Mental Health

Mood disorder: depression

Depression is characterised by persistent low mood and/or loss of pleasure in most activities and a range of
associated emotional, cognitive, physical, and behavioural symptoms.

When only depression occurs, it is termed as unipolar disorder. Other mood disorders, termed bipolar disorders,
involve episodes of depression alternating with episodes of mania. Mania without depression (called unipolar
mania) is very rare.

CAUSE of DEPRESSION: is unknown but is likely to result from a complex interaction of biological, psychological, and
social factors.

 Psychosocial issues such as unemployment, divorce, and poverty.

 Genetic factors.
 Personality.
 Failure of adaptive mechanisms to stressors.
 Chronic comorbidities such as diabetes, chronic obstructive pulmonary disease, cardiovascular disease and
especially people with chronic pain syndromes.
 A past head injury, including hypopituitarism following trauma

Complications

 Exacerbates the pain, disability, and distress associated with a range of physical diseases
 Increases mortality:
 In a range of comorbid conditions including coronary heart disease

From suicide.

 Suicide in people who are depressed accounts for nearly 0.6% of all deaths in the general population
 There is a four-times higher risk of suicide in depressed people compared with the general population, and
the risk of suicide is nearly 20-times higher in the most severely ill.

Impairs a person's ability to function normally, which may result in:

 Employment problems.
 Neglect of dependants
 Family problems and relationship break-ups.

Increases the risk of substance abuse.

DX It is defined: by the presence of at least five out of a possible nine defining symptoms, present for at least 2
weeks, of sufficient severity to cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning

 Sleep changes
 Interest
 Guilt
 Energy
 Concentration
 Appetite
 Psychomotor
 Suicide

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Types of depression
The term depression is used to describe several related disorders:

 Major depressive disorder People with major depressive disorder are depressed most days for at least 2
weeks. They may appear miserable. Their eyes may be full of tears, their brows may be furrowed, and the
corners of the mouth may be turned down. They may slump and avoid eye contact. They may hardly move,
show little facial expression, and speak in a monotone.
 Persistent depressive disorder- Symptoms are considered persistent if they continue despite active
monitoring and/or low-intensity intervention, or have been present for a considerable time, typically several
months. (For a diagnosis of dysthymia, symptoms should be present for at least 2 years

 'subthreshold depressive symptoms', which fall below the criteria for a diagnosis of major depression,
and are defined as at least one key symptom of depression but with insufficient other symptoms and/or
functional impairment to meet the criteria for full diagnosis

Bipolar disorder
Bipolar disorder (also o A manic episode is a distinct period during which there is abnormally and persistently
known as bipolar elevated, expansive, or irritable mood lasting at least 1 week, accompanied by at least
affective disorder or three additional
manic depressive  Is severe enough to cause marked impairment in social or occupational
disorder) is a serious functioning or necessitate hospitalization, or
mental illness, with a  Includes psychotic features such as delusions or hallucinations.
long course that is o A hypomanic episode symptom has lasted for 4 days, the episode is not severe
usually characterized by enough to cause marked impairment in social or occupational functioning or
both episodes of necessitate hospitalization, and there are no psychotic features
depressed mood and o A depressive episode is a period of at least 2 weeks during which there is either
episodes of elated depressed mood or loss of interest or pleasure in nearly all activities (or irritability in
mood and increased children and adolescents), accompanied by at least four additional symptoms.
activity (hypomania or o A mixed episode is:
mania)  A mixture or rapid alternation of manic and depressive symptoms
 A period of time (at least 1 week) in which the criteria are met for either a
manic or hypomanic episode and at least three symptoms of depression are
present during the majority of the days of the current or most recent episode of
mania or hypomania
 A period of time (at least 2 weeks) in which the criteria for a major depressive
episode are met and at least three manic or hypomanic symptoms are present
during the majority of the days of the current or most recent episode of
depression

Pathology  There is likely to be a large genetic contribution to bipolar disorder:

o There is a substantial difference in concordance rates between monozygotic and
dizygotic twins, leading to an estimate that 85% of the tendency towards bipolar
disorder is inherited.
 Dysfunction of the hypothalamic-pituitary-adrenal axis (with abnormal secretion of
cortisol, as found in unipolar depression) and dysfunction of the hypothalamic-
pituitary-thyroid axis may contribute to bipolar disorder

 Psychosocial influences (for example childhood maltreatment, traumatic events and

social exclusion) may be both predisposing and precipitating factors in the
development of bipolar disorder.

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Risk Factors o Age 19 and above
o Incidence of bipolar is higher in black and other minorities than in white populations
Clinical Features Irritability
I DIG FASTER Distractibility
Increased Libido
Grandiose delusions
Flight of ideas
Activity increased
Sleep decreased
Talkative
Elevated mood/energy increased
Reduced concentration/Reckless behaviours

ICD-10 criteria for Mania and Bipolar affective disorder

Mania requires 3/9 symptoms to be present

Bipolar affective disorder requires at least two episodes in which a person mood and
activity levels are significantly-one of which must be Mania or hypomania
ICD-10 divides bipolar disorder into 5 states
1. Currently hypomanic
2. Currently manic
3. Currently depressed
4. Mixed disorder
5. In remission

Diagnosis o Mood questionnaire

o Bipolar I disorder is o Blood and urine tests to rule out other disorders –
characterized by at 1. FBC
least one manic 2. TFT  rule out hypo& hyperthyroidism
episode with or 3. LFT Baseline hepatic function with view to starting mood stabilizers
without a history of 4. U&E baseline renal function with view to starting lithium
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 major depressive 5. Glucose, calcium  biochemical disturbance
episodes. 6. Urine drug test  illicit drugs may cause manic symptoms
o Bipolar II disorder is o CT head to rule out space occupying lesions
characterized by o The diagnosis of bipolar disorder is based on specific lists of symptoms (criteria).
one or more major However, people with mania may not accurately report their symptoms because they
depressive episodes do not think anything is wrong with them. So, doctors often have to obtain
and by at least one information from family members.
hypomanic episode, o Doctors also ask people whether they have any thoughts about suicide.
but no evidence of
mania
Classification of bipolar Bipolar I
affective disorder Involves severe mood episodes from mania to depression

Bipolar II
Milder form of mood elevation involving milder episodes of hypomania that alternate with
periods of severe depression

Rapid cycling
More than 4 mood swings in a 12-month period with intervening asymptomatic periods
Complications  The most important complication of bipolar disorder is suicide and deliberate self-
harm.
 Other consequences of acute episodes are:
o Financial ruin arising from overspending.
o Traumatic injuries and accidents.
o Sexually transmitted infections and unplanned pregnancy arising from
disinhibition and increased libido.
o Damage to reputation, occupation, and relationships.
o Alcohol and substance misuse.
o Reduced quality of life and functioning.
o Harm to others from:
 Neglect.
 Depressive or paranoid delusions.
 Grandiosity, overspending, poor judgement, and erratic or chaotic
behaviour (e.g. resulting in road traffic accidents).
 Rarely, violence and aggression (particularly if there is a personal history
of violent behaviour).
 Cardiovascular disease - people with bipolar disorder have an increased risk of
cardiovascular disease.
o Lifestyle factors (for example poor diet and smoking).
o Adverse effects of antipsychotic drugs, such as weight gain.
o Substance misuse (for example alcohol and illegal drugs).
Management and ♠ Full Risk Assessment is vital  rule out suicidal risk and risk to self (financial ruin from
Treatment overspending)
♠ Ask about Driving  DVLA has clear guidelines about driving
♠ The Mental Health Act compulsory admission and treatment of people who: Have a
mental disorder of a nature and degree that warrants treatment in hospital, and
♠ Compulsory admission is arranged using the appropriate section of the Mental
Health Act:
♠ Section 2  compulsory admission for up to 28 days for assessment.
♠ Section 3  compulsory admission for up to 6 months for treatment (in people with
an established diagnosis).
♠ Section 4  exceptional cases to permit compulsory admission for up to 72 hours
♠ Section 136 used by police to take people from a public place to a place of
safety to enable examination by a registered medical practitioner and interview by an
AMHP.
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 Pharmacological intervention
For the 1st line treatment of mania, options include:
 A therapeutic trial of an oral antipsychotic (haloperidol, olanzapine,
quetiapine, or risperidone).
 If the first antipsychotic is not tolerated or not effective, a second
antipsychotic (from one of the four antipsychotics listed above) is usually
offered.
2nd line treatment  lithium may be added, or if this is not suitable, sodium valproate
may be added instead.

Lithium  standard long-term therapy: Lithium can lessen the symptoms of mania and
depression. Lithium helps prevent mood swings in many people with bipolar disorder.
Because lithium takes 4 to 10 days to work, a drug that works more rapidly, such as an
anticonvulsant or a newer (second-generation) antipsychotic drug, is often given to
control excited thought and activity. Lithium can have side effects. It can cause
drowsiness, confusion, involuntary shaking (tremors), muscle twitching, nausea,
vomiting, diarrhoea, thirst, excessive urination, and weight gain. It often worsens a
person's acne or psoriasis
♠ Four weeks after the acute episode has resolved, the secondary care team will
usually discuss the long-term management plan.
o To prevent relapses, the person is usually offered a choice to:
 Start long-term treatment with lithium to prevent relapses, or
 If lithium is not effective, valproate may be added to lithium treatment.
♠ Benzos for sleep and agitation.

♠ Lorazepam is a sedation/tranquilizer.

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Personality disorders

☺ A deeply ingrained and enduring pattern of inner experience and behaviour that deviates markedly from
expectations in the individuals culture is Pervasive and inflexible has an onset in adolescence or early
adulthood, is stable over time and leads to distress or impairment

Pathophysiology and Risk factors

The cause of personality disorders involves both biological and environmental factors

1. Society  both low socioeconomic status and social reinforcement of abnormal behaviour are liked to PD
2. Genetics  Twins
3. Dysfunctional Family  poor parenting and parental deprivation are a risk for the development of PD
4. Abuse during childhood  physical, sexual and emotional abuse as well as neglect

There are 8 specific PDs classified by the ICD 10 however I have added the remaining two

Cluster A weird
Paranoid Personality disorder
A pervasive distrust and suspiciousness of others such that their
motives are interpreted as malevolent
Beginning by early adult hood and may presents as
 Suspects without sufficient basis that others are exploiting, harming
or deceiving him/her

 Is preoccupied with unjustified thoughts about the loyalty or

trustworthiness of friends or associates

 Is reluctant to confide in others because of an unwarranted fear that

the info will be maliciously used against him/her

 Reads hidden demeaning or threatening meaning into benign

remarks or events
 Bears grudges
 Suspicious about fidelity of spouse
Schizoid Distant Pervasive detachment to social relationships and restricted range of
Detached expression of emotions in interpersonal settings, beginning by early
Indifferent to praise and critism childhood and present in a variety of contexts
Sexual drive reduced
Task done alone  Neither desired nor enjoys close relationships including being part of
Absence of close friends a family
No emotion  Almost always chooses solitary activities
Takes pleasure in few activities  Has little if any interest in having sexual experiences with another
person
 Lacks friends and close confidants

Schizotypal- Odd People with schizotypal personality disorder:

 Behave oddly, are uncomfortable around other people, and are
somewhat out of touch with reality
 Avoid social situations and choose to be alone
 Don't have close friends
 Have trouble interpreting other people's emotions
 Think in odd, magical ways, such as believing they can control
someone with their mind
 Are suspicious and mistrustful, such as mistakenly believing that
someone wants to hurt them
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  Use words in unusual ways, so their speech is strange
 Dress oddly, such as wearing dirty or wrongly-sized clothes
They may also have depression or abuse drugs or alcohol.
Schizotypal personality disorder is similar to but milder than
schizophrenia which causes more severe and bizarre thinking and
behaviour.
Cluster B wild
Emotionally Unstable (Borderline) Pattern of inability of interpersonal relationship self-image and affects
and marked impulsivity beginning by early adulthood and present in
Am Suicide variety of context
Abandonment feared  Frantic efforts to avoid real or imagined abandonment
Mood stability  A pattern of unstable and intense interpersonal characterised by
alternating between extremes of idealization and devaluation
Suicidal behaviour  Recurrent suicidal behaviour, gestures, threats or self-mutilating
Unstable relationships behaviour
Intense relationships  Chronic feeling of emptiness
Control of anger poor  Inappropriate intense anger or difficulty controlling anger
Impulsivity  Impulsivity in at least two areas that are potentially self-
Disturbed sense of self (identity) damaging (spending, sex, substances abuse reckless driving binge
Emptiness eating )
Dissocial (Antisocial) Pattern for disregard and violation of the rights of others occurring since
“Corrupt” age 15 years
Callous
Others blamed  Failure to conform to social norms with respect to lawful
Reckless disregard for safety behaviours repeatedly performing acts that are grounds for
Remorseless arrest
Underhanded  Deceitfulness, indicated by repeated lying of aliases conning
Poor planning others for personal gain
Temper/tendency to violence  Impulsivity and failure to plan ahead
 Irritability and aggressiveness
 Reckless disregard for safety of others
 Consistent irresponsibility as indicated by repeated failure to
sustain consistent work.
Histronic Pattern of excessive emotionally attention seeking.
“Praise”  Is uncomfortable in situations where he or she is not the centre of
Provocative behaviour attention
Real concern for physical  Interactions with others is often characterised by inappropriate
attractiveness sexually seductive or proactive behaviour
Attention seeking  Displays rapidly shifting and shallow expressions of emotions
Influenced easily  Consistently uses physical appearance to draw attention to self
Shallow/seductively inappropriate  Shows dramatization theatrical exaggerated expression of
Egocentric emotion
 Is suggestible
 Considers relationship to be more intimate than they actually are
Narcissistic Pattern of grandiosity (in fantasy or behaviour) need for admiration and
lack of empathy beginning by early adulthood and present in a variety of
context.
 Has a grandiose sense of importance
 Exaggerates achievements and talents
 Preoccupied with fantasies of unlimited success, power brilliance,
beauty or ideal love
 Believes he or she is special and can only be understood by or
associated with high status people
 Interpersonally exploitative
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  Lack empathy
 Often envious of others
 Shows arrogance and haughty attitudes
Cluster C  Worriers
Dependence Dependent personality disorder is:
 A pattern of feeling extremely dependent on other people to
take care of them
People with dependent personality disorder often:

 Fear they can't take care of themselves and worry about being
abandoned
 Appear submissive and needy so others will want to take care of
them
 Lack confidence and need a lot of reassurance
 Let others make decisions for them, for example, having their spouse
tell them what to wear, what job to take, and who their friends are
 Let others take advantage of them, such as by agreeing to do
unpleasant tasks for them
 Tolerate physical, emotional, or sexual abuse for fear of losing the
abuser's support
 Have a hard time disagreeing with others even when they're in the
right
 Have a hard time starting projects on their own or working
independently, but when they feel reassured that someone is
supporting them, they usually function all right

What causes dependent personality disorder?

Dependent personality disorder is probably caused by a combination of:

 Traits that run in families

 Bad experiences in childhood
 Anxiety

Avoidant ( anxious ) Pattern of social inhibition, feelings of inadequacy and hypersensitivity to

negative evaluation beginning by early adulthood and present as

 Avoids occupational activities that involve significant interpersonal

contact because of fear of criticism, disapproval or rejection
 Is unwilling to get involved with people unless certain of being liked
 Shows restraint within intimate relationships because of the fear of
being shamed or ridiculed
 Is inhibited in new interpersonal situations because of feeling of
inadequacy
 Views themselves as undesirable and inferior to others
Anankastic Obsessional Loses point of activity due to preoccupation with detail
Ability to complete task is compromised
Workaholic at expense of leisure
Fussy
Inflexible
Rigid
Meticulous attention to detail
Stubborn

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Diagnosis Q and Questionnaire

1. Personality Questionnaire.--> Eysenck personality questionnaire

2. Psychological testing MMPI Minnesota multiphasic personality inventory
3. Substance Misuse

Management
1. Identify and treat co-morbidity mental health disorders
2. Risk assessment is crucial especially in case of emotionally unstable PD where patients may be suicidal
potential stressors that induce crises should be identified and reduced
3. Several psychosocial interventions exist in the treatment of PD  social support groups
4. Pharmacological management will not resolve the PD, but may be used to control symptoms.
a. Low dose antipsychotics for ideas for reference, impulsivity and intense anger
b. Mood stabilisers
c. Antidepressant
5. Psychological  cognitive behavioural therapy , psychodynamic psychotherapy, dialect individual therapy
6. Give the patient a written crisis plan. At times of crisis if dangerous and violent or if there is a suicide risk
consider Crisis Resolution Team and detention under the Mental Health Act

 Biopsychosocial Model

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 Anxiety Disorders

Disorder
Generalized  (GAD) is characterized by disproportionate, pervasive, uncontrollable, and widespread worry and a
anxiety disorder range of somatic, cognitive, and behavioural symptoms that occur on a continuum of severity
 GAD is defined in
o The DSM-V criteria require core symptoms of excessive widespread worry for more days than
not, which is difficult to control and present for at least 6 months
o The ICD-10 criteria require symptoms of anxiety to be present for most days for several months
and should include elements of apprehension, motor tension and autonomic over activity

(GAD) is one of a range of anxiety disorders which also include acute stress disorder, obsessive-
compulsive disorder, panic disorder, post-traumatic stress disorder, social phobia, and specific
phobias

Risk Factor and Clinical Features

 Female sex.
 Childhood adversity such as:
o Maltreatment (for example, sexual or physical abuse).
o Parental problems  partner violence, alcoholism, drug use, and/or mental illness.
o Exposure to an overprotective or overly harsh parenting style, Bullying
 Environmental stressors such as:
o Physical or emotional trauma.
o Domestic violence, Unemployment, Low socioeconomic status.
 Substance dependence or exposure to organic solvents — these can exacerbate the development
of anxiety disorders
Clinical Features
☺ Worry, Autonomic hyperactivity ( sweating, ↑Pupil size, ↑HR)
☺ Tension in muscles/ tremor
☺ Muscle tension
☺ Difficulty in breathing
☺ Concentration difficulty/ Chronic aches
☺ Headache/hyperventilation , Energy loss
☺ Restlessness, Startled easily/sleep disturbance

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 Diagnosis
1. Generalized anxiety disorder questionnaire
 The generalized anxiety disorder questionnaire (GAD-7) consists of 7 questions. The score is
calculated by assigning scores of 0, 1, 2, and 3, to the response categories of 'not at all', 'several
days', 'more than half the days' and 'nearly every day' adding up to a possible total of 21.
Scores of 5, 10, and 15 are taken as cut-off points for mild, moderate, and severe anxiety
respectively. The person should be asked 'over the last 2 weeks, how often have you been
bothered by any of the following problems’?
o Feeling afraid, as if something awful might happen.
o Becoming easily annoyed or irritable.
o Being so restless that it is hard to sit still.
o Trouble relaxing.
o Worrying too much about different things.
o Not being able to stop or control worrying.
o Feeling nervous, anxious, or on edge.
2. Other questionnaires  Beck’s anxiety Inventory, Hospital Anxiety and depression scale
3. Check appearance, speech, mood (anxious), Thought, Perception, Cognition, Insight
4. Do blood test FBC (infection), TFT (hyperthyroidism), Glucose, ECG tachycardia

Management
 Step 1 —
o Assess the severity of GAD. Ask about:
 The number, severity, and duration of symptoms.
 The degree of distress and functional impairment.
 Consider using validated assessment tools such as the GAD-7 questionnaire, to help
determine GAD severity.
o Provide written material about the nature of GAD and its treatment options:
 Step 2 — For people who have not improved following step 1 interventions, offer low-
intensity psychological interventions based on cognitive behavioural therapy (CBT) principles,
such as :
o Individual non-facilitated self-help — should include suitable written or electronic materials that
the person works through systematically over a period of at least 6 weeks. Minimal therapist
contact, for example an occasional short telephone call of no more than 5 minutes, is required.
o Individual guided self-help — should include suitable written or electronic materials, and be
supported by a trained practitioner who facilitates the programme and reviews progress and
outcome. This usually consists of five to seven weekly or fortnightly face-to-face or telephone
sessions, each lasting 20–30 minutes
o Psychoeducational groups — should have an interactive design and encourage observational
learning through presentations and self-help manuals. They should have a ratio of
approximately one trained practitioner to 12 participants and usually consist of six weekly 2
hour sessions
 Step 3 —
o high-intensity psychological intervention CBT or applied relaxation,
o Psychological interventions - Inform the person that response to psychological treatment is not
immediate and that a prolonged course is usually needed to maintain an initial response.

o Drug treatment

 1st -line treatment is usually with a selective serotonin reuptake inhibitor (SSRI) such as
sertraline, paroxetine, or escitalopram.
 A selective serotonin-noradrenaline reuptake inhibitor (SNRI), such as duloxetine or
venlafaxine is a possible alternative.

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 Pregabalin can be offered if SSRIs or SNRIs are contraindicated or not tolerated.
Discuss the potential for adverse effects and withdrawal symptoms before drug treatment is initiated.
Explain that adverse effects early in treatment with an SSRI or SNRI may include increased anxiety,
agitation, and sleeping problems.
 Do not offer an antipsychotic for the treatment of GAD in primary
care.
 Step 4 — Refer for specialist treatment when patient is at risk of:
o Self-harm.
o Self-neglect.
o A significant comorbidity such as substance misuse, personality disorder, or complex physical
health problem.
o Suicide

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Phobias A phobia is an intense, irrational fear of an object, situation, place or person that is recognized as
excessive or unreasonable

Agoraphobia:
“Fear of marketplace”. It is the fear of Public spaces or fear of entering a public space from which
immediate escape would be difficult in event of a panic attack
Social Phobia
Is characterized by intense fear in social situations, causing significant distress and impaired ability to
function in parts of daily life. Social phobia can be subdivided into generalized social phobia (aka social
anxiety disorder) and specific social phobia, in which anxiety is triggered only by very specific social
situation
Specific Phobia
A fear restricted to a specific object or situation

Diagnostic Criteria For Specific Phobia

1. Marked and persistent fear that is excessive or unreasonable, cued by the presence or
anticipation of a specific object or situation.
2. Exposure to the phobic stimulus almost invariably provokes an immediate anxiety response,
which may take the form of a situationally bound or situationally predisposed panic attack.
3. The avoidance, anxious anticipation, or distress in the feared situation(s) interferes
significantly with the person’s normal routine, occupational (or academic) functioning, or
social activities or relationships, or there is marked distress about having the phobia.
4. The anxiety, panic attacks, or phobic avoidance associated with the specific object or
situation are not better accounted for by another mental disorder

☺ Fear of animal
 Spider – arachnophobia
 Insects – entomophobia
 Dogs – Cynophobia
 Birds – ornithophobia
☺ Nature forces
 Thunder – Astraphobia
 Storms - Lilapsophobia
 Water – aquaphobia
☺ Blood/injection/injury
 Sight of blood- haemophobia
 Physical injury- traumatophobia
☺ Situational
 Closed Spaces –claustrophobia
 Heights or flight – acrophobia

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 Clinical features
Biological: Tachycardia, a vasovagal response, fainting
Psychological: include unpleasant anticipatory anxiety, inability to relax, urge to
avoid feared situation and at extremes a fear of dying

Agoraphobia strongly linked to panic disorder.

Aetiology
1. Psychodynamic Theory
Anxiety is usually dealt with the defense mechanism of repression. When repression fails to
function
adequately, other secondary defense mechanisms of ego come into action
In phobia  , this secondary defense mechanism is displacement. By using dis placement,
anxiety is transferred from a really dangerous or frightening object to a neutral object. These
two objects are often connected by symbolic associations. The neutral object chosen
unconsciously is the one which can be easily avoided in day-to-day life, in contrast to the
frightening object (frightening to the patient only, due to oedipal genital drives).
In agoraphobia,  loss of parents in childhood and separation anxiety have been theorised to
contribute to causation.

Differential Diagnosis
The differential diagnoses include anxiety disorder, panic disorder, major
depression, avoidant personality disorder, obsessive compulsive disorder,
delusional Disorder, hypochondriasis, and schizophrenia.

Management
1. Try and establish a good rapport with the patient. Remember that it may be
challenging for the patient to attend the appointment
2. Advise avoidance of anxiety inducing substances – caffeine
3. Screen for significant co-morbidities such as substance misuse and personality
disorders
4. Psychotherapy – Cognitive behavioural therapy
5. Gradual exposure techniques such as increased walking distances
(Agoraphobia)

Pharmacological treatment
1. SSRI – first Line for agoraphobia
2. SSRi, SNRi Venlafaxine if no response... MAOi (moclobemide)
3. Psychodynamic psychotherapy for those who decline CBT or medication
4. Don’t use Benzodiazepines unless  may be used but for short term due to
tolerance and dependence.

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  Obsessive-compulsive disorder (OCD) is characterized by recurrent obsessional thoughts or
compulsive acts or, commonly, both, which may cause significant functional impairment and/or
Obsessive distress.
Compulsive o An obsession is defined as an unwanted intrusive thought, image, or urge that repeatedly enters
Disorders the person's mind, and that usually causes marked anxiety or distress. Common obsessions in
OCD include:
 Contamination from dirt, germs, viruses (e.g. HIV), bodily fluids or faeces, chemicals,
sticky substances, dangerous materials (e.g. asbestos).
 Fear of harm.
 Excessive concern with order or symmetry.
 Superstition, fear of 'bad' numbers 'magical' thinking, religious obsessions.
o Compulsions are repetitive behaviours or mental acts that the person feels driven by their
obsession(s) to perform. Common compulsions in OCD include:
 Repetitive hand washing — due to fear of contamination.
 Checking (e.g. that doors are locked, electrical items unplugged, gas taps are off) — due
to fear of harm to self or others, Ordering, arranging, and/or repeating
 Mental compulsions (e.g. special words or prayers repeated in a set manner, asking for
forgiveness, excessive counting) — due to religious beliefs, 'magical' thinking,
superstitions.
 Memory checking and avoidance of triggers — due to concerns about 'forbidden'
thoughts or images.
o In children and young people:
 Young children's obsessional thoughts are more likely to include 'magical' or superstitious
thinking (e.g. If I don't count up to 20, my parents will die).
 Members of the family are almost always involved in a young person's compulsive rituals.

Risk factors for the development of obsessive-compulsive

disorder (OCD) include:
o Family history:
o Age
 A bimodal onset has been observed, with peak mean ages of onset at
approximately 10 years and 21 years.
 Onset over the age of 30 years is rare.
o Developmental factors
 Emotional, physical, and sexual abuse, neglect, social isolation, bullying.
o Pregnancy and the postnatal period
 Common obsessions in these periods are worries about harming or abusing the
baby and/or not being careful enough e.g. with sterilizing feeding equipment.
Compulsions include avoidance behaviour, repeatedly seeking approval, checking
the baby is still breathing.
Complications of obsessive-compulsive disorder (OCD) include:
 Reduced quality of life — adverse effects on daily life, personal relationships, and ability
to work and/or study. Fear of contamination can prevent the accessing of appropriate
health care. Childhood or adolescent onset may prevent the person from socialising with
peers and may eventually cause difficulties with independent living.
 Dermatitis — due to excessive handwashing.
 Self-harm and suicide — people with OCD, particularly those who also have depression,
may be at increased risk of self-harm and/or suicide.

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 Clinical Features

Diagnosis
1. (ICD-10) criteria for a diagnosis of obsessive-compulsive disorder (OCD) are the presence
of recurrent, obsessional thoughts or compulsive acts:
o Obsessional thoughts are:
 Ideas, images, or impulses that enter the person's mind again and again in
stereotyped form.
 Almost invariably distressing, and the person often tries, unsuccessfully, to resist
them.
o Compulsive acts or rituals are:
 Stereotyped behaviours that are repeated again and again.
 Not inherently enjoyable, nor do they result in completion of inherently useful
tasks.
 Performed to prevent some objectively unlikely event,
2. Yale-Brown obsessive compulsive scale Y-BOCS10 item questionnaire with each graded
from 0-4 ( time occupied by obsessive thoughts
3. Behavioural Avoidance Tests: They are designed to assess in vivo fear and avoidance
behaviour. Several types of BAT has been developed for use in OCD
4. National Institute of Mental Health Global Obsessive- Compulsive Scale(NIMH-GOCS)
5. Assessment of psychiatric co-morbidity
6. Past Medical History and Family History and Mental Health assessment
Differential diagnosis
The differential diagnoses of obsessive-compulsive disorder (OCD) include:
 Obsessive-compulsive personality disorder (OCPD) — suggested by a preoccupation
with orderliness, details, rules, organisation, or schedules, to the degree that the point
of the activity is lost, with absence of obsessions and compulsions, but may involve
discomfort if things are sensed not to have been done completely.
 Body dysmorphic disorder (BDD) — suggested by obsessive preoccupation with a
perceived defect in physical appearance.
 Somatic symptom disorder — suggested by excessive thoughts, feelings, or behaviours
related to somatic symptoms or associated health concerns.

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  Illness anxiety disorder (hypochondriasis) — suggested by a preoccupation with having
or acquiring serious illness and excessive health-related behaviours, such as repeatedly
checking for signs of illness. May demonstrate maladaptive avoidance, such as avoiding
medical appointments.
 Delusional disorder — suggested by a false belief that is firmly sustained and based on
incorrect inference about reality. Compulsions may be absent.
 Hoarding disorder — suggested by persistent difficulty in discarding or parting with
possessions, regardless of actual value, due to perceived need to save items and
distress associated with discarding them.
 Trichotillomania (hair-pulling disorder) — suggested by recurrent pulling out of hair,
resulting in hair loss.
 Excoriation (skin-picking) disorder
Management and Treatment
1. Assess their degree of distress and functional impairment as mild, moderate, or severe
a. Ask about the effects on work or school, relationships, social life, and quality of life.
2. Consider using a severity rating scale such as the Yale–Brown Obsessive-Compulsive Scale (Y-
BOCS)
3. OCD may exist with other mental health disorders including depression, anxiety, alcohol or
substance misuse, body dysmorphic disorder, and/or an eating disorder.
4. Refer for specialist treatment people whose OCD and marked functional impairment are
assessed as 'severe', and/or those exhibiting, or at risk of:
a. Self-harm.
b. Self-neglect.
5. A significant comorbidity such as substance misuse, severe depression, anorexia nervosa, or
schizophrenia.
6. Following assessment, a low intensity cognitive-behavioural therapy (CBT), including exposure
and response prevention (ERP) may be offered. The format for low-intensity CBT should be
up to 10 therapist-hours per person, of one of the following:
a. Brief individual CBT (including ERP) with structured self-help materials.
b. Brief individual CBT (including ERP) by phone.
c. Group CBT (including ERP) which may be for more than 10 hours.
7. Pharmacological therapy- SSRI - Escitalopram, fluoxetine, fluvoxamine, paroxetine, and
sertraline. Citalopram can also be prescribed as a treatment for OCD, but this is an unlicensed
use.
(a) Discuss the potential for adverse effects and withdrawal symptoms before drug
treatment is initiated. Explain that adverse effects early in treatment with an SSRI may
include increased anxiety, agitation, and sleeping problems.
(b) prescribing clomipramine (as an alternative first-line drug treatment to an SSRI)

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19 | P a g e
Post-Traumatic Stress Disorder

Post-traumatic stress disorder can develop following a major traumatic event

(such as a serious accident, a violent personal assault, or military combat)

Post
Traumatic Clinical Features
Stress
 Re-experiencing symptoms — which may occur in the daytime when the person is
Disorder
awake (flashbacks, or intrusive images or thoughts) or as nightmares when asleep.
 Avoidance of people or places that remind the person of the event.
 Emotional numbing/negative thoughts, where the person expresses a lack of ability
to experience feelings or feels detached from other people, or has negative thought
about themselves.
 Hyperarousal/hyper reactivity, where the person is on guard all the time, looking for
danger (hypervigilance), or the person has irritable behaviour or angry outbursts with
little or no provocation.

The person is said to have post-traumatic stress disorder if a defined number

of symptoms persist for more than 6 month after the major traumatic event

What is a major traumatic event?

☺ The ICD-10 describes a major traumatic event as 'a stressful event or situation of an
exceptionally threatening or catastrophic nature, which is likely to cause pervasive
distress in almost anyone'
☺ The DSM-5 describes a traumatic event as 'exposure to actual or threatened death, serious
injury, or sexual violence

 Examples of major traumatic events include

o Serious accidents, Military combat, Violent personal assault (sexual assault, physical
attack, abuse, robbery, mugging), Being taken hostage.
o Terrorist attack, being a prisoner-of-war.
o Torture.
 Upsetting events that do not lead to post-traumatic stress disorder include
o Divorce, Job loss, failing an examination.

Exposure to a major traumatic event is a risk factor for post-traumatic stress

disorder.

☺ Members of the armed forces (including combat veterans and ex-service

personnel).
☺ Police, prison and fire services, Ambulance and emergency personnel
☺ Nursing and medical professions (especially in front-line situations, such as
casualty).
☺ Journalists, Refugees and asylum seekers (especially those from conflict zones).

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 Factors which are associated with developing post-traumatic stress disorder

Pre-trauma factor→→ Previous trauma, History of psychiatric illness (personal and family), Female,
Lower socioeconomic background, childhood abuse

Peri-trauma factors →→Severity of the trauma, Perceived threat to life, Dissociative experiences,
Adverse emotional reaction during, or immediately after, the event.

Post-trauma factors →→ Concurrent life stressors, Absence of social support.

A child is at risk of developing post-traumatic stress disorder (PTSD) following exposure

to a major traumatic event. →→ Female gender, Previous trauma exposure, Pre-existing psychiatric
disorders, Low social support.

The risk of PTSD is reduced by good family support and when there is less parental distress.

ICD-10 Criteria for diagnosis of PTSD

1. Exposure to stressful event or situation of extremely threatening or catastrophic nature
2. Persistent remembering of stressful situation
3. Actual or preferred avoidance of similar situation resembling or associated with a stressor
4. Either
a. Inability to recall some important aspects of the period of exposure to the stressor
b. Persistent symptoms of increased psychological sensitivity and arousal

History taking
 Has there been any traumatic incident or event in your life recently which may account for
how you are feeling?(Exposure to stressful event)
 Do you ever get any flashbacks, vivid memories or nightmares about the events that took
place? (reliving the situation)
 Do you find yourself constantly thinking about the same thing
 Have you had any problems with sleep since the event? Are you feeling more irritable or
having trouble concentrating? Do you get startled easily? (Hyperarousal)

Mental State Examination

Appearance →→ hyper vigilant, on edge, poor eye contact
Speech →→ slow rate trembling
Mood →→ anxious
Thought →→ pessimistic. Reliving or remembering of the event
Perception →→ no hallucination but may have illusions
Cognition →→ poor attention and concentration

Investigation
1. Questionnaires →→ Trauma Screening Questionnaire, Post ytraumatic diagnostic
scale
2. CT head if injury is suspected

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 DDX
1. Adjustment disorder, bereavement, acute reaction to stress, anxiety disorders
2. Organic  head injury, alcohol abuse

Management
How should I manage an adult with post-traumatic stress
disorder?
 Risk assessment for suicide:
Suicide risk assessment  Directly ask about suicidal thoughts and
intent.
Ask if the person feels hopeless or that life is not worth living.
Suggested questions are:

 Do you ever think about suicide?

 Have you made any plans for ending your life?
 Do you have the means for doing this available to you?
 What has kept you from acting on these thoughts?
Follow up on 'not really' answers.

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  Offer trauma-focused psychological treatments such as Trauma focused CBT, EMDR, Exposure
Therapy
 Exposure therapy — the person confronts traumatic memories (usually by
recounting the event) and is repeatedly exposed to situations which they have
been avoiding that elicit fear.
 Trauma-focused cognitive therapy — this identifies and modifies
misrepresentations of the trauma and its aftermath that lead the person to
overestimate the threat. For example, rape victims may blame themselves, war
veterans may feel that it was their fault a friend was killed.
 EMDR uses bilateral stimulation (eye movements, taps, and tones) while the
person focuses on memories and associations. This is thought to help the brain
process flashbacks and to make sense of the traumatic experience

 Consider treatment with an antidepressant such as paroxetine or mirtazapine,

amitriptyline and phenelzine if:
1. Little benefit comes from psychological therapy
2. Patient prefers medication
3. Co-morbid depression or Hyperarousal

NICE found evidence that trauma-focused psychological treatments (trauma-focused CBT

and EMDR) were effective for treating post-traumatic stress disorder, depression, and
anxiety compared with no treatment (being placed on a waiting list), stress management,
and other therapies (supportive therapy and non-directive counselling, psychodynamic
therapies, and hypnotherapy). Trauma-focused CBT has the largest evidence base of all the
psychological therapies.

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Eating Disorders
An eating disorder is characterized by a persistent disturbance of eating or eating related behaviour that
results in altered consumption or absorption of food that significantly impairs physical health or
psychosocial functioning
 The main types of eating disorders are:

o Anorexia nervoa
o Bulimia nervosa
o Binge eating disorder — characterized by recurring episodes of eating significantly more
food in a short period of time (usually less than 2 hours) than most people would eat under
similar circumstances. These episodes are marked by feelings of lack of control.
Compensatory behaviour (for example vomiting, fasting, or excessive exercise) is absent.
o Atypical eating disorders (also known as 'other specified feeding or eating disorder'
[OSFED]) — characterized by symptoms of an eating disorder such as anorexia nervosa, or
bulimia nervosa, but does not meet the precise diagnostic criteria for them. For example, all
of the criteria for anorexia nervosa are met, there is significant weight loss, but the person's
weight is within or above normal range.

Anorexia Nervosa
Anorexia An eating disorder characterised by deliberate weight loss, an intense fear of fatness, distorted
Nervosa body image and endocrine disturbances
Pathophysiology Biological  Female, adolescence, early menarche, Family history of eating disorders
Social  western society pressure to diet in a society that emphasizes that being thin is beauty.
bullying revolving round weight
Occupational pressure to lose weight for your occupation- ballet, dancers, models
Psychological  Sexual abuse, low self-esteem, perfectionism obsessional/Anakastic personality
= criticism regarding eating , body shape or weight

Clinical features  Weight maintained at least 15% below that expected for the person- in adults this normally
represents a BMI of less than 17.5 kg/m2.
 Self-avoidance of foods thought to be fattening to achieve weight loss
 Self-induced purging (by vomiting or excessive use of laxatives).
 Use of appetite suppressants, Use of diuretics.
 Weight loss may also be supported by excessive exercising
 Distorted body image
 A widespread endocrine disorder involving the hypothalamic–pituitary–gonadal axis.
o Women may present with amenorrhoea
o Loss of sexual interest and potency in males
o Before puberty, growth and physical development can be affected
 Other symptoms, such as constipation, headache, fainting, dizziness, fatigue, and cold
intolerance.

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  Physical signs, such as cachexia, acrocyanosis (hands or feet are red or purple in colour), dry
skin, hair loss, bradycardia, orthostatic hypotension, hypothermia, loss of muscle mass and
subcutaneous fat, oedema, and lanugo hair (downy hair on the upper part of the body and
face).

Investigative 1. Some people find body shape and weight to be very important to their identity. Do
Questions you ever find yourself feeling concerned about your weight?
2. What would be your ideal target weight?
3. The obvious methods people use to lose weight are to eat less and exercise more are
these things that you personally do?
4. When women lose significant weight, their periods have a tendency to stop has this
happened in your case?
5. ASK about – physical symptoms of anorexia – fatigue, headache

MSE
Appearance and behaviour – thin, weak, slow, anxious, may try to disguise emaciation
with makeup. Baggy clothes, Dry skin, Lanugo hair.
Speech – May be slow, slurred or normal
Mood – low mood, depression
Perception – preoccupation with food, overvalued ideas about weight and Appearance
Cognition – Either normal or poor if physically unwell with complications
Insight- often poor

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 Investigation  Blood Test : FBC (anaemia, thrombocytopenia, leukopenia),
 U&E( ↑urea and creatinine if dehydrated , ↓potassium, phosphate, magnesium and
chloride)
 TFTs – (↓T3 and T4)
 LFTs, Lipids, Cortisol↑, Sex Hormones , ↓Glucose, Amylase (pancreatitis is a
complication)
 Venous Blood Gas: metabolic alkalosis(vomiting), metabolic acidosis(laxatives)
 Dexa scan: To rule out osteoporosis
 ECG: Arrhythmias such as sinus bradycardia and prolonged QT are associated with AV
patients
 Questionnaires- Eating Attitude Test (EAT)
Complications Metabolic Hypokalaemia, hypercholesterolemia, hypoglycaemia, impaired
of AN Glucose tolerance, deranged LFTs, ↑urea and creatinine,
↓potassium, ↓phosphate, ↓magnesium, ↓albumin and
↓chloride
Endocrine ↑cortisol, ↑Growth hormone, ↓T3 and T4. ↓LH, FSH.
Oestrogens and progesterone leading to amenorrhoea.
↓Testosterone in men
GI Enlarged salivary Glands, pancreatitis, constipation, peptic ulcers,
hepatitis
Cardiovascular Cardiac failure, ECG abnormalities, arrhythmias, ↓BP, Bradycardia
Renal Renal Failure, Renal stones
Neurological Seizure, peripheral neuropathy, autonomic dysfunction
Haematological Iron deficiency anaemia, thrombocytopenia, leucopenia
Musculoskeletal Proximal myopathy, osteoporosis
Others Hypothermia, dry skin, brittle nails ,lanugo hair, infections, Suicide
Management Management of AN is outlined using the Biopsychosocial model

Biological Psychological Social

1. TX of medical
complications
2. SSRIs for co-morbid
depression or OCD
 Psycho-education  Voluntary organisation
 CBT  SELF HELP GROUPS
 Interpersonal
Psychotherapy
 Family therapy

1. Risk assessment for suicide and medical complications is absolutely vital

2. Psychological treatments should normally be for atleast 6 months
3. The aim of treatment as an inpatient is for a weight gain of 0.5- 1kg/week and as an
outpatient of 0.5 kg/week
4. Patients are at risk of refeeding syndrome which causes metabolic disturbances such as
low phosphate
5. Hospitalization is necessary

LOOK INTO REFEEDING SYNDROME!!!!!!!!!!!!

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Bulimia Nervosa
BULIMIA Eating disorder characterized by repeated episodes of binge eating followed by compensatory
NERVOSA weight loss.
No genetic role.
Binge due to strong cravings, feel guilty compensate by vomiting, laxatives, excess exercise and
starvation.

2 types:
Purging type the patient uses self-induced vomiting, enemas.
Non-purging excess exercise or fasting.

Patho The Cycle of BN

 Sense of compulsion to eat
 Binge eats
 Fear fatness
 Compensatory weight loss behaviour

Occurs in young women.

Risk factors are  female, FH, alcohol abuse, early puberty, type 1 DM, obesity in childhood.
Physical abuse as child, bullying, parental pressure.
Developed country, dancers, and athletes.

Clinical ICD 10 criteria to diagnose : BPFO- Bulimia patients fear obesity

Features Behaviours to prevent weight gain
Preoccupation with eating.
Fear of fatness.
Over eating – 2 episodes per week for 3 months.

Normal weight
Depression and low self esteem
Irregular periods
Signs of dehydration- ↓BP, dry mucous membranes, ↑capillary refill time, ↓skin turgor,
sunken eyes
Consequence of repeated vomiting any Hypokalemia- low potassium can result in weak
muscles cardiac arrhythmias and renal damage

Investigative - Do you ever feel like your eating is getting out of control
Q? - After eating what you later feel is too much do you ever make yourself sick so that you
feel better?
- Have you ever used medication to help control your weight?
- Do you ever feel a strong craving to eat?
- Do you ever get muscle aches? Do you ever have sensation that your heart is beating
abnormally fast?

DX ICD 10 criteria to diagnose : BPFO- Bulimia patients fear obesity

Behaviours to prevent weight gain
Preoccupation with eating.
Fear of fatness.
Over eating – 2 episodes per week for 3 months.

Blood tests usuals including mgn

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 Complication Metabolic/Renal Hypokalaemia, dehydration, renal stones, renal failure
Endocrine Amenorrhoea, irregular menses hypoglycaemia, osteopenia

GI Mallory Weiss tars, ↑size of salivary glands especially the parotid

Cardiovascular Arrhythmias, mitral valve prolapse, peripheral oedema

Dental Permanent erosion of dental enamel secondary to vomiting of
gastric acid
Neurological Cognitive impairment peripheral neuropathy seizures
Dermatological Russell’s sign calluses on the back of hand due to abrasion
against teeth)
Pulmonary Aspiration pneumonitis
Others Hypothermia, dry skin, brittle nails ,lanugo hair, infections, Suicide
DDX 1. Anorexia nervosa
2. EDNOS
3. Kleine-Levin Syndrome : sleep disorder in adolescent males characterised by binge eating
4. Depression
5. Obsessive compulsive disorder

Management Biological
Anti-depressants offered, fluoxetine at high dose.
Replace potassium.
Psychological education about nutrition, CBT-BN.
Social
Small regular meals, self-help programmes.
Food diary.

Risk assessment for suicide and electrolyte should be monitored for any imbalance.

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Autism
Definition Autism is a pervasive developmental disorder characterised by a triad of impairment in social
interaction, impairment in communication and restricted stereotyped interest and behaviour

Path: The aetiology can be divided in three

Prenatal Antenatal Postnatal

1. Genetics Obstetric 1. Toxins – Lead and

2. Parental age- studies show complication: mercury
40yr olds have a 50% hypoxia during 2. Pesticide exposure
chance of having a child childbirth,
with autism
gestational age
3. Drugs- sodium valproate in
at birth, low birth
particular in the womb
4. Infection – prenatal viral weight
infection (rubella) ↑ risk of
autism

Clinical Autism Triad  ABC mneumonic

features  Asocial-
a) Few social gestures – waving, nodding and pointing at objects
b) Lack of : eye contact (gaze avoidance), social smile, response to name, interest in
others, emotional expression, sustained relationships, awareness of social rules

 Behaviour restricted
a) Restricted, repetitive and stereotyped behaviour – rocking and twisting
b) Upset at any change in daily routine
c) May prefer the same food insist on the same clothes and play the same games
d) Obsessively pursued interest
e) Fascination with sensory aspects of environment

 Communication impaired
a) Distorted and delayed speech – often first sign
b) Echolalia repetition

The onset of autism is before the age of 3 years. There is also atypical autism after the
age of 3 years
Other features include  intellectual disability , temper tantrums, impulsivity,
cognitive impairment
 Epileptic seizures , Visual impairment , Hearing impairment
 ~~Psychiatric  ADHD, Bipolar, Psychosis, OCD, anxiety
 Pica –eating inedible objects
 Sleep disorders
 Underlying mental condition  PKU, Fragile X, Tuberous sclerosis, toxoplasmosis,
congenital Rubella

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 History 1. Does your child ever engage in pretend alone or with others? Does your child
struggle to interact with others and make friends? (poor social interaction)
2. Have you notices any pattern in their behaviour? Does your child insist on the same
toys activities or foods? Have you noticed them making any abnormal movements
such as flapping their hands or walking on their tiptoes? (repetitive stereotypical
behaviour)
3. Do they struggle to communicate with you? Have you noticed their speech is
monotonous and repetitive? (impaired communication)
4. What sort of games does your child play and with what toys?
5. Do you have any concerns about your child’s development?
Diagnosis ICD-10 criteria for diagnosis
A. Presence of abnormal or impaired development before the age of 3
B. Qualitative abn0ormalities in social interaction
C. Qualitative abnormalities in communication
D. Restrictive repetitive and stereotyped patterns of behaviour interests and
activities
E. The clinical picture is not attributable to other varieties of pervasive
developmental disorder

- Full developmental assessment – including family history, pregnancy, birth medical

history, developmental milestones, daily living skills and assessment of
communication, social interaction and stereotyped behaviours
- Hearing test
- Screening tools including CHAT- Checklist for autism in toddlers
DDX - Asperger’s syndrome
- Rett’s syndrome
- Childhood disintegrative disorder
- Learning disability
- Deafness, Childhood schizophrenia
Management 1. Dx should be done by a specialist- at age 3
2. Local autism teams including Peads psychiatrist, educational psychologist, speech
and language therapist and occupational therapists: should ensure that all those
diagnosed with autism have a key worker to manage and coordinate treatment
3. CBT
4. Intervention for life skills include support developing their daily living skills, their
coping strategies and enabling access to education and community facilities such as
those related to leisure and sports
5. Ensure all physical health, mental health and behavioural issues are addressed
6. Families and carers should also be offered personal social emotional support. Self-
help groups such as the National Autistic society (NAS).
7. Special schooling
8. Melatonin may be considered for sleep disorders that persist despite behavioural
intervention
Intervention for the core features of autism
- Social –communication intervention
- Do not use pharmacological agents such as antipsychotics, antidepressants or
exclusion diets
Intervention for behaviour that challenges
- Treat co-existing physical disorder ( epilepsy and constipation) and mental health
(e.g. anxiety depression ) and behavioural problems

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 - Modification of environmental factors which initiate or maintain challenging
behaviour, are the First line in management (e.g. lighting, noise, social,
circumstances and inadvertent reinforcement of challenging behaviour

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Psychotherapies
The basis of psychological therapy is to help people better understand the way that they feel and aim to support
patients in changing the way they interact with and perceive the world to come to terms with past stressors

The principles of psychotherapy

Develop therapeutic relationship

Listen to patients concerns

Empathetic approach

Provide information, support and advice

allow expression of emotion

encourage self help

CBT
Developed in 1960by Aaron Beck

Indication

a. Mild-moderate depressive illness, eating disorders, anxiety disorder, BPAD, substance misuse disorder
schizophrenia

Aim: initially help individuals to identify and challenge their automatic negative thoughts and then to modify core
beliefs.

Behavioural therapies
Based on the learning theory and particularly operant conditioning – operant conditioning states that behaviour is
reinforced if it has positive consequences for the individuals

1. Relaxation training – for stress related anxiety disorders

2. Systemic desensitization – phobic anxiety disorder gradual exposed to a hierarchy of anxiety producing
situations
3. Flooding – involves the patient rapidly being exposed to the phobic object without any attempt to reduce
anxiety beforehand
4. Exposure and response prevention – used for a variety of anxiety disorders  OCD and phobias. Patients are
repeatedly exposed to situations that cause them anxiety
5. Behavioural activation – used for depressive illness – rationale behind this is to avoid doing certain things as
they feel they will not enjoy them or fear of not completing them. BA- involves making realistic and achievable
plans to carry out activities and then gradually increasing the amount of activity

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Psychodynamic therapy
Developed by Freud, Jung and Klein

Indication: Dissociative disorders somatoform disorders, psychosexual disorders certain personality disorders,
chronic dysthymia recurrent depression

Rationale: it is based upon that childhood experiences past unresolved conflicts and previous relationships
significantly influence an individual current situation

AIM: the unconscious is explored using free association (whatever comes to their mind) and the therapist interprets
these statements. Conflicts and defence mechanism are explored and client subsequently develops insights

Psychoeducation
PE is delivery of information to people in order to help them understand and cope with their mental illness.

Informing the patient of the name and nature of their illness, likely causes of the illness in their particular case, what
the health service can do to help them and what they can do to help themselves

Problem solving therapy

Consists of structured combination of counselling and CBT. It facilitates individuals to learn to deal actively with their
life by selecting an option for tackling each one

Indication are mild anxiety and depressive disorders

Interpersonal therapy
IPT  used to treat depression and eating disorders

The focus is on the interpersonal problem – such as relationship difficulties, complicated bereavement

Eye movement desensitisation and reprocessing EMDR

Aims to help patients access and process traumatic memories

Effective in PTSD treatment

Involves Client recalling emotionally traumatic material while focusing on external stimulus

Dialectical behavioural therapy

DBT used with individuals with Borderline PD

Cognitive analytic therapy CAT

Combines cognitive theories and psychoanalytic approaches into integrated therapy

Used in problems such as – eating and personality disorder

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Psychotherapy indications
Adverse life events PE, counselling, relation techniques

Depression PE, counselling, CBT, psychodynamic therapy, IPT, Behavioural activation

PTSD PE, Trauma focused CBT, EMDR

Schizophrenia PE CBT, Family therapy

Eating disorders PE, CBT, IPT, family therapy CAT

Anxiety disorders PE, CBT, Behavioural therapies

Substance Misuse PE, CBT, motivational interviewing group therapy

Borderline personality PE,DBT, Psychodynamic therapy , CAT

disorder

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 ECT
Definition  ECT is a passage of a small electrical current through the brain with a view to inducing a modified
epileptic seizure which is therapeutic

Background an electric current is applied via electrodes to the patient skull aiming to induce a seizure for at least
30 seconds – done under general anaesthetic. A muscle relaxant (suxamethonium) is given which limits the motor
effects of the seizure

Bilateral ECT has been shown to be more effective but with more cognitive side effects

- The Seizure threshold – minimum electrical stimulus required to induce a seizure and its used in calculating an
electrical current dose
- Drugs which ↑ seizure threshold: benzos, anticonvulsants, barbiturates
- Drugs that ↓ Seizure threshold = antipsychotics, antidepressants, lithium

Indication

1. Prolonged or severe mania

2. Catatonia
3. Severe depression :
a. Treatment resistant depression
b. Suicidal ideation or serious risk to others
c. Life threatening depression
d. NOTE!!!!! Severe depression is the most common indication for the use of ECT

Side effects

‘PC DAMS’

Peripheral nerve palsies

Cardiac arrhythmias, Confusion

Dental or oral trauma

Anaesthetic risks  laryngospasm, sore throat, N+V

Muscular aches and headaches

Short term memory impairment, status epilepticus

Long term side effects

Anterograde and retrograde amnesia
Contraindications  ‘MARS’
1. MI, major unstable fracture
2. Aneurysm
3. Raised ICP intracranial bleed
4. Stroke, Hx of Status Epilepticus, severe anaesthetic risk

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Acute reaction to stress
Stress – a force Stress is atypical if it is prolonged, and/or too intense for the stressor.
from the outside
acting on an Normal stress over a long period of time can lead to psychiatric problems.
individual

Normal The stress respone uses the sympathetic nervous system and the HPA
response to (hypothalamic-pituitary-adrenal axis)
stressful events
Upon perceived threatening situation (2 systems activated):

Sympathetic nervous system activates, releasing Adrenaline from the

adrenal medulla. This produces flight or fight response (flee or deal with the
threat). Adrenaline ellicits the physiological response to stress in regards
to haemodynamics, increased muscle contractility, respiratory rate and
alertness.

Stress it’s self, combined with neuronal firing from the locus coruleius
(Pons) activate the HPA axis – leads to glucocorticoid release from the
adrenal cortex – concerned with chemical energy production and
catabolic state (see diagram)

Emotional response: - 3 kinds:

 Response to danger – fear

 Response to threat - anxiety
 Response to separation or loss – depression.

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 Physiological Difficulty in recall and numbering
changes that People who have experienced stressful circumstances tend to have
reduce the difficulty in recalling events.
impact of They may feel unexpected absence of feeling about event – numbing
stressful events Together, these = freudian repression – active but unconscious mental
process.

Coping strategies
Adaptive strategies – reduce distress short and long term.
 Avoidance of situation that caused stress (can be maladaptive in the
long term if it prevents the following two:)
Histrionic:  Working through problems
melodramatic
 Coming to terms with situation
behaviour
designed to attract
attention. Maladaptive strategies – effective in short term, may lead to difficulties long
term
 Alcohol or drugs
 Discharging emotion through histrionic / aggressive behaviour, or
deliberate self harm
 Long term avoiodance of situation
Culturally determined strategies – open and extreme displays of distress
are a socially accepted and adaptive means of discharging emotion – e.g. in
the sudden death of a loved one.
 In cultures where this is not the norm, this is maladaptive as it may
seem excessive and lose sympathy of potential helpers.

Acute stress = An abnormal reaction to sudden events.

disorder
(Acute stress  Same basic stress response, but more severe and longer.
reaction ICD-
10) Normal stress response generally shows symptoms for up to 48 hours.

Typical symptoms:

37 | P a g e
 1. The emotional response – intense anxiety, restlessness,
purposeless activity, insomnia, panic attacks. Sometimes
depersonalisation and derealisation.
2. Somatic symptoms – sympathetic activation – commonly sweating,
tremor, palpitations.
3. Dissociative symptoms – numbing and difficulty in recall (can feel
like the event never took place, or being in a daze. Flashbacks:
Sudden re-experiencing the event with visualisation of traumatic
images which can’t usually be recalled. Can manifest as frightening
dreams.
4. Coping strategies – avoiding reminders or talking about stressful
event. Social contacts may be avoided. Maladaptive: flight (e.g.
running from the scene of a road accident), histrionic or aggressive
emotional release, alcohol, self harm

Acute stress order lasts no more than 4 weeks. Longer = PTSD.

Prevalence 13-14% road traffic accident (RTA) survivors meet diagnostic criteria
19% assult victims

The highest values recorded are for witnesses of mass shootings – 1/3rd of
people develop acute stress reaction.
Comorbidities Depression. Substance misuse. People who have a psychiatric history,
previous abnormal stress reactions or have suffered from previous traumatic
events.

38 | P a g e
 Differential PTSD – is acute stress disorder lasts more than 4 weeks. Requires an
diagnosis “exceptionally threatening or catastrophic event”

Adjustment disorder – Distress considered out of proportion to the severity

of the stressor. Can be any life event (not just a percieved threat to life) –
Symptoms are more generalised, usually less severe.

Brief psychotic disorder – hallucinations, dellusions, disorganised speech,

grossly abnormal behaviour

Dissociative disorders – presence of dissociative symptoms in the absence

of a stressor.

Organic disorder – Head injury. Space occupying lesion causing acute

stress reaction symptoms. History of headaches or finding of neurological
signs should raise suspicion. Investigate as appropriate (neurology referrals,
CT/MRI scans etc.)

39 | P a g e
 Aetiology Stressful events: Fire, rape, accident, physical assult.
Can occur among bystanders, and those involved in rescuing.

Psychological theories:
 Probably multifactorial, but dissociation is the most studied
 Thought dissociation reduces negative consequences of trauma by
restricting awareness, preventing person being overwhelmed
 Prevents recovery as person fails to deal with it (does not allow the
experience to be processed and integrated into existing coping
mechanism)

Biological theories. – based on classical conditioning

 When a traumatic event occurs (unconditioned stimulus), people
respond with fear (unconditioned response).
 As reminders of the event occur (conditioned stimulus), people respond
with fear reactions (conditioned response).
 It is thought that in some people, the stress response becomes
sensitised to repeated stimuli. A larger response is produced to each
stimuli
 People who suffer a panic attack during a traumatic event are likely to
experience increasing panic attacks in the few weeks afterwards.

Prognosis  Either remission or development of PTSD.

 50-60% road traffic accident survivors may develop PTSD.

Management Most may be managed in primary care. Only severe needs specialist
treatment.
One aim is to reduce the occurance of PTSD. As you will see, CBT
contributes towards this quite well/

General measures
Provide emotional support.
 Usually the person can be comforted effectively by relatives or friends,
and can talk to them about the stressful experience.
 If no close friend or relative is available, or if the response is severe,
comfort may be offered by a healthcare professional. It is important to
explain the course and prognosis of an acute stress disorder

Provide practical support.

 The period after a traumatic event is usually very busy and confusing.
 The person involved will need advice regarding police procedures,
support in obtaining medical care, help with insurance claims,
assistance with dealing with the media, and help with domestic tasks

Help with residual problems.

 Sometimes an acutely stressful situation results in lasting adversity to
which the person has to adjust; for example, a serious car accident may
lead to permanent disability.
 When this happens the treatment of an acute reaction should be
followed by help inreadjustment.

40 | P a g e
 Psychological treatments
 Encourage recall. As anxiety is reduced, the person is usually able to
recall and come to terms with the experience. When memories of the
events remain fragmented, help may be needed to remember the
events and integrate them into memory.
Develop more effective coping strategies.
Cognitive behavioural therapy.
o CBT differs from debriefing crucially in its emphasis on integrating
recovered memories with existing ones, and on self-help.
o Evidence suggests the most effective strategy is a brief intervention,
typically five sessions of individual therapy.
o Studies vary in their results but on average CBT reduces the proportion
of people developing PTSD by 20–50 per cent.

Pharmacological treatments

-Benzodiazepines. SSRIs. Sometimes hypnotics. -

Anxiolytics.- A short course (3–5 days) of a benzodiazepine

may be indicated in patients with a high level of anxiety
immediately after the event.

Occasionally, insomnia is severe, and a hypnotic drug (e.g. temazepam)

should be given, but again only for a short period to avoid the development
of tolerance and dependence.

Antidepressants. SSRIs are the most effective drug treatment for PTSD.
Consider prescribing an SSRI if the symptoms continue to be severe, there is
evidence of depression, or the patient is too unwell to engage in psychological
therapy. It is also an option for those patients who fail to improve after CBT

41 | P a g e
ADHD
What is ADHD?
Hyperkinetic disorder = ADHD

Behaviour: Overactivity, impulsiveness, inattentiveness.

Can arise from a complex web of problems. Clinically useful to identify

as it has a strong impact on the child development and can be treated.

3 subtypes: Inattentive Type, hyperactive-impulsive type, combined

type.

Arose from this idea of a “minimal brain dysfunction (MBD)” – that

this set of behavioural changes arose from brain development, not
from social setting. – Now outdated term due to wide range of
psychological impairment (not all brain dysfunction is “minimal”).

Most commonly affects children. Adults can still meet diagnostic /

subdiagnostic criteria.

Needs specialist assessment for formal diagnosis

Clinical features
Overactivity
= Excess of movement (compared with control’s, even during sleep)

Paradoxically, this excess of movement can be inhibited by new

environments – makes diagnosis difficult (especially on a first clinical
visit)

Non-evident in areas where high activity is expected (e.g. game field).

Key situation for ADHD detection – area which is familiar to the child,
but where calm is expected:
 Visiting family friends
 Attending church
 Mealtimes
 Homework
 At school, during class (often the most troublesome).

Impulsiveness
Action without reflection – a failure to stop and think.
 Interrupting others
 Giving too little time to appreciate what’s in a school task or or
a social situation

42 | P a g e
 Inattentiveness
Disorganised and forgetful behaviour
 Short-sequence activities, changing before they are completed
 Lack of attention to detail and failure to correct mistakes.

 Yet they do maintain attention whilst on that short sequence

of that task. (They just move onto something else very
quickly).
 Proportional (to ordinary people) reaction to distractors.

Other behavioural changes may be present (not exclusive to ADHD

or diagnostic) (can simply be a defiant child)
 Irritable with swings of mood when provoked
 Sleep badly (can contribute to [poor])
 Can be aggressive towards others
 Can be non-compliant to authority
 Can be charming, humorous, inquisitive, intuitive
 Temper tantrums

Direct observation can usually make the distinction:

 Watching child doing tasks that require them to stop and think
 Their natural behaviour in the classroom

For Diagnosis, the behaviours need to be excessive for that child’s age
and developmental level – demands considerable familiarity with the
usual range of variation.

Comorbidity with ADHD It is common for children with features of ADHD to show other disturbance
as well. Clinician must understand the relationships so:
 They do not make or miss diagnosis of ADHD
 They can make good treatment strategies for treating ADHD in the
presence of other disorders + vice versa.

Common co-morbidities
 Conduct and oppositional disorders – Child shows abnormally high defiant and
aggressive behaviour. ICD10: “hyperkinetic conduct disorder”
 Tourette disorder and multiple tics
 Autism spectrum disorder
 Attachment disorders
 Bipolar disorders

Aetiology  Genetic (82% concordance rate identical twins)

 Neurochemical (abnormality in dopaminergic pathway)
 Neurodevelopmental (prefrontal cortex – recklessness, inattention, learning
difficulties)
 Social (Association with social deprivation, family conflict, parental cannabis and alcohol
exposure)

43 | P a g e
 Aetiology is almost always Multifactorial
 Genetics
 Brain structure and function abnormalities
MRI scans of ADHD patients have repeatedly shown smaller frontal lobe,
cerebellum and striatum, persisting into adulthood.
Restlessness and difficulty in concentrations indicates a difference in
prefrontal cortex and related subcortical structures involved in guiding and
sustaining behaviour and delaying responses. These brain areas are rich in
catecholamine’s (hence response to stimulants).
 Psychological
Lesser impact than genetics
Early deprivations (emotional, nutrition, stimulatory)
 Environmental
Prenatal / postnatal.
Prenatal: maternal stress. Maternal use of benzodiazepines, nicotine,
cocaine, alcohol, anti-convulsants = predisposition to ADHD [
Postnatally: head injuries, other brain disease (Autism/ Tourette’s) =
strong link to ADHD
Some question about dietary factors (Wheat, dairy, artificial sweeteners)

Epidemiology Present in 2.4% of children

3x more common in males
Age of onset – 3-7 years
Sibling with ADHD = other sibling more at risk

44 | P a g e
 Diagnosis Remember the 3 criteria: Inattention, impulsivity,
hyperactivity
History:
Inattention – Do you find that your child:
1. “Is reluctant to engage in activities which require sustained mental
effort, such as school work?”
2. “Often leaves play activities unfinished?”
3. “Regularly loses their possessions?
4. “Does not listen when spoken to?”
Hyperactivity
1. “Is constantly fidgeting, jumping or running around?”
2. “Is unable to remain still?”
3. “Is difficult to engage in quiet activities?

Impulsivity
 “Cannot wait their turn to play in groups?”
 “Blurts out the answers to questions before they have been
completed?”

Assessment of hyperkinetic disorder (OSCE hint)

Observe the child
 Hyperactivity is often obvious
 New setting may dampen hyperactivity though.
 Child may interrupt parents = impulsivity
Speak to the child
 Does the child engage with you and make eye contact?
 Offer a toy and see if they get bored or easily distracted
Speak to the parents
 Elicit whether symptoms are present in more than one
environment

Mental state examination

 Appearance and behaviour: Fidgety. Unable to sit still.
Running around. Jumping or climbing inappropriately. If toys
are offered, will flit between one to another. If parents are
asked a question, child replies with answer before parents
can
 Speech Talks loudly, even at appropriate times. Makes
excessive noise.
 Mood Normal, may be low if co-morbid depressive disorder
 Cognition Poor attention levels
 Insight poor

Differential diagnosis  Normal childhood behaviour.

 Attachment disorder.
 Hearing impairment.
 Learning difficulty.
 High IQ child insufficiently stimulated/challenged in a mainstream
school. Behavioural disorder.
 Anxiety disorder.
 Medication side effects.

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 Investigations NICE recommends no blood test unless clinically indicated (TFTs would be a
suggestion if they have other symptoms of hyperthyroid).

Before starting medication for ADHD (specialist),

 a review to confirm they continue to meet the criteria for ADHD and
need treatment
 a review of mental health and social circumstances, including:
presence of coexisting mental health and neurodevelopmental
conditions, current educational or employment circumstances risk
assessment for substance misuse and drug diversion care needs
 a review of physical health, including: a medical history, taking into
account conditions that may be contraindications for specific
medicines
 current medication
 Height and weight (measured and recorded against the normal
range for age, height and sex)
 baseline pulse and blood pressure
 a cardiovascular assessment
 An electrocardiogram (ECG) if the treatment may affect the QT
interval.
Management Psychoeducation
 Taught courses that allow the parents to meet other families with an
ADHD child, and to reinforce behavioural work being done in school
and therapy sessions.
 Helps parents identify and understand exact problem behaviours,
their triggers, and effective strategies for reducing them
 Very effective at allowing parents to manage ADHD at home
 May be all that is needed in mild to moderate cases

Behavioural modification at school

 Coordinated by a special need’s coordinator
 Gives appropriate classroom assistance.
 Class teacher trained to recognise behaviours + manage them e.g. sit
near front of class
 Similar reward and punishment system to home

Medication (more severe cases)

Other considerations:
 Behavioural interventions e.g. encouraging realistic expectations,
positive reinforcement of desired behaviours (small immediate
rewards)
Treat comorbidity
 Evidence base for dietary changes (e.g. oily fish) poor at the moment
 Voluntary organisations: ADDIS – Attention deficit disorder
information and support service.

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 Medication for ADHD
Drug treatment for children and young people with ADHD should always form part of a
comprehensive treatment plan that includes psychological, behavioural and educational advice
and interventions

Medication for ADHD should only be prescribed after expert advice:

 when a decision has been made to treat children or young people with ADHD with drugs,
healthcare professionals:

methylphenidate First line children aged 5 years and over and young people with
(either short or long ADHD
acting)
Controlled drug. Potential for abuse
Ritalin
Monitor: Weight/height, pulse, BP, Tics, Agitation/anxiety, drug
misuse
Lisdexamfetamine Switch to this when inadequate response to methylphenidate
after 6 weeks

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 (prodrug of dexamfetamine. Monitor: Weight/height, pulse, BP, Tics, Agitation/anxiety, drug
Hydrolysed in blood = less misuse
abuse potential)

Elvanse
Dexamfetamine  Responding to lisdexamfetamine
 But can’t tolerate side effects
Dexamfetamine sulfate

Amfexa
Atomoxetine  Cannot tolerate lisdexamfetamine / dexamphetamine
 No response to above drugs, after dose/preparation
Straterra adjustments

or Guanfacine No potential for abuse

Intuniv Weight/height, pulse, BP, (+suicidal ideation (atomoxetine))

48 | P a g e
Psychotic Disorders
Functional  Schizophrenia is a functional psychosis.
disorder –  There is a spectrum of severity.
Disorder of the
brains  Schizophrenia is characterised by delusions AND hallucinations
functioning with
no structural  Delusional disorder: Delusions, but no hallucinations.
abnormality.
 It is frequently chronic and relapsing

 Can be simplified into acute syndrome and chronic syndrome

Diagnosis and Main clinical features
clinical  Hallucinations
presentation –  Persecutory ideas
The Acute  The false idea of being referred to (a delusion of reference)
syndrome  Social withdrawal
 Impaired performance at work

Positive syndrome – refers to appearance of hallucinations and delusions

Appearance and behaviour

 Some appear normal
 Awkward, preoccupied and withdrawn, odd
 Smile and laugh with no obvious reason
 Appear perplexed by what is happening to them
 Restless and noisy
 Some show sudden unexpected changes in behaviour
 Spend time alone in room – often lying immobile on bed deep in thought.

Mood
I) Mood change such as depression, anxiety, irritability or euphoria. Causes:
II) Develop by same mechanism as delusions and hallucinations
III) As a response to insight into their disorder
IV) Side effect of anti-psychotic medication

2: Flattening / blunting mood – reduction in the normal variations of mood.

3: incongruity of affect – emotion not in keeping with the situation. E.g. laughing upon
news of the death of mother

Speech and form of thought.

Speech may be difficult to follow.
Early stages - Talk may be vague + difficult to grasp the meaning.
Later - definite abnormalities (formal thought disorder)
 Difficulty in dealing with abstract ideas (concrete thinking)
 Become preoccupied with vague / pseudoscientific / mystical ideas
 Loosening of associations (lack of connection between ideas).
 Extreme – word salad.

May also be disorder in the stream of thought. Pressure of thought. Poverty of thought.
Thought blocking.

Perception
49 | P a g e
 Auditory hallucinations: (earliest at top)
 Simple noises
 Complex sounds of voices or music
 Voices uttering single words, phrases or entire conversations.
 Voices giving commands to patient
 Voices speaking patients own thoughts.
 Two or more voices discussing the patient in 3rd person
 Commenting on patients’ actions or narrating.
Visual hallucinations:
 Less frequent than auditory in schizophrenia

Tactile, olfactory, gustatory, somatic hallucinations.

e.g. Hallucinatory sensations in lower abdomen may

be attributed to unwanted sexual interference.

Abnormalities in the content of thought

Delusions: - belief that is held firmly but on adequate grounds, is not affected by rational
argument or evidence to the contrary, and is not conventional to the belief that the person
might be expected to hold given his cultural background and level of education.

See the sections + table on delusions for definitions! (Go forward a few pages)

 Mostly secondary delusions in schizophrenia

 Can be preceded my delusional mood and hallucinations

 Types common in schizophrenia = Persecutory delusions, Delusions of reference,

Delusions of control, delusions of possession #

Insight
Insight is Usually impaired in schizophrenia.
Patients may blame their experiences on the malevolent actions of others.

50 | P a g e
 Disturbed behaviour + Dellusions + Hallucinations = Positive symptoms
of schizophrenia.

Chronic syndrome Negative symptoms

 underactivity or disorganized behaviour;

 lack of drive;
 social withdrawal;
 emotional apathy;
 thought disorder;
 Cognitive impairment.

Diagnosis  The diagnosis of schizophrenia is based entirely on the clinical presentation (history
and examination).
 exclude other disorders when there is clinical
51 | P a g e
 DSM-5 diagnosis
Characteristic symptoms: two of the following, for most of a month (or less if treated):
1. delusions;
2. hallucinations;
3. disorganized speech (e.g. frequent derailment or
4. incoherence);
5. grossly disorganized or catatonic behaviour;
6. negative symptoms, i.e. affective flattening, alogia, or avolition.

Only one Criterion A symptom is required if delusions are bizarre or hallucinations

consist of a voice keeping up a running commentary, or two or more voices
conversing with each other.

B Social/occupational dysfunction: Disturbance in

 Work,
 Interpersonal relations
 Self-care
 faliure to achieve expected level of interpersonal, academic, or occupational
achievement (Adolescent onset).

C Duration: continuous signs of the disturbance persist for at least 6 months.

 This 6-month period must include at least 1 month of symptoms (or less if
successfully treated) that meet Criterion A (i.e. active-phase symptoms)
 May include periods of prodromal or residual symptoms.
 - During these prodromal or residual periods, the signs of the disturbance may
be manifested by only negative symptoms or two or more symptoms listed in
Criterion a present in an attenuated form (e.g. odd beliefs, unusual perceptual
experiences).

D Exclude Schizoaffective and mood disorder: schizoaffective disorder and mood

disorder with psychotic features have been ruled out because either :
 no major depressive episode, manic episode, or mixed episode has occurred
concurrently with the active-phase symptoms
 Mood episodes have occurred during active-phase symptoms, but total
duration has been brief relative to the duration of the active and residual
periods.

E Exclude Substance/general medical condition: the disturbance is not due to the

direct physiological effects of a substance (e.g. a drug of abuse, a medication) or a
general medical condition.

F Relationship to a pervasive developmental disorder: if there is a history of autistic

disorder or another pervasive developmental disorder, the additional diagnosis of
schizophrenia is made only if prominent delusions or hallucinations are also present for
at least a month (or less if successfully treated).
 DSM5 differs from ICD-10; requires only one of the category A symptoms (if
very clear-cut) and a minimum duration of 1 month.
52 | P a g e
 Symptoms included in the ICD10 /DSM5 diagnostic criteria:

1symptoms highly specific for schizophrenia have high positive predictive value. These are
called Schneider’s ‘first rank’ symptoms (occur in 70% of cases)

2 Symptoms that are more frequent but less discriminating than first-rank symptoms (e.g.
prominent hallucinations, loosening of association, and flat or inappropriate affect).

3 Impaired social and occupational functioning.

4 A minimum duration (6 months in DSM-IV but, unfortunately, a different period—1 month—

in ICD-10).

5 The exclusion of (i) organic mental disorder, (ii) major depression, (iii) mania, or (iv) the
prolongation of autistic disorder (which is a mental disorder of childhood, see
p. 430).

Differential
diagnosis
 Organic syndromes – drug induced states, temporal lobe
epilepsy, delirium, dementia
 Psychotic mood disorder
 Personality disorder
 Schizoaffective disorder

older patients:
Delirium- especially when there are prominent hallucinations and delusions; the cardinal
feature of this disorder is clouding of consciousness

53 | P a g e
 Dementia can resemble schizophrenia (persecutory delusions common). The finding of
memory disorder suggests dementia.

Diffuse brain diseases can present a schizophrenia-like picture without any neurological signs
or gross memory impairment; e.g. general paralysis of the insane (paralytic dementia –
meningitis from syphilis)

Psychotic mood disorder.

The distinction between mood disorder and schizophrenia depends on:

(i) Degree and persistence of mood disorder;
(ii) Congruence (agreement) of hallucinations or delusions with prevailing mood;
(iii) previous mood disorder

Personality disorders. Differential diagnosis from personality disorder may be difficult,

especially when there have been insidious changes of behaviour in a young person who does
not describe hallucinations or delusions.
As well as interviewing relatives it may be necessary to make prolonged observations for first-
rank and other features of schizophrenia before a definite diagnosis can be reached.

Schizoaffective disorder.
 Some patients have schizophrenic symptoms and affective (depressive or manic)
symptoms of equal prominence.
 These disorders are classified separately because it is uncertain whether they are a
subtype of schizophrenia, or of affective disorder.
 Usually require both antipsychotic and antidepressant drug treatment.
 When they recover, affective and schizophrenic symptoms improve together,
 Upon recovery most, patients lose all their symptoms, although many have further
episodes.
Assessment Non-urgent cases
Patient presents with – e.g. odd behaviour. Withdrawn. Elderly woman who is
reclusive and paranoid.. family concerned

GP: Take history of symptoms and behavious from patient and/or informant (family).
Assess:
 Functional imparment – still working? Relationships okay?
 Patient at risk to self/others?

Then: - encorage patient to accept referral to mental health services for further
assesment;

if declined: d/w psychiatrist – GP may commence treatment under specialist advice.

f/up patient.

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Adjustment Disorder
Adjustment Normal adjustment
disorder  Adjustment refers to the psychological reactions involved in adapting to
new circumstances.
 It is a normal process that is expected after major life changes.

Typical events where an adjustment period would be expected include divorce and
separation, a change in job or home situation, transition between school and
university, and the birth of a child.
Adjustment
disorder Adjustment is judged to be abnormal if the distress
involved is:
 greater than that which would be expected in response to the particular
stressful events (this judgement is subjective, and the diagnostic manuals
offer no objective criteria); or
 is close in time to the life change (ICD specifies within 1 month and DSM
allows up to 3 months); and
 is not severe enough to meet the criteria for the diagnosis of another
psychiatric disorder.

Clinical features
Patients usually present with mild symptoms of depression, anxiety, emotional
or behavioural disturbance.

Diagnosis of adjustment disorder is often a judgement call; it can be useful to

consider the following two questions:
1. Does the patient have a diagnosable mental disorder?
2. If there is a diagnosable mental disorder, does it fit criteria for another
condition better than those for adjustment disorder?

Differential  Acute stress disorder or PTSD.

diagnosis  Mood disorder.
 Anxiety disorder.
 Alcohol or substance misuse.
 Grief reaction.
 Organic disorder causing psychological symptoms.

Aetiology
Adjustment disorders may be caused by any identifiable stressful event.

Risk factors for an adjustment disorder are:

● age—young people have fewer established coping mechanisms;
● female gender;
● past experiences of stressful events;
● past psychiatric history;
● Low self-esteem.

55 | P a g e
 Management The aim of any treatment is to help to relieve the acute symptoms caused by the
stressor, and to teach the person a wider range of coping skills to protect
against future episodes.

General measures

Practical support. It is important to try to relieve any stress that is still ongoing; for
example, by providing financial support, childcare, helping to arrange a funeral, or
getting an occupational therapy assessment.

Psychoeducation. Give the patient and their family information about adjustment
disorders and reassure them that it is not a serious psychiatric condition and that
they are not going mad. Information leaflets, support groups, and websites can all
be valuable.

Anxiety reduction can usually be achieved by encouraging patients to talk

about the problems and to express their feelings to a sympathetic listener. A
friend or family member can provide this, and many patients will not need any more
formal therapeutic input.

Psychological treatments

Self-help materials. A good first step is to provide the patient with appropriate self-
help materials, varied according to the predominant symptoms. CBT-based and
problem-solving materials (e.g. books, computerized courses) are particularly
useful.

Brief psychotherapy or counselling.

Pharmacological treatments

Short term benzodiazepines = hopefully only treatment required.

Short-term anxiolytics. It may be necessary to provide a short-term supply (a few

days) of an anxiolytic in the immediate Aftermath of the stressful event. A low-dose
relatively short-acting benzodiazepine is the best choice. They should
not be continued longer term due to the risks of tolerance and dependence.

Antidepressants. There is no good evidence that antidepressants are effective

in relieving the symptoms of adjustment disorders. However, if there are
prolonged/distressing mood or anxiety symptoms, a low-dose SSRI may provide
some relief. Other antidepressants are not recommended as the risks outweigh the
benefits.

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Dementia
Dementia

Permanent loss of intellectual function.

5% >65, 20% >85
Typically progressive.
Alzheimer’s and vascular dementia = most common.

Types
Neoplastic
Vascular
Common
Common:
 Secondary deposits
 Diffuse small vessel disease
Less common:
Less common:  Primary cerebral tumour
 Amyloid angiopathy Rare
 Multiple emboli (e.g. from Atrial fibrillation).  Paraneoplastic syndrome (limbic encephalitis)

Rare: Inflammatory
 Cerebral vasculitis Less common:
 Systemic Lupus Erythematosus  Multiple sclerosis
Rare
Inherited  Sarcoidosis
Common: Traumatic
 Alzheimer’s disease Common:
Rare:  Chronic subdural haematoma post head-injury
 Mitochondrial encephalopathies Less common
 Cortic-Basal degeneration  Punch drunk syndrome
Hydrocephalus (less common)
Infective  Communicating/non-communicating
Less common
 Syphilis Toxic/nutritional
 HIV Common:
Rare  Alcohol
 Post encephalitis Less common
 Whipple’s disease  Thiamine deficiency
 Subacute sclerosis panencephalitis  Vitamin b12 deficiency

Prion diseases
(less common):
 Sporadic Creutzfeldt Jakob disease (CJD)
Rare:
 Varient CJD
 Kuru
 Gerstmann-Sträussler-Scheinker disease

Pathogenesis Clinical features

Dementia is either cortical or subcortical in type.
Investigations
Aim is to seek a treatable cause, estimate prognosis.
 Disturbance of personality or memory
 Low performance on MoCA (Montreal cognitive
assessment test)

57 | P a g e
 Exclude focal brain lesion by determining cognitive
disturbance is in more than one area.
Mental state examination needed to rule out / identify
Initial investigations depression.
Imaging of head (CT +/- MRI)
Bloods: CJD: Quickly progressive, associated with myoclonus.
 FBC
Other dementias: slower, difficult to distinguish during
 ESR
life.
 U&E Fronto temporal dementia: - Signs of frontal and
 Glucose temportal lobe dysfunction
 Calcium
 LFTs Lewy body: may have hallucinations.
 TFTs
 B12 Course: Gradual worsening may suggest Alzheimer’s
Stepwise deterioration may suggest vascular dementia.
 Syphilis serology
 ANA, anti-dsDNA
CXR Management:
Electroencephalography
Address treatable causes
Provide support for patients and carers.
In selected patients:
Lumbar puncture Tackling risk factors may slow deterioration:
HIV serology  Manage hypertension (Vascular dementia)
Brain biopsy  Abstinance and vitamin replacement
(toxic/nutritional dementias)
Investigations information
Imaging can exclude potentially treatable structural Psychotrophic drugs
lesions (Hydrocephalus, cerebral tumour, chronic
subdural haematoma). These may alleviate symptoms (sleep disturbance,
Usual finding will be generalised atrophy. perception, mood) – but treat with care as they may
increase mortality long term.
?CJD? – EEG is useful. CJD has characteristic generalised
sharp wave pattern. If negative, consider lumbar Sedation = bad. In later stages, they may require good,
puncture, or (rare) brain biopsy. attentive residential nursing care.

Alzheimer’s: Cholinesterase inhibitors and Memantine

may slow progression.

Alzheimer’s disease Pathogenesis

Genetics plays a role.
15% are familial.

Early onset – Autosomal dominant

inheritance
Later onset: - Polygenic aetiology.

Many genes play either strong or weak

contributary roles. Presence of any of these
alleles is not necessary for Alzheimer’s :
 Apolipoprotein ε gene: (Specific
allele = Apoε4)

58 | P a g e
 The most common form of dementia. Rare under 45 years of age
(although there is an inherited early-onset form).
Amyloid - Amyloids are aggregates of proteins that become
folded into a shape that allows many copies of that protein to
stick together, forming fibrils (Polymeric rods). Pathogenic
amyloids form when previously healthy proteins lose their normal
physiological functions and form fibrous deposits in plaques
around cells which can disrupt the healthy function of tissues and
organs.
Apraxia: the individual has difficulty with the motor planning to
perform tasks or movements when asked, provided that the
request or command is understood, and the individual is willing to
perform the task.
Aphasia is an impairment of language, affecting the production or
comprehension of speech and the ability to read or write.
Anosognosia = “without disease knowledge” – person is unaware
of the existence of their disease/disability
59 | P a g e
Heterozygotes: 2-4x higher risk
Homozygotes: 6-8x higher risk
(Not tested for or clinically useful…so
who knows why the book bothers to
mention it.)
Brain in Alzheimer’s
Atrophic (especially in hippocampus and
cerebral cortex (enlarged ventricles also).
Histology
Senile plaques. And neurofibrillary tangles of
Tau proteins (Microtubule associated).
Significant amyloid build up: Seen in
Ubiquitin staining (positive for ubiquitin
content).
Exact cause of plaque formation is unknown.
Plaques and tangles occur initially in the
hippocampi then spread more widely.
Cerebellum and occipital lobe tend to be
unscathed.
Disease course
Inability to remember new information.
Short term memory loss is the most
pronounced. Long term memory will be
affected progressively also.
Later: Apraxia, visuo-spatial impairment,
aphasia – initially noticed by patient, but
progresses to anosognosia
Depression and aggression is common in
Alzheimer’s.
Patients often present with subjective
memory loss: Getting lost in familiar
locations
Key to making a diagnosis: Hx of Progressive
memory loss, associated functional
impairment, corroborated by an informant
Cognitive tests and neuroimaging are helpful,
but not diagnostic.
Investigations
Exclude treatable causes of dementia.
1: Detailed history taking.
Any suspicion of dementia should lead to
detailed questioning about intellectual
function and neurological symptoms.

“is it reversable? Will he ever get his memory back?”
 MMSE
If all items are answered
correctly, the score is 30. The
mean score for a community-
dwelling population over 65
years of age is 27, with a
standard deviation of 1.71 The
score is lower in those who
completed comparatively fewer
years of education and who have
diagnosable diseases. Patients
with dementia, delirium, mental
retardation, Parkinson’s disease,
stroke and some cases of
depression score lower than
normal controls1,12. Alzheimer’s
disease patients lose 3–4 points
per year of illness after the onset
of memory disturbance,
although there is wide variability
in this phenomenon
60 | P a g e
Interview other informants as well (some
patients have anosognosia). Also assess
mood.
2: full physical examination focusing on
neurological system.
3: Cognitive testing Standardized procedures
for assessing cognitive state may be of value.
Take previous education/achievement into
account. MMSE (mini-mental state
examination) is widely used. Combines
standard questions with tests of spatial
ability. High sensitivity and specificity. (First
hit on google to left:  (print and use
clinically))
4: Bloods: FBC, LFT, TFT, U+E, B12, Folate,
Thiamine, Calcium, Glucose.
Consider HIV or syphilis testing only if there is
clinical suspicion from exam.
5: Imaging: CT and or MRI head. Look for
focal or diffuse cerebral pathology.
Management:
 Maintain any remaining ability
 Relieve distressing symptoms
 Arrange for the practical
requirements for the patient (Bio-
psycho-social)
 Support the family. (e.g. signpost to
local carers support).
Psychoeducation
Carers, family, relatives should be informed
of following:
 Symptoms of dementia
 Course
 Prognosis
 Treatments
 Support groups
 Financial and legal considerations
(capacity and driving).
 Where to look for further
information.
Written care plan
Draw up soon after diagnosis. Includes:
 Views on residential accommodation
 End of life care
 Resuscitation status
 Input from occupational therapist,
physiotherapist, dietician should be offered.

Support for carers

 Training courses run by voluntary
sector
 Short-time respite care is invaluable
to carers – especially in later stages.
 CBT or psychological councilling for
carers who suffer distress during
illness.

Structured group cognitive stimulation

programmes – can improve MMSE scores
and quality of life in mild-moderate dementia

Agitation and challenging behaviour:

-carers and healthcare professionals can be
taught how to manage these.
-NICE recommends: Aromatherapy,
music/dance therapy/ animal assisted
therapy, massage therapy to reduce
agitation.

Medication options

Treat with acetylcholinesterases (Donepezil /

Rivastigmine/Galantamine)
May show some benefit in slowing the
progression of cognitive impairment in the
early stages while post-synaptic cholinergic
receptors are still present. doesn’t slow
disease course. Only temporarily offers
some potential relief to some symptoms.

NMDA receptor antagonist Memantine –

slightly enhances learning and memory in
early stages of the disease – can also be
useful in patients with more advanced
disease.

Non-pharmacological approaches: Provision

of a familiar environment.
Support for carers.
Antidepressants if depressed.

61 | P a g e
 Drugs:

AChE inhibitors:
Donepezil/galantamine/rivastigmine

Memantine

1. Monotherapy of AChE inhibitors

donepezil / galantamine /
Rivastigmine
2. Memantine monotherapy – Mild
Alzheimer’s with intolerance to AChE
inhibitors.
/ Severe Alzheimer’s
3. Add memantine as a dual therapy for
mild/strong alzheimer’s If already on
AChE, primary care prescribers may
start treatment without taking
specialist advice from a clinician.

Non-Alzheimer's dementia
Offer donepezil or rivastigmine to people
with mild to moderate dementia with Lewy
bodies.

Only consider galantamine for people with

mild to moderate dementia with Lewy
bodies if donepezil and rivastigmine are not
tolerated.

Consider donepezil or rivastigmine for

people with severe dementia with Lewy
bodies.
;
Consider memantine for people with
dementia with Lewy bodies if AChE inhibitors
are not tolerated or are contraindicated.

Only consider AChE inhibitors or memantine

for people with vascular dementia if they
have suspected comorbid Alzheimer's
disease, Parkinson's disease dementia or
dementia with Lewy bodies.

Do not offer AChE inhibitors or memantine to

people with frontotemporal dementia.

Do not offer AChE inhibitors or memantine to

people with cognitive impairment caused by
multiple sclerosis.

Early onset alzheimer’s

62 | P a g e
 One cause: Mutations in beta-amyloid, APP, encoded by APP gene
chromosome 21. (exceptionally rare)

Mutations in Presenilin genes – encode proteins in the cleavage of

APP to beta-amyloid.
Pharmacology
Pharmacological treatments should be initiated by a specialist experienced in the
management of dementia.
Treatment should be reassessed on a regular basis
 AChE inhibitors: Donepezil HCL, Galantamine, Rivastigmine – treatment of cognitive
impairment of mild-moderate Alzheimer’s.
 Memantine HCL = suitable alternative for patients with moderate Alzheimer’s with
AChE intolerance or contraindicated (e.g. due to seizures/ epilepsy).
 Memantine HCL = drug of choice for Severe Alzheimer’s

Anti-psychotic drugs
 Only offered if patient severely distressed is at risk of harming self / others.
 Used to treat cognitive symptoms: Delusions, anxiety
 Behaviour changes: e.g. aggression, agitation
 Offered in In Lewey body, alzheimer’s, mixed dementia, vascular dementia causing
significant distress.
 Increases risk of stroke / death. Weigh risks and benefits. E.g. pmh of stroke, TIAs,
hypertension, smoking, AF.
 Start small, titrate up. Beware of adverse reactions in lewey body dementia (LBD): -
“Severe neuroleptic sensitivity affects up to 50% of the LBD patients who are treated
with traditional antipsychotic medications, and is characterized by worsening
cognition, sedation, increased or possibly irreversible acute onset parkinsonism, or
symptoms resembling neuroleptic malignant syndrome, which can be fatal.”
Book view on anti-psychotic drugs (based on results of studies)
Study 1: improvement in agitation, aggression, psychosis with olanzapine and risperidone
compared with placebo
Study 2: olanzapine and risperidone show greater clinical improvement than other anti-
psychotics in alzheimer’s
Study 3: atypical antipsychotics are associated with greater risk of cardiovascular events
and mortality in alzheimer’s patients. 3x increase in cardiovascular events (commonly
ischaemic stroke)

63 | P a g e
Consensus: It is appropriate to prescribe them for aggression / agitation causing stress, but
only in the short term at the lowest possible dose
Drug + indications M of A Side effects
Memantine Glutamate receptor antagonist  Balance disorders
 Constipation
Hydrochloride Uncompetitive NMDA receptor  Dizziness
Alzheimer’s antagonism, binding preferentially to the  Drowsiness
NMDA receptor-operated cation channels.  Dysponea
Initially 5mg daily  Headache
Increase by 5mg weekly The pathology:  Hypertension
Prolonged increased levels of glutamate in
20mg maintenance dose. the brain of demented patients are Uncommon
sufficient to counter the voltage-  Abnormal gait
dependent block of NMDA receptors by  Confusion
Caution in epilepsy. Mg2+ ions and allow continuous influx of
 Fatigue
Ca2+ ions into cells (= the problem),
 Hallucinations
ultimately resulting in neuronal
 Heart failure
degeneration.
 Thrombosis
M of A  Vomiting
Studies suggest that memantine binds Very rare
more effectively than Mg2+ ions at the  Seizures
NMDA receptor, and thereby effectively Unknown:
blocks this prolonged influx of Ca2+ ions  Hepatitis
through the NMDA channel whilst  Pancreatitis
preserving the transient physiological  Depression
activation of the channels by [synaptically  Suicidal ideation
released glutamate]. Thus memantine  Psychosis
protects against chronically elevated
concentrations of glutamate

64 | P a g e
 Donepezil Reversible inhibiter of acetylcholine Common:
esterase  Aggression; agitation; appetite
(AChE inhibitor) decreased;
Alzheimer’s
 common cold;
5mg OD for 1 month
Pathophysiology:  diarrhoea; dizziness;
Increase if necessary to 10mg
Alzheimer's disease that is associated with  fatigue;
memory loss and cognitive deficits is  gastrointestinal disorders;
OD
associated with a deficiency of  hallucination; headache;
acetylcholine as a result of selective loss  injury;
Give dose at bedtime.
of cholinergic neurons in the cerebral  muscle cramps;
cortex, nucleus basalis, and hippocampus.  nausea;
Treatment given on advice of a
specialist  pain;
M of A
 skin reactions; sleep disorders;
Leads to an increased concentration of
If patient has learning disability, syncope;
acetylcholine at cholinergic synapses.
do not rely on cognitive tests to  urinary incontinence; vomiting
Mostly CNS selective.
monitor disease progression Uncommon

Only give this treatment if there Bradycardia; gastrointestinal

are cognitive, global, functional haemorrhage; hypersalivation; seizure
or behavioural benefits. Rare or very rare

Cardiac conduction disorders;

extrapyramidal symptoms; hepatic
disorders; neuroleptic malignant
syndrome; rhabdomyolysis

65 | P a g e
 Galantamine Reversible acetylcholine esterase inhibitor. Common or very common
Also has nicotinic receptor antagonistic Appetite decreased; arrhythmias;
Mild to moderately severe
properties. asthenia; depression; diarrhoea;
dementia in Alzheimer’s disease
dizziness; drowsiness; fall;
increases concentration of acetylcholine at gastrointestinal discomfort;
By mouth (immediate release)
cholinergic synapses. Galantamine also hallucinations; headache;
4mg BD 4 weeks.
binds allosterically with nicotinic hypertension; malaise; muscle spasms;
Maintence up to 8-12mg BD
acetylcholine receptors and may possibly nausea; skin reactions; syncope;
potentiate the action of agonists (such as tremor; vomiting; weight decreased
Modified release
acetylcholine) at these receptors.
8mg OD 4 weeks. Increase to
Uncommon
16mg OD for at least 4 weeks.
Atrioventricular block; dehydration;
Maintenance up to 16-24mg OD
flushing; hyperhidrosis; hypersomnia;
hypotension; muscle weakness;
Avoid in:
palpitations; paraesthesia; seizure;
Gastro/urinary obstruction; post
taste altered; tinnitus; vision blurred
bladder surgery;
Post gastro-intestinal surgery;
Rare or very rare
Hepatitis; severe cutaneous adverse
Cautions:
reactions (SCARs)
cardiac disease;
chronic obstructive pulmonary
disease; congestive heart
failure; electrolyte disturbances;
history of seizures; history of
severe asthma; pulmonary
infection; sick sinus syndrome;
supraventricular conduction
abnormalities; susceptibility to
peptic ulcers; unstable angina

66 | P a g e
 Rivastigmine AChE inhibitor Common or very common
 Anxiety; appetite decreased;
Inactivates chlolinesterase (eg. arrhythmias; asthenia;
See BNF for doses and dose-
equivalent conversions:
acetylcholinesterase,  dehydration; depression;
butyrylcholinesterase), preventing the diarrhoea; dizziness;
Can be transdermal or oral
hydrolysis of acetycholine, and thus drowsiness;
Oral example: 1.5mg BD, 2 week
leading to an increased concentration of  fall;
interval increases according to
acetylcholine at cholinergic synapses. The  gastrointestinal discomfort;
anticholinesterase activity of rivastigmine  headache; hyperhidrosis;
response and tolerance. 3-6mg
is relatively specific for brain hypersalivation; hypertension;
typical / max maintenance dose.
acetylcholinesterase and  movement disorders; nausea;
butyrylcholinesterase compared with  skin reactions; syncope;
Retitrate from 1.5mg if
those in peripheral tissues.  tremor;
treatment is interrupted.
 urinary incontinence; urinary
Cautions: tract infection;
 vomiting; weight decreased
Bladder outflow obstruction;
conduction abnormalities; Uncommon
duodenal ulcers; gastric ulcers; Aggression; atrioventricular block
history of asthma; history of
chronic obstructive pulmonary Rare or very rare
disease; history of seizures; risk Pancreatitis; seizure
of fatal overdose with patch
administration errors; sick sinus
syndrome; susceptibility to
ulcers
67 | P a g e
 Vascular dementia (aka Multi-infarct
dementia)
Prognosis
4-5 year lifespan average, but Wide variations. Half die
from ischaemic heart disease. Others die from cerebral
infarction or renal complications.
Treatment
Continue with cardiovascular medications to reduce
cholesterol, control blood pressure, control atrial
fibrillation. To slow down disease progression
Adopt healthy lifestyle (Less salt/fat/sugar)
Diabetes control.
“The drugs that are routinely prescribed for Alzheimer's
disease do not have benefits for vascular dementia and
are not recommended for it. These drugs may, however,
be prescribed to treat mixed dementia
68 | P a g e
Second most common dementia – 15-20% of cases
Caused by various cerebrovascular pathologies,
including multiple small infarcts
Pathology
Vascular dementia is associated with ischaemic and
non-ischaemic changes in the brain.
Can involve large and small vessels
 Multiple infarctions and ischaemic lesions in
white matter
 Atrophy of old infarcted areas
 Bilateral infarcts (tend to be)
 Lesions involve the full thickness of white-
matter.
 Changes in the blood flow in unaffected
regions.
 Entire brain is smaller, and the ventricles
expanded.
Clinical features
 Late 60’s – early 70’s.
 More sudden onset than Alzheimer’s
 May present with stroke or sudden decline
infunction
 Emotional and personality changes tend to
occur early (unlike Alzheimer’s)
 Depression is prominent
 Fits, TIAs, other signs of cerebral ischaemia.
 O/E – Focal neurology: Often upper motor
neuron deficits. Signs of cardiovascular
disease elsewhere.
Diagnosis
 Difficult to distinguish from Alzheimer’s unless
there’s a clear hx of stroke / neurological
localising signs.
Suggestive features:
 Patchy deficits in cognitive function
 Stepwise progression (not slow and steady)
 Presence of Hypertension
 Presence of atherosclerosis in peripheral or
retinal vessels
Prevelance:
1-4% of people over 65. 6-12 per 1000 per year over
70’s. more common in men.
Aetiology
PMH cardiovascular disease or high cholesterol.
Smoking., Family history of cardio/cerebrovascular
disease
Atrial fibrillation (multiple small emboli)
Diabetes mellitus, Coagulopathies, Polycythaemia
 Sickle cell anaemia
Carotid disease

Lewy body dementia Spherical inclusion bodies “lewy bodies” are

seen on histology (post-mortem).

Lewy body has 3 main clinical

manifestations:

 Parkinson’s disease
 Dementia with Lewy bodies
 Associated with degeneration of
sympathetic neurons in the spinal
cord.

Cross-over in the 3 syndromes: many

patients with Parkinson’s develop both
dementia and autonomic dysfunction in the
latter years.

Pathology

Mixture of Lewy bodies and Alzheimer’s

type amyloid plaques and tangles.

Lewy bodies are dense intracytoplasmic

inclusions made of phosphorylated
neurofilament proteins associated with α-
synuclein. These are primarily found in the
basal ganglia, and later spread into the
cortex. Neuronal loss is prominent, and
there is a slight reduction in total brain
volume.

Often inherited – mutations in α-synuclein

and β-synuclein genes – leads to abnormal
protein aggregates containing α-synuclein,
ubiquitin, other proteins.
Clinical features
 Dementia—relative sparing of memory, with fluctuating Cognitive state often fluctuates. High
cognitive ability and level of consciousness is typical. incidence of visual hallucinations
● Parkinsonism—postural instability and shuffling gait;
only 20 per cent have a tremor. Particularly sensitive to the side effects of
● Visual hallucinations. anti-psychotic medications (exacerbate
● Falls. parkinsonian symptoms) and anti-Parkinson
● Depression. medication.
● Sleep disorders—daytime somnolence
No cure, but acetylcholine-esterase drugs
may help slow progression of cognitive
impairment (but not the disease).

69 | P a g e
 Frontotemporal dementia  Encompasses many syndromes
 Behaviour abnormalities, impairment of
language.
 Usually begins before 60 years old
 15 / 100,000 people get this between 45-60
years

3 subtypes:
 Behavioural-variant fronto-temporal
dementia
 Primary progressive aphasia
 Semantic dementia

Pick’s disease can cause the first two in particular

Cause

 Mutations in genes that result in the abnormal

accumulation of tau and other proteins in brain
tissue – seen as inclusion bodies on histology
 Gene mutations also associated with ALS
(Amyotrophic lateral sclerosis) – similar
pathologic basis?

Clinical presentation
 Personality change (frontal lobe involvement)
 Language change (Temporal lobe
involvement)
 Memory usually well preserved in early stages
(unlike Alzheimer’s disease)

Treatment
 No specific, but consider:
 SSRI’s for disinhibition and compulsive behaviours
 Do not offer AChE inhibitors or memantine to people with frontotemporal Dementia (NICE)

More treatment suggestions (BMJ best practice)

 Benzodiazepines or neuroleptics (anti-psychotics) for acute irritability, restlessness, agitation,

and aggression.

 SSRIs for compulsions that dominate significantly or interfere with everyday life.

 Antipsychotics: Mirtazapine is preferred for sleep disturbances; zolpidem, trazodone, and

clonazepam can also be considered, but benzodiazepines are a last resort.#

 Amantadine for distractibility, perseveration, and restlessness. [Amantadine is a weak dopamine

agonist with modest antiparkinsonian effects.]

70 | P a g e
  Valproate semisodium (valproic acid and sodium valproate in a 1:1 ratio) for euphoria,
excitability, mania, impulsivity, irritability and persistent restlessness, agitation, and aggression

71 | P a g e
Alcohol Abuse
Consumption of alcohol at a sufficient level to cause physical or psychiatric and/or social
harm…

Binge drinking = 2x recommended level of alcohol in one session. (>8 units male, >6
female)

Harmful use = drinking above safe levels with evidence of alcohol related problems. (>50
units/week male, >30 female).

Antiolytic = reduces Alcohol effects

anxiety  Affects GABA in brain. Anxiolytic / sedative effects in brain.
 Dopaminergic pathway – stimulant and pleasurable effects. Repeated ingestion =
sensitised dopamine pathways in brain = dependence.
 Long term use – downregulation of inhibitory GABA receptors, Upregulation of
excitatory glutamate receptors. Result = CNS hyper-Excitability
 Craving – linked to dopaminergic, serotonergic, opioid systems that mediate
positive reinforcement, then withdrawal mediated by GABA, glutaminergic and
Craving – conscious noradrenergic systems.
urge to drink alcohol  Social learning theory: imitation of friends / relatives.
Risk factors Male: increased risk of alcohol abuse and increased metabolism of alcohol, allowing them
to have more.

Genetics: Monozygotic twins have higher concordance rates than dizygotic.

Antisocial behaviour: Pre-morbid antisocial behaviour may predict alcoholism.

Life stressors: financial problems, marital issues, certain occupations.

Advice Male / female – 14 units/week. No more than 2-3 units a day.

Clinical features Alcohol intoxication Slurred speech, labile affect, impaired judgement, poor
coordination.
Severe: Hypoglycaemia, stupor, coma, hypothermia (if exposed to elements).

Alcohol dependence: SAW DRINK

Subjective awareness
Avoidance
Withdrawal symptoms
Drink-seeking behaviour,
Reinstatement
Increased tolerance
Narrowing of drinking repertoire. (routinely stick to one or two drinks e.g. tenants or
special brew).

Medical
 Heatic: Fatty liver, hepatitis, cirrhosis, hepatocellular carcinoma

72 | P a g e
  Gastrointestinal: Peptic ulcer disease, oesophageal varices, pancreatitis,
oesophageal carcinoma.
 Cardiovascular: Hypertension, cardiomyopathy, arrhythmias,
 Haematological: Anaemia, thrombocytopenia
 Neurological: Seizures, peripheral neuropathy, cerebellar degeneration,
Wernicke’s encephalopathy, Korsakoff’s psychosis, head injury from fall (alcohol
may mask acute symptoms)
 Obstetrics: foetal alcohol syndrome
Psychiatric
 Morbid jealousy
 Self-harm and suicide
 Mood disorders, Anxiety
 Alcohol-related dementias
 Alcoholic hallucinations, Delirium tremens
Social
 Domestic violence
 Drink driving, Employment difficulties, Financial problems, Homelessness ETC
Withdrawal Symptoms
6-12 hours abstinence: Malaise, tremor, nausea, insomnia, transient hallucinations,
autonomic hyperactivity,
36+ hours: seizure peak incidence
72 hours: delirium tremens

ICD 10 criteria for withdrawal:

Evidence drinking has stopped after high-level use.
Not accounted for by medical disorder

+ any three of: Tremor, sweating, nausea/vomiting, tachycardia, increased BP, headache,
psychomotor agitation, insomnia, malaise, transient hallucinations, grand-mal
convulsions.

Delirium After 24 hours, peak 72 hours

Physical illness may pre-dispose
tremens Dehydration / electrolyte disturbance
Cognitive impairment
Vivid perceptual abnormalities
Paranoid delusions
Marked tremor
Autonomic arousal (tachy, fever, pupillary dilatation, increased sweating,

Medical treatment
large doses of benzodiazepines (e.g. Clordiazepoxide), Haloperidol (To treat psychotic
features), IV pabrinex (=injection that contains vitamins B and C (thiamine, riboflavin,
pyridoxine, nicotinamide and ascorbic acid).

73 | P a g e
 Peripheral
stigmata of
alcoholic liver
disease

Osce tips 1:
Cage
questionnaire

74 | P a g e
 Mental state
exam for
alcohol

OSCE tips: 1: screen for alcohol depence via cage questionnaire – score
Specific alcohol of 1 or more may warrant further question
history: 2: Establish drinking pattern and quantity consumed
 “can you describe what drinks you have in a typical day?”
 “How much alcohol do you consume in a typical week?”
 “How much money do you spend on drinking?”
 “how often do you consume alcohol?”
 “do you drink steadily, or have periods of binge drinking?”
 “is there anything in particular which causes you to drink
more?”
3: Explore features of alcohol dependence
 “When and where do you normally drink?” (Narrowing of
drinking repertoire)
 “Do you often feel the urge to drink?” (Comulsive need to
drink)
 “Have you noticed that alcohol has less effect on you than it did
in the past?” (Tolerance)
 “Is alcohol the first thing that comes to your mind when planing
a social gathering?” (Drink-seeking behaviour predominates)
 “Do you ever feel shakey and anxious when you haven’t had a
drink?”
 “have you ever tried to give up drinking? If so, what happened?”
 “Do you ever drink to get rid of this feeling?”

4: Explore possible risk factors

 “is there any family history of alcohol-related problems?

75 | P a g e
  Explore other risk-factors: e/g. financial difficulties, relationship
difficulties etc “is there anything going on in your life at the
moment that is particularly difficult to deal with or causing ou a
lot of stress?”
5: Establish impact
 “Has alcohol affected your mental health?” (Psychiatric impact)
 “Has alcohol affected your physical health?” Ask about e.g. liver
disease, cardiovascular disease, neurological disorders (Physical
impact)
 “Has alcohol caused any problems with work, relationships or
the law?” (Social impact)
Investigations:  Bloods
Blood alcohol level, Blood alcohol concentration
FBC,U&E (Dehydration, low urea), LFTs + Gamma GT (may be raised),
MCV (macrocytosis indicated vitamin B12 depletion), B12/folate,
TFTs, (alternate causes of raised MCV), Amylase (pancreatitis)
Hepatitis serology, Glucose (Hypolycaemia)
 Alcohol questionnaires:
AUDIT – Alcohol use and disorders identification test
SADQ – Severity of alcohol dependence questionnaire
FAST – 4 items, good in bust settings

 CT head (If head injury is suspected)

 ECG (For arrythmias)

Differential Psychiatric disorders:
diagnosis Psychosis
Mood disorders
Anxiety disorders
Delerium

Medical disorders
Head injury
Cerebral tumour
Cerebrovascular accident (Stroke)

76 | P a g e
 Key fact:
Wernike’s
Encephalopathy

Acute encephalopathy due to thiamine deficiency: Delerium,

nystagmus, opthalmoplegia, hypothermia, ataxia. If you don’t treat, it
will progress to irreversable Korsakov’s syndrome. Treat with
Parenteral thiamine (Pabrinex).
OSCE tip

How many
units?

Biopsychosocial Biological
approach to  Chlordiazepoxide detox regiment + thiamine (withdrawal)
management  Disulfiram/Naltrexone/Acamprosate
 Treatment of medical and psychiatric complications.

Psychological
 Motivational interviewing +CBT
 Social network and environment based therapies

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 Social
 Alcoholics anonymous
 Social support including family involvement.

Driving  It is the patients responsbility to contact the DVLA if there is

alcohol misuse or dependence.
 If at follow up you find that the patient has not informed the
DVLA, Consider first contacting your Medical defence union for
advice, inform the person in writing of your intended actions so
as to give them another opportunity. If this does not work,
contact the DVLA personally.
Alcohol
withdrawal Management of withdrawal:
 High dose benzodiasepines (commonly chlordiazepoxide) –
Reducing regime (dose is tapered down over 5-9 days)
 Thiamine (Vitamin B1) – to prevent wernike’s encephalopathy –
Oral (200-300mg) or IV (Pabrinex)

Alcohol Long term management

dependence 1. Disulfiram – causes a build up of acetylaldehyde on consumpion
(Long term) of alcohol. Unpleasent symptoms (Anxiety, flushing,
headaches). Basically, causes an instant hangover upon drinking
2. Acamprosate – Reduces craving by enhancing GABA
transmission
3. Naltrexone – Blocks opioid receptors (antagonist) in body,
reducing pleasurable effects of alcohol.

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 Motivational interviewing
guides the person into wanting to
change. Motivational interviewing is
the most effective during the Pre-
contemplation and contemplation
phases (see stages of change )

CBT

Alcoholics anonymous – 12 step approach for patients who accept

they have a drinking problem. Utilizes psychosocial techniques in
order to change behaviour (Social suport networks, rewards).

Prophylactic oral thiamine (50mg OD) for harmful drinkers if they are
at risk of malnourishment or have decompensated liver disease.

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 Drug M of A Side effects
Chlordiazepoxide Chlordiazepoxide binds to drowsiness
10–30 mg 4 times a stereospecific benzodiazepine (BZD) light-headedness
day, dose to be binding sites on GABA (A) receptor confusion
gradually reduced over complexes at several sites within the unsteadiness (especially in older
5–7 days, consult local central nervous system, including people, who may have falls and injur
protocols for titration the limbic system and reticular themselves as a result)
regimens. formation. This results in an dizziness
increased binding of the inhibitory slurred speech
neurotransmitter GABA to the muscle weakness
GABA(A) receptor.BZDs, memory problems
constipation
Therefore, enhance GABA-mediated nausea (feeling sick)
chloride influx through GABA dry mouth
receptor channels, causing blurred vision
membrane hyperpolarization. Less common:
headaches
The net neuro-inhibitory effects low blood pressure
result in the observed sedative, increased saliva production
hypnotic, anxiolytic, and muscle digestive disturbances
relaxant properties. rashes
sight problems (such as double vision)
See slide below on GABA tremors (shaking)
transmission changes in sexual desire
incontinence (loss of bladder control)
difficulty urinating
Disulfiram Disulfiram blocks the oxidation of Allergic dermatitis; breath odour;
alcohol at the acetaldehyde stage depression; drowsiness;
200 mg daily, increased during alcohol metabolism following encephalopathy; fatigue;
if necessary up to disulfiram intake causing an hepatocellular injury; libido decreased;
500 mg daily. accumulation of acetaldehyde in mania; nausea; nerve disorders;
the blood producing highly paranoia; schizophrenia; vomiting
unpleasant symptoms. Disulfiram
blocks the oxidation of alcohol
through its irreversible inactivation
of aldehyde dehydrogenase, which
acts in the second step of ethanol
utilization
Naltrexone Naltrexone is a pure opiate Common or very common
antagonist and has little or no Abdominal pain; anxiety; appetite
Initially 25 mg daily, agonist activity. Naltrexone is abnormal; arthralgia; asthenia;
then increased to thought to act as a competitive Chest pain; chills; constipation;
50 mg daily, total antagonist at mc, κ, and δ receptors diarrhoea; dizziness;
weekly dose may be in the CNS, with the highest affintiy eye disorders;
divided and given on 3 for the μ receptor. Naltrexone headache; hyperhidrosis;

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 days of the week for competitively binds to such mood altered; myalgia;
improved compliance receptors and may block the effects nausea;
(e.g. 100 mg on of endogenous opioids. This leads to palpitations;
Monday and the antagonization of most of the sexual dysfunction; skin reactions;
Wednesday, and subjective and objective effects of sleep disorders;
150 mg on Friday); opiates, including respiratory tachycardia; thirst;
maximum 350 mg per depression, miosis, euphoria, and vomiting
week. drug craving. The major metabolite
of naltrexone, 6-β-naltrexol, is also Uncommon
an opiate antagonist and may Alopecia; confusion; cough;
contribute to the antagonistic depression; drowsiness; dry mouth;
activity of the drug. dysphonia; dyspnoea; ear discomfort;
eye discomfort; eye swelling; feeling
Longer acting than Naloxone hot; fever; flatulence; flushing;
hallucination; hepatic disorders;
lymphadenopathy; nasal complaints;
oropharyngeal pain; pain; paranoia;
peripheral coldness; seborrhoea; sinus
disorder; sputum increased; tinnitus;
tremor; ulcer; urinary disorders;
vertigo; vision disorders; weight
changes; yawning
Acamprosate Chronic alcohol exposure is
hypothesized to alter the normal
Maintenance of balance between neuronal excitation Abdominal pain; diarrhoea; flatulence;
and inhibition. in vitro and in
abstinence in alcohol- vivo studies in animals have nausea; sexual dysfunction; skin
dependent patients provided evidence to suggest reactions; vomiting
Acamprosate may interact with
666 mg once daily at glutamate and GABA
breakfast and 333 mg neurotransmitter systems centrally
twice daily at midday and has led to the hypothesis that
acamprosate restores this balance. It
and at night. seems to inhibit NMDA receptors
while activating GABA receptors.
Pabrinex Replaced depleated Vitamin B1
(thiamine) and more.
( VITAMIN B
SUBSTANCES WITH
ASCORBIC ACID) For Adult – IV infusion:
2–3 pairs 3 times a day for 2 days,
Treatment / discontinue if no response, continue
prophylaxis of treatment if symptoms respond
Wernicke's after 2 days; (by intravenous
encephalopathy infusion or by deep intramuscular
Initially by intravenous injection) 1 pair once daily for 5 days
infusion or for as long as improvement
. continues, give deep intramuscular
injection into the gluteal muscle

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Tobacco Misuses
What is nicotine?
Tobacco  Selective agonist of nicotinic acetylcholine receptor (nAChR)
smoking  nAChRs may play an important role in cognitive processes (loss of Ach releasing
neurons in Alzheimer’s
 Tobacco may be smoked, snuffed, chewed (e.g. chewing tobacco)

How does nicotine produce a rewarding effect?

 Addiction (e.g. gambling, cocaine, sugar, scrolling to the next post on

Instagram, pulling a leaver on a slot machine) is often driven by the release of
dopamine in the nucleus accumbens: this = the reward.
 Nicotine: Involves Dopaminergic neurons with NAChR’s in the Ventral
tegmental area (VTA).
 Upon excitation of projecting neurons in the VTA, Dopamine is released in the
Nucleus accumbens and the prefrontal cortex (fulfils the dopamine
requirement of addictive drugs).
 Specifically, the α4β2 NAChR is implicated in nicotine addiction (knock-out mice
are not interest in nicotine)
 Homomeric α7 receptor may also be implicated in nicotine-evoked dopamine
release

Dangers of  Smoking is associated with heart disease, multiple types of cancer, and COPD.
smoking Every year, almost 500,000 people in the US die from smoking-related illnesses
 Large proportion of the risk of coronary heart disease and stroke comes from
smoking only a few cigarettes.
Aetiology  Biological, genetic, behavioural, social, and environmental factors.

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 more likely in households with current smokers where parental approval is more
likely and there is greater access to cigarettes
 Low socio-economic status is associated with increased smoking rates
 Smoking is more prevalent in patients with a history of mental health, illness or
substance abuse. The rate of smoking among those with schizophrenia
approaches 90%.
 Patients with HIV/AIDS have high smoking rates (47% to 72%), and the
proportion of deaths among HIV/AIDS patients from diseases related to
tobacco use is substantial and increasing.
Withdrawal There are 7 symptoms of nicotine withdrawal described in DSM-5. If 4 or more of the
following symptoms appear within 24 hours after cessation or reduction in the amount
of tobacco used.

1. Irritability, frustration, or anger

2. Anxiety

3. Difficulty concentrating

4. Increased appetite

5. Restlessness

6. Depressed mood

7. Insomnia
Tobacco History
“Do you smoke?”
“How many per day” (20/day for 1 year = one pack year).
“How soon after waking do you have your first cigarette?”

Assess
Assess readiness to stop smoking:
"How important is it for you to try to stop smoking now?"
“between 0 (not at all) and 10 (Extremely) If you decide to stop, how confident are you
that you can succeed?".
"Why did you select 4 instead of 0?".
The patient may then be asked: "Are you willing to try to stop in the next month?".

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 Management
1) Ask about a patients' smoking status.
Ask
Advise 2) Advise those who smoke to stop. Open patient centred discussion. What is stopping
Assess them from stopping? How would stopping help them to achieve their personal goals?
Assist
Arrange 3) Assess their readiness to stop.

4) Assist smokers in their stopping attempts.

Pharmacological smoking cessation aids are recommended to all smokers who want
to quit: nicotine replacements bupropion and varenicline have strong efficacy for
smoking cessation.

Medications
First-line agents
 Nicotine replacement therapies (NRTs)
 with patches, gum, lozenges, nicotine inhaler, or nasal spray double the
success rate of a stopping attempt.
 Nicotine replacement (gum, patch, lozenge, inhaler, nasal spray):
 Bupropion and varenicline are both considered first-line medications for
smoking cessation.
Second-line agents

 Clonidine is not approved in the US for smoking cessation and has the potential
for serious adverse effects, but it may have a role for those with severe
cravings.
 Nortriptyline is also considered second-line therapy due to higher rates of
adverse events than with bupropion.

Clonidine (Hypertension drug)

 Second-line therapy for smoking cessation due to significant adverse effects of

hypotension and sedation (10%).
 Blood pressure monitoring essential.
 Taper patients off the medication over 2 to 7 days.

Nortriptyline (Depression drug / neuropathic pain)

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  Second-line therapy for smoking cessation due to higher rates of adverse
events; these include arrhythmias and changes in contractility and blood flow.

NICE does not recomment NRT mixed with buproprion or varenicline

Unwilling to stop smoking abruptly?

 alternative approach is to provide NRT to support a reduction in cigarette

consumption as a first step towards abstinence.
 For patients who are not willing to quit in the next month, but are willing to
reduce cigarette consumption and quit in 3 months, varenicline therapy for 24
weeks has been shown to significantly increase smoking cessation rates.

Pharmacological treatment, including NRT, bupropion, and varenicline, is not

recommended for pregnant or breastfeeding women, or for adolescents.

Adolescents <18 years

o Pharmacological treatment, including NRT, bupropion, and varenicline, is not

recommended for adolescents.

o High intensity, family-based interventions

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 Bupropion (buproprion hydrochloride / amfebutamone hydrochloride)
Zyban modified release tablet. 150mg OD 6 days, BD 7-9
weeks.
o Bupropion selectively inhibits the neuronal reuptake
of dopamine (Quite pronounced blockade)
norepinephrine, and serotonin (weak blockades
compared with other tricyclic antidepressants)
o The increase in norepinephrine may attenuate
nicotine withdrawal symptoms
o the increase in dopamine at neuronal sites may
reduce nicotine cravings and the urge to smoke.
o Bupropion exhibits moderate anticholinergic effects.

Contraindicated in: Cautions

 Acute alcohol withdrawal;  Alcohol abuse;
 acute benzodiazepine withdrawal;  Diabetes;
 bipolar disorder;  Elderly;
 CNS tumour;  History of head trauma;
 Eating disorders;  Predisposition to seizures (prescribe only
 history of seizures; if benefit clearly outweighs risk)
 severe hepatic cirrhosis

Side effects Less common

More common
 Buzzing or ringing in the ears
 Anxiety  headache (severe)
 dry mouth  skin rash, hives, or itching
 hyperventilation
Rare
 palpitations
 irritability  Confusion
 restlessness  fainting
 shaking  false beliefs that cannot be changed by
facts
 trouble sleeping
 having extreme distrust of people
 seeing, hearing, or feeling things that
are not there
 seizures
 trouble concentrating

Varenicline
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 (Chantix and Champix) – the most effective option
M of A
The drug competitively inhibits the ability of nicotine to bind to and activate the alpha-4 beta-2
receptor. The drug exerts mild agonistic activity at this site, though at a level much lower than nicotine;
it is presumed that this activation eases withdrawal symptoms.

Patients should be advised to stop taking + seek medical advice if they develop agitation, depressed
mood or suicidal thoughts.

Cautions:
 Conditions that may lower seizure threshold;
 history of cardiovascular disease;
 history of psychiatric illness (may exacerbate underlying illness including depression);
 predisposition to seizures

Side effects common: Side effects – rare / more serious

feeling and being sick
difficulty sleeping (insomnia), sometimes with  Mood swing
vivid dreams  Suicidal ideation
dry mouth  Depression
constipation or diarrhoea  Hallucination
headaches  Seizures
drowsiness  arrhythmias
dizziness

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Extra
Anorexia nervosa
Individuals with anorexia nervosa who are at risk medically or psychiatrically require inpatient treatment.

Indications for hospital admission include the following:

 Low weight (85% or less of expected weight and/or less than the third percentile for BMI)

 Lack of any weight gain

 Significant oedema

 Physiologic decompensation including, but not limited to, the following: (1) severe electrolyte imbalance
(life-threatening risks created by sodium and potassium derangements), (2) cardiac disturbances or other
acute medical disorders, (3) altered mental status or other signs of severe malnutrition, and (4) orthostatic
differential greater than 30/min

 Temperature less than 36°C

 Pulse below 45 beats per minute

 Psychosis or a high risk of suicide

 Symptoms refractory to outpatient treatment

Hallucination
 Hypnogogic hallucinations occur when an individual is falling asleep. They occur most commonly in the
auditory modality but can also be visual, tactile or kinaesthetic. They occur in approximately 30% of adults.
 Hypnopompic hallucinations occur as a person awakes; the hallucinatory experience continues once the
individual's eyes open from sleep.
 Hypnogogic and hypnopompic hallucinations do not suggest psychopathology but psychiatrists consider
them true hallucinatory experiences. They can be the side-effect of medication (e.g SNRIs) or a symptom of
narcolepsy.
 A reflex hallucination occurs when a true sensory stimulus causes an hallucination in another sensory
modality (like a loud noise creating an unpleasant smell).
 Autoscopy is the experience of seeing oneself and knowing that it is oneself. It is sometimes called the
'phantom mirror image'.
 Auditory illusions occur when an auditory stimulus is misrepresented or misinterpreted by the listener

Lithium toxicity
Lithium has a very narrow therapeutic window and the development of lithium toxicity is not uncommon. Thiazide
diuretics are most commonly associated with toxicity. Thiazide diuretics have been shown to have the greatest
propensity to induce this interaction because of their distal renal tubular site of action causing compensatory
proximal tubular reabsorption of sodium and lithium.

 Ramipril can also increase Lithium levels, but not to the same extent as Bendroflumethiazide.
 Acetazolamide and Theophylline decrease Lithium levels by increasing renal clearance.

Clinical features of Lithium toxicity can include:

 Anorexia, diarrhoea and vomiting

 Drowsiness, restlessness.
 Dysarthria
 Dizziness, ataxia, incoordination, muscle twitching, coarse tremor
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  Hyperreflexia, convulsions
 Acute renal failure
 Collapse, coma, death

Illusions
Illusions can occur in any sensory modality and occur commonly in humans. They are not generally signs of mental
illness or psychiatric pathology. The most commonly reported are visual.

Illusions are divided into three broad types:

 Affect illusion - associated with specific mood states, for example, someone who has recently been
bereaved may 'see' their loved one
 Completion illusion - due to inattention when reading, such as misreading words or completing faded letters
 Pareidolia - occurs when an individual perceives a vivid picture in an otherwise vague or obscure stimulus,
such as seeing faces or animals in clouds.

Schizophrenia – First rank symptoms

The first rank symptoms are:

1. Delusional perception ("I knew by looking at the man on the bus that I was right about the conspiracy.")

2. Auditory hallucinations

Audible thoughts

Voices arguing or discussing, (3rd person auditory hallucinations)

Voices commenting on patient's actions. (‘Running commentary')

3. Thought disorder:

Thought withdrawal

Thought insertion, and

Thoughts broadcasting.

4. Passivity experience

Somatic passivity ("They're making me feel cold all the time!")

Passivity of affect ("It's not me getting angry, it's the Man that sends me the anger.")

Passivity of impulse ("The Devil gave me the urge to slap the nurse.")

Passivity of volition ("The Government was controlling me, so I couldn't help it.")

Second-rank-symptoms are common in schizophrenia, but also occur in other types of mental illness.

 Mood changes (depression or elation)

 Emotional blunting
 Perplexity, and
 Sudden delusional ideas.

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Binge eating disorder
This is the typical description of a Binge-Eating Disorder.

Clinical features

 Eating large quantities of food in a certain time frame.

 Eating until uncomfortably full
 Eating when she does not feel hungry
 Eating rapidly
 Feeling embarrassed by, or guilty about, these behaviours.
 Eating alone because of the embarrassment

These episodes have occurred ≥1 per week, for ≥3 months, No compensatory behaviours, such as purging, laxatives,
exercise (this is key to differentiating between Bulimia Nervosa)

Anorexia of Binge-Eating Type: This requires a low body weight for diagnosis. The question states that her BMI is 28.

Avoidant Food Intake Disorder: This is characterised by low food intake, without any disturbances in body image

Bulimia Nervosa: Crucially, she does not have any compensatory behaviours (purging, exercise, emetics, laxatives).
The presence of these would switch the diagnosis to Bulimia Nervosa.

Obsessive-Compulsive Disorder (OCD): Overeating may be considered a compulsion, but this is classified as an
eating disorder, not OCD.

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