtazepine
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81
Q

Biological Management

MoA of TCAs?

A

5-HT & NA re-uptake inhibition
Most will also inhibit re-uptake of Dopamine
Anticholinergic effects
Antihistaminergic effects
Amitriptyline; Nortiptyline; Clomipramine; Lofepramine

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82
Q

Biological Management

Give examples of TCAs?

A

Amitriptyline; Nortiptyline; Clomipramine; Lofepramine

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83
Q

Biological Management

SEs of TCAs?

A

Sedation
Anticholinergic effects
Dry mouth, blurred vision, constipation, urinary retention
Cardiotoxic – QT prolongation, ST elevation, AV block
Discontinuation syndrome
Manic switch in bipolar patients

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84
Q

Biological Management

MoA of SSRIs?

A

Inhibit re-uptake of 5-HT
No significant effect on re-uptake of NA

Most widely prescribed antidepressants
Relative safety in overdose
Relatively less side effects

Fluoxetine; Paroxetine; Sertraline

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85
Q

Biological Management

Give examples of SSRIs?

A

Fluoxetine; Paroxetine; Sertraline

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86
Q

Biological Management

SEs of SSRIs?

A

Nausea +/- Vomitting
Diarrhoea & Headaches
Tolerance usually develops to these within 7-10 days
Sexual dysfunction
Risk of GI bleed, especially in the elderly
Withdrawal syndrome of restlessness/ agitation & increased suicidal ideation

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87
Q

Biological Management

What is serotonin syndrome? What can it be caused by?

A

SSRIs can cause

Acute toxic syndrome due to increased 5-HT activity
Confusion 
Myoclonic jerks, hyperreflexia
Pyrexia, sweating, autonomic instability
GI symptoms
Mood change, mania
Convulsions
Death
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88
Q

Biological Management

MoA of MOAIs?

A

Increase the availability of 5-HT & NA in the synapse

Phenelzine, Tranylcypromine, Isocarboxazid
‘Irreversible’
Tyramine Interaction
After cessation, recovery occurs slowly, over days
Moclobemide - Reversible Inhibitor of MAO-A

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89
Q

Biological Management

Give examples of MOAIs?

A

Phenelzine, Tranylcypromine, Isocarboxazid
‘Irreversible’
Tyramine Interaction
After cessation, recovery occurs slowly, over days
Moclobemide - Reversible Inhibitor of MAO-A

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90
Q

Biological Management

What is the reversible inhibitor of MOAIs?

A

Moclobemide - Reversible Inhibitor of MAO-A

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91
Q

Biological Management

What happens if someone on MOAIs eats mature cheeses; yeast extracts; some red wines; hung game; pickled herrings?

A

Tyramine interaction (Cheese effect)

Tyramine is indirect sympathomimetic

Can cause hypertensive crises;
Flushing
Severe throbbing headache
Severe hypotension
Tachycardia 
Pallor
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92
Q

Biological Management

What foods contain tyramine?

A

Found in; mature cheeses; yeast extracts; some red wines; hung game; pickled herrings

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93
Q

Biological Management

What is antidepressant discontinuation syndrome. When does it occur?

A
Experienced with cessation of antidepressant
All antidepressants at risk
1/3rd of all patients
Receptor rebound
Usually within 5 days of stopping
Variable intensity
Usually mild and self limiting
Occasionally severe & life threatening
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94
Q

Biological Management

What symptoms are seen with antidepressant discontinuation syndrome?

A
Six broad categories;
Affective e.g irritability
Gastrointestinal e.g nausea
Neuromotor e.g ataxia
Vasomotor e.g diaphoresis
Neurosensory e.g paraesthesia
Other neurological e.g increased dreaming
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95
Q

Biological Management

List NaSSA, SNRI, and NRIs examples?

A

Mirtazepine (NaSSA) blocks presynaptic alpha-2 adrenergic receptors. Side effects include drowsiness, increased appetite, and weight gain
Venlafaxine (SNRI) similar side effects to SSRI’s
Reboxetine(NRIs) noradrenaline reuptake inhibitors

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96
Q

Biological Management
What are mood stabilisers used for?
Give examples of some?

A

Lithium and anticonvulsant drugs used to treat bipolar affective disorder
Treats both poles of bipolar disorder without causing a switch
Lithium
Sodium valproate
Carbamazepine
Lamotrigine
Atypical antipsychotics

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97
Q

Biological Management

Give examples of mood stabilisers?

A
Lithium 
Sodium valproate
Carbamazepine
Lamotrigine 
Atypical antipsychotics
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98
Q

Biological Management

Problems of lithium?

A
Narrow therapeutic range (0.4-1mmol/L)
Regular serum levels required
Weekly monitoring at initiation
Then every 3-4 months
Renal function Pre Lithium.
Risk of Hypothyroidism in 10-15%
Lithium toxicity
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99
Q

Biological Management

Describe the procedure of ECT?

A
Electric current:
 passed briefly through the brain
via scalp electrodes applied to the scalp
induces generalised seizure activity
Patient is given a general anaesthetic
Muscle relaxants to prevent body spasms
Bilateral or unilateral electrodes
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100
Q

Biological Management

SEs of ECT?

A

Commonest complaint is of muscle pain – 8%
5% complain of confusion or dizziness at some point
30% complain of headache post ECT
20% will complain of memory problems
No evidence of structural damage to the brain

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101
Q

Biological Management

What are the indications for ECT?

A
Severe depression with psychosis and psychomotor retardation
Alternative treatments have failed
Rapid response is required
Dangerous self neglect
Resistant psychotic depression 

Severe depressive illness
Catatonia
Prolonged or severe manic episode

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102
Q

Biological Management

Contraindications to ECT?

A
Raised ICP
Recent cerebrovascular accident
Unstable vascular aneurysms
Recent MI with unstable rhythm 
Treatment of co-existing medical conditions should be optimised before elective treatment
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103
Q

Psych in the hospital setting

What is the ABC mnemonic for risk assessment?

A

Antecedent
Behaviour
Consequences

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104
Q

Psych in the hospital setting
What questions would be asked when assessing antecedents to suicide?
ABC

A
Impulsive or Planned? 
Last acts? 
Attempts to avoid being found?
Disinhibiting factors? 
Prevailing mood? 
Psychotic symptoms?
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105
Q

Psych in the hospital setting
What questions would be asked when assessing behaviour aspect of suicide?
ABC

A

Method chosen?
Actual lethality v perceived lethality
Drugs or alcohol have additive effect

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106
Q

Psych in the hospital setting
What questions would be asked when assessing the consequences aspect of suicide?
ABC

A
How were they found?
How did they end up in hospital? 
Regret about attempt v failure of attempt? 
Compliance with medical intervention? 
Future plans? 
Hopelessness
What has changed since the attempt?
Protective factors
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107
Q

Psych in the hospital setting

What are the three criteria required for MHA to be applied?

A

Mental Disorder of a nature or degree which warrants detention in hospital (for Ax, & or treatment)
Admission necessary in the interests of at least one of these:
patient’s health
patient’s safety
safety of others

Patient is unwilling or unable to consent to informal admission

ALL 3 of the above have to be present for the MHA to be able to be applied

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108
Q

Psych in the hospital setting

How is capacity assessed?

A

ALL 4 criteria to be fulfilled:
Understand nature and purpose of treatment
Retain information for long enough to make an effective decision
Be able to weigh up the information provided, as part of the decision making process
Communicate the decision

Specific to each decision!

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109
Q

Systemic thinking and Family influences

What are the four P’s for systematic thinking?

A

Predisposing - why this family
Precipitating - why now
Perpetuating - what will keep it going
Protective

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110
Q

Systemic thinking and Family influences

What is high expressed emotion?

A

– emotional over-involvement
– criticism/hostility
– lack of warmth.

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111
Q

MHA MCA

Role of the AMPH?

A

Co-ordinator and takes the lead in the process
Will have detailed local knowledge
Conveys the patient to the hospital
Lots of experience of the practicalities

Doctors make medical recommendations and the AMHP has the final decision.

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112
Q

MHA MCA

What is a section 135?

A

Section 135 (1) – Warrant to search and remove
AMPH applies to Magistrates Court for warrant to gain access to property to look for and remove an ill patient to a ‘place of safety’ (usually a hospital)
Executed by the police who must be accompanied by an AMHP and a doctor.
Can result in 72 hour admission for assessment (Rx under MCA)

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113
Q

MHA MCA

How long can someone be held on a section 135?

A

Section 135 (1) – Warrant to search and remove
AMPH applies to Magistrates Court for warrant to gain access to property to look for and remove an ill patient to a ‘place of safety’ (usually a hospital)
Executed by the police who must be accompanied by an AMHP and a doctor.
Can result in 72 hour admission for assessment (Rx under MCA)

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114
Q

MHA MCA

What is a section 136?

A

Section 136 – Police power of arrest
Power for police to remove a mentally ill person from a public place to a place of safety
Can result in 72 hour admission for assessment. (Rx under MCA)

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115
Q

MHA MCA

How long can someone be held on a 136?

A

Section 136 – Police power of arrest
Power for police to remove a mentally ill person from a public place to a place of safety
Can result in 72 hour admission for assessment. (Rx under MCA)

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116
Q

MHA MCA

What is a section 2, and when is it used?

A

Section 2 (Admission for Assessment)
To be used when the diagnosis is unclear or (rarely) for the non-compliant not
obviously ill patient. Lasts up to 28 days. Requires two doctors, one Section 12
Approved, and an Approved Mental Health Professional (AMHP)

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117
Q

MHA MCA

How long can a patient be held on a section 2?

A

Section 2 (Admission for Assessment)
To be used when the diagnosis is unclear or (rarely) for the non-compliant not
obviously ill patient. Lasts up to 28 days. Requires two doctors, one Section 12
Approved, and an Approved Mental Health Professional (AMHP)

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118
Q

MHA MCA

What is a section 3?

A
Section 3 (Admission for Treatment)
To be used where the diagnosis is clear, usually a known patient. Lasts up to six months and renewable. Requires two doctors, one Section 12 Approved, and an AMHP
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119
Q

MHA MCA

How long can a patient be held on a section 3?

A
Section 3 (Admission for Treatment)
To be used where the diagnosis is clear, usually a known patient. Lasts up to six months and renewable. Requires two doctors, one Section 12 Approved, and an AMHP
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120
Q

MHA MCA

Can a section 2 be appealed?

A

Yes

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121
Q

MHA MCA

Can a section 2 be used post a 135, 136 or 5(2)

A

Yes

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122
Q

MHA MCA

Can a section 3 be renewed?

A

Section can be renewed for 6/12 and then 1 year.

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123
Q

MHA MCA

Can a section 3 be appealed?

A

Legal right to appeal to the MH review tribunal

Can obtain leave under section 17

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124
Q

MHA MCA

No Rx after 3/12 without patient consent or with SOAD treatment review

A

Section 3

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125
Q

MHA MCA

What is a section 4?

A

Admission for assessment in cases of emergency, where waiting for a second doctor would cause undesirable delay.

Requires one doctor and an AMHP

Rarely used – eg. If 2 drs cannot be found in time for S2

Lasts up to 72 hours

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126
Q

MHA MCA

How long can a patient be detained under a section 4?

A

Admission for assessment in cases of emergency, where waiting for a second doctor would cause undesirable delay.

Requires one doctor and an AMHP

Rarely used – eg. If 2 drs cannot be found in time for S2

Lasts up to 72 hours

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127
Q

MHA MCA
What is a section 5(2)?
Who can perform one?

A

Consultant Psychiatrist or nominated deputy (with full GMC registration IE FY1)
Patient suspected to be suffering from a mental disorder
Detention for up to 72 hours
Allows time for an MHA Assessment
Does not authorise treatment for mental disorder.

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128
Q

MHA MCA

What are the criteria of a section 5(2)

A

Must be an inpatient.
Cannot be used in A&E or in outpatients.
To detain a patient receiving care for a physical condition on a general ward who is suspected of having a mental disorder.

  • MCA cannot be used to detain a patient
  • Nurse’s holding power S5(4) lasts up to 6 hours
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129
Q

MHA MCA

What is a community treatment order?

A

Can be used once a patient is discharged from a section 3 (and certain forensic sections)

Gives the Responsible Clinician power to recall the patient back to hospital

Can’t be used to compel a patient with capacity to take treatment

Can last initially for 6 months, renewed for 6/12, then 1 year

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130
Q

MHA MCA

What is the MCA?

A

Framework for decision-making on behalf of people who lack capacity
Identifies how best interests are determined
Applies to people aged 16 and over
Decisions can be wide-ranging, simple or complex and include decisions regarding medical treatment for both physical and mental disorder

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131
Q

MHA MCA

How is capacity assessed?

A

Understand the risks, benefits and alternatives related to their decision

Retain that information long enough to make the decision

Weigh up that information

Communicate the decision through any means

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132
Q

MHA MCA
“No treatment without consent”

                                    Unless.....?
A

1) the person lacks capacity – the MCA applies

Or

2) the person is detained under MHA - which can provide an authority to treat mental disorder

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133
Q

MHA MCA

When is DOLs used?

A

18 years and over, with mental disorder, lacking capacity in relation to their care and Rx and would come to harm if not detained

IE BEING TREATED NOT FOR THE MENTAL HEALTH CONDITION

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134
Q

Define acute stress reaction

A

Acute stress disorder (ASD) is characterized by acute stress reactions that may occur in the initial month after a person is exposed to a traumatic event (threatened death, serious injury, or sexual violation). The disorder includes symptoms of intrusion, dissociation, negative mood, avoidance, and arousal.

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135
Q

Epidemiology of acute stress reaction

A

5-20% point prevalence

Epidemiology varies by types of trauma:

●Motor vehicle accident – 13 percent, 21 percent
●Mild traumatic brain injury – 14 percent
●Assault – 16 percent, 19 percent
●Burn – 10 percent
●Industrial accident – 6 percent, 12 percent
●Witnessing a mass shooting – 33 percent

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136
Q

Aetiology of acute stress reaction

A

Dissociating trauma memories and their associated affect from normal awareness impedes processing of these reactions and thereby leads to subsequent PTSD

Fear conditioning - fear elicited during a traumatic event results in conditioning - subsequent reminders of the trauma elicit anxiety in response to trauma reminders.

Extreme sympathetic arousal at the time of a traumatic event -> release of stress neurochemicals (including norepinephrine and epinephrine) that results in overconsolidation of trauma memories

Most trauma survivors successfully engage in extinction learning in the days and weeks after trauma as they learn that the reminders are not signaling further threat.

Evidence that people who eventually develop PTSD display elevated heart rate in the days after the trauma

People with elevated respiration rate after trauma are more likely to develop PTSD.

These findings underscore the proposal that elevated arousal in the acute phase is important in the etiology of ASD and PTSD.

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137
Q

RFs for acute stress reaction

A

●History of a pretrauma psychiatric disorder
●History of traumatic exposures prior to recent exposure
●Female gender
●Trauma severity
●Neuroticism
●Avoidant coping

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138
Q

Sx of acute stress reaction

A

Acute stress disorder (ASD) typically presents with severe levels of re-experiencing and anxiety in response to reminders of the recent trauma.

Nightmares
Intrusive memories
Vivid recollections
Perceptual memories
Avoidant behaviour 
Flat / blunted affect 
Emotional numbing
Distress on recall of trauma 
Amnesia of core aspects of the event
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139
Q

Ix for acute stress reaction

A

A. Exposure to actual or threatened death, serious injury, or sexual violation in one (or more) of the following ways:
•1. Directly experiencing the traumatic event(s)
•2. Witnessing, in person, the event(s) as it occurred to others
•3. Learning that the event(s) occurred to a close family member or close friend
Note: In cases of actual or threatened death of a family member or friend, the event(s) must have been violent or accidental.
•4. Experiencing repeated or extreme exposure to aversive details of the traumatic event(s) (eg, first responders collecting human remains, police officers repeatedly exposed to details of child abuse)
Note: This does not apply to exposure through electronic media, television, movies, or pictures, unless this exposure is work-related.
●B. Presence of nine (or more) of the following symptoms from any of the five categories of intrusion, negative mood, dissociation, avoidance, and arousal, beginning or worsening after the traumatic event(s) occurred:
•Intrusion symptoms
-1. Recurrent, involuntary, and intrusive distressing memories of the traumatic event(s).

Note: In children, repetitive play may occur in which themes or aspects of the traumatic event(s) are expressed.
-2. Recurrent distressing dreams in which the content and/or affect of the dream are related to the event(s).

Note: In children, there may be frightening dreams without recognizable content.
-3. Dissociative reactions (eg, flashbacks) in which the individual feels or acts as if the traumatic event(s) were recurring. (Such reactions may occur on a continuum, with the most extreme expression being a complete loss of awareness of present surroundings.)

Note: In children, trauma-specific reenactment may occur in play.
-4. Intense or prolonged psychological distress or marked physiological reactions in response to internal or external cues that symbolize or resemble an aspect of the traumatic event(s).
•Negative mood
-5. Persistent inability to experience positive emotions (eg, inability to experience happiness, satisfaction, or loving feelings).
•Dissociative symptoms
-6. An altered sense of the reality of one’s surroundings or oneself (eg, seeing oneself from another’s perspective, being in a daze, time slowing).
-7. Inability to remember an important aspect of the traumatic event(s) (typically due to dissociative amnesia and not to other factors such as head injury, alcohol, or drugs).
•Avoidance symptoms
-8. Efforts to avoid distressing memories, thoughts, or feelings about or closely associated with the traumatic event(s).
-9. Efforts to avoid external reminders (people, places, conversations, activities, objects, situations) that arouse distressing memories, thoughts, or feelings about or closely associated with the traumatic event(s).
•Arousal symptoms
-10. Sleep disturbance (eg, difficulty falling or staying asleep, restless sleep)
-11. Irritable behavior and angry outbursts (with little or no provocation), typically expressed as verbal or physical aggression toward people or objects
-12. Hypervigilance
-13. Problems with concentration
-14. Exaggerated startle response
●C. Duration of the disturbance (symptoms in Criterion B) is three days to one month after trauma exposure.
Note: Symptoms typically begin immediately after the trauma, but persistence for at least three days and up to a month is needed to meet disorder criteria.
●D. The disturbance causes 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 (eg, medication or alcohol) or another medical condition (eg, mild traumatic brain injury) and is not better explained by brief psychotic disorder.

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140
Q

Rx of acute stress reaction

A

Trauma survivors often display symptoms of marked distress in the initial days and weeks after a traumatic event, but then the majority of people tend to adapt, and these symptoms remit.

CBT first line
Mindfullness
Pharmacological - antidepressants may help

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141
Q

Complications of acute stress reaction

A

Although there is considerable variability across studies, between 40 and 80 percent of those with ASD develop subsequent PTSD; that is, half or more of people with ASD do not experience chronic PTSD.

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142
Q

Prognosis of acute stress reaction

A

Trauma survivors often display symptoms of marked distress in the initial days and weeks after a traumatic event, but then the majority of people tend to adapt, and these symptoms remit.

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143
Q

Define adjustment disorder

A

An adjustment disorder (AD)—sometimes called exogenous, reactive, or situational depression—occurs when an individual is unable to adjust to or cope with a particular stress or a major life event. Since people with this disorder normally have symptoms that depressed people do, such as general loss of interest, feelings of hopelessness, and crying, this disorder is sometimes known as situational depression. Unlike major depression, the disorder is caused by an outside stressor and generally resolves once the individual is able to adapt to the situation.

According to the DSM-IV-TR, if the AD lasts less than six months, then it may be considered acute. If it lasts more than six months, it may be considered chronic.

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144
Q

Epidemiology of adjustment disorder

A

5–21% among psychiatric consultation services for adults
M:F 1:2
M=F in adolescents

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145
Q

Aetiology of adjustment disorder

A

A stressor is generally an event of a serious, unusual nature that an individual or group of individuals experience. The stressors that cause adjustment disorders may be grossly traumatic or relatively minor, like loss of a girlfriend/boyfriend, a poor report card, or moving to a new neighborhood. It is thought that the more chronic or recurrent the stressor, the more likely it is to produce a disorder. The objective nature of the stressor is of secondary importance. Stressors’ most crucial link to their pathogenic potential is their perception by the patient as stressful. The presence of a causal stressor is essential before a diagnosis of adjustment disorder can be made.

There are certain stressors that are more common in different age groups:

Adulthood:

Marital conflict
Financial conflict
Health issues with oneself, partner or dependent children
Personal tragedy such as death or personal loss
Loss of job or unstable employment conditions e.g. corporate takeover or redundancy
Adolescence and childhood:

Family conflict or parental separation
School problems or changing schools
Sexuality issues
Death, illness or trauma in the family

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146
Q

RFs for adjustment disorder

A

Younger age;

More identified psychosocial and environmental problems;

Increased suicidal behaviour, more likely to be rated as improved by the time of discharge from mental healthcare;

Less frequent previous psychiatric history;

Shorter length of treatment.

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147
Q

Sx of adjustment disorder

A

According to the DSM IV-TR, the development of the emotional or behavioral symptoms of this diagnosis have to occur within three months of the onset of the identifiable stressor(s).[6] Some emotional signs of adjustment disorder are:

Sadness
Hopelessness
Lack of enjoyment
Crying spells
Nervousness
Anxiety
Worry
Desperation
Trouble sleeping
Difficulty concentrating
Feeling overwhelmed and thoughts of suicide
Reckless driving
Ignoring important tasks such as bills or homework
Avoiding family or friends
Performing poorly in school/work
Skipping school/work
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148
Q

Ix for adjustment disorder

A

The DSM-5 defines adjustment disorder as “the presence of emotional or behavioral symptoms in response to an identifiable stressor(s) occurring within 3 months of the onset of the stressor(s)”

One or both of these criteria exist:

Distress that is out of proportion with expected reactions to the stressor
Symptoms must be clinically significant—they cause marked distress and impairment in functioning
Further, these criteria must be present:

Distress and impairment are related to the stressor and are not an escalation of existing mental health disorders
The reaction isn’t part of normal bereavement
Once the stressor is removed or the person has begun to adjust and cope, the symptoms must subside within six months.

6 SUBTYPES:

The DSM-5 criteria for each type of adjustment disorder relate to its specific symptoms. The manual specifies adjustment disorder with

Depressed mood
Anxiety
Mixed depressed mood and anxiety
Disturbance of conduct
Mixed disturbance of emotions and conduct
Unspecified (symptoms don’t quite meet the criteria for any of the defined categories)

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149
Q

Rx of adjustment disorder

A

Psychotherapy - for symptom relief and behaviour change
Counselling
Crisis intervention
Family therapy
Behaviour therapy
Self-help group treatment
= are often used to encourage the verbalization of fears, anxiety, rage, helplessness, and hopelessness.

Small doses of antidepressants / anxiolytics

Because natural recovery is the norm, it has been argued that there is no need to intervene unless levels of risk or distress are high.

FOR CHILDREN:
offering encouragement to talk about their emotions;
offering support and understanding;
reassuring the child that their reactions are normal;
involving the child’s teachers to check on their progress in school;
letting the child make simple decisions at home, such as what to eat for dinner or what show to watch on TV;
having the child engage in a hobby or activity they enjoy.

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150
Q

Prognosis of adjustment disorder

A

Because natural recovery is the norm, it has been argued that there is no need to intervene unless levels of risk or distress are high.

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151
Q

Define prolonged grief disorder

A

Prolonged grief disorder (PGD) refers to a syndrome consisting of a distinct set of symptoms following the death of a loved one. The affected person is incapacitated by grief, so focused on the loss that it is difficult to care about much else. He or she often ruminates about the death and longs for a reunion with the departed, while feeling unsure of his or her own identity and place in the world. The victim will develop a flat and dull outlook on life, feeling that the future holds no prospect of joy, satisfaction or pleasure. The bereaved person who suffers from PGD feels devalued and in constant turmoil, with an inability to adjust to (if not a frank protest against) life without the beloved.

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152
Q

Epidemiology of prolonged grief disorder

A

PGD is relatively rare – experienced by about 10 percent

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153
Q

Aetiology of prolonged grief disorder

A

Loss of a loved / close person

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154
Q

RFs for prolonged grief disorder

A
Miscarriage
Childhood separation anxiety
Controlling parents
Parental abuse or death
Close kinship relationship to the deceased (e.g., parents)
Insecure attachment styles
Emotional dependency
Lack of preparation for death
Death in hospital
No shortened rapid eye movement (REM) latency
Activation of the nucleus accumbens
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155
Q

Sx of prolonged grief disorder

A
Intense yearning 
Identity confusion
Difficulty accepting the loss
Bitterness
Emotional numbness
Loss of trust 
Feeling of trapped in grief

These are present every day, causing significant distress and functional impairment, and remaining intense, frequent, and disabling for six months or more after the death.

Normal grief differs from PGD in that it is not as intense, persistent, disabling and life-altering and is not experienced as a severe threat to the survivor’s identity, sense of self-worth, feeling of security, safety or hopes for future happiness.

156
Q

Ix for prolonged grief disorder

A

Category
A) Event - bereavement
B) Yearning to disabling degree
C) Cognitive, emotional and behavioural symptoms: (need 5)
Confusion about role in life
Difficulty accepting loss
Avoidance of reminders of reality of the loss
Loss of trust
Bitterness/anger
Difficulty moving on
Numbness
Feeling that life is unfulfilling/empty/meaningless
Stunned/shocked
D) Timing: diagnosis should not be made until 6 months have elapsed
E) Impairment on daily functioning
F) Disturbance is not accounted for by another mental illness

157
Q

Rx of prolonged grief disorder

A

TCAs

Interpersonal psychotherapy

158
Q

Prognosis / complications prolonged grief disorder

A

Elevated rates of suicidal ideation and attempts
Cancer
Immunological dysfunction
Hypertension
Cardiac events
Functional impairment
Adverse health behaviors
Reduced quality of life in adults and in children
Increased health service use and sick leave

159
Q

Define generalised anxiety disorder

A

Generalised anxiety disorder (GAD) is defined as at least 6 months of excessive worry about everyday issues that is disproportionate to any inherent risk, causing distress, or impairment.

The worry is not confined to features of another mental disorder, or as a result of substance abuse or a general medical condition. At least 3 of the following emotional, somatic, and cognitive symptoms are present most of the time: restlessness or nervousness, being easily fatigued, poor concentration, irritability, muscle tension, or sleep disturbance. Other common complaints are autonomic in nature, such as sweating, lightheadedness, palpitations, dizziness, and epigastric discomfort.
Anxiety may be ‘free-floating’ (i.e., not restricted to, or even strongly predominating in, any particular environmental circumstances).

160
Q

Epidemiology of generalised anxiety disorder

A

76% of people who had more than 1 mental disorder for 12 months had GAD.

Estimates for 1-month prevalence in Europe are 0.2% to 1% with a lifetime prevalence of 0.1% to 21.7%.

In women, there is an increased risk of GAD during pregnancy (with a 4.1% prevalence during pregnancy overall according to one large study) and also in the postnatal period (5.7% prevalence in the first 24 weeks after birth).

161
Q

Aetiology of generalised anxiety disorder

A

No single aetiology exists, but an increase in minor life stressors, presence of physical or emotional trauma, and genetic factors seem to contribute.

162
Q

RFs generalised anxiety disorder

A
STRONG
Fix
Physical/emotional stress
Hx physical or emotional trauma
Other anxiety disorder
Female

WEAK
DM
Adolescence / early adulthood

163
Q

Sx of generalised anxiety disorder

A
COMMON
RFs
Excessive worry for at least 6 months
Anxiety not confined to another disorder
Anxiety not due to medication/substance
Not due to organic cause
Muscle tension
Sleep disturbance
Fatigue
Restlessness
Irritability 
Poor concentration 
OTHER COMMON
Headache
Sweating 
Dizziness
GI symptoms 
Muscle aches 
Increased heart rate 
SOB
Trembling
Exaggerated startle response
Chest pain
164
Q

Ix generalised anxiety disorder

A

DSM-V
Excessive anxiety and worry regarding several issues are present most of the time for more than 6 months.

Difficulty controlling worry.

At least 3 symptoms associated with anxiety for the past 6 months:

Restlessness or feeling on edge
Easily fatigued
Difficulty concentrating
Irritability
Muscle tension
Sleep disturbance (difficulty falling or staying asleep, or restless sleep).
Anxiety causes significant distress or impairment in social, occupational, or other important areas of functioning.

The disturbance is not better explained by another mental disorder (e.g., worries about having a panic attack in panic disorder), worries about embarrassment in public (social phobia), fear of contamination (OCD), separation anxiety; fear of gaining weight (anorexia nervosa), multiple physical complaints (somatisation disorder), fear of a serious illness (hypochondriasis), or exclusively due to PTSD.

The disturbance is not attributable to the physiological effects of a substance or another medical condition.

CONSIDER:
TFTs
Urine drug screen
24hr urine collection
Pulmonary FTs
ECG
Echocardiogram 
EEG
165
Q

Rx of generalised anxiety disorder

A
1) Pharmacology:
Sertraline
Duloxetine 
...basically any SSRI/SNRI/TCA
2) BDZ - clonazepam
CBT
Applied relaxation
Meditation training 
Sleep hygiene education
Exercise
Self-help 
Augmented treatment 

PREGNANT
CBT 1st line
Then all the other non-pharmacological interventions

166
Q

Complications/prognosis of generalised anxiety disorder

A

Depression
Substance abuse
Over-use of healthcare resources

Pharmacotherapy should be given for at least 6 to 8 weeks to determine efficacy, and in the author’s clinical experience should be continued for at least 12 months if effective.

Depression co-occurs in 30% to 60% of patients and increases the risk for suicidality. Patients with depression and GAD have a more severe and prolonged course.

167
Q

A 25-year-old woman presents to her general practitioner with complaints of muscle tension, especially in her shoulders and neck, contributing to tension headaches. She describes decreased sleep, chronic fatigue and constant restlessness in addition to poor concentration at work, with repeated run-ins with her co-workers. She has been a worrier since childhood, with worsening bouts when under stress; currently she reports having a hard time controlling her worry, which extends into several topics. Physical examination reveals a healthy, tense woman with normal vital signs and generalised muscular tension. She does not abuse substances, and medical history is unremarkable.

A

generalised anxiety disorder

168
Q

Patients may try to reduce anxiety by drinking alcohol or taking central nervous system depressants, thereby increasing the risk of substance abuse and dependence. Depression or panic attacks may co-occur, with symptoms including shortness of breath, palpitations, hot and cold flushes, or fear of dying or going crazy.

A

generalised anxiety disorder

169
Q

Define anxiety disorder: obsessive compulsive disorder

A

Obsessive-compulsive disorder (OCD) is a frequently debilitating and often severe anxiety disorder that affects approximately 2% of the population.

OCD is characterised by: (a) obsessions, defined as unwanted, disturbing, and intrusive thoughts, images, or impulses that are generally seen by the patient as excessive, irrational, and ego-alien; and (b) compulsions, defined as repetitive behaviours and mental acts that neutralise obsessions and reduce emotional distress.

OCD causes significant distress and impairment in daily functioning and can have a substantial effect on the sufferer’s quality of life.

Obsessions and/or compulsions that cause marked distress, are time consuming (take more than 1 hour per day), or interfere substantially with the person’s normal routine, occupational or academic functioning, or usual social activities or relationships.

If the content of the obsessions or compulsions is limited to the scope of another psychiatric disorder, such as an obsession with food in the context of an eating disorder, then an additional diagnosis of OCD should not be made.

The Yale-Brown Obsessive-Compulsive Scale is useful in grading severity initially and following trials of therapy.

Patients tend to seek treatment from 3 to 4 doctors and spend on average around 9 years in treatment before a correct diagnosis is made. The average amount of time that lapses between onset of symptoms and appropriate treatment is 17 years.

Cognitive behavioural therapy in the form of exposure and response prevention, alone or in combination with a selective serotonin-reuptake inhibitor (SSRI) or clomipramine, is a first-line therapy.

While controlled trials with SSRIs have demonstrated a selective efficacy in OCD, up to 40% to 60% of patients do not have a satisfactory outcome.

170
Q

Epidemiology of anxiety disorder: obsessive compulsive disorder

A

OCD affects 2% to 3% of the population and it is estimated that OCD is the fourth most common mental illness.
M=F
22-36yo onset

171
Q

Aetiology of anxiety disorder: obsessive compulsive disorder

A

OCD most probably results from a confluence of aetiologies. Genetic factors are important, as monozygotic twins are much more likely to exhibit OCD symptoms than dizygotic twins.

In addition, there is an association between pregnancy and the development of obsessive-compulsive symptoms. In one study of 59 female OCD patients, 39% of participants described an onset of OCD symptoms during pregnancy.

172
Q

RFs for anxiety disorder: obsessive compulsive disorder

A

STRONG
FHx
PANDAS - PANDAS (paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection) - OCD symptoms can be caused or exacerbated by an autoimmune reaction in which antibodies to beta-haemolytic streptococci cross-react with proteins in the basal ganglia

WEAK
Pregnancy
Male - earlier onset/more chronic/Rx resistance

Rx Resistance RFs:
Earlier onset
Hospitalisations for OCD
Higher freq. complulsions
Schizotypical personality disorder 
Tic disorder 
Poor motor control 
Sensory perceptual difficulties
173
Q

Sx of anxiety disorder: obsessive compulsive disorder

A

COMMON

Obsessions:

Intrusive, unwanted, anxiogenic thoughts that result in marked distress.

Patient typically recognises that these thoughts are irrational.

Common obsessions include fear of contamination, need for symmetry or exactness, fear of causing harm to someone, sexual obsessions, religious obsessions, fear of behaving unacceptably, and fear of making a mistake.

Compulsions:

Repetitive behavioural or mental acts that are designed to neutralise the anxiety that results from obsessions.

Compulsions result in a temporary relief of anxiety and are self-reinforcing.

Common behavioural compulsions include cleaning, hand washing, checking, ordering and arranging, hoarding, and seeking reassurance from others.

Common mental compulsions include counting, repeating words silently, ruminating, and attempting to ‘neutralise’ thoughts.

174
Q

Ix for anxiety disorder: obsessive compulsive disorder

A

Structured clinical interview for the DSM (SCID)
- The SCID is a structured instrument that can be used to determine whether or not a patient meets DSM criteria for OCD.

Yale-Brown Obsessive-Compulsive Scale
- Not a diagnostic tool, but a reliable measure of symptom severity. Should be administered at the start of treatment and periodically (every 6 months) in order to track treatment progress. [

175
Q

Rx of anxiety disorder: obsessive compulsive disorder

A

Mild-Mod
CBT 1st line - involves exposure and response prevention
Pharm:
Fluoxetine / Sertraline / clomipramine

At 12 weeks, if a patient has exhibited a partial response to an agent, one might prefer to utilise augmentation strategies instead of switching to a different drug. Augmentation strategies include: increasing the current medication to the highest tolerable dose; using intravenous citalopram or clomipramine (however, these formulations are not available in general clinical settings in the US); or combining regimens (e.g., selective serotonin-reuptake inhibitor [SSRI] plus clomipramine, [90] or SSRI plus an antipsychotic medication).

Caution is advised when using citalopram, due to association with QT interval prolongation. Special caution is advised in those over 60 years of age or in those who have pre-existing potential for QTc prolongation/arrhythmias either due to inherent disease or due to other concomitant medications.

If the patient does not respond to the highest tolerated dose of SSRI for 12 weeks, augmentation with an antipsychotic medication may be considered.

176
Q

Complications / prognosis of anxiety disorder: obsessive compulsive disorder

A

Suicide

177
Q

A 45-year-old woman presents describing obsessive concerns that she has harmed or will accidentally harm someone. Her most debilitating symptoms occur in the context of driving. She reports being troubled by obsessions and compulsions for approximately 4 hours each day. When she drives over a pothole or speed bump, she experiences overwhelming uncertainty about whether she may have accidentally run over a child. In an attempt to ease the anxiety she drives back and forth on her street in order to search for any indication that a child has been injured. When she completes these compulsions, she returns to her home and engages in checking compulsions for any evidence of blood or clothing under her car or on her tyres. She then calls her husband repeatedly at work to ask for reassurance that she has not harmed anyone. Although she is aware that her concerns are irrational, she finds it very difficult to resist her impulses to engage in these rituals.

A

anxiety disorder: obsessive compulsive disorder

178
Q

A 45-year-old woman presents describing obsessive concerns that she has harmed or will accidentally harm someone. Her most debilitating symptoms occur in the context of driving. She reports being troubled by obsessions and compulsions for approximately 4 hours each day. When she drives over a pothole or speed bump, she experiences overwhelming uncertainty about whether she may have accidentally run over a child. In an attempt to ease the anxiety she drives back and forth on her street in order to search for any indication that a child has been injured. When she completes these compulsions, she returns to her home and engages in checking compulsions for any evidence of blood or clothing under her car or on her tyres. She then calls her husband repeatedly at work to ask for reassurance that she has not harmed anyone. Although she is aware that her concerns are irrational, she finds it very difficult to resist her impulses to engage in these rituals.

A

anxiety disorder: obsessive compulsive disorder

179
Q

Define panic disorder

A

Panic disorder is characterised by recurring unexpected panic attacks over a 1-month period and associated worry about their recurrence or implications. Panic attacks involve the sudden onset of intense physical and cognitive symptoms of anxiety that may be triggered by specific cues or occur unexpectedly. Panic disorder may also be characterised by avoidance of situations that may trigger the panic sensations.

180
Q

Epidemiology of panic disorder

A

8-28% have a panic attack
Panic disorder prevalence - 2% to 3% for adolescents and adults
Develop in 20s
Men present earlier than women
Panic disorder is highly comorbid with other anxiety, mood, and substance use disorders, including nicotine dependence.
Comorbidity with depressive disorders is common (33% to 85%) especially among those with agoraphobia.

181
Q

Aetiology of panic disorder

A

Genetic factors: the risk of panic disorder increases fivefold among first-degree relatives.

Environmental factors: panic attacks, by definition, initially occur unexpectedly. However, they do happen in context, and thus certain features of the environment may become triggers that elicit intense anxiety symptoms. Significant histories of unpredictable and uncontrollable life stressors and trauma are common.
Psychological factors: cognitive behavioural models of panic assume that repeated, unpleasant experiences with external (e.g., crowds) and internal (e.g., rapid heartbeat) triggers lead to selective attention and hypervigilance.

182
Q

RFs for panic disorder

A
STRONG 
Hx in 1st deg relative
18-39
Female
White
Major life event 
Comorbid disorders
Psychological factors 
Asthma/respiratory association
CS + caffeine use 

WEAK
Cardiac abnormalities

183
Q

Sx of panic disorder

A
COMMON
RFs
Unexpected onset - Up to 70% of patients report at least 1 nocturnal panic attack.
Apprehension/worry
Behavioural avoidance 
Tachycardia 
PRIME-MD panic screen (4 points)
Panic disorder severity scale - A 7-item measure assessing the frequency, avoidance, degree of distress, and functional impairment of panic attacks
Palpitations, chest pain, discomfort
Nausea
Abdo pain
Dizziness
Perceptual abnormality [derealisation/depersonalisation]
Hyperventilation, shortness of breath, smothering sensations, and a feeling of choking.
Paraesthesias
Muscle shaking 
Sweating
Fainting
Chills/hot flushes
184
Q

Ix for panic disorder

A

Clinical

Potential:
ECG
BG - hypoglycaemia rule out
TFTs - hyper
Toxicology screen
185
Q

Rx of panic disorder

A

ACUTE
Benzo+reassurance

ONGOING
1. CBT - CBT for panic disorder involves a combination of education, self-monitoring, relaxation training, challenging negative styles of thinking, situational exposure training, and systematic exposure to uncomfortable physical sensations.
2. SSRI/SNRI
Sertraline/fluoxetine/citalopram
3. BDZ - lorazepam/clonazepam - although physiological dependence can occur in as little as 2 to 4 weeks.
Dual therapy

186
Q

Complications / prognosis of panic disorder

A

Serotonin withdrawal syndrome
Substance abuise
Ambivalence towards mental health referral or excessive fears of cognitive behavioural psychotherapy

187
Q

A 22-year-old woman in her first year of college reports waking in the middle of the night with a pounding heart, hot flushes, smothering sensations, and intense nausea. The attack came suddenly and unexpectedly, was not in reaction to a nightmare, and the symptoms subsided within a few minutes. Over the last few months, she is feeling more anxious and has experienced similar episodes each week at varying levels of intensity. She is worried that she might be on the verge of a “nervous breakdown” and admits to being overly aware of her “fast breathing and heart rate”.

A

panic disorder

188
Q

A 38-year-old man presents to the emergency department for the second time in 4 weeks with sudden-onset chest pain, tachycardia, shortness of breath, dizziness, and sweating. He says he is afraid of having a heart attack and is afraid of “losing his mind”. He is no longer driving his car and has started avoiding crowded areas for fear of inducing further attacks. Past medical history is unremarkable. Cardiac testing during both admissions is normal.

A

panic disorder

189
Q

Define social anxiety disorder

A

The condition involves an excessive fear of social or performance situations. The individual will often fear being embarrassed, or worry about being negatively evaluated by others. Anticipatory anxiety and situational avoidance are common, and the individual may endure social situations with a high level of discomfort. The scope of the anxiety may be focused on specific types of social situations or generalised to almost any social encounter.

Characterised by an excessive fear of social and performance situations where the individual is afraid of being embarrassed or negatively evaluated by others.

One of the most common and impairing mental disorders with a high risk for comorbid anxiety, depressive, and substance-use/abuse-related disorders.

Assessment is based on self-reporting, clinical interview, and behavioural observation.

Selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and cognitive behavioural therapy are considered the first-line treatments.

Long-term clinical management and monitoring are typically required, as patients are prone to relapse following discontinuation of acute treatment.

190
Q

Aetiology of social anxiety disorder

A

A combination of biological, familial, experiential, and cultural factors contributes to the risk of developing social anxiety.

Temperament factors, such as behavioural inhibition, shyness, introversion, and anxiety sensitivity, have also been implicated as risk factors for social anxiety.

Familial factors, such as parental over-control, over-protection, and lack of warmth, may also contribute to insecure attachment styles and social anxiety risk.

Adverse life experiences, including transitions, humiliation, losses, and poverty, may also play a role in the development of social anxiety.

Conditioning models of anxiety propose that multiple social cues can develop the capacity to elicit anxiety-related symptoms. Learned escape and avoidance behaviours maintain the anxiety, interfere with skill development, and can lead to increasing levels of functional impairment and disability over time. Similarly, safety behaviours, such as only entering into social situations with a trusted companion, averting eye contact, and staying on the periphery of social gatherings, may also maintain anxiety-related impairments.

191
Q

Epidemiology of social anxiety disorder

A

Late childhood - adolescence
5-12% lifetime estimates
The prevalence of social anxiety in pre-adolescence is 3.5%, with rates increasing to about 14% during adolescence
Gender distribution tends to be generally equal during pre-adolescence, becoming increasingly more common in females than in males through adolescence and adulthood.

192
Q

RFs for social anxiety disorder

A
STRONG
Psychiatric comorbidity
Genetic
Temperamental factors
Parenting style
Psychological disorder
Life stressors
Environmental factors
193
Q

Sx of social anxiety disorder

A
COMMON
RFs
Anticipatory anxiety 
Tachycardia
Hyperventilation
Sweating
Flushing
Muscle tension
Post-event processing 
Attentional biases
Social skills deficits 
Crying, tantrums or freezing
194
Q

Ix for social anxiety disorder

A

Clinical - DSMV

Diagnostic and statistical manual of mental disorders, fifth edition (DSM-5)

Marked fear or anxiety in one or more social or performance situations in which the person is exposed to possible scrutiny by others.
Fear that they will act in a way (or show anxiety symptoms) that will be humiliating, embarrassing, or they will be rejected by others.
Exposure to the feared social situation almost invariably provokes anxiety or a panic attack. The fear or anxiety is out of proportion to the actual threat of the situation.
Feared social or performance situations are either avoided or endured with intense anxiety or distress.
The fear or avoidance interferes significantly with the person’s normal routine, occupational functioning, relationships, or social activities.
For children and adults, the duration of symptoms must be at least 6 months.
The fear or avoidance is not due to the direct physiological effects of a substance or a general medical condition, and is not better accounted for by another mental disorder.
If a general medical condition or another mental disorder is present, the social anxiety disorder is unrelated to it.
The diagnosis can be further specified as ‘performance only’ if the anxiety is focused specifically on public speaking or performing in public to a degree that there is marked functional impairment (e.g., interfering with ability to work).

In children:

The anxiety must occur in peer settings, and not just in interactions with adults
The anxiety may also be expressed by crying, tantrums, ‘freezing’, or shrinking from social situations with unfamiliar people.

Consider
Blood glucose (hypo)
TSH - normal/abnormal
Urine/blood toxicology

195
Q

Rx of social anxiety disorder

A

1) 12 week CBT

1) Sertraline
Citalopram
Fluoxetine
Duloxetine
For those patients who prefer pharmacological therapy, SSRIs or SNRIs are first-line therapies.
The treatment period needs to be at least 12 weeks.
Following response, treatment for up to 12 months or longer is recommended to prevent relapse.
2) Clonazepam/alprazolam - caution abuse
3) MAOI - phenelzine or moclobemide
3) Gabapentin/pregabalin

196
Q

Prognosis / complications of social anxiety disorder

A

This is among the most common and disabling mental disorders. It can be chronic, and access to treatment is often delayed or avoided. About 70% to 80% of cases have a lifetime history of concurrent anxiety, depression, and/or substance abuse-related disorders.

Relapse may occur in 30% to 50% of patients following medication discontinuation.

Complications:
Serotonin withdrawal syndrome
Substance abuse
Risk of suicide with SSRI Rx

197
Q

Many individuals with social anxiety will often report panic-like sensations brought on by the anticipation of, or actual engagement in, feared situations. Relative to other anxiety disorders, social anxiety is associated with a high risk of comorbid depressive and substance-related disorders. In more severe presentations, the social anxiety is often long-standing and the individual may be avoidant of almost any social encounter, thereby making treatment engagement difficult. Childhood presentations of social anxiety may include behavioural inhibition, crying, tantrums, school refusal, and separation anxiety from caregivers that would be considered developmentally abnormal.

A

Social anxiety disorder

198
Q

Define specific phobia

A

Phobias involve intense fears of specific objects or situations that are triggered upon actual or anticipated exposure to phobic stimuli. Situations in which phobic cues are present are usually avoided or endured with intense anxiety. Excessive fears can cause functional impairments or lifestyle disruptions.

One of the most common and treatable psychiatric conditions.

Marked by fear or anxiety in the presence of a specific object or situation.

Assessments are based on self-reports, clinical interviews, and behavioural observations.

Cognitive behavioural therapy, especially exposure therapy, is considered the first-line treatment for patients with frequent symptoms.

Therapy can also be delivered through self-help, computer-assisted, and/or therapist-assisted modalities.

Patient motivation and available resources are important to consider when reviewing treatment options.

199
Q

Epidemiology specific phobia

A

Lifetime prevalence is between 9% and 13%

12-month prevalence is between 7% and 9%

18 per 1000

F:M 3:1

Approximately 70% of specific phobics report more than one clinically relevant fear.

Animals and heights tend to be the most common stimuli, followed by flying, enclosed spaces, and blood-injection-injury.

200
Q

Aetiology of specific phobia

A

Intense anxiety or unexpected panic responses in the presence of specific objects or situations can mark phobia onset, but this is not necessarily the only causal route to phobic acquisition.

Disgust, either alone or in combination with fear, may be involved in the onset and maintenance of various animal (e.g., spiders, snakes, worms) and blood-injection-injury phobias.

Onset can also occur through indirect means, such as observing others reacting fearfully or receiving negative information.

However, a past event or specific reason for the onset of a phobia is not always possible to identify.

Some phobias (e.g., animal phobias) may arise solely due to the evolutionary threat relevance of their stimuli.

Familial concordance rates among first-degree biological relatives tend to be moderate. Heritability studies suggest that animal and blood-injection-injury phobias have the greatest heritability indices, of roughly 32% and 33%, respectively; however, there is limited research in this area.

201
Q

RFs of specific phobia

A
STRONG
somatisation disorder
anxiety disorders
mood disorders
first-degree relative with phobia
twin with phobia
WEAK
aversive experiences
stress and negative life events
female sex
white ethnicity
parental anxiety and overprotectiveness
negative affectivity and behavioural inhibition
cognitive/attentional bias
202
Q

Sx of specific phobia

A
COMMON
Anticipatory anxiety 
Behavioural avoidance 
Onset during childhood/early adulthood
Nausea 
Dizziness 
Disgust 
Fainting 
Tachycardia
Hyperventilation
Exaggerated startle 
Sleep disruption
203
Q

Ix for specific phobia

A

Self report
Behaviour observation/approach test

DSMV:

Marked and persistent fears that are cued by the presence or anticipation of specific objects or situations.
Exposure to phobic stimuli almost invariably provokes immediate anxiety responses, including increased physiological arousal. In children, anxieties may be expressed by crying, tantrums, freezing, or clinging.
Phobic situations are avoided or endured with intense anxiety or distress.
The fear or anxiety is out of proportion to the actual danger posed by the threatening object or situation.
Avoidance, anxious anticipation and/or distress of feared situations interferes significantly with normal routines, occupations or academic functions, social activities, and/or relationships.
Symptoms have been present for at least 6 months in both children and adults.
Symptoms are not better accounted for by other mental disorders.
Subtypes are specified based on the following phobia categories.

Animal: dogs, snakes, insects, etc.
Situational: driving, flying, enclosed spaces, etc.
Natural environment: storms, heights, dark, etc.
Blood-injection-injury: injections, blood draws, medical procedures, etc.
Other: choking, vomiting, clowns, etc.

204
Q

Rx of specific phobia

A

Education:
Advise patients that fear is an inevitable and normal part of life, but that avoidance behaviours can feed a particular fear to the point it interferes with everyday life and becomes a phobic disorder.

Encourage patients to face their fears, rather than avoid them.

CBT and exposure therapy

If fainting - applied tension

BDZ
Alprazolam
Clonazepam
Lorazepam
Diazepam
205
Q

Prognosis / complications of specific phobia

A
Complications
Anxiety disorder
Depression
Non-compliance with medical regimens
Apprehension/stigma of MH referrals
Resistance to exposure therapy 

Up to 90% of patients reach clinically significant levels of improvement after treatment with exposure therapy.

206
Q

Prognosis / complications of specific phobia

A
Complications
Anxiety disorder
Depression
Non-compliance with medical regimens
Apprehension/stigma of MH referrals
Resistance to exposure therapy 

Up to 90% of patients reach clinically significant levels of improvement after treatment with exposure therapy.

207
Q

Define agoraphobia

A

Agoraphobia is a fear of being in situations where escape might be difficult or that help wouldn’t be available if things go wrong.
Many people assume agoraphobia is simply a fear of open spaces, but it’s actually a more complex condition. Someone with agoraphobia may be scared of:
travelling on public transport
visiting a shopping centre
leaving home

May be related to:
Attachment theory
Spatial theory (discussed)
Evolutionary theory 
Substance abuse (chronic BDZ use)
208
Q

Epidemiology of agoraphobia

A

M:F 1:2
Agoraphobia affects about 1.7% of adults
1/3 of this population with panic disorder have comorbid agoraphobia

209
Q

Aetiology of agoraphobia

A

Individuals without agoraphobia are able to maintain balance by combining information from their vestibular system, their visual system, and their proprioceptive sense. A disproportionate number of agoraphobics have weak vestibular function and consequently rely more on visual or tactile signals. They may become disoriented when visual cues are sparse (as in wide-open spaces) or overwhelming (as in crowds).

210
Q

Sx of agoraphobia

A
rapid heartbeat
rapid breathing (hyperventilating)
feeling hot and sweaty
feeling sick
chest pain
difficulty swallowing (dysphagia)
diarrhoea 
trembling
dizziness 
ringing in the ears (tinnitus)
feeling faint
They'll avoid situations that cause anxiety and may only leave the house with a friend or partner. They'll order groceries online rather than going to the supermarket. This change in behaviour is known as avoidance.

Cognitive symptoms may include fear that:
a panic attack will make you look stupid or feel embarrassed in front of other people
a panic attack will be life threatening – for example, you may be worried your heart will stop or you’ll be unable to breathe
you would be unable to escape from a place or situation if you were to have a panic attack
you’re losing your sanity
you may lose control in public
you may tremble and blush in front of people
people may stare at you
There are also psychological symptoms that aren’t related to panic attacks, such as:
feeling you would be unable to function or survive without the help of others
a fear of being left alone in your house (monophobia)
a general feeling of anxiety or dread
Behavioural symptoms
Symptoms of agoraphobia relating to behaviour include:
avoiding situations that could lead to panic attacks, such as crowded places, public transport and queues
being housebound – not being able to leave the house for long periods of time
needing to be with someone you trust when going anywhere
avoiding being far away from home
Some people are able to force themselves to confront uncomfortable situations, but they feel considerable fear and anxiety while doing so.

211
Q

Ix for agoraphobia

A

A diagnosis of agoraphobia can usually be made if:
you’re anxious about being in a place or situation where escape or help may be difficult if you feel panicky or have a panic attack, such as in a crowd or on a bus
you avoid situations described above, or endure them with extreme anxiety or the help of a companion
there’s no other underlying condition that may explain your symptoms

Check TFTs

212
Q

Rx of agoraphobia

A

Antidepressant medications most commonly used to treat anxiety disorders are mainly selective serotonin reuptake inhibitors. Benzodiazepines, monoamine oxidase inhibitor, and tricyclic antidepressants are also sometimes prescribed for treatment of agoraphobia

CBT
Applied relaxation
Eye-movement desensitisation therapy 
Support groups
Self-help groups 
SSRI SEs:
feeling sick
loss of sex drive (libido)
blurred vision
diarrhoea or constipation
feeling agitated or shaky
excessive sweating
213
Q

Prognosis /complications of agoraphobia

A

Depression
Reclusion
Substance abuse disorder

Resolution in half with treatment

214
Q

Prognosis /complications of agoraphobia

A

Depression
Reclusion
Substance abuse disorder

Resolution in half with treatment

215
Q

Define somatisation and conversion disorders

A

Conversion and somatic symptom disorders are psychiatric conditions that fall under the somatic symptoms and related disorders category of the DSM-5. Somatic symptom and related disorders are those with distressing physical symptoms that are not fully explained by other medical, neurological, or psychiatric disorders (also known as somatisation).

Conversion disorder is characterised by voluntary motor or sensory function deficits that suggest neurological or medical conditions but are rather associated with clinical findings that are not compatible with such conditions. Somatic symptom disorder is characterised by one or more somatic symptoms that are distressing or result in significant disruption of daily life.

To meet DSM-5 criteria, these patients must have 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 levels of anxiety about health or symptoms; excessive time or energy devoted to these symptoms or health concerns. Importantly, even if any one somatic symptom is not continuously present, the state of being symptomatic is persistent (typically more than 6 months).

Somatic symptom and related disorders are psychiatric conditions where patients experience distressing physical symptoms that are not fully explained by other medical, neurological, or psychiatric disorders, as well as abnormal thoughts, feelings, and behaviours in response to these symptoms. They may result from psychological stress that is unconsciously (without awareness) expressed somatically, though the underlying cause is not fully understood.

Risk factors include being female, having a history of abuse or adverse childhood events, and having personality traits of alexithymia (difficulty expressing emotions) or neuroticism. Symptoms that persist with an external focus of control, and without awareness of the psychological and stress-related interplay, can lead to considerable functional impairment and distress.

Diagnosis is made by clinical interview, behavioural observation, physical examination suggestive of pseudoneurological causes, and tests to rule out medical or neurological causes. The diagnosis should not be made solely on the basis of medically unexplained symptoms; rather, it should be based on evidence from the clinical examination and the patient’s abnormal thoughts, feelings, and behaviours in response to the medically unexplained symptoms.

Good doctor-patient relationships and validation of the patient’s suffering are essential for effective management. Treatment includes cognitive behavioural therapy and avoiding unnecessary medicines, tests, and procedures. Diagnosis and treatment of associated comorbid psychiatric conditions benefit overall functioning and recovery.

Long-term management involves interrupting perpetuating factors, maintaining the same doctor, and providing strategies for self-efficacy, distress tolerance, coping, and modulating the interaction of anxiety, stress, and physical symptoms.

216
Q

Epidemiology of somatisation and conversion disorders

A

M:F
1:3

Somatic symptom disorder

10% to 15% of primary care patients have multiple unexplained symptoms that are present for >2 years
The prevalence of somatic symptom disorder is not known but may be around 5% to 7%.

Conversion disorder
5-22 per 100k

10% of patients referred to general neurology outpatient clinics have purely medically unexplained symptoms;

Psychogenic tremor, dystonia, myoclonus, and parkinsonism occurs in 2% to 3% of patients evaluated in specialty neurology clinics;

217
Q

Aetiology of somatisation and conversion disorders

A

Chronic and/or acute intrapsychic (emotional/psychological) stress or conflict, in combination with either emotional processing deficits, avoidance tendencies, or social, cultural, or family taboos against emotional expression, seems to be important in the aetiology of somatisation.

Societal attitudes in which people exhibiting psychological distress are less tolerated than those who are physically ill are also likely to reinforce somatisation.

Cognitively, disturbances in attention and control through dissociation, misattribution, and misinterpretation probably contribute to both conversion and somatic symptom disorder symptoms.

218
Q

RFs for somatisation and conversion disorders

A
STRONG
Hx sex/physical abuse
Hx unstable childhood
Hx trauma related disorders
Female
Alexithyma (difficulty describing emotions)
Neuroticism

WEAK
Previously poor dr-pt relationships

219
Q

Sx of somatisation and conversion disorders

A
COMMON
Unconventional behaviour during Hx
Emotional processing problems
Recent life stressor
Remote life stressor
Multiple illness behaviours 
Unusual neurological deficit (ie not confined to dermatomal distribution)
Give way weakness
Inconsistent exam findings (ie leg weakness on testing an ambulatory pt)
False sensory findings
Distractable symptoms
Inions
220
Q

Ix for somatisation and conversion disorders

A

At initial presentation, all patients should have laboratory testing to rule out potential medical or neurological conditions. Repeat laboratory evaluations may be necessary when new symptoms arise.

In established conversion disorder, it is not necessary to repeat and exhaust all medical evaluations when there is clear evidence of pseudoneurological disorders (and no other indication of neurological conditions) on neurological examination.

Continuous video-EEG monitoring can be useful in establishing a psychogenic non-epileptic seizures diagnosis when typical spells are captured.

standardised personality testing - mental illness trait, personality disorder trait, hypochondriasis, depression, hysteria, anxiety, somatisation, pain disorder, or health concern

221
Q

Rx of somatisation and conversion disorders

A

Eclectic psychotherapy - Includes a combination of cognitive behavioural therapy (CBT), mindfulness, and/or short-term dynamic psychotherapy, interpersonal psychotherapy, re-attribution training, and general psychotherapy. CBT for this group involves reducing physiological arousal through relaxation techniques; enhancing activity regulation through increased exercise, and pleasurable and meaningful activities; pacing activities; increasing awareness of emotions; modifying dysfunctional beliefs; enhancing communication of thoughts and emotions; and reducing spousal reinforcement of illness behaviour.

Psychiatric consultation - Involves regular, rather than as-needed, scheduling of appointments; conducting brief physical examinations focusing on areas of discomfort at each visit; avoiding unnecessary diagnostic procedures, invasive treatments, and hospital admissions; and avoiding explanations such as “Your symptoms are all in your head”

Graded physical exercise
Biofeedback training

Antidepressant:
Duloxetine
Sertraline
Citalopram
Fluoxetine 

SNRIs, nortriptyline, and amitriptyline are used as first line in order to target chronic pain symptoms.

SSRIs include sertraline, citalopram, fluoxetine, paroxetine, escitalopram, and fluvoxamine.

SNRIs include venlafaxine, desvenlafaxine, and duloxetine.

TCAs include nortriptyline, amitriptyline, desipramine, imipramine, and doxepin.

Doses should be started low and increased gradually according to response.

222
Q

Prognosis of somatisation and conversion disorders

A

Depression
Anxiety
Suicide
Substance abuse

223
Q

Complications of somatisation and conversion disorders

A

Conversion disorder

Between 50% and 90% of patients with conversion disorder exhibit short-term resolution of symptoms after reassurance, but up to 25% of these responders relapse or develop new conversion symptoms over time.

Somatic symptom disorder

Reported remission rates range from very low (<10%) to a 50% recovery within 1 year.

224
Q

A 21-year-old woman presents to the accident and emergency department with acute onset of left-sided body twitching after a minor accident in which she hit her head. Physical examination, laboratory investigations, and imaging studies are normal. Over the next several weeks, she begins experiencing episodes of full-body movements. In the week before the initial symptom onset, her boyfriend (for whom she also worked) broke up with her, and she had a conflict with her parents. She and her boyfriend have since reconciled. There is no reported history of abuse, but there is a family dynamic of high expectations of the patient. Neurological examination and EEG during a typical episode are normal.

A

Conversion and somatic symptom disorders

225
Q

A 35-year-old married woman seeks treatment for pelvic pain. On review of systems, she reports several years of various symptoms, including GI problems (constipation, abdominal pain, nausea, and vomiting); headaches; vulvodynia; fatigue; all-over body pains; paraesthesias; and several sensitivities to environmental factors and medications. She has visited the accident and emergency department on several occasions and has been previously admitted to hospital for persistent GI symptoms. Extensive GI work-up, laboratory studies, and laparoscopy to rule out endometriosis have been unrevealing. She reports a stressful childhood, with an alcoholic father and sexual abuse by her grandfather.

A

Conversion and somatic symptom disorders

226
Q

Define PTSD

A

Post-traumatic stress disorder (PTSD) may develop following exposure to 1 or more traumatic events such as deliberate acts of interpersonal violence, severe accidents, disasters, or military action. According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), it is characterised by 4 types of symptoms: intrusions (e.g., flashbacks, intrusive images and sensory impressions, dreams/nightmares); avoidance (e.g., avoiding people, situations, or circumstances resembling or associated with the event); negative alterations in mood and cognition (e.g., feeling alienated from others, constricted affect, diminished interest in significant activities, distorted negative beliefs about oneself or the world, and inability to remember key features of the traumatic event); and alterations in arousal or reactivity (e.g., hypervigilance for threat, exaggerated startle response, irritability, difficulty concentrating, and sleep problems). These symptoms must impair function for a diagnosis to be made.

SUMMARY
Disorder that may develop (either immediately or delayed) following exposure to a stressful event or situation of an exceptionally threatening or catastrophic nature.

According to DSM-5, it is characterised by 4 groups of symptoms: intrusion symptoms, avoidance, negative alterations in cognition and mood, and alterations in arousal and reactivity. These symptoms must impair function for a diagnosis to be made.

More often than not, presentation is comorbid with problems such as depression, anxiety, anger, and substance misuse.

Clinicians should ask whether patients presenting with such symptoms have suffered a traumatic experience.

Assessment should cover physical, psychological, and social needs, and an assessment of risk: this can be facilitated by the use of screening questionnaires and a clinical interview schedule.

Trauma-focused psychological treatments are the most effective treatment. Pharmacotherapy may be used in patients who do not respond to, cannot tolerate, do not want, or do not have access to psychological therapies.

227
Q

Epidemiology of PTSD

A

In the UK, although exposure to potentially traumatic experiences since the age of 16 was reported in only 33% of adults, current PTSD was reported in 3%.

Certain groups are more likely to be exposed to PT

Es: these include military personnel, emergency-service workers, police, and refugees.

228
Q

Aetiology of PTSD

A

People who are at risk of PTSD include those who have been exposed to, or have witnessed, extreme traumatic stressors, such as intentional acts of violence, physical and sexual abuse, accidents, disaster, or military action. People who have experienced threat to their own life or the life of others while in medical care, such as during anaesthesia, complications during childbirth, or as a result of medical negligence, are also at risk.

Emotional processing theory: implicates complex fear structures, which exist in memory and which produce cognitive, behavioural, and physiological reactions when activated. It is argued that in PTSD, these have become pathological. Alterations in beliefs about the world and the self, brought about by difficulties in processing information about the traumatic event, lead to misinterpretation of benign stimuli as dangerous and of the self as being incompetent.

Dual representation theory: based on research into memory processing, and argues the existence of different types of memory, namely verbally accessible memories (VAMs) and situationally accessible memories (SAMs). Whereas VAMs are easily recalled, SAMs remain unconscious until triggered, whereupon they give rise to symptoms such as dreams and flashbacks, during which the emotions felt during the traumatic event are re-experienced with the same degree of intensity.

Cognitive model of PTSD: argues that negative appraisals of the traumatic event lead to the development of views of the world as a dangerous place and of the self as incompetent. This leads to a sense of current threat in which situations are misinterpreted as threatening.

229
Q

RFs for PTSD

A
STRONG
Serious accident
Witness of school violence / domestic
Natural disaster
Terrorist attack 
Torture
Combat exposure
Traumatic brain injury 
Sudden death of loved one 
Molestation
Rape
Victimisation by attacker 
Previous trauma
Multiple major life stressors
Low social support
Hx mental disorder
Hx of drug and alcohol abuse 

WEAK
Female
Younger age

230
Q

Sx of PTSD

A

4 groups of symptoms: intrusion symptoms, avoidance, negative alterations in cognition and mood, and alterations in arousal and reactivity.

Exposure and response to trauma 
Intrusion Sx (re-experiencing)
(e.g., flashbacks, intrusive images and sensory impressions, dreams/nightmares, emotional and physiological reactivity to internal and external cues)
Avoidance Sx - persistent effortful avoidance of reminders of the trauma.
Negative alterations in cognition/mood - diminished ability to experience positive feelings and feelings of closeness to others, persistent negative/distorted beliefs, distorted ideas of blame, loss of interest in significant activities, and inability to recall key aspects of the traumatic event.
Alterations in arousal + reactivity - hypervigilance for threat, exaggerated startle response, irritability, angry outbursts, self-destructive or reckless behaviours, difficulty concentrating, and sleep problems.

OTHER COMMON
Depression
Alchohol/substance misuse
Anxiety

231
Q

Ix for PTSD

A

PTSD Checklist for DSMV
IES - Impact of event scale
TSQ - Trauma screening questionnaire
PSSI - PTSD symptom scale interview version

232
Q

Rx of PTSD

A

Symptoms <3 months = watch and F/U in one month

SEVERE
Trauma focussed CBT
Eye-movement desensitisation and reprocessing - Procedures are based on stimulating the person’s own information processing in order to help integrate the targeted event as an adaptive contextualised memory. People are made ready to attend to the memory and associations while their attention is also engaged by a bilateral physical stimulation (e.g., eye movements, taps, or tones).

Antidepressants are effective in reducing severity of the core symptoms of PTSD as well as associated depression and disability. However, owing to the small effect sizes in systematic reviews, pharmacotherapy should be considered only after trauma-focused psychological treatment has been initiated, or failure to adhere/respond

Sertraline, fluoxetine, amytriptyline

If there is a response to drug treatment, the drug should be continued for at least 12 months before gradual withdrawal, usually over a 4-week period, although some patients may require a longer period of withdrawal.

Non-trauma focussed CBT

233
Q

Complications of PTSD

A
Increase in distress due to exposure therapy 
Anxiety 
Depression
Psychosis
Substance misuse
Suicide
234
Q

Prognosis of PTSD

A

Whereas most people who go through traumatic events experience a brief acute response to the stressful situation and never develop an enduring pathological reaction, a smaller proportion of people will develop PTSD, either alone or complicated with comorbid disorders such as depression, generalised anxiety disorder, or substance abuse.

The average duration of symptoms, if treated, is 36 months, and the average duration of symptoms among those untreated is 64 months. Moreover, while almost 50% experience significant reduction in symptoms, more than one third of people never fully remit.

235
Q

A 25-year-old woman presents to the accident and emergency department complaining of sad mood, nervousness, difficulty falling asleep, and disinterest in her friends for the past 2 months. She notes these symptoms started following a rape by a former male friend after a party. She appears visibly uncomfortable when asked further questions about the attack. The patient has disclosed the incident to some of her peers, but did not report it to authorities. She reports nightmares about the rape, concerns for her safety, difficulties in intimate relationships with men, and repeated avoidance of non-dangerous situations reminding her of the assault.

A

Post-traumatic stress disorder

236
Q

A 35-year-old male combat veteran presents with symptoms of poor sleep, crying episodes, flashbacks, and nightmares. He also reports that his marriage and friendships have been suffering, in addition to poor work performance. When in a bad mood, he tends to smoke cigarettes and drink alcohol. He has tried to overcome these symptoms on his own, but has been largely unsuccessful and now recognises a need for formal help. He speaks openly about his experiences and recognises a direct connection between his combat exposure and current symptoms.

A

Post-traumatic stress disorder

237
Q

Define bipolar disorder

A

Bipolar disorder, previously termed manic depression, is a psychiatric diagnosis characterised by abnormally elevated or irritable mood episode(s) accompanied by disruptive symptoms of distractibility, indiscretions, grandiosity, flight of ideas, hyperactivity, decreased need for sleep, and talkativeness. Manic episodes include a clustering of these symptoms over at least a period of 1 week, and are more disruptive than hypomania (milder symptoms, >4 days’ duration). It is marked by alternating mood elevation (mania or hypomania) and depression.

A recurrent and sometimes chronic mental illness marked by alternating periods of abnormal mood elevation and depression associated with a change or impairment in functioning.

The long-term course of illness is characterised by a predominance of depression, although a history of at least one manic, hypomanic, or mixed episode is required to make the diagnosis of a bipolar disorder.

Diagnosis is based on interviews with the patient and family, using diagnostic criteria for bipolar disorder.

Misdiagnosis of bipolar disorder is common, with unipolar major depressive disorder the most frequent diagnostic error made.

The management of acute mania requires the use of mood stabilisers or atypical antipsychotics, as monotherapy or in combination. There are fewer approved treatment options for acute bipolar depression; traditional antidepressants are not indicated.

Bipolar disorder requires individualising a long-term management plan that includes maintenance medication(s), adjunctive psychosocial therapies, and careful monitoring for any treatment-emergent complications.

238
Q

Epidemiology of bipolar disorder

A

Bipolar disorder is the sixth leading cause of disability in the developed world among those between the ages of 19 and 45 years. The total lifetime cost of illness in the US is estimated at 202 billion US dollars.

1% lifetime prevalence

Thirty-five percent of the patients were symptomatic for >10 years before being accurately diagnosed, with women significantly more likely than men to be misdiagnosed.

Up to 50% of all people with bipolar disorder have been estimated to make at least 1 suicide attempt in their lifetime, with 10% to 15% of untreated patients with bipolar disorder completing suicide.

The lifetime prevalence of any substance misuse disorder among patients with bipolar I disorder is 61%, and among those with bipolar II disorder is 48%; these rates are higher than those observed among patients with schizophrenia (47%), obsessive-compulsive disorder (33%), and major depressive disorder (27%).

239
Q

Aetiology of bipolar disorder

A

The exact aetiology of bipolar disorder is unknown, although the risk for disease is thought to be influenced by several genes.

Family and twin studies substantiate the importance of genetic factors influencing a person’s risk for bipolar disorder, with environmental stressors or triggers being likely to contribute to the phenotypic expression of the underlying mood disorder.

240
Q

RFs for bipolar disorder

A
STRONG
FHx
Onset of mood disorder prior to 20yrs old
Stressful life event
Hx depression
Lifetime history substance misuse
Presence of an anxiety disorder

WEAK
Obesity
CV disease

241
Q

Sx of bipolar disorder

A
COMMON
Major depress episode(s)
Episode(s) of manic or mixed episodes
Episode(s) of hypomania
Grandiosity 
Decreased sleep
Talkative
Flight of ideas/racing thoughts 
Distractibility 
Increased goal directed activity
Excessive involvement in pleasurable activities that have a high potential for adverse consequences
Functional impairment 
No substance misuse
No underlying medical cause 
Not due to somatic antidepressant
242
Q

Ix for bipolar disorder

A

Bipolarity index
Young mania rating scale
Patient Health Questionnaire-9
PRIME-MD - primary care evaluation of mental disorders
FBC
TFTs
Vit D
Lipid derangements often found in patients with BPD
MRI - Test should not routinely be ordered except in the case of new onset of mania or atypical presentations, to rule out an organic aetiology, such as brain tumour or multiple sclerosis.

243
Q

Rx of bipolar disorder

A

IF AGITATED
IM neuroleptic / BDZ
- olanzipine/aripiprazole/Lorazepam

ORAL MONOTHERAPY = MOOD STABILISER OR ATYPICAL ANTIPSYCHOTIC
Lithium / Carbamazepine / risperidone / olanzipine / quetiapine

For patients who do not respond to monotherapy, consideration of dose optimisation and medication adherence is recommended. However, switching to an alternative mood stabiliser or atypical antipsychotic agent should be tried if the original agent is ineffective.

CAN ADD TYPICAL ANTIPSYCHOTIC IF FAILS
EG haloperidol

Patients with symptoms of mania who have not responded to several trials of medications should be considered candidates for either clozapine or ECT.

The addition of psychosocial interventions for bipolar depression has been associated with higher recovery rates at 1 year as well as shorter times to recovery.

244
Q

Complications of bipolar disorder

A
Valproate SE hyperammonaemic encephalopathy 
Lamitrigine induced rash
Obesity SE
Lithium nephrotoxicity 
Lithium induced hypothyroidism 
Metabolic syndrome 
Suicide
Disability 
Lithium toxicity 
SCD 
Atypical SE - Extra-pyrimidal/tardive dyskinesia
Valproate induced hepatitis
Blood dycrasias due to carbemazepine (Aplastic anaemia and agranulocytosis)
245
Q

Prognosis of bipolar disorder

A

Likelihood of recurrence is almost certain, as the vast majority of patients have more than 1 lifetime episode. Although considerable variability exists regarding relapses across individuals with bipolar disorder, it is generally believed and supported by the evidence that, over time, episodes become more frequent and that the euthymic intervals become shorter in between episodes. Subsyndromal symptoms may be chronic for some patients with bipolar disorder.

Manic episodes typically have an abrupt onset, developing over a few days, while depressive episodes usually develop more gradually. With treatment, episodes of mania, depression, or mixed states last for approximately 3 months.

Mortality is higher among patients with bipolar disorder when compared with the general population. The standardised mortality ratio for bipolar disorder due to cardiovascular disease is reported to range between 1.2 and 3.0, while the standardised mortality ratio for suicide is between 14.0 and 23.4.

246
Q

A 20-year-old man presents to the accident and emergency department accompanied by his parents, owing to a change in mental status and behaviour, marked by uncharacteristic argumentativeness, eruptions of laughter, excessive talking, and unusual thoughts. He is being treated for depression and insomnia, and has recently been drinking more alcohol. For the past 2 weeks he has missed college classes, while staying up most nights until 4 or 5 a.m., writing feverishly in several notebooks. When asked, he reports that he is writing 2 novels at the same time and also documenting his accomplishments in an autobiography. He denies any illicit substance use while admitting to increasing alcohol consumption “like all the great novelists do”. Efforts by his family to understand his recent change in thinking and behaviour have been met with loud and rambling discourses, and he angrily accuses them of wanting him to stay “subjugated by the tyranny of depression”.

A

Bipolar disorder in adults

247
Q

A 32-year-old nurse presents to her primary care provider complaining of frequent headaches, irritable bowel, insomnia, and depressed mood. She currently takes no medication and has no history of substance misuse or major medical problems beyond treatment for a single depressive episode in her first year at university. Her physical examination, routine labs, and computed tomography of the brain are all within normal limits. Her family history is notable for several ancestors who have been affected by psychiatric illness, including depression, bipolar disorder, and schizophrenia. Her paternal grandfather and a maternal aunt committed suicide. She has had 3 prior episodes of several weeks’ duration characterised by insubordinate behaviour at work, irritability, high energy, and decreased need for sleep. She regrets impulsive sexual and financial decisions that she took during these episodes, and has recently filed for personal bankruptcy. For the past month her mood has been persistently low, and she has had reductions in sleep, appetite, energy, and concentration, with some passive thoughts of suicide.

A

Bipolar disorder in adults

248
Q

In addition to the common presentations of bipolar disorder in classic manic or depressed phases of the illness, individuals may present with other variants or with complex comorbidities that can make diagnosis challenging. Mixed episodes are marked by the co-existence of simultaneous symptoms of depression and mania and may represent a more difficult-to-treat state. Rapid-cycling bipolar disorder is characterised by 4 or more mood episodes in a 12-month period; it is more resistant to pharmacological treatment and may be worsened by traditional antidepressants. In some patients, severe psychotic symptoms and thought disorder may mimic schizophrenia. Most patients with bipolar disorder suffer with at least 1 comorbid condition that may complicate diagnosis and treatment. The most common comorbidities include alcohol or substance misuse disorders, anxiety disorders, attention-deficit disorder, personality disorder, and common medical conditions such as obesity, diabetes, hypertension, migraine, and irritable bowel syndrome.

A

Bipolar disorder in adults

249
Q

Define anorexia nervosa

A

Anorexia nervosa (AN) is an eating disorder characterised by restriction of caloric intake leading to low body weight, an intense fear of gaining weight, and a body image disturbance.

Patients with anorexia nervosa (AN) typically have low body weight, intense fear of gaining weight, and a body image disturbance.

While more often detected in women, cases of AN in young men may be under-represented.

Weight restoration with re-feeding techniques is essential for prevention of sequelae, such as heart failure, fertility problems, and osteoporosis.

Patients with AN are often identified through family referral and the patient’s physical complaints.

Early intervention is key in order to prevent long-term psychiatric and physical complications of AN.

Among psychiatric illnesses, AN has one of the highest premature mortality rates (with a risk of premature death of approximately 5-fold greater than that of peers).

250
Q

Epidemiology of anorexia nervosa

A

According to strict diagnostic criteria, about 0.3% of people in westernised countries, with about 0.5% to 1% of college-aged women, are affected.

It is estimated that 3 in 10 patients are male, but many males may not present for treatment; thus, about 90% of patients diagnosed are female

White women are more likely to be diagnosed with AN than women from ethnic minority groups.

251
Q

Aetiology of anorexia nervosa

A

No single aetiology has been identified for AN. Multiple biological, psychological, and social factors likely contribute to its development and persistence.

252
Q

RFs for anorexia nervosa

A
STRONG
Female
Adolescence and puberty
Obsessive/perfectionist traits
Exposure to western media 
Genetic influence

WEAK
Middle / upper socioeconomic classes

253
Q

Sx of anorexia nervosa

A
COMMON
Significantly low body weight
Fear of gaining weight
Disturbed body image
Calorie restriction
Binge eating/purging
Misuse of laxatives, diuretics or diet pills
Amenorrhoea 
Decreased subcutaneous fat 
General weakness
Poor concentration
Fatigue 
Orthostatic hypotension
Non-specific GI Sx
Hair/skin/nail changes
Cardiac Sx 
Dependent oedema
Osteopenia/porosis
254
Q

Ix for anorexia nervosa

A

The key elements of the DSM-5 diagnostic criteria for AN are as follows:

A. Restriction of energy intake relative to requirements, leading to a significantly low weight in the context of age, sex, developmental trajectory, and physical health
B. Intense fear of gaining weight or persistent behaviour that interferes with weight gain
C. Disturbance in body image.
Specific subtype:

Restricting subtype: no episodes of binge eating or purging in the preceding 3 months; weight loss has been achieved by dieting, fasting, and/or excessive exercise
Binge-eating/purging subtype: recurrent episodes of binge eating or purging behaviour (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or enemas) in the preceding 3 months.
Specific level of severity for adults. The level of severity can be increased based on other indicators such as medical instability and illness duration:

Mild: BMI ≥17 kg/m²
Moderate: BMI 16-16.99 kg/m²
Severe: BMI 15-15.99 kg/m²
Extreme: BMI <15 kg/m².

CHECK:
FBC anaemia
U+E - metabolic alkalosis and hypokalaemia (if vomiting is present); metabolic acidosis, hyponatraemia and hypokalaemia (if laxative use is present), hypomagnesaemia, hypophosphataemia, hypocalcaemia, hypoglycaemia, elevated urea levels
TFTs
LFTs
Urinalysis - low specific gravity may indicate consumption of large quantities of free water; ketonuria may indicate significant semi-starvation

255
Q

Rx of anorexia nervosa

A

Structured eating plan with oral nutrition

Low weight patients who are not at significant risk of developing re-feeding syndrome will commonly begin therapeutic feeding at caloric prescriptions of 1500-1800 kcal/day. Caloric prescriptions may increase by 400 kcal/day every 48-72 hours if patients tolerate prior caloric level, in order to achieve consistent weight change approximating 1-2 kg/week for inpatients (with 0.5-1 kg/week more common in outpatient programmes). Peak caloric requirements in treatment programmes that aim to help patients achieve full weight restoration reach >3500 kcal/day for females and >4000 kcal/day for males. Meal plans may include liquid supplements in addition to solid foods.

Vitamins and minerals (e.g., multivitamin, phosphorus, magnesium, and calcium) should be given until the patient’s diet contains enough to meet his or her dietary reference values. Thiamine supplementation should be considered.

Psychotherapy

UK-based guidance from the National Institute for Health and Care Excellence (NICE) recommends AN-focused family therapy for children and young people with AN delivered as single-family therapy or a combination of single- and multi-family therapy (with children and young people offered the option to have some sessions separately from their family or carers).

REFEEDING
May need potassium/magnesium/sodium/calcium replacement

Monitor fluid intake

Hospital care may be either medical or psychiatric depending on the degree and severity of physical symptoms, and the experience of the psychiatric unit in managing malnutrition. [36] Inpatient care is generally recommended for patients with exceedingly low weight (e.g., <75% expected), precipitous loss of weight, and/or evidence of medical complications of illness, including significant bradycardia, hypotension, or hypothermia, laboratory abnormalities (e.g., electrolyte disturbance, hypoglycaemia), and psychiatric instability including suicidality.

Can try SSRIs or olanzipine

256
Q

Prognosis of anorexia nervosa

A

The prognosis for AN is best when identification and treatment begin early in the illness course, and when full weight restoration is achieved. Recovery-focused treatment is always recommended, and recovery does occur, even among patients who have been ill for an extended period, but younger patients are thought to have the best prognosis. Follow-up studies suggest that approximately 75% of adolescent patients with AN achieve full recovery, although time to recovery may be 3-5 years.

Mortality associated with AN is high, estimated at 5% per decade of illness.

Among psychiatric illnesses, AN has one of the highest premature mortality rates (with a risk of premature death of approximately 5-fold greater than that of peers).

Deaths are due primarily to medical complications or suicide.

257
Q

Complications anorexia nervosa

A
Peripheral oedema secondary to refeeding
Refeeding syndrome
Anaemia
Hypophoshataemia 
Thiamine deficiency 2nd to refeeding
Primary amenorrhoea
Infertility 
Osteopenia
Osteoporosis
Growth retardation
Skeletal fractures
Lip/mous fissures
Glossitis
Bleeding gums
Congestive heart failure
Slowed GI motility 
Acute+chronic renal failure 
Pregnancy complications
258
Q

A 15-year-old girl, accompanied by her mother, presents to her primary care physician complaining of fatigue and sleeplessness for 6 months’ duration. The doctor notes the patient is quite petite and is wearing an oversized, baggy dress. There are no physical findings, but, during the examination, the patient is reluctant to step on the scale, mentioning that she is sure she has gained too much weight since her last visit, and that she ought to spend more time exercising at the gym. She is weighed and is found to be 88% of the minimum weight requirements for her age and height. Her mother is concerned as her daughter has been eating little and exercising daily, and seems disinterested in her friends.

A

Anorexia nervosa

259
Q

As with females, males tend to present in adolescence and early adulthood, although diagnosis may occur after a longer illness duration than is typical for females. In a study of 135 males receiving treatment for eating disorders at an academic medical centre, patients reported feeling ashamed of assignment to a culturally identified ‘female’ disorder, often seeking help only late in disease development.

Patients who present with sub-threshold and atypical symptoms are categorised as having an ‘other specified eating disorder’ in the Diagnostic and statistical manual of mental disorders, 5th edition (DSM-5). For example, a patient who meets all of the criteria for AN but is at a normal or above normal weight would receive the diagnosis of atypical AN, which is briefly described in the section on ‘other specified eating disorders’ in DSM-5.

A

Anorexia nervosa

260
Q

Define schizoaffective disorder

A

Schizoaffective disorder is an illness defined by a course that combines significant affective and psychotic symptoms. The Diagnostic and statistical manual of mental disorders (DSM) definition requires the presence of schizophrenia symptoms concurrent with the mood symptoms (depression or mania), and lasting for a considerable part of a 1-month period. Schizoaffective disorder is further classified as manic type (when manic symptoms are prominent) or depressive type (when only schizophrenia and major depressive symptoms have been present).

Schizoaffective disorder has features of both schizophrenia and mood disorders.

The lifetime prevalence is in the range of 0.32% to 1.1%.

The depressive type of schizoaffective disorder is more common in older patients, whereas the bipolar type is more common in younger patients.

Patients have a better prognosis than patients with schizophrenia but a worse prognosis than patients with mood disorder.

Patients tend to have a non-deteriorating course and better response to mood stabiliser medications than patients with schizophrenia.

Patients with schizoaffective disorder are a heterogeneous group with a variable predominance of schizophrenia and affective disorder symptoms.

261
Q

Epidemiology of schizoaffective disorder

A

Schizoaffective disorder is estimated to be less common than schizophrenia.

Age of onset: 30% of cases have their onset under the age of 25 years, 30% between ages 25 and 35 years, and 30% above the age of 35 years.

Gender distribution: appears to occur more frequently in women.

In regional studies, lifetime prevalence for schizoaffective disorder varies from 0.32% to 1.1%.

262
Q

Aetiology of schizoaffective disorder

A

Most aetiopathological studies cluster schizoaffective disorder together with schizophrenia or bipolar disorder. As such, there is no specific pathophysiology that is ascribed exclusively to this disorder.
Genetic data suggest that chromosome 1q42 (near DISC1 gene location) and the BDNF gene may be associated with schizoaffective disorder.

263
Q

RFs for schizoaffective disorder

A

STRONG
FHx
Substance abuse

WEAK
Age of father at patients birth
Psychological stress
Environment

264
Q

Sx of schizoaffective disorder

A

COMMON
+ve Sx:
Such symptoms include hallucinations, delusional ideation, thought disorder, and bizarre behaviour.

-ve Sx:
Examples of negative symptoms include anhedonia, amotivation, social isolation, or flat affect.

Disorder of perceptions
Delusions- Common delusional themes in schizoaffective disorder, as in schizophrenia, are persecutory, grandiose, nihilistic (also common in depression), religious, and somatic.
Disturbance in emotion
Disorder of stream and form of thought
Cognitive abnormalities
Deficit Sx - asociality (withdrawal from interpersonal interactions), avolition (decrease in interests and activities), affective blunting, alogia (quantitative and qualitative decrease in speech), and anhedonia (lack of enjoyment in any previously pleasurable activities).
Neurological deficit
FHx
Disorders of behaviour - mannerisms (goal-directed behaviour carried out in a stilted fashion), stereotypies (uniformly repetitive movements), parakinesis (e.g., grimacing, twitching, and jerking), echopraxia (repetition of a movement seen in others), automatic obedience (automatic execution of directions), and waxy flexibility (ability to maintain imposed positions for long periods of time).

Catatonia can be seen with psychomotor agitation or retardation.

265
Q

Ix for schizoaffective disorder

A

Urine drug screen
STI screen
FBC
TFTs

CRITERIA DSMV

Schizoaffective disorder debut has an uninterrupted period of illness, during which there is an episode of mood disorder (manic or major depressive disorder) concurrent with a schizophrenia episode characterised by 2 or more of the following symptoms present for a considerable part of a 1-month period:
delusions
hallucinations
disorganised speech (e.g., frequent derailment or incoherence)
grossly disorganised or catatonic behaviour
negative symptoms (i.e., affective flattening, alogia, or avolition).
During this time, there should be a period of at least 2 weeks with delusions and hallucinations, in the absence of prominent mood symptoms during the lifetime duration of illness.
Mood symptoms have been present for the majority of the total duration of the active and residual period of illness.
Other possible etiologies such as substances (e.g., drug abuse, medication) or general medical conditions have been ruled out.
Specify whether bipolar type (if manic episode is part of the presentation; major depressive episodes may also occur) or depressive type (if only major depressive episodes are part of the presentation).

Specify if: with catatonia.

Specify if: (the following course specifiers are only to be used after a 1-year duration of the disorder and if they are not in contradiction to the diagnostic course criteria)

First episode, currently in acute episode
First episode, currently in partial remission
First episode, currently in full remission
Multiple episode, currently in full episode
Multiple episode, currently in partial remission
Multiple episode, currently in full remission
Continuous
Unspecified.

266
Q

Rx of schizoaffective disorder

A

ACUTE
Start or review oral typical/a antipsychotic

MAY NEED IM Antipsychotic:
Olanzipine / aripiprazole / ziprasidone

+/- Lorazepam anxiolytic

MULTIPLE EPISODE DISORDER
1st line: atypical antipsychotic
The benefits of these agents over older antipsychotics, in terms of decreased risk for extrapyramidal adverse effects and tardive dyskinesia, need to be balanced on an individual basis against the increased risk for weight gain and metabolic syndrome, which is especially seen with olanzapine. 2week minimum trial length

Mood stabiliser lithium can be given alongside atypical if refractory

CBT
Social skill training

2 failures of treatment -> try clozapine (worry of agranulocytosis though)

Can try typical antipsychotic if all else fails: eg haloperidol or fluphenazine - The efficacy of these medications is well established, but they are not generally recommended as initial treatment because they carry a higher likelihood of tardive dyskinesia and worsening of negative symptoms.

267
Q

Complications of schizoaffective disorder

A
Orthostatic hypotension (SE)
Dystonia (Parenteral diphenhydramine or benztropine produces reversal of dystonia in minutes.)
Neuroleptic malignant syndrome 
Suicide
Substance abuse
Tardive dyskinesia 
Parkinsonism
Weight gain (atypical)
Metabolic (atypical)
Anticholinergic 
Prolactin elevation 
Prolonged QT
Agranulocytosis
268
Q

Prognosis of schizoaffective disorder

A

The prognosis of patients with schizoaffective disorder, measured in terms of overall poor outcome and parameters such as work functioning and cognitive impairments, appears to be better than the prognosis of patients with schizophrenia but worse than the prognosis of patients with mood disorders.

As in schizophrenia, predictors of poor prognosis include an insidious course, prior history of poor functioning, a family history of schizophrenia, predominant psychotic symptoms and negative symptoms, poor recovery in between episodes, mood-incongruent psychotic symptoms, and lack of clear precipitants.

269
Q

A 26-year-old single woman is seen in the outpatient clinic with her mother. She is dressed provocatively and states that she is Whitney Houston’s daughter and a very important person who knows many famous actors. Her thought content is significant for thought blocking. At times, she is observed to direct her attention to random parts of the room, presumably as a result of active auditory hallucinations. She also believes that everything that she thinks will, in fact, happen. The patient reports that she has always been shy, with few or no friends as she grew up. She started to experience perceptual disturbances around the age of 18, when she “saw spirits but did not hear them”. Around that time she also became aware of her ability to know the future. For example, once she looked towards the airport and knew that 2 planes would crash in the future. She wanted to call someone to report it but did not know whom to call. Days later there were 2 accidents. Despite such unusual experiences she was able to train as a dental technician and had a steady job for 5 years. During that time, she started to experience more auditory hallucinations. She described them as voices conversing, at times yelling or giving her directions, even telling her to kill herself, when under stress. She also reported that she resisted the voices by distracting herself, as she did not want to die. Last year she also had a mixed episode, during which she was manic, did not sleep for more than a week, felt “hyper”, impulsive, and “tingling”, and also depressed. At that time she decided that she could not continue to work in the same place and left; she has not since held a job. At the time of her initial evaluations she was living with her parents and brother. About 1 year ago, she started an antipsychotic medication, which decreased the intensity of the voices and the fear that other people could read her thoughts. During the past year she has had manic symptoms most of the time (including grandiosity, impulsivity, decreased sleep, and mixed mood symptoms). This culminated with an exacerbation about 6 months ago that prompted psychiatric hospitalisation. On examination, she was sitting in a somewhat provocative position on the couch. Her speech was high-pitched. She appeared relaxed, although at random times she would get tense. Her thought process was slow and tangential, with intermittent thought blocking. Her attention span was moderately diminished. No active suicidal or homicidal thoughts were present; however, she reported that the voices insisted that she should jump out of the window. Her insight and judgement were poor.

A

Schizoaffective disorder

270
Q

The Diagnostic and statistical manual of mental disorders, fifth edition, based on the history and type of affective symptoms, defines 2 types of schizoaffective disorder: [1] bipolar type, which is diagnosed when there is at least one manic episode (major depressive episodes may also occur); and depressive type, which is diagnosed if all the mood episodes have been exclusively major depressive episodes (i.e., no history of manic or mixed episodes).

The WHO International statistical classification of diseases and related health problems, 10th revision (ICD-10), based on the history and type of affective symptoms, defines 3 types of schizoaffective disorder: [2] manic type, which is diagnosed when both schizophrenia and manic symptoms are prominent during the same episode (if a single episode) or during the majority of the episodes (if recurrent); mixed type, which is diagnosed when both schizophrenia and mixed symptoms are prominent during the same episode (if a single episode) or during the majority of the episodes (if recurrent); and depressed type, which is diagnosed when schizophrenia and depressive symptoms are both prominent during the same episode (if a single episode) or during the majority of the episodes (if recurrent).

A

Schizoaffective disorder

271
Q

Define Alcohol-use disorder

A

Alcohol-use disorder is a term used to refer to the misuse of alcohol. Several specifically defined conditions better categorise patterns of alcohol misuse.

It is characterised by increased tolerance to the effects of alcohol, the presence of characteristic withdrawal signs and symptoms, and impaired control over the quantity and frequency of drinking. Alcohol-use disorder can be associated with a variety of medical and psychiatric sequelae.

Alcohol-use disorder is diagnosed when, over a 12-month period, the patient’s drinking has caused clinically significant impairment or distress.

Alcohol-use disorder is a common psychiatric disorder that is multifactorial in aetiology, chronic in nature, and is associated with a wide variety of medical and psychiatric sequelae.

Tolerance, withdrawal, impaired control of drinking behaviour, and continued alcohol use despite adverse consequences are some important features of alcohol dependence.

Alcohol withdrawal syndrome can follow cessation or reduction in alcohol consumption. Withdrawal can be a serious medical condition. It is best monitored by use of a structured instrument: the Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar). Benzodiazepines are the definitive medical treatment.

Binge-drinking, alcohol abuse, and mild alcohol dependence may be addressed by brief physician-based interventions, or psychological interventions such as cognitive behavioural therapy.

Moderate or severe alcohol-use disorder requires multi-modal treatment. Detoxification in an inpatient or outpatient setting may be necessary. The goal of detoxification is to minimise withdrawal symptoms and to facilitate entry into an ongoing, multi-modal treatment programme directed towards assisting the patient in maintaining abstinence.

Medications, including naltrexone, nalmefene, acamprosate, and disulfiram, can be successfully utilised for selected patients to improve their chances of maintaining abstinence.

272
Q

Epidemiology of Alcohol-use disorder

A

Alcohol-use disorder is a common psychiatric disorder with lifetime prevalence estimates of 7% to 10% in most Western countries.

M:F 2:1

In primary care settings, the prevalence of alcohol-use disorders ranges from 20% to 36%.

It is estimated that alcohol causes a significant global disease mortality burden, accounting for 3.2% of global deaths.

273
Q

Aetiology of Alcohol-use disorder

A

Alcohol-use disorder is a chronic illness with a multifactorial aetiology, combining several components, genetic as well as social, psychological, and environmental.

Approximately 50% of the risk of developing alcohol-use disorder is genetically determined, but the influence of genes is complex, as there are genes that increase risk and genes that are protective. Alcohol-use disorder is frequently associated with psychiatric disorders, especially affective disorders, anxiety disorders, post-traumatic stress disorder, and schizophrenia.

Alcohol affects many brain neurotransmitters and their receptors, including dopamine, gamma-aminobutyric acid, glutamate, serotonin, adenosine, noradrenaline (norepinephrine), and opioid peptides.

The clinical course of patients with addictive disorders is characterised by phases of repeated intoxication, withdrawal, and abstinence, with the disorder progressing from impulsivity to compulsivity. Chronic exposure of the brain to alcohol is thought to result in long-term adaptive changes that initially produce increased reinforcement for alcohol use, and over time progress to withdrawal and negative affective states, so that regular alcohol use is required to feel normal.

274
Q

RFs for Alcohol-use disorder

A

STRONG
FHx
Antisocial behaviour
High trait anxiety level

WEAK
Lack of facial flushing on exposure to alcohol
Low responsively to effects of alcohol
Hx gastric bypass

275
Q

Sx of Alcohol-use disorder

A

COMMON
RFs
Withdrawal Sx: Increased autonomic activity, agitation, and nervousness are common symptoms. Generalised seizures and a confusional state (delirium) are seen in more severe cases of alcohol withdrawal.
Tolerance
Sx of liver disease
Nicotine dependence
Social, economic,legal or psychological problems
Gastritis/pancreaitis - N+V, abdo pain, haematemesis
Muscle cramps, pain, tenderness, altered sensory perception
Hypertension and tachycardia
Possible skin manifestations of alcoholism include increased superficial cutaneous vasculature, urticarial reactions, porphyria cutanea tarda, flushing, cutaneous stigmata of cirrhosis, psoriasis, pruritus, seborrhoeic dermatitis, and rosacea.
Impaired nutritional status
Dental hygeine
Broad based gait

276
Q

Ix for Alcohol-use disorder

A

Diagnostic interview using DSMV criteria
OR A QUESTIONNAIRE:
AUDIT - Alcohol Use Disorders Identification Test
OR
Severity of alcohol dependence questionnaire
Alcohol level (breath/blood)
(CIWA-Ar) - The revised Clinical Institute Withdrawal Assessment for Alcohol

277
Q

Rx of Alcohol-use disorder

A

(CIWA-Ar) - The revised Clinical Institute Withdrawal Assessment for Alcohol SCORE >8 = need BDZ
- May need inpatient/outpatient speciality Rx

Mild:
Motivational interviewing, cognitive-behavioural therapy with 12 steps, cognitive-behavioural therapy with aftercare, multidimensional family therapy

Mod-Severe
Motivational interviewing
CBT
Alcoholics Anonymous

Frequent relapse = pharmacotherapy

Naltrexone - opioid antagonist
Acamprosate - maintains abstinence
Disulfiram - blocks metabolism
Nalmefene - mu opioid antagonist

278
Q

Complications of Alcohol-use disorder

A
Mallory Weiss
Delerium tremens 
Seizure 
Alcoholic liver disease
Cirrhosis 
Nutritional disorders
Cardiomyopathy 
Wernick-korsakoff syndrome
279
Q

Prognosis of Alcohol-use disorder

A

Alcohol-use disorder tends to run a chronic course. While treatment does impact the condition positively, relapse is common, particularly in the first 12 months after treatment initiation.

Medication treatments are relatively under-utilised for alcohol-use disorders, despite their shown efficacy.

280
Q

Define bulimia nervosa

A

Bulimia nervosa is an eating disorder characterised by recurrent episodes of binge eating, followed by behaviours aimed at compensating for the binge. Binge-eating episodes are characterised by eating an amount of food that is definitely larger than most people would eat (e.g., at least twice the normal amount of food ingested) over a discrete period of time (it must be ingested more quickly than normally). Binges are accompanied by a sense of lack of control over eating during the episode. Recurrent inappropriate compensatory behaviours occur in order to prevent weight gain. These behaviours include self-induced vomiting; fasting; excessive exercise; and misuse of laxatives, diuretics, enemas, or other medication. Binge-eating episodes typically occur, on average, at least weekly for 3 months.

An eating disorder, characterised by severe preoccupation about weight and body shape. Includes recurrent episodes of binge eating with compensatory mechanisms, such as self-induced vomiting, to prevent weight gain.

Most common in women in their 20s and 30s.

Patients usually appear physically normal, although they may have low self-esteem and depressive thoughts, as well as lack of confidence.

Parotid hypertrophy and erosion of the teeth are the most common physical signs and may prompt diagnosis.

Cognitive behavioural therapy (CBT) is considered optimal primary treatment for bulimia, but it may not always be available.

Selective serotonin-reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors (SNRIs) may be used adjunctively to CBT, or as an alternative when CBT is not available.

Treatment of comorbid psychiatric disorders, such as major depressive disorder and obsessive-compulsive disorder, is necessary to optimise the chance of recovery from bulimia nervosa. SSRIs are effective in additional treatment of comorbid psychiatric disease.

281
Q

Epidemiology of bulimia nervosa

A

Lifetime prevalence of DSM-5-defined bulimia nervosa by age 20 is 2.6% in women.

W>B

282
Q

Aetiology of bulimia nervosa

A

The aetiology of bulimia nervosa is uncertain. A biopsychosocial theory of causation posits a combination of coexisting biological (genetic abnormalities in receptors or neurotransmitters), psychological, and social factors.

Risk factors that are strongly associated with bulimia nervosa include female sex; perfectionism; body dissatisfaction; impulsivity; history of sexual abuse; family history of alcoholism, depression, or eating disorder; past obesity; and exposure to media pressure. An association with urbanisation has been reported.

283
Q

RFs for bulimia nervosa

A
STRONG
Female
Personality disorder
Body image dissatisfaction
Hx sex abuse
Impulsivity 
FHx alcoholism
FHx depression 
FHx eating disorder
Childhood obesity 
Exposure to media
Early onset puberty 

WEAK
Urbanisation
FHx obesity

284
Q

Sx of bulimia nervosa

A

Recurrent binge eating
Recurrent compensatory behaviour - There must always be some form of compensatory behaviour to attempt to burn off calories. This may be purging (vomiting, laxatives, enemas, suppositories) or non-purging (exercise, fasting).
Occurs, on average, at least once a week for 3 months.

Eating disturbance not exclusively anorexia
Depression
Low self esteem
Concern about body image
Dental erosion
Parotid hypertrophy 
Russels sign - Scarring over the dorsum of the hands.
Arrythmia 
Menstrual irregularity 
Drug seeking behaviours
Self injurious behaviour
Insulin misuse
GI Sx - oesophageal reflux, diarrhoea, constipation, and abdominal pain 
Hx dieting
Marked fluctuations in weight 

UNCOMMON
Use of ipecac
Needle marks on skin
Vomiting in pregnancy

285
Q

Ix for bulimia nervosa

A

U+E - may show hypokalaemia or alkalosis
Serum Creatinine - may be elevated
Magnesium - may be low
Urine preg test
LFTs - Drug overdose, alcohol ingestion, or excess exercise may elevate aminotransferases.
Serum creatine kinase - Drug overdose, alcohol ingestion, or excess exercise may elevate CK.
FBC - patients may self-phlebotomise as a form of purging, but rarely give this history. Anaemia and the presence of needle marks may be the only clues
Urinalysis - may show ketones

CONSIDER
ECG
B12
DEXA

286
Q

Rx of bulimia nervosa

A
  1. CBT / CBT self-help
    +/- nutritional and meal support
    Meal support means that a therapist actively supports the patient at mealtimes regarding their concerns, feelings, habits, and beliefs about eating.

+/- SSRI/SNRI
Fluoxetin/sertraline OR Venlafaxine
These are used to temporarily reduce the frequency of binge eating and purging. Only 1 to 2 weeks of medication should be prescribed.

  1. Interpersonal Therapy
    Core dysfunctional thoughts, attitudes, motives, conflicts, and feelings should be addressed.

If the patient presents with physical symptoms such as loss of consciousness, syncope, and seizures, referral for emergency department assessment is advised.

If the patient has diabetes, referral to an endocrinologist is recommended.

Alcoholism or other substance abuse, borderline personality disorder, or ongoing self-injurious behaviour also indicates the need for immediate specialised psychiatric or psychological referral.

287
Q

Prognosis of bulimia nervosa

A

Bulimia nervosa has an average onset at an age of about 18 years, but bingeing and purging to a lesser degree is much more common. Many, if not most patients, who meet the diagnostic criteria for bulimia do not access medical help. Of those who do, 45% to 75% recover completely, 27% improve considerably, and 23% have a chronic course. The crude mortality rate is approximately 0.32% to 3.9%. Most patients with bulimia nervosa continue an active life despite the disorder.

288
Q

Complications of bulimia nervosa

A
Volume depletion
Hypomagnesaemia
Tooth erosion
Pancreatitis
Ipecac related cardiomyopathy 
Hypokalaemia
Cardiac dysrythmia
Haematemesis
Oesophageal rupture
Death 
Suicide
289
Q

A 30-year-old woman presents with marked weight fluctuations. She says that her weight has changed by just over 3 kg over a few days, unrelated to menstruation. Physical examination is normal except for bilateral parotid hypertrophy.

A

Bulimia nervosa

290
Q

A 25-year-old woman complains that she is obsessed with eating and weight. She has tried unsuccessfully to lose weight. She becomes so hungry that she overeats to the point of regurgitating.

A

Bulimia nervosa

291
Q

Bulimia nervosa usually begins as an attempt at weight control. It soon becomes a compulsion that the patient considers shameful and a sign of weakness. Most commonly it presents as bingeing and purging, with marked weight fluctuation. It is associated with depression and low self-esteem. Hypokalaemia or parotid hypertrophy may be found. Less common presentations are self-injurious behaviour, shoplifting, suicidality, vomiting in pregnancy, refractory poor control of diabetes mellitus, rupture of the oesophagus, or pancreatitis.

Men with bulimia nervosa may be more weight- and shape-conscious, and these patients tend to focus on muscle gain and fat loss. The research on men with bulimia nervosa is poor due to the condition not being as common in men, and because they are often excluded from research trials to reduce the number of confounding factors.

A

Bulimia nervosa

292
Q

Define personality disorders

A

Personality disorders refer to enduring patterns of thinking and feeling about oneself and others that significantly and adversely affect how an individual functions in the various aspects of life. In the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5), [1] the personality disorders fall into 10 distinct types: paranoid, schizoid, schizotypal, antisocial, borderline, histrionic, narcissistic, avoidant, dependent, and obsessive-compulsive. None of the criteria for personality disorders has changed in the DSM-5 compared with the previous edition, DSM-IV.

Relatively common, chronic pattern of perceptual and behavioural abnormalities. These manifest as problems in at least two of the following domains: cognitive-perceptual, affect regulation, interpersonal functioning, or impulse control.

Onset of symptoms in childhood/adolescence with stability over time.

Typical presentation involves comorbid disorders (more than one personality disorder or additional diagnoses of depression, anxiety, somatoform, or substance abuse disorder).

Ongoing relationship with primary care physician is essential but may be challenging to maintain.

Potential for self-harm must be monitored. There is also potential for social withdrawal.

Psychotherapy is indicated in most cases. Selective use of pharmacotherapy can provide added benefit.

293
Q

Epidemiology of personality disorders

A

Prevalence rates for DSM-IV personality disorders range from 9% to 11.2%

Schizoid personality disorder was found to be more common in men, with schizotypal personality disorder diagnosed equally between men and women.

Prevalence of antisocial personality disorder appears to decline with increasing age.

294
Q

Aetiology of personality disorders

A

There is evidence for both environmental and genetic effects on the development of personality disorders; however, the relative contribution of each is variable.

Similarly, an investigation of exposure to antenatal adversities (i.e., tobacco use, alcohol consumption, anxiety, and depression) found that exposure to increased stress in utero was associated with borderline personality disorder in children 11 to 12 years later.

Environmental factors that have been linked to development of personality disorders include: childhood maltreatment, particularly a history of childhood physical abuse; sexual abuse; and neglect.

295
Q

RFs for personality disorders

A
STRONG
Hx abuse
FHx schizophrenia 
Negative parenting interactions
Emotional/disruptive disorder in childhood
296
Q

Sx of antisocial personality disorder

A

Failure to conform to social norms with respect to lawful behaviors as indicated by repeatedly performing acts that are grounds for arrest;
More common in men;
Deception, as indicated by repeatedly lying, use of aliases, or conning others for personal profit or pleasure;
Impulsiveness or failure to plan ahead;
Irritability and aggressiveness, as indicated by repeated physical fights or assaults;
Reckless disregard for safety of self or others;
Consistent irresponsibility, as indicated by repeated failure to sustain consistent work behavior or honor financial obligations;
Lack of remorse, as indicated by being indifferent to or rationalizing having hurt, mistreated, or stolen from another

297
Q

Ix for personality disorders

A

Clinica interview - symptoms dating from adolescence/early adulthood; not occurring solely in the presence of another disorder such as depression or anxiety; significant difficulties in interpersonal interactions may lead to suspected diagnosis of personality disorder

CONSIDER
Suicide risk screening
Standardised assessment of personality abbreviated scale - SAPAS
Structured clinical interview for DSM-IV axis 2 personality disorders

Urine drug screen
MRI/CT brain (ie potential picks Sx)
Depression screen - mood disorder questionnaire

298
Q

Rx of personality disorders

A

AT RISK OF SELF HARM
?Hospitalisation
- May need referral for substance abuse assessment

CLUSTER A - Odd/eccentric IE paranoid/schizoid/schizotypal

Communication that is straightforward with an unintrusive style is recommended in this group. The physician should display interest in those concerns that the patient is willing to share.

Low dose antipsychotics - aripiprazole / haloperidol

First-generation antipsychotic agents (e.g., haloperidol, perphenazine) are associated with hyperprolactinaemia and early (akathisia and parkinsonism) and late (tardive dyskinesia) movement abnormalities, as well as the neuroleptic malignant syndrome. Second-generation antipsychotics (e.g., aripiprazole) are associated with the metabolic syndrome and are not free of the same risks as first-generation antipsychotics: acute and tardive movement disorders and neuroleptic malignant syndrome.

Consider antidepressants - sertaline/fluoxetine

CLUSTER B (Dramatic) Borderline

Same communication style (caution re-nonadherence/loss of trust)
Psychotherapy
Mood stabilisers, such as lithium and anticonvulsants (lamotrigine), may have some effectiveness in treating impulsivity and aggression in borderline personality disorder.

Narcissistic
Substance abuse Rx referral

Antisocial
Psychotherapy

CLUSTER C - ANXIOUS 
Avoidant
Psychotherapy 
1st - Fluoxetine / sertraline 
2nd - gabapentin / pregabalin 

Dependent
Psychotherapy

Obsessive compulsive
Psychotherapy

299
Q

Complications of personality disorders

A

Self harm
Suicide
Impairment in social functioning -

300
Q

Prognosis of personality disorders

A

For example, in one study of 290 inpatients with borderline personality disorder, 88% achieved remission; factors were identified to predict an earlier time to remission, including the absence of childhood sexual abuse. Some have suggested symptoms may attenuate with age. Symptoms are often exacerbated in response to stressors. Personality disorders have been shown to respond to treatment, particularly if relatively intensive treatment is provided over an extended time-frame. The 10-year course of borderline personality disorder is also characterised by severe and persistent impairment in social functioning.

301
Q

Sx of narcissistic personality disorders

A
Grandiose sense of self importance
Preoccupation with fantasies of unlimited success, power, or beauty
Sense of entitlement
Taking advantage of others to achieve own needs
Lack of empathy
Excessive need for admiration
Chronic envy
Arrogant and haughty attitude
302
Q

Sx of obsessive-compulsive personality disorders

A

Is occupied with details, rules, lists, order, organization, or agenda to the point that the key part of the activity is gone
Demonstrates perfectionism that hampers with completing tasks
Is extremely dedicated to work and efficiency to the elimination of spare time activities
Is meticulous, scrupulous, and rigid about etiquettes of morality, ethics, or values
Is not capable of disposing worn out or insignificant things even when they have no sentimental meaning
Is unwilling to pass on tasks or work with others except if they surrender to exactly their way of doing things
Takes on a stingy spending style towards self and others; and shows stiffness and stubbornness

303
Q

Sx of paranoid personality disorders

A

Hypersensitivity and an unforgiving attitude when insulted
Unwarranted tendency to questions the loyalty of friends
Reluctance to confide in others
Preoccupation with conspirational beliefs and hidden meaning
Unwarranted tendency to perceive attacks on their character

304
Q

Sx of schizoid personality disorders

A
Indifference to praise and criticism
Preference for solitary activities
Lack of interest in sexual interactions
Lack of desire for companionship
Emotional coldness
Few interests
Few friends or confidants other than family
305
Q

Sx of schizotypal personality disorders

A
Ideas of reference (differ from delusions in that some insight is retained)
Odd beliefs and magical thinking
Unusual perceptual disturbances
Paranoid ideation and suspiciousness
Odd, eccentric behaviour
Lack of close friends other than family members
Inappropriate affect
Odd speech without being incoherent
306
Q

Sx of schizotypal personality disorders

A
Ideas of reference (differ from delusions in that some insight is retained)
Odd beliefs and magical thinking
Unusual perceptual disturbances
Paranoid ideation and suspiciousness
Odd, eccentric behaviour
Lack of close friends other than family members
Inappropriate affect
Odd speech without being incoherent
307
Q

Define BDZ abuse and OD

A

Benzodiazepine (BZD) overdose occurs when excessive amounts of BZD medications are taken. Commonly known as minor tranquilisers or sleeping pills, BZDs are prescribed for sedative, anxiolytic, hypnotic, and anticonvulsant purposes. BZDs are also widely abused. Acute overdose is characterised by excessive sedation with impaired mental status and diminished postural stability and reflexes. Although BZDs are relatively safe medications, acute overdose may induce respiratory depression resulting in coma and uncommonly death. Diagnosis is suggested by the history and by exclusion of other aetiologies. Chronic overuse increases the risk of many other pathologies.

Benzodiazepines (BZDs) are the most commonly prescribed medications for anxiety, sedation, and sleep. Overdose can be intentional in suicidal patients, accidental in combination with other CNS depressants such as alcohol and opioids and in older people, and occasionally by medication error. Older people, who commonly have diminished drug clearance and polypharmacy, are at especially high risk of overdose.

The key feature is excessive sedation with unremarkable vital signs and anterograde amnesia. Larger doses can cause coma and respiratory depression.

Treatment of overdose is by symptom management, not by quantitative assay. Acute management consists of maintaining airway, respiration, and haemodynamic support while excluding other diagnoses. Assisted ventilation may be necessary.

Death is uncommon. Most deaths from BZD overdose are from respiratory depression as a result of mixed overdoses with BZD and other respiratory depressants, particularly alcohol and opioids.

The BZD antagonist flumazenil can be used in first-time or infrequent BZD users to reverse CNS depression. It is contraindicated in BZD-dependent patients because of the risk of provoking seizures. The risks associated with its use often outweigh the benefits.

308
Q

Epidemiology of BDZ abuse and OD

A

Since initial development in the 1950s, benzodiazepines (BZDs) have become popular in the treatment of various medical disorders and as a drug of abuse. BZDs are the most common hypnotic or sedative medications, other than alcohol, used for recreation.

his figure is as high as 36% for adults receiving treatment for depression in mental healthcare settings.

BZD use is higher in white people than in other ethnic groups. Twice as many females as males use BZDs. Sedatives, anxiolytics, and hypnotics are commonly prescribed for people in the sixth and seventh decades of life.

Non-medical use of BZDs is highest in people aged 18 to 25 years, with rates of 0.7% to 1.9%. Use is especially common in those who abuse alcohol, with up to 40% reporting inter-current or concurrent self-medication with BZDs.

BZDs account for approximately 31% of fatal overdoses involving prescription drugs in the US, while 75% of these fatal overdoses also involve opioids.

309
Q

Aetiology of BDZ abuse and OD

A

Benzodiazepines are the most commonly prescribed medications for anxiety, sedation, and sleep. Overdose can be intentional in suicidal patients; accidental in combination with other CNS depressants such as alcohol and opioids, and in older people; and occasionally by medication error (patient administered or iatrogenic).

BZDs enhance the activity of the inhibitory neurotransmitter gamma-aminobenzoic acid (GABA) in the CNS. GABA receptors are located on postsynaptic neurons. The binding of a BZD molecule to a site on the GABA receptor complex potentiates the inhibitory effect of GABA. The clinical effects depend on the location of GABA neurons in the CNS and include sleep induction, excitement inhibition, anxiolysis, other sedative/hypnotic and antiseizure action, and generalised CNS depression.

310
Q

RFs for BDZ abuse and OD

A
STRONG
Depression
Hx illicit drug use
Drug administration error
Comorbidity
Hx BDZ use
Hx polypharmacy 
Suicidal ideation
Older age

WEAK
Drug interaction
Biogenetic susceptibility

311
Q

Sx of BDZ abuse and OD

A

COMMON
RFs
Impaired mental status
Drowsiness, slurred speech, ataxia

UNCOMMON
Coma
Respiratory Depression 
Dec deep tendon reflexes
Nystagmus 
Paradoxical stimulation
312
Q

Rx of BDZ abuse and OD

A

Supportive - Management of pure benzodiazepine (BZD) overdose is supportive, consisting of airway maintenance, cardiorespiratory monitoring and support, and intravenous fluids. Mixed overdose and other causes of CNS depression should be ruled out.

Flumenazil

Drug abuse referral - ARC - addiction, recovery, community centre
CBT/Motivational therapy

313
Q

Complications of BDZ abuse and OD

A

Resp arrest
Coma
Death

314
Q

Prognosis of BDZ abuse and OD

A

Most patients make a full physical recovery after acute benzodiazepine overdose, but the underlying psychiatric and social issues that precipitated the overdose in many cases need to be addressed in the long term. Patients who have taken an intentional overdose are at risk of future episodes of deliberate self-harm.

A greater challenge is treating long-term abuse or dependence. An extensive review of 25 clinical trials, with a total of 1666 subjects, found that cognitive behavioral therapy offers limited benefit, whereas there is insufficient evidence to support motivational therapy or other common approaches in treating abuse or dependence.

315
Q

Ix for BDZ abuse and OD

A
Pulse Ox
FBC
Serum chem
Serum ethanol
Urine toxicology screen 
ECG
Flumazenil
316
Q

A 24-year-old woman is brought to the emergency department (ED) by her classmate, who is concerned that she may have ingested an excessive number of ‘sleeping pills’. She has been distraught over a relationship and has admitted to taking an unknown number of pills an hour earlier. Before ingestion, she had drunk approximately 2 to 3 glasses of wine. On examination the patient has slurred speech and ataxia, but is oriented, with a Glasgow Coma Scale score of 12. She has a normal physical examination with no focal neurological signs. Medical records show that the patient has a prescription for alprazolam for panic attacks. She denies co-ingestions other than alcohol, or other morbidity.

A

Benzodiazepine overdose

317
Q

Define cocaine abuse and overdose

A

Cocaine is a drug of abuse that is usually either insufflated (snorted), injected, or smoked in its freebase form (crack). Cocaine is a type IA antidysrhythmic, local anaesthetic, and sympathomimetic. It can also bind the hERG (slowly depolarising inward potassium channel), which is prodysrhythmic.

Episodic cocaine use leads to short-lived states of autonomic arousal. Chronic use can lead to scarring of heart tissue and myocardial hypertrophy and other changes collectively known as myocardial remodelling. These changes constitute the substrate for the occurrence of lethal arrhythmias.

Cocaine binds to the hERG (rapid repolarising potassium) channel, disrupting the normal process of depolarisation in heart muscle. Cocaine should not, therefore, be used concomitantly with drugs known to cause QT interval prolongation.

While chest pain related to cocaine use is a common reason for seeking medical care, occasional use is rarely associated with acute myocardial infarction (AMI) unless there is pre-existing coronary artery disease.

Psychosis can be seen in chronic users as an isolated condition or as a feature of ‘excited delirium’. It is an agitated confusional state associated with potentially lethal hyperthermia.

There is no evidence to support the use of antipsychotic agents for cocaine dependence. Antipsychotic agents may cause QT interval prolongation and, when used concomitantly with cocaine, may compound the risk of sudden death.

OVERDOSE:
Occurs within minutes to hours of excessive cocaine use.

Some patients may die suddenly before treatment is given.

Presentation includes tachycardia, hypertension, hyperthermia, diaphoresis, mydriasis, and agitation.

Urine cocaine screen confirms recent cocaine use, but treatment should not be delayed pending results of the test.

Treatment may involve supportive care and benzodiazepines; hyperthermia requires rapid cooling to prevent death.

Complications such as dysrhythmias, acute coronary syndrome, and intracranial haemorrhage can occur.

318
Q

Aetiology of cocaine abuse and overdose

A

It is also known that dopamine-rich neurons in the shell of the nucleus accumbens are deeply involved in the process of addiction to all drugs, and that numerous polymorphisms can alter dopamine metabolism. Genome-wide linkage and association studies have implicated several regions and genes in addiction to alcohol and, more recently, tobacco, but progress in this area has been slower than expected.

319
Q

Epidemiology of cocaine abuse and overdose

A

Cocaine is the most commonly used illegal stimulant in Europe, and its use is most common in southern and western countries. It is estimated that around 17.5 million European adults aged 15 to 64 years (5.2% of this age group) have used cocaine at some time in their lives. Of these, there are about 2.3 million young adults aged 15 to 34 years (1.9% of this age group) who have used cocaine in the past year.

320
Q

RFs for cocaine abuse and overdose

A

Hx alcohol drug abuse

Hx mental illness

321
Q

Sx of cocaine abuse and overdose

A
COMMON
HTN
Tachycardia
Chest pain
Mydriasis
Diaphoresis
Tremulousness
Agitation
Mood changes
Anxiety 
Drug induced formication
Hx hospitalisation
Body packing Sx
Nasal septum ulceration/perforation
Seizure
LOC
Skin lesions 
Dyspnoea
322
Q

Ix for cocaine abuse and overdose

A
Urine Tox - 
Also do mass spec for Levamisole. Levamisole is now almost a universal cocaine adulterant.
ECG
CT head
EEG 
Glucose
323
Q

Rx of cocaine abuse and overdose

A

Anxiolytic - BDZ lorazepam, clonazepam, diazepam
Tachycardia and hypertension often respond to treatment with sedatives such as benzodiazepines. Lorazepam and alprazolam have shorter durations of action. In patients with mild anxiety, lorazepam or diazepam is preferred. Intravenous use of diazepam requires close monitoring of vital signs.
Glyceryl trinitrate, aspirin administration, and cardiac work-up (ECG and cardiac enzymes) are indicated for significant/persistent chest pain.

Drug counselling/mental health referral

ARC - addiction, rehabilitation and community

324
Q

Complications of cocaine abuse and overdose

A
Cocaine overdose
Excited delirium 
Psychosis (magnum syndrome) 
Crack keratitis 
Hypertensive crisis
Haemorrhagic stroke
Seizures
Crack lung 
HepB/C/HIV
MI
Cardiomyopathy 
Chronic skin ulcers
Ventricular arrythmias -> sudden cardiac death
325
Q

A 28-year-old man presents to an emergency department with anxiety, complaining of a racing pulse and chest pain. He reports a history of 10 pack-years of cigarette smoking. He has recently begun smoking crack cocaine. His symptoms clear during observation, after reassurance and mild sedation.

A

Cocaine abuse

326
Q

A 22-year-old man is brought from the airport with high fever and convulsions. No other history is available, other than that he started vomiting soon after the flight had left Jamaica. His abdomen is soft and non-tender but he is tachycardiac with an elevated systolic BP. Abdominal x-ray reveals the presence of several foreign bodies in the gastrointestinal tract.

A

Cocaine abuse

327
Q

Prognosis of cocaine abuse and overdose

A

Detoxification and rehabilitation
Abrupt withdrawal from stimulants does not require detoxification and many patients can be safely discharged from the emergency department with referral to a drug-counselling centre.

The odds of relapse to drug use are high (about 50%).

Patients can benefit from treatment, even those with severe problems related to use. Treatment programme participation of over 90 days has been shown to lead to greater improvement for all patient groups.

Occasional user
People who have only experimented with the drug rarely require further medical treatment. Education about the dangers of cocaine use, and the offer of resources, may be of benefit.

Injection and skin-popping (subcutaneous injection)
Intravenous abusers are potentially subject to organ damage and to hepatitis B, hepatitis C, and HIV infection, and will require thorough medical examination before addiction treatment entry.

328
Q

A 22-year-old man is brought from the airport with high fever and convulsions. No other history is available, other than that he started vomiting soon after the flight had left Jamaica. His abdomen is soft and non-tender but he is tachycardiac with an elevated systolic BP. Abdominal x-ray reveals the presence of several foreign bodies in the gastrointestinal tract.

A

Cocaine abuse

329
Q

Define opioid abuse

A

An opioid is any synthetic or natural agent that stimulates opioid receptors and produces opium-like effects. Opiates are opioids naturally derived from the opium poppy, Papaver somniferum , and include morphine and codeine. Opioids are used in the treatment of pain but are often sold illicitly and abused for their euphoric effects. An overdose occurs when larger quantities than physically tolerated are taken, resulting in central nervous system and respiratory depression, miosis, and apnoea, which can be fatal if not treated rapidly.

OD:
The patient’s history from bystanders/friends/family can assist diagnosis.

Signs include central nervous system and respiratory depression, miosis, and apnoea.

Initial treatment consists of ensuring adequate ventilation followed by administration of the opioid antagonist naloxone.

Monitor patients for re-sedation and repeat antidote dose if necessary.

330
Q

Epidemiology of opioid abuse

A

Opioids are powerful pain killers that are highly addictive. Opioid dependence affects nearly 5 million people in the United States and leads to approximately 17,000 deaths annually. Half of deaths due to drug overdose are related to prescription drugs, according to a report on the leading cause of deaths from injury in the United States.

331
Q

Aetiology of opioid abuse

A

Opioid overdose can result from the following:

Complications of substance abuse in regular users/abusers of illicit or prescription opioids
Unintentional overdose in patients prescribed opioids for pain by taking larger amounts than tolerated
Intentional overdose and intent of self-harm (suicidality)
Therapeutic drug error; iatrogenic overdose by a practitioner unfamiliar with opioid prescribing, or an adverse drug reaction.

332
Q

RFs of opioid abuse

A

STRONG
Chronic pain / prescription
Recent abstinence in chronic user
Hx abuse/dependence

333
Q

Sx of opioid abuse

A

Symptoms of opioid abuse can be categorized by physical state.
Intoxication state

Patients with opioid use disorders frequently relapse and present with intoxication. Symptoms vary according to level of intoxication. For mild to moderate intoxication, individuals may present with drowsiness, pupillary constriction, and slurred speech. For severe overdose, patients may experience respiratory depression, stupor, and coma. A severe overdose may be fatal.

Withdrawal state
Symptoms of withdrawal include the following:
Autonomic symptoms - diarrhea, rhinorrhea, diaphoresis, lacrimation, shivering, nausea, emesis, piloerection
Central nervous system arousal - sleeplessness, restlessness, tremors
Pain - abdominal cramping, bone pains, and diffuse muscle aching
Craving - for the medication

DSMV (at least 2 of):
Taking larger amounts of opioids or taking opioids over a longer period than was intended
Experiencing a persistent desire for the opioid or engaging in unsuccessful efforts to cut down or control opioid use.
Spending a great deal of time in activities necessary to obtain, use, or recover from the effects of the opioid.
Craving, or a strong desire or urge to use opioids.
Using opioids in a fashion that results in a failure to fulfill major role obligations at work, school, or home.
Continuing to use opioids despite experiencing persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of opioids.
Giving up or reducing important social, occupational, or recreational activities because of opioid use.
Continuing to use opioids in situations in which it is physically hazardous.
Continuing to use opioids despite knowledge of having persistent or recurrent physical or psychological problems that are likely to have been caused or exacerbated by the substance.
Tolerance, as defined by either a need for markedly increased amounts of opioids to achieve intoxications or desired effect, or a markedly diminished effect with continued use of the same amount of an opioid.
Withdrawal, as manifested by either the characteristic opioid withdrawal syndrome, or taking opioids to relieve or avoid withdrawal symptoms.

334
Q

Ix for opioid abuse

A

DSMV (at least 2 of):
Taking larger amounts of opioids or taking opioids over a longer period than was intended
Experiencing a persistent desire for the opioid or engaging in unsuccessful efforts to cut down or control opioid use.
Spending a great deal of time in activities necessary to obtain, use, or recover from the effects of the opioid.
Craving, or a strong desire or urge to use opioids.
Using opioids in a fashion that results in a failure to fulfill major role obligations at work, school, or home.
Continuing to use opioids despite experiencing persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of opioids.
Giving up or reducing important social, occupational, or recreational activities because of opioid use.
Continuing to use opioids in situations in which it is physically hazardous.
Continuing to use opioids despite knowledge of having persistent or recurrent physical or psychological problems that are likely to have been caused or exacerbated by the substance.
Tolerance, as defined by either a need for markedly increased amounts of opioids to achieve intoxications or desired effect, or a markedly diminished effect with continued use of the same amount of an opioid.
Withdrawal, as manifested by either the characteristic opioid withdrawal syndrome, or taking opioids to relieve or avoid withdrawal symptoms.

335
Q

Rx of opioid abuse

A

Medical:
Opioid substitution with methadone or buprenorphine, followed by a gradual taper
abrupt opioid discontinuation with the use of clonidine to suppress withdrawal symptoms
clonidine-naltrexone detoxification

Psychological:
Behavioral therapies (e.g., community reinforcement, contingency management)
cognitive-behavioral therapies (CBTs) (e.g., relapse prevention, social skills training)
psychodynamic therapy/interpersonal therapy (IPT)
group and family therapies

336
Q

Complications/prognosis of opioid abuse

A

The progression from illicitly using opioids to opioid dependence has dire consequences, including a yearly mortality rate of approximately 2%. Moreover, sustained remission from opioid dependence is difficult to achieve.

337
Q

Define dissociative disorder

A

Dissociative disorders (DD) are conditions that involve disruptions or breakdowns of memory, awareness, identity, or perception. People with dissociative disorders use dissociation as a defense mechanism, pathologically and involuntarily. Some dissociative disorders are triggered by psychological trauma, but dissociative disorders such as depersonalization/derealization disorder may be preceded only by stress, psychoactive substances, or no identifiable trigger at all.

Dissociative identity disorder (formerly multiple personality disorder): the alternation of two or more distinct personality states with impaired recall among personality states. In extreme cases, the host personality is unaware of the other, alternating personalities; however, the alternate personalities can be aware of all the existing personalities.

Dissociative amnesia: the temporary loss of recall memory, specifically episodic memory, due to a traumatic or stressful event. It is considered the most common dissociative disorder amongst those documented. This disorder can occur abruptly or gradually and may last minutes to years depending on the severity of the trauma and the patient.

Dissociative fugue is now subsumed under the dissociative amnesia category. It is described as reversible amnesia for personal identity, usually involving unplanned travel or wandering, sometimes accompanied by the establishment of a new identity. This state is typically associated with stressful life circumstances and can be short or lengthy.

Depersonalization disorder: periods of detachment from self or surrounding which may be experienced as “unreal” (lacking in control of or “outside” self) while retaining awareness that this is only a feeling and not a reality.

Dissociative seizures also known as psychogenic non-epileptic seizures: seizures that are often mistaken for epilepsy but are not caused by electrical pulses in the brain and are in fact another form of dissociation.

338
Q

Epidemiology of dissociative disorder

A

Emerge in adulthood
Rare after 50Y
The lifetime prevalence of dissociative disorders varies from 10% in the general population to 46% in psychiatric inpatients.

339
Q

Aetiology of dissociative disorder

A

Usually related to stress, ongoing childhood trauma, mechanism of coping with trauma

340
Q

RFs for dissociative disorder

A

Stressful life event
Way to cope with trauma
Childhood abuse/trauma

341
Q

Sx of dissociative disorder

A

Dissociative identity disorder (formerly multiple personality disorder): the alternation of two or more distinct personality states with impaired recall among personality states. In extreme cases, the host personality is unaware of the other, alternating personalities; however, the alternate personalities can be aware of all the existing personalities.

Dissociative amnesia: the temporary loss of recall memory, specifically episodic memory, due to a traumatic or stressful event. It is considered the most common dissociative disorder amongst those documented. This disorder can occur abruptly or gradually and may last minutes to years depending on the severity of the trauma and the patient.

Dissociative fugue is now subsumed under the dissociative amnesia category. It is described as reversible amnesia for personal identity, usually involving unplanned travel or wandering, sometimes accompanied by the establishment of a new identity. This state is typically associated with stressful life circumstances and can be short or lengthy.

Depersonalization disorder: periods of detachment from self or surrounding which may be experienced as “unreal” (lacking in control of or “outside” self) while retaining awareness that this is only a feeling and not a reality.

Dissociative seizures also known as psychogenic non-epileptic seizures: seizures that are often mistaken for epilepsy but are not caused by electrical pulses in the brain and are in fact another form of dissociation.

342
Q

Ix for dissociative disorder

A

Structured clinical interview for DSM-V (SCID-D)

Dissociative experiences scale (DES)

343
Q

Rx of dissociative disorder

A

Dissociative identity disorder (multiple personality disorder):
Long-term psychotherapy that helps the patient merge his/her multiple personalities into one personality

Dissociative amnesia: Psychotherapy, hypnosis, art therapy, cognitive therapy, MED: antidepressants/anti anxiety

Dissociative Fugue: hypnosis often used to helped patient recall true identity, psychotherapy

Depersonalization disorder: Psychotherapy, hypnosis, art therapy, cognitive therapy, MED: antidepressants/anti anxiety

344
Q

Prognosis of dissociative disorder

A

Dissociative identity disorder (multiple personality disorder) - many years, can relapse, less of a problem after midlife

Dissociative amnesia / depersonalisation disorder - as brief as a few seconds or continue for several years.

Dissociative fugue - many people recover quickly. The problem may never happen again

345
Q

Define delusional disorder

A

Delusional disorder is a generally rare mental illness in which the patient presents delusions, but with no accompanying prominent hallucinations, thought disorder, mood disorder, or significant flattening of affect.

Delusions are a specific symptom of psychosis. Delusions can be “bizarre” or “non-bizarre” in content; non-bizarre delusions are fixed false beliefs that involve situations that occur in real life, such as being harmed or poisoned. Apart from their delusions, people with delusional disorder may continue to socialize and function in a normal manner and their behavior does not necessarily generally seem odd. However, the preoccupation with delusional ideas can be disruptive to their overall lives.

For the diagnosis to be made, auditory and visual hallucinations cannot be prominent, though olfactory or tactile hallucinations related to the content of the delusion may be present.

The Diagnostic and Statistical Manual of Mental Disorders (DSM) defines six subtypes of the disorder characterized as erotomanic (believes that someone is in love with them), grandiose (believes that they are the greatest, strongest, fastest, richest, or most intelligent person ever), jealous (believes that the love partner is cheating on them), persecutory (delusions that the person or someone to whom the person is close is being malevolently treated in some way), somatic (believes that they have a disease or medical condition), and mixed, i.e., having features of more than one subtype.

346
Q

Epidemiology of delusional disorder

A
24-30/100k
1-2% of psychiatric admissions
Mid-late adulthood
W>M
Increased in migrants
347
Q

Aetiology of delusional disorder

A

Erotomanic type (erotomania): delusion that another person, often a prominent figure, is in love with the individual. The individual may breach the law as he/she tries to obsessively make contact with the desired person.

Grandiose type (megalomania): delusion of inflated worth, power, knowledge, identity or believes themself to be a famous person, claiming the actual person is an impostor or an impersonator.

Jealous type: delusion that the individual’s sexual partner is unfaithful when it is untrue. The patient may follow the partner, check text messages, emails, phone calls etc. in an attempt to find “evidence” of the infidelity.

Persecutory type: This delusion is a common subtype. It includes the belief that the person (or someone to whom the person is close) is being malevolently treated in some way. The patient may believe that he/she has been drugged, spied upon, harmed, harassed and so on and may seek “justice” by making reports, taking action or even acting violently.

Somatic type: delusions that the person has some physical defect or general medical condition

Mixed type: delusions with characteristics of more than one of the above types but with no one theme predominating.

Unspecified type: delusions that cannot be clearly determined or characterized in any of the categories in the specific types

348
Q

RFs for delusional disorder

A
FHx
Drug abyse
Stress
Being married
Low Socio
Celibacy among men
Widowhood among women
349
Q

Sx of delusional disorder

A

The following can indicate a delusion:

The patient expresses an idea or belief with unusual persistence or force, even when evidence suggests the contradictory.

That idea appears to have an undue influence on the patient’s life, and the way of life is often altered to an inexplicable extent.

Despite their profound conviction, there is often a quality of secretiveness or suspicion when the patient is questioned about it.

The individual tends to be humorless and oversensitive, especially about the belief.

There is a quality of centrality: no matter how unlikely it is that these strange things are happening to them, the patient accepts them relatively unquestioningly.

An attempt to contradict the belief is likely to arouse an inappropriately strong emotional reaction, often with irritability and hostility. They will not accept any other opinions.

The belief is, at the least, unlikely, and out of keeping with the patient’s social, cultural, and religious background.

The patient is emotionally over-invested in the idea and it overwhelms other elements of their psyche.

The delusion, if acted out, often leads to behaviors which are abnormal and/or out of character, although perhaps understandable in light of the delusional beliefs.

Individuals who know the patient observe that the belief and behavior are uncharacteristic and alien.

Additional features of delusional disorder include the following:

It is a primary disorder.
It is a stable disorder characterized by the presence of delusions to which the patient clings with extraordinary tenacity.
The illness is chronic and frequently lifelong.
The delusions are logically constructed and internally consistent.
The delusions do not interfere with general logical reasoning (although within the delusional system the logic is perverted) and there is usually no general disturbance of behavior. If disturbed behavior does occur, it is directly related to the delusional beliefs.
The individual experiences a heightened sense of self-reference. Events which, to others, are nonsignificant are of enormous significance to him or her, and the atmosphere surrounding the delusions is highly charged.

350
Q

Ix for delusional disorder

A

Differential diagnosis includes ruling out other causes such as drug-induced conditions, dementia, infections, metabolic disorders, and endocrine disorders.

Other psychiatric disorders must then be ruled out. In delusional disorder, mood symptoms tend to be brief or absent, and unlike schizophrenia, delusions are non-bizarre and hallucinations are minimal or absent.

MSE

351
Q

Rx of delusional disorder

A

Most patients Rx as outpatients
Individual psychotherapy

No real data for antipsychotic use - good if agitated though

352
Q

Define Alzheimer’s

A

Alzheimer’s disease (AD) is a chronic neurodegenerative disease with an insidious onset and progressive but slow decline. AD is the most common type of dementia.
It often co-exists with other forms such as vascular (mixed-type dementia). The histopathology of AD is characterised by senile plaques, neurofibrillary tangles, and neuronal loss. The hallmark symptoms are memory loss, impairment of daily activities, and neurobehavioural abnormalities.

Definition of severity varies according to country, but a commonly accepted categorisation is mild, moderate, and severe. The Mini-Mental State Examination can be used as a guide to cognitive impairment, but education and language must be taken into consideration when interpreting scores.

Chronic, progressive neurodegenerative disorder characterised by a global, non-reversible impairment in cerebral functioning.

Characterised by memory loss, loss of social and occupational functioning, diminished executive function, speech and motor deficits, personality change, plus behavioural and psychological disturbance.

Deteriorating course over up to 8-10 years.

Brain lesions are marked by neurofibrillary tangles, senile plaques, neuronal loss and brain atrophy, with defects in acetylcholine synthesis at the cellular level.

Treatment requires a multidisciplinary approach with increasing emphasis on behavioural and psychological symptoms.

Psychosocial interventions and carer support are key to managing disease course. Caregiver support groups are beneficial to caregivers and should be considered, where available.

353
Q

Epidemiology of Alzheimer’s

A

5.4% >65yo
30% >90

AD is estimated to account for between 35% and 50% of dementia in older people, depending on geographical, cultural, and racial factors.

WM

B>W

Early onset AD (age <60 years) is often autosomally dominantly inherited and accounts for <1% of cases.

AD is the most common type of dementia worldwide.

354
Q

Aetiology of Alzheimer’s

A

There are several theories behind the formation of senile plaques and neurofibrillary tangles. The amyloid hypothesis is currently the most commonly accepted explanation. Brains from Alzheimer’s patients have an excess of interneuronal amyloid (Abeta) peptides, due to overproduction or diminished clearance of beta-amyloid. This leads to the formation of dense amyloid oligomers, which are deposited as diffuse plaques. These plaques cause an inflammatory process through microglial activation, cytokine formation, and activation of the complement cascade. Inflammation leads to the formation of neuritic plaques, causing synaptic and neuritic injury and cell death.

Lifestyle factors including smoking, midlife obesity, and a diet high in saturated fats have also been correlated with an increased risk for the development of AD.

355
Q

RFs for Alzheimer’s

A
STRONG
Increased age
Fix
Genetics (Presenilin 1 + APP)
Down's syndrome
Cerebrovascular disease
Hyperlipidaemia
Lifestyle (smoking, obesity, high satfat)
Less than secondary school education
WEAK
Low IQ
Traumatic brain injury
Depression
DM
Female sex
Elevated plasma homocysteine level
Artificial sweetened soft drink consumption
356
Q

Sx of Alzheimer’s

A
COMMON
RFs
Memory loss
Disorientation
Nominal dysphasia 
Misplacing items/getting lost 
Apathy
Decline in activities of daily living
Personality change 
Normal initial physical examination

OTHER COMMON
Mood changes
Poor abstract thinking
Constructional dyspraxia - Parietal lobe deficits may lead to difficulties completing the clock-drawing test or intersecting pentagons in the Mini-Mental State Examination.

UNCOMMON
Prosopagnosia

357
Q

Ix for Alzheimer’s

A

Minimental state examination MMSE - impaired recall, nominal dysphasia, disorientation (to time, place, and eventually person), constructional dyspraxia, and impaired executive functioning 24/30 = N
Below this, scores can indicate severe (≤9 points), moderate (10–18 points) or mild (19–23 points) cognitive impairment. The raw score may also need to be corrected for educational attainment and age.

FBC - Rule out anaemia
U+E - rule out abnormal
TSH - Rule out hyperthyroid- or hypothyroid-associated dementia.
B12 - rule out B12 deficiency-induced dementia
Urine drug screen
CT - may exclude space-occupying lesions or other pathology
MRI - generalised atrophy with medial temporal lobe and later parietal predominance

358
Q

Rx of Alzheimer’s

A
  1. Supportive treatment
    - OT input - home safety evaluation
    - Prepare power of attorney for healthcare
  2. Environmental control
    - Measures such as identification bracelets or installing sound and motion detectors make the environment safe for wandering patients and minimise the burden on carers.
MEDICAL
CHOLINESTERASE INHIBITORS
Donepezil max 23mg oral
Rivastigmine max 12mg oral
Galatamine max 24mg oral day

SEVERE DISEASE
ADD OR CHANGE TO MEMANTINE

COTREAT DEPRESSION - MAY HELP SX
Sertaline 50-100mg orally OD
Citalopram 10-40mg OD
Mirtazapine: 15-45 mg orally once daily

ANTIPSYCHOTIC USE

Antipsychotic use in patients with Alzheimer’s disease is increasingly controversial.

Many clinicians continue to use these medications for symptoms such as agitation, wandering, hallucinations, and delusions. If there is any evidence of vascular dementia their use should be avoided.

INSOMNIA MANAGEMENT
Trazodone: 25-50 mg orally once daily at bedtime, maximum 200mg/day

AGGRESSION MANAGEMENT
Aggression has multiple causes in Alzheimer’s disease (AD). These include acute confusion, paranoid delusions, agitation or irritability stemming from comorbid depression, or adverse effects of medication.
Citalopram 10mg max 30
Lorazepam 0.5mg orally/OM

359
Q

Complications of Alzheimer’s

A
Pneumonia
Insitutionalisation
UTI
Falls + complications
Elder abuse
Weight-loss
360
Q

Prognosis of Alzheimer’s

A

The natural course is of progressive decline with some plateaus. Some data exist showing that current medications slow the rate of progression or temporarily improve cognition, but overall the current treatment options do not provide solid evidence of improving cognitive function. Cholinesterase inhibitors and NMDA receptor antagonists should be discontinued if there are intolerable adverse effects or there is poor compliance because of financial or other social issues. Family education and referral to resources such as the Alzheimer’s Association are vital, as patient care requires coordination between physician, carer, family, friends, social worker, psychologist, and community supports.

361
Q

A 76-year-old white woman is brought to her general practitioner by her children because she is becoming more forgetful. She used to pay her bills independently and enjoyed cooking but has recently received overdue notices from utility companies and found it difficult to prepare a balanced meal. She has lost 3.5 kg in the past 3 months, and left the water running in her bathtub and flooded the bathroom. When her children express their concerns, she becomes irritable and resists their help. Her house has become more cluttered and unkempt. On a past visit to her physician, she had normal laboratory tests for metabolic, haematological, and thyroid function. The current evaluation reveals no depressive symptoms and 2/15 on the Geriatric Depression Scale short-form. Her Mini-Mental State Examination score is 20/30.

A

Alzheimer’s dementia

362
Q

A 54-year-old black woman is referred to the neurology clinic by her general practitioner for evaluation of memory problems. The patient is brought to the clinic by family members who are concerned that she has been forgetful in the past year. They report that she has difficulty in recalling birthdays and anniversaries and is not managing common household tasks such as cooking and paying bills. The patient’s sister had onset of dementia in her early 40s and was institutionalised because she was unable to care for herself. The patient was last seen by her primary care physician 3 months ago, when she had a routine work-up, which was reported to be unremarkable. Neurological examination revealed no significant abnormalities. Neuropsychological testing demonstrated severe impairment in executive function, deficits in visuo-spatial testing, and delayed speed of processing information. Mini-Mental State Examination score is 20/30.

A

Alzheimer’s dementia

363
Q

Define dementia with Lewy bodies

A

Essential for a diagnosis of dementia with Lewy bodies (DLB) is dementia, defined as a progressive cognitive decline of sufficient magnitude to interfere with normal social or occupational functions, or with usual daily activities. DLB is characterised by the following core clinical features (the first 3 typically occur early, and may persist throughout the course): fluctuating cognition; recurrent visual hallucinations; REM sleep behaviour disorder; and one or more spontaneous cardinal symptoms of parkinsonism: bradykinesia, rest tremor, or rigidity. Prominent or persistent memory impairment may not necessarily occur in the early stages but is usually evident with progression. Deficits on tests of attention, executive function, and visuoperceptual ability may be especially prominent and occur early.
Disease course is progressive, although treatment may help some cognitive, sleep, motor, and behavioural symptoms. DLB should be distinguished from neurocognitive disorder associated with Parkinson’s disease, although there are areas of clinical overlap.

A neurodegenerative disorder with parkinsonism, progressive cognitive decline, prominent executive dysfunction, and visuospatial impairment.

Core clinical features include: recurrent visual hallucinations; cognitive fluctuations; REM sleep behaviour disorder; and one or more spontaeous cardinal features of parkinsonism: bradykinesia, rest tremor, or rigidity. Supportive clinical features include sensitivity to antipsychotic agents, postural instability and falls, syncope, autonomic dysfunction, delusions and non-visual hallucinations, apathy, anxiety, and depression.

Diagnosis is made clinically and can only be confirmed pathologically by the presence of Lewy bodies. Many patients have concomitant Alzheimer’s disease (AD)-type pathology.

Meta-analyses support the use of cholinesterase inhibitors for the cognitive and the neurobehavioural symptoms. Memantine may be of some value in the treatment of dementia and behavioural symptoms.

The use of antipsychotic medication must be minimised due to the increased sensitivity to these medicines’ adverse effects, including increased mortality.

Levodopa/carbidopa can be used for the motor symptoms, though adverse effects may be restrictive and response limited; clonazepam is effective for REM sleep behavioural disorder.

364
Q

Epidemiology of dementia with Lewy bodies

A

10% of all dementia cases

Incidence 0.1%/yr

365
Q

Aetiology of dementia with Lewy bodies

A

The aetiology of DLB is not known. Possible causative mechanisms include:
Toxic protein aggregation
Abnormal phosphorylation
Other molecular mechanisms such as nitration, inflammation, oxidative stress, and lysosomal dysfunction.

Almost all DLB cases are sporadic

However, familial clusters have been reported. It is likely that genetic factors contribute to DLB pathogenesis. Most are autosomally dominantly inherited, though autosomal recessive inheritance has also been implicated. Genes identified in families with DLB include the alpha-synuclein gene on chromosome 4, and apolipoprotein E e4 allele. Other genes implicated include SNCA and glucocerebrosidase (GBA). There does not appear to be an association with MAPT locus, unlike that found in Parkinson’s disease.

366
Q

RFs for dementia with Lewy bodies

A

STRONG
Older age

WEAK
Male
Fix

367
Q

Sx of dementia with Lewy bodies

A

COMMON
RFs
Cognitive fluctuations/arousal/attention
Visual hallucinations - well formed + visual
Motor symptoms - Spontaneous parkinsonian features, not due to antidopaminergic medications or stroke, are present in over 85% of patients with DLB. Parkinsonism in Parkinson’s disease is defined as bradykinesia in combination with rest tremor, rigidity, or both.
REM sleep behavioural disturbance - vivid dreams are accompanied by loss of associated atonia of REM sleep. Patients tend to act out their dreams. Vocalisation, as well as violent and unpredictable movements, may occur.

OTHER COMMON
Antipsychotics worsen motor symptoms and consciousness DO NOT USE.
Depression
Repeated falls and syncope (autonomic dysfunction)
Orthostatic hypotension (autonomic dysfunction)
Urinary incontinence (autonomic dysfunction)
Constipation (autonomic dysfunction)
Attention + visuospatial abnormalities
Delusions
Hypersomnia
Hyposomnia

UNCOMMON
Auditory hallucinations

368
Q

Ix for dementia with Lewy bodies

A
FBC - rule out (RO) anaemia
Met panel - rule out derangements
TSH - rule out (RO) hyper- or hypothyroid-associated dementia.
B12 - RO b12 ass.
Folate - RO deficiency 
VDRL - RO syphilis dementia
Urine drug - RO rec drug use
Urinalysis - RO UTI 
HIV test - rule out HIV (at risk with dementia)
369
Q

Rx of dementia with Lewy bodies

A

ACUTE + Agitated
BDZ: Lorazepam 0.5mg orally/IM
Oxazepam 10-15mg orally QDS

ONGOING
Cholinesterase inhibitors:
Donepezil 
Rivastigmine 
Galantamine

IF VERY PSYCHOTIC
Atypical anti-psychotics
Risperidone/olanzapine/quetiapine
(typical antipsychotics worsen Parkinsonism => CONTRAINDICATED)

COMORBID DEPRESSION
Sertraline 50mg orally OD
Citalopram 10mg orally OD

WITH REM DISORDER
Melatonin
Clonazepam

SEVERE PARKINSONISM:
Dopaminergic agents, typically levodopa, should be given in small doses and titrated slowly. Few controlled trials are available, and caution should be exercised due to possible worsening of cognition, hallucinations, and behaviour; may worsen cognitive and/or behavioural deficits; lowest possible dose should be used and only if necessary. Because of these potential adverse effects, motor symptoms should be treated only if they are severe and interfere with activities of daily living. A significant motor response is seen in approximately one third of patients, with younger patients responding better.

Non-pharmacological approaches to psychosis include providing a comfortable environment with adequate lighting, correcting vision, and decreasing visual triggers. Increasing social engagement and ongoing activities may help mask psychotic symptoms.

370
Q

Complications of dementia with Lewy bodies

A
Pneumonia
Institutionalisation 
Dysphagia 
Antipsychotic sensitivity 
Urinary incontinence and catheterisation complications 
Falls
Elder abuse
371
Q

Prognosis of dementia with Lewy bodies

A

Treatment is symptomatic and is unlikely to entirely prevent cognitive and behavioural disturbance. The course of disease is progressive, and a steady decline in functioning leads to eventual institutionalisation, loss of independence, and death.

A retrospective study of DLB cases confirmed by autopsy showed an average survival of about 5 years. A further study demonstrated a survival time of around 7 years after symptom onset, with higher mortality than with Alzheimer’s disease.

372
Q

A 78-year-old woman presents with confusion, agitation, and visual hallucinations. She has become progressively confused over the past 2 years and has had trouble managing her affairs, including shopping and paying bills. It is unclear when her confusion started. Initially, she was having trouble following conversations and got lost on several occasions. Her memory, which was previously good, has begun to deteriorate. At night, she sees children playing in her house and has called the police on several occasions. She gets angry easily and has been paranoid about her relatives and their intentions. Her behaviour tends to fluctuate from day to day. She started to shuffle about 6 months ago and had difficulty getting out of chairs, and getting dressed to go out seemed to take hours. On one occasion, she fell and was taken to the emergency department but was subsequently discharged with no diagnosis given.

A

dementia with Lewy bodies

373
Q

DLB can present in myriad ways. In most instances, cognitive or neurobehavioural features (e.g., delusions, agitation) lead to medical attention being sought. Other presentations include parkinsonism, excessive night-time motor activity (rapid eye movement [REM] sleep behaviour disorder), and fluctuating levels of attention or alertness. Less commonly, syncope, depression, or autonomic dysfunction can be the presenting feature.

A

dementia with Lewy bodies

374
Q

Define frontotemporal dementia

A

Frontotemporal dementias (FTDs) are the second most frequent primary neurodegenerative brain diseases (after Alzheimer’s disease) in adults <65 years of age. The FTD spectrum comprises a heterogeneous group of conditions that appear heritable in some cases. Prominent early symptoms include progressive coarsening of personality, social behaviour, self-regulation (of emotions, drives, and behaviour), and language. FTDs typically appear in mid-life, with peak onset in the sixth decade.

Gross changes in social behaviour and language are often seen, including indifference to self-care and others’ needs, loss of speech and comprehension, loss of empathy, distractibility, impulsiveness, disinhibition, stereotyped behaviours and rigid routines, and compulsions.

Manifests primarily as disruption in personality and social conduct, or as a primary language disorder.

Almost 50% of all affected people display parkinsonism; a smaller subset may have motor neuron disease.

Clinical diagnosis derives primarily from examination and brain imaging.

Diagnostic confirmation is based on pathological examination or identification of gene mutation.

Treatment is supportive, combining medications with carer guidance, community services, and social work interventions.

375
Q

Epidemiology of frontotemporal dementia

A

15 cases per 100,000 in adults aged 45 to 64 years

M>F

When the therapeutic aim is to slow the progress of dementia, the lack of reliable criteria to distinguish early FTD from other pre-dementia syndromes remains a major obstacle in the design of clinical trials.

The Zuid-Holland epidemiological study reported a positive family history in 43% of cases

376
Q

Aetiology of frontotemporal dementia

A

The Zuid-Holland epidemiological study reported a positive family history in 43% of cases

Genes found:
MAPT chr 17
PGRN chr 17

Known mutations (in MAPT and PGRN genes) could account for <20% of cases.

377
Q

Sx of frontotemporal dementia

A

COMMON
Disregard for social conventions, slovenly appearance, impatience and irritability, argumentativeness, lewd and tactless remarks, child-like and impulsive actions, loss of empathy and concern for others, compulsions, and rigid adherence to routines.

In FTD, changes in personality, language, habits, and activity generally precede the development of memory impairment, disorientation, or apraxias.

Development of memory impairment, disorientation, or apraxias

OTHER COMMON
Age at onset peak in mid-50s
Fix
Altered eating habits - (fads, gorging, and gluttony)
Inattentiveness, puerile preoccupations, economy of effort, and impulsive responding

UNCOMMON
Sx of Amytrophic lateral sclerosis - progressive asymmetrical weakness of spinal or bulbar muscles and muscle wasting.
Parkinsonian Sx
Fasciculations, atrophy, hyper-reflexia, and other signs of motor neuron disease
Glabellar, snout, sucking, rooting, or grasp reflex
Loss of bladder/bowel control

378
Q

Ix for frontotemporal dementia

A

MMSE - < score <24= impairment - disproportionately poor performance in test-taking behaviour and/or in tests of executive functioning; poor emotional processing

MOCA (montreal cognitive assessment) - disproportionately poor performance in test-taking behaviour and/or in tests of executive functioning; poor emotional processing

Brain MRI/CT - focal atrophy in the frontal and/or anterior temporal lobes; frequently the atrophy is characterised by left-right asymmetry

RULE OUT:
FBC - anaemia
ESR/CRP - inflammatory conditions
TSH/T4 - hypothyroidism
Met panel
Urea+creatinine - renal failure
B12/folate
Syphilis
HIV testing 
ELISA for B.burgdorferi - rule out lyme
379
Q

Rx of frontotemporal dementia

A

The first step in the care of a patient with FTD is to educate the patient and carer about the illness, focusing on its key features and how these translate to care needs. The discussion also serves as the context for presenting preliminary plans for managing present-day needs and any behavioural complications and for tailoring these to the patient’s needs. It is also important to address long-term care needs early, because early planning and action maximise options and the patient’s ability to participate. The clinical team should initiate processes that empower carers to assist the patient in making decisions regarding health and property, managing finances, taking medicines, cooking meals, etc.

Aggression/restlessness
BDZ - lorazepam
Neuroleptic - quetiapine/olanzapine

Many patients cannot be managed at home without a professional aide in the home to provide respite to the family, and supervision and assistance to the patient. In many cases, continued home care is no longer possible due to the nature of the care environment (e.g., a spouse who cannot retire) or of the problem behaviours (e.g., night-time roaming, belligerent behaviour). Daycare services can offer respite to weary carers and patients, and may be used in combination with in-home care. Patients who require residential care should generally be cared for in a specialised dementia unit.

WITH COMPULSIONS
Citalopram, sertraline, fluoextine

WITH Hyposomnia
Mirtazipine/trazodone/lorazepam

WITH Mania
valproate semisodium: consult specialist for guidance on dose

WITH gluttony
Topiramate - 25mg OD

380
Q

Prognosis of frontotemporal dementia

A

Median survival is 80 months from diagnosis

Compared with patients with Alzheimer’s disease, FTD patients have shorter survival and faster rates of cognitive and functional decline.

Survival appears to be shorter for patients with parkinsonism and those with motor neuron disease,

381
Q

Complications of frontotemporal dementia

A

Financial crisis
Dangerous driving
Parental relationship breakdown
Legal crisis

382
Q

A 55-year-old man who worked as a technician developed difficulty finding words 2 years earlier, which has evolved into dysfluency, frequent repetition of remarks and questions, stereotypies (purposeless behaviours or fragments of speech frequently repeated, without regard to context), and echolalia (reflexive repetition of another’s speech). In the past year, he has also become forgetful. His work efficiency deteriorated due to his poor comprehension, reasoning, planning, and completion, resulting in disability leave. He also became unfeeling, intrusive (indiscriminately approaching strangers), child-like, and impulsive. He developed rigid routines (e.g., insistence on the same TV shows) and coarse manners (e.g., eating out of serving bowls, jumping queues, and walking away from conversation). Restlessness is marked: each day he bikes, swims many laps, runs 10 km, and ‘volunteers’ at a local nursing home, making the rounds with all maintenance crews. On examination, he is pleasant and cooperative. Given opportunity, he quizzes the examiner on trivial facts (such as listing capital cities). Depression is not evident, and he does not have euphoria, psychosis, or paranoia. Speech is mildly non-fluent. Verbal fluency is impaired. Mini-mental state examination score is 29.

A

frontotemporal dementia

383
Q

A 58-year-old male teacher developed dysnomia, spelling errors, impaired comprehension of reading and conversation, and diminished singing ability. He also has impaired attention, planning, and organisation, along with declining self-care, child-like behaviour, and altered social habits (e.g., eating meals with his fingers). He developed anxiety. Two years into the illness, a neurologist suspected early dementia. Folstein mini-mental state examination score was 27 points and the neurological examination was normal. Brain magnetic resonance imaging showed temporal lobe atrophy, predominantly left-sided. Three years later, his partner complains about impulsive, obstinate, and gluttonous behaviour. Formal neuropsychological testing shows mini-mental state examination score of 28, impaired memory and learning, impaired word and sentence comprehension, marked dysnomia, grammatical and spelling errors, and poor copying of a complex figure.

A

frontotemporal dementia

384
Q

Language presentations are well established, with patients presenting with progressive loss of fluency, syntax, and grammar (primary non-fluent aphasia) that progresses to mutism, or with progressive loss of word (and object) knowledge that results in profound agnosia. Apathetic presentations are also commonly observed, with absent or markedly diminished emotions, self-neglect, and social detachment the predominant features. Parkinsonism may accompany the behavioural or language features, or dominate the presentation with unilateral parkinsonism, apraxia, and alien hand (a phenomenon in which the upper limb performs complex involuntary movements, and may be seen in corticobasal degeneration [CBD]), or with bilateral parkinsonism, falling, and vertical gaze palsy (progressive supranuclear palsy [PSP]). Sometimes an overlapping CBD/PSP presentation is seen. FTD may also present with features of amyotrophic lateral sclerosis (ALS); with a strong male family history of ALS; and presenting features of several months of aloofness, emotional detachment, irritability, rudeness, forgetfulness, and gluttonous eating. Hyper-reflexia and tongue fasciculations may be present, although insufficient for formal diagnosis of ALS.

A

frontotemporal dementia

385
Q

Language presentations are well established, with patients presenting with progressive loss of fluency, syntax, and grammar (primary non-fluent aphasia) that progresses to mutism, or with progressive loss of word (and object) knowledge that results in profound agnosia. Apathetic presentations are also commonly observed, with absent or markedly diminished emotions, self-neglect, and social detachment the predominant features. Parkinsonism may accompany the behavioural or language features, or dominate the presentation with unilateral parkinsonism, apraxia, and alien hand (a phenomenon in which the upper limb performs complex involuntary movements, and may be seen in corticobasal degeneration [CBD]), or with bilateral parkinsonism, falling, and vertical gaze palsy (progressive supranuclear palsy [PSP]). Sometimes an overlapping CBD/PSP presentation is seen. FTD may also present with features of amyotrophic lateral sclerosis (ALS); with a strong male family history of ALS; and presenting features of several months of aloofness, emotional detachment, irritability, rudeness, forgetfulness, and gluttonous eating. Hyper-reflexia and tongue fasciculations may be present, although insufficient for formal diagnosis of ALS.

A

frontotemporal dementia