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Phase 3a > Psychiatry > Flashcards

Psychiatry Flashcards

1
Q

Define generalised anxiety disorder (GAD)

A

GAD is defined as at least 6 months of excessive, uncontrollable worry about everyday issues that is disproportionate to any inherent risk. The anxiety is not due to substance misuse or another condition.

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2
Q

Describe the epidemiology of GAD

A
  • Around 3.6% of the world’s population is affected
  • More common in high-income countries
  • Twice as common in females
  • Higher prevalence during pregnancy and people with chronic health conditions
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3
Q

Name the risk factors for developing GAD

A
  1. FHx of anxiety
  2. Physical or emotional stress - bullying, work-related, relationship etc
  3. History of physical, sexual or emotional trauma
  4. Other anxiety conditions - panic disorder, social and other phobias
  5. Female sex
  6. Chronic physical health condition
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4
Q

What are the emotional/cognitive symptoms of GAD?

A
  • Excessive worrying for at least 6 months
  • Unable to control worry
  • Restlessness
  • Poor concentration
  • Irritability
  • Easily tired
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5
Q

What are the physical signs and symptoms of GAD?

A
  • Muscle tension
  • Trembling
  • Sleep disturbance
  • Palpitations
  • Signs of Hyperarousal (sweating, increased HR, SOB)
  • GI symptoms
  • Headaches
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6
Q

How is GAD diagnosed?

A

GAD is made by clinical diagnosis with the help of screening tools.

Consider other tests to rule out other causes:
- TFT
- Urine drug screen - will be negative
- 24 hr urine catecholamines, metanephrines, normetanephrines and creatinine - to rule out pheochromocytoma
- ECG
- Pulmonary function

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7
Q

What is the ICD 11 criteria for GAD?

A
  1. Excessive anxiety and worry - More days than not for at least 6 months
  2. At least 3 symptoms of (Restlessness, fatigue, poor concentration, irritability, muscle tension, sleep disturbance)
  3. Causes significant distress or impairment in important areas of function (social, work etc)
  4. Not attributable to a substance, another medical condition or better explained by another mental disorder
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8
Q

What are the diagnostic criteria for GAD7 scale?

A

Assesses symptoms over the past 2 weeks: Each item 0-3 (not at all - nearly everyday)

  1. Feeling nervous, anxious, or on edge.
  2. Not being able to stop or control worrying.
  3. Worrying too much about different things.
  4. Trouble relaxing.
  5. Being so restless that it’s hard to sit still.
  6. Becoming easily annoyed or irritable.
  7. Feeling afraid as if something awful might happen.

0-4: Minimal anxiety.
5-9: Mild anxiety.
10-14: Moderate anxiety.
15-21: Severe anxiety.
(Above 10 suggests GAD)

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9
Q

What is the Non-pharmacological management for GAD?

A

Non-pharmacological treatment is valuable at all stages of treatment.

  • CBT
  • applied relaxation
  • mindfulness or meditation training
  • attention/perception modification
  • sleep hygiene education
  • exercise
  • self-help
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10
Q

What is the pharmacological management for GAD?

A

Pharmacological:
1st line: SSRI - escitalopram (10mg daily, max 20mg) or sertraline (25mg daily, max 200mg).

Consider Mirtazapine in patients with contraindication or caution to SSRI (uncontrolled epilepsy, Hx of bleeding disorders, HX of mania)

2nd line: serotonin-noradrenaline reuptake inhibitor (SNRI) such as Duloxetine or Venlafaxine

3rd line: Under specialist guidance use Buspirone or Pregabalin (addictive, less suitable in patients with addiction issues)

4th line: tricyclic antidepressant (imipramine or clomipramine) or quetiapine or benzodiazepine (diazepam or clonazepam)

Others: Propranolol (non-selective BB) for physical symptoms

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11
Q

What are the differentials for GAD?

A

Panic disorder
Social anxiety disorder
Depression
PTSD
OCD
Substance induced/withdrawal
Hyperthyroidism
IBS
Pheochromocytoma

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12
Q

What are potential complications associated with GAD

A
  • Comorbid depression
  • Comorbid substance use/dependance
  • Behavioral/mental health problems in offspring
  • Comorbid anxiety disorder (panic disorder, social phobia)
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13
Q

Define ADHD

A

Attention deficit hyperactivity disorder is a neurodevelopmental disorder characterised by persistent inattention, hyperactivity, and impulsivity. Symptoms manifest in at least 2 settings e.g school, home etc

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14
Q

Outline the epidemiology of ADHD

A
  • Around 5% of children globally are affected by ADHD.
  • Higher prevalence in boys (3:1) - this is thought to be due to underdiagnosis in girl (more likely to present with inattention).
  • Associated with poverty and low SES
  • Comorbidity with other mental health disorders is common
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15
Q

What is the aetiology of ADHD?

A

Exact cause is unknown. Thought to be multifactorial:

  • Genetic predisposition: Heritability estimated at 70-80%. Several associated genes
  • Environmental - LBW, maternal smoking/alcohol/drugs, premature birth, poverty
  • Neurobiological - lower levels of the neurotransmitters noradrenaline and dopamine.
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16
Q

What are the risk factors for developing ADHD?

A
  • FHx of ADHD
  • Male sex
  • Low birth weight
  • Epilepsy
  • Issues in pregnancy (smoking, drug use etc)
  • Other neurodevelopmental disorders (autism, dyspraxia, tic disorders)
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17
Q

What are the subtypes of ADHD?

A

Combined presentation: if both criterion for inattention and hyperactivity-impulsivity are met for the past 6 months. (6 symptoms of each)

Predominantly inattentive presentation: Inattention is met but hyperactivity-impulsivity is not met for the past 6 months.

Predominantly hyperactive/impulsive presentation: if hyperactivity-impulsivity is met and inattention is not met for the past 6 months.

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18
Q

What are the inattention symptoms of ADHD?

A

Inattention symptoms:
1. Fails to give close attention to details or makes careless mistakes in school work, work, or during other activities
2. Difficulty sustaining attention
3. Does not seem to listen when spoken to directly
4. Does not follow through on instructions and fails to finish school work, chores, or duties in the workplace
5. Difficulty organising tasks and activities
6. Avoids/reluctant to engage in tasks that require sustained mental effort
7. Loses things necessary for tasks or activities
8. Easily distracted by extraneous stimuli.
9. Forgetful in daily activities

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19
Q

What are the hyperactivity/impulsivity symptoms of ADHD?

A
  1. Fidgets with hands or feet or squirms in seat.
  2. Leaves seat in situations when remaining seated is expected
  3. Runs/climbs excessively in inappropriate situations
  4. Unable to play or engage in leisure activities quietly.
  5. Often ‘on the go’, acting as if ‘driven by a motor’
  6. Talks excessively.
  7. Blurts out an answer before a question has been completed.
  8. Difficulty awaiting his or her turn
  9. Interrupts or intrudes on others
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20
Q

According to the DSM-5-TR/ICD-11 criteria, what other requirements need to be met for ADHD to be diagnosed?

A

A. At least 6 inattention, hyperactivity/impulsivity symptoms which persist for at least 6 months. Inappropriate for development.

B. Symptoms must have been present before 12 years of age.

C. Several inattentive or hyperactive-impulsive symptoms are present in two or more settings.

D. Significant impairment in the quality of, social, academic, or occupational functioning.

E. Symptoms not better explained by another mental disorder. (e.g present only in times of psychosis as part of schizophrenia)

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21
Q

How do symptoms of ADHD differ in adults?

A
  • Symptoms may manifest as chronic disorganisation, poor time management, difficulty prioritising, and emotional dysregulation.
  • Adults often report feelings of restlessness rather than overt hyperactivity.
  • Relationship and occupational difficulties are common.
  • Only 5 symptoms of each are required for diagnosis.
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22
Q

What are the investigations for ADHD in children?

A

Diagnosis is purely clinical and made with the help of screening tools (always done in secondary care)

ADHD Rating scale - 18 item test based on DSM V
Vanderbilt Scale - assesses ADHD and comorbid conditions
Snap IV

Neuropsychological testing - to distinguish between learning disability (normal cognitive but difficulty with executive function)

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23
Q

What are the investigations for ADHD in adults?

A

ASRS - self reported scale may be used
Functional impairment scores and assessment

Children are usually assessed with the help of third party assessors (teachers). Adults symptoms tend to be self reported.

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24
Q

What are the differential diagnoses for ADHD?

A

Learning/language disorder
Oppositional defiant disorder
Depression
Bipolar disorder
Autism
Auditory/visual impairment
Anxiety disorder
Absent seizures

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25
Q

How is ADHD treated in children and adults?

A

Age 4-6:
1st line - Parent training in behaviour management (PTBM) and/or behavioural classroom intervention + psychoeducation.
2nd line - Methylphenidate
3rd line - Guanfacine

Age 6-18:
1st line - Psychoeducation + behavioral therapy in all lines. Consider methylphenidate or amfetamine/lisdexamfetamine (stimulant)
2nd line - Atomoxetine (selective norepinephrine reuptake inhibitor)
3rd line - Guanfacine or clonidine (alpha-2-adrenergic agonists) - especially effective for hyperactivity

Adults:
1st line: Lisdexamfetamine or methylphenidate
2nd line: Atomoxetine (non-stimulant)
Off licence: Bupropion, venlafaxine etc

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26
Q

What are the complications and prognosis of ADHD?

A

Medication induced: anorexia, insomnia, headache, cardiac issues, growth delay, mood lability

Untreated: Suicidal behaviour, obesity

ADHD symptoms persist into adulthood but the majority enter a partial remission.
Symptoms in adulthood often lead to academic/professional difficulty, maladaptive relationship, antisocial behaviours, increased accident risk.

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27
Q

Define depression

A

Depression and depressive disorders are characterised by persistent low mood, loss of interest, anhedonia and reduced energy. Causing varying levels of social and occupational dysfunction

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28
Q

What is the epidemiology of depression?

A
  1. Depression is a major global cause of disability and premature death.
  2. Incidence in women is double to men
  3. Risk of depression is 2-3 fold in people who have a 1st degree family member affected.
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29
Q

What is the aetiology of depression?

A

Multifactorial although exact cause still unknown

  1. Genetic - strong evidence but no specific factors
  2. Psychosocial/environmental - trauma, loss, stressful life events
  3. Neurobiological - dysregulation of neurotransmitters e.g serotonin
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30
Q

What is the pathophysiology of depression?

A

Not fully understood, probably due to a combination of complex mechanisms. Including dysregulation of the HPA which leads to disturbance in neurotransmitter activity in the CNS, including low levels of serotonin.

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31
Q

What are the risk factors for depression?

A
  1. FHx of depression/suicide
  2. Personal Hx of depression/other mental illness
  3. Female sex
  4. Chronic health condition - Dementia
  5. Medications - corticosteroids, propranolol, oral contraceptive
  6. Postnatal status
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32
Q

What are the main signs and symptoms of depression?

A

Core:
- Persistent depressed/low mood
- Anhedonia (reduced pleasure)
- Low energy/fatigue

Additional:
- Weight change
- Reduced libido
- Sleep disturbance
- Psychomotor change
- Excessive guilt
- Poor concentration
- Functional impairment
- Suicidal ideation
- Substance/medication SE excluded
- Manic episode in bipolar patient excluded
- Medical illness excluded

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33
Q

According to the DSM-V-TR criteria, when should a major depressive disorder be diagnosed?

A

A patient must have at least 5 of 9 symptoms during the same 2 week period, which is different to normal. At least one of the symptoms must be low mood or anhedonia. Symptoms should occur in all areas/nearly everyday

  1. Depressed/low mood
  2. Anhedonia
  3. Significant weight change
  4. Sleep disturbance - in/hypersomnia
  5. Psychomotor symptoms -agitation/retardation
  6. Fatigue/low energy
  7. Feelings of worthlessness/excessive guilt
  8. Poor concentration/indecisiveness
  9. Thoughts of death, suicidal ideation, or suicide attempt

Further criteria -
- Functional impact
- Not better explained by substance abuse, medication side effects, or other psychiatric or somatic medical conditions.

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34
Q

How is depression investigated?

A
  1. Clinical diagnoses based on a MSE - according to the DSM-V or ICD 11 criteria
  2. Metabolic panel - should be normal
  3. FBC - rule out other causes of fatigue
  4. TFTs - rule out hypothyroidism
  5. PHQ 9
  6. Other scales - e.g Edinburgh postnatal, geriatric or cornell dementia scale where appropriate
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35
Q

How does the ICD-11 criteria differ to the DSM-V-TR criteria for depression?

A

ICD 11 criteria requires 1 symptom of (low mood, anhedonia, fatigue) + additional symptoms. No minimum amount of symptoms and focuses on severity and impact on function. Relies more on clinical judgement.

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36
Q

What is dysthymia?

A

Also known as persistent depressive disorder is a chronic form of depression which lasts at least 2 years, usually milder symptoms but cause a significantly reduced QofL.

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37
Q

What is the non-pharmacological management for depression?

A

In patients with subthreshold/mild depression non-pharmacological options should be offered 1st line. This includes:

  1. Psychotherapy - CBT, low or high intensity
  2. Computer based interventions
  3. Lifestyle factors - exercise, diet, sleep hygiene etc
  4. Social support - especially for people with caring roles
  5. Safety net - support groups, helplines
  6. Early follow up - 2-4 weeks
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38
Q

What is the pharmacological management for depression?

A

Non-suicidal, non-pregnant, no psychosis or severe psychomotor symptoms:
1st line - Antidepressant
Consider immediate management with benzodiazepine (+/-) antipsychotic
2nd line - switch antidepressant class

Treatment resistant cases:
1st line: Consider combination antidepressant therapy, antipsychotic therapy and lithium
2nd line: MAOI (monoamine oxidase inhibitor)
3rd line: ECT

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39
Q

How should a patient with severe depression and suicidal thoughts be managed?

A

Psychiatric referral (+/-) hospitalisation + antidepressant or ECT (in some severe cases)

Consider immediate management with benzodiazepine (+/-) antipsychotic

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40
Q

What are the differentials for depression?

A
  • Bipolar disorder - will have manic symptoms
  • Anxiety disorders
  • Hypothyroidism
  • Cushing’s
  • Adjustment disorder w/ depressed mood
  • Substance/medication induced or somatic illness
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41
Q

What is the prognosis for depression?

A

Treatment should be continued for 9-12 months

  • 1/3 of patients will have a recurrence within a year of stopping treatment
  • More than 50% will have a recurrence in their lifetime
  • Maintenance therapy may be required for people who have relapsed 3 times
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42
Q

Define Autism Spectrum Disorder?

A

ASD is a neurodevelopmental condition characterised by persistent impairments in social communication/interaction and restricted/repetitive patterns of behaviour, interests or activities.

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43
Q

What is the epidemiology of ASD?

A
  1. Prevalence is around 1% of children in the UK
  2. More common in males (3-4 times)
  3. Coexisting ADHD, learning disability, sleep difficulty and other mental health conditions are common
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44
Q

What is the aetiology and pathophysiology of ASD?

A

Development of ASD is associated with genetic and environmental factors:
Genetic - specific factors are found in 20-25% of patients. Including known genetic syndromes (fragile x, retts, Downs)
Environmental - Advanced paternal age, maternal medication, infections, traumatic birth

These factors result in modified brain development and abnormalities in neural connections.

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45
Q

What are the risk factors for developing ASD?

A
  1. Male sex
  2. Positive FHx
  3. Gestational valproate exposure
  4. Genetic variants
  5. Increasing age
  6. Prematurity/antenatal complications
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46
Q

What are the signs and symptoms of ASD?

A

Symptoms:
- Language regression/delay
- Verbal/Non-verbal communication impairment (limited eye contact and facial expressions)
- Social impairment (play alone, inappropriate, one sided)
- Repetitive, rigid, stereotyped behavior, interests + activities
- Motor stereotypies
- Sensory sensitivity

Signs:
- Placid or very irritable baby
- Feeding difficulties

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47
Q

What are the investigations for ASD?

A
  1. ASD diagnosis are done by trained specialist (e.g community paediatrician, psychiatrist).
  2. Initial screening tools in primary care can be useful (e.g SCQ, CAST, CARS)

Further tests:
Hearing and language assessment - if delayed speech
Genetic testing - to test syndromic causes like fragile X
EEG or MRI brain - in some cases e.g language regression

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48
Q

What are the differentials for ASD?

A
  1. Other causes of disordered development, LD
  2. ADHD
  3. Social pragmatic communication disorder
  4. Schizoid personality disorder
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49
Q

How is ASD managed?

A

No specific medication:
1. Behavioural & educational interventions (e.g. high staff-to-student ratio, highly supportive teaching environment, predictability and structure)
2. Psychosocial interventions (e.g. be appropriate for the child or young person’s developmental level and sensitive and responsive to their patterns of communication and interaction, include techniques to expand communication, interactive play and social routines)
3. Interventions for life skills (e.g. coping strategies for leisure activities, public transport and employment)
4. Interventions for speech and language problems (e.g. involvement of speech and language team)
5. Intervention for sleep disorders
6. Managing comorbidities

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50
Q

What is the DSM-V-TR criteria for ASD?

A

A. Persistent deficits in social communication and social interaction (all 3 of):
- Deficits in social-emotional reciprocity. (conversation, communicating emotion)
- Deficits in nonverbal communicative behaviors used for social interaction (e.g. eye contact, body language).
- Deficits in developing, maintaining, and understanding relationships.

B. Restricted, Repetitive Patterns of Behavior, Interests, or Activities (at least 2 of the following):
- Stereotyped or repetitive motor movements, use of objects, or speech.
- Insistence on sameness, inflexible adherence to routines, or ritualized patterns.
- Highly restricted, fixated interests that are abnormal in intensity or focus.
- Hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of the environment.

C. Symptoms must be present in the early developmental period, but may not fully manifest until social demands exceed limited capacities.

D. Symptoms cause clinically significant impairment in social, occupational, or other important areas of functioning.

E. These disturbances are not better explained by intellectual disability. Intellectual disability and ASD frequently co-occur, but to diagnose ASD, social communication should be below that expected for general developmental level.

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51
Q

What are the complications/prognosis of ASD?

A

Complications:
- Epilepsy
- Anxiety
- Depression
- Developmental regression

With appropriate support patients will have fulfilling lives.
- Depends on severity of ASD
- ASD patients with higher IQ have less severe symptoms in adulthood

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52
Q

Define bipolar disorder

A

Bipolar disorder is an episodic mood disorder characterised by manic, or hypomanic, and depressive episodes. Two subtypes are recognised: bipolar I disorder and bipolar II disorder.

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53
Q

What is the epidemiology of bipolar disorder?

A
  • Lifetime prevalence of 1-2% in the UK
  • Onset is usually adolescence to early adulthood (usually before 30)
  • Misdiagnosis with Major depressive disorder is common
  • Equal sex prevalence (slight female predominance in bipolar II)
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54
Q

What is the aetiology of bipolar disorder?

A

Exact cause is unknown, likely due to a combination of genetic and environmental factors.

Genetic - 8 fold increase if 1st degree relative is affected
Environmental - Childhood trauma/abuse, adverse life events, history of substance use disorder
Biological - Hormone abnormalities (HPA issues), also systemic inflammatory pathways

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55
Q

What are the risk factors for developing bipolar disorder?

A
  1. FHx of bipolar or schizophrenia
  2. Onset of mood disorder (depression) <20 years
  3. Adverse life events
  4. Childhood trauma/adversity
  5. Hx of Depression
  6. Hx of substance use disorder
  7. Presence of anxiety disorder
  8. Hx of obesity or CVD
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56
Q

What are the clinical features of bipolar disorder?

A

Symptoms:
- Major depressive episode
- Mania (elated mood/energy, psychotic symptoms, affect social function)
- Hypomania (milder symptoms, no psychotic features, few days)

  • Inflated self esteem/grandiosity
  • Decreased need for sleep
  • Racing thoughts + speech
  • Disinhibition - excessive spending, sexual behaviour
  • Psychotic features - delusions/hallucinations (auditory)
  • No underlying cause - substance misuse, underlying medical cause, medication (steroids)
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57
Q

How is bipolar disorder classified?

A

Based on discrete episodes:
- Manic episode: abnormal and persistently elevated, expansive, or irritable mood. Symptoms last >1 week, 3 additional symptoms for mania.

  • Hypomanic episode: abnormal and persistently elevated, expansive, or irritable mood. (lasting at least 4 days)
  • Depressive episode: depressed mood or loss of interest/pleasure in nearly all activities. Symptoms last ≥2 weeks.
  • Mixed episode: rapid alternating between manic and depressive symptoms. (manic/hypomanic criteria + 3 depressive for 1 week or opposite for 2 weeks)
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58
Q

What is the DSM-V criteria for bipolar diagnosis?

A
  1. Bipolar I - at least one manic episode (lasting 1 week or requiring hospitalisation). Depression episode not required for diagnosis.
  2. Bipolar II - at least one major depressive episode and one major hypomanic episode.
  3. Cyclothymic disorder - At least 2 years (1 year in children), numerous periods of hypomanic and depressive symptoms that don’t meet full criteria for hypomanic or major depressive episodes.
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59
Q

What are the investigations for bipolar disorder?

A

Made by specialist assessment. Using DSM 5

In primary care:
- Primary care eval of mental disorders (PRIME-MD)
- PHQ-9
- Mood disorder questionnaire (MDQ)
- FBC
- TFT
- Vit D
- Toxicology

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60
Q

What are the differentials for bipolar?

A
  1. Major or persistent depressive episode
  2. Cyclothymic disorder
  3. Substance induced
  4. Medical disorder induced (thyroid,cushing’s,MS)
  5. Other mental health disorders (Schizophrenia,Schizoaffective,ADHD,OCD, PTSD)
  6. Iatrogenic (antidepressants, levodopa, steroids)
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61
Q

How is an acute manic episode managed?

A

1st line: Atypical antipsychotic (olanzapine, risperidone, quetiapine)
2nd line: Valproate, Lithium, lamotrigine or combination therapy

Consider ECT if no response

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62
Q

How is an acute depressive episode managed?

A
  • Olanzapine w/ fluoxetine
  • Quetiapine alone
  • lamotrigine
  • Combination therapy

Be careful using SSRIs. Consider ECT if no response

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63
Q

What is the maintenance therapy for bipolar disorder?

A

Non pharmacological:
- Psychoeducation
- CBT
- Mood diary, regular sleep pattern

Pharmacological:
- Lithium
- Antipsychotic (e.g. olanzapine, quetiapine or risperidone)
- Sodium valproate (teratogenic)
- Combination therapy (sodium valproate + antipsychotic)

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64
Q

Why does using antidepressants in bipolar disorder need to be closely monitored?

A

Can cause mania or lead to a rapid cycling mood (frequent, distinct episodes)

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65
Q

Why do patients on maintenance therapy for bipolar need to be closely monitored?

A

The medications have many complications:

  1. Lithium - renal impairment, thyroid dysfunction, cardiotoxicity, lithium toxicity (tremor, confusion, coma, seizures)
  2. Sodium Valproate - Hepatotoxicity, pancreatitis, weight gain, teratogenicity
  3. Antipsychotics - Metabolic syndrome (weight gain, T2DM), tardive dyskinesia (EPS), cardiac arrhythmias.
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66
Q

What is the prognosis for people with bipolar disorder?

A
  • Bipolar episode relapse
  • Higher mortality (from CVD and suicide)
  • Difficult management, often patients are not well over maintenance therapies
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67
Q

What is Obsessive Compulsive Disorder?

A

OCD is a mental health condition characterised by persistent obsessions and/or compulsions that are performed in response to the obsessions. It causes significant distress and impact on function.

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68
Q

What is the epidemiology of OCD?

A
  1. Equal sex prevalence
  2. Age of onset - late adolescence to early 20s
  3. Earlier presentation in boys
  4. 1-3% of UK affected
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69
Q

What is the aetiology/risk factors for OCD?

A

Multifactorial aetiology

  1. Genetic - genes related to serotonin, dopamine + glutamate neurotransmission
  2. Environmental - Childhood trauma, stress, PANDAS (paediatric autoimmune neuropsychiatric disorders associated w/ Strep), pregnancy,
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70
Q

What are risk factors for developing treatment resistant OCD?

A

Male sex
Higher frequency of compulsions
Early age of onset
Previous OCD hospitalisation
Comorbid psychiatric disorders (tic, schizotypal personality disorder)

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71
Q

What are obsessions?

A

Intrusive, unwanted thoughts that caused marked stress/anxiety. (e.g. contamination, harm, sexual, symmetry)

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72
Q

What are compulsions?

A

Repetitive behaviours (e.g. handwashing, checking) or mental acts (e.g. counting, repeating words) which are aimed at reducing the anxiety caused by obsessions.

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73
Q

How is OCD diagnosed?

A

Using the DSM-V or ICD 11 criteria:

DSM:
1. Obsessions and/or compulsions
2. These are time consuming (>1 hour/day)
3. Not attributable to substance use, medical conditions, or other mental disorders.

ICD-11:
Same
Symptoms present for at least several weeks

Both include insight specifiers (Delusional/absent to good)

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74
Q

How is symptom severity assessed?

A

Yale-Brown Obsessive compulsive scale (0-40)
Clinical Global Impression (0-7)

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75
Q

What are potential differentials for OCD?

A
  • Obsessive compulsive personality disorder
  • Body dysmorphic disorder - compulsions connected to appearance
  • ASD
  • Delusional disorder
  • Substance/medication induced
  • Trichotillomania
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76
Q

How is OCD managed?

A

Non-pharmacological: For mild -moderate symptoms
- CBT
- Exposure + response prevention

Pharmacological:
1st line: SSRI
2nd line: Clomipramine (tricyclic)
Consider atypical antipsychotic if unresponsive

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77
Q

When should a patient with OCD be referred to a specialist?

A
  • Treatment resistance
  • Severe symptoms, significantly limiting function
  • Safeguarding concerns
  • Suicide/self harm risk
  • Significant comorbidities
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78
Q

Define postnatal depression?

A

Refers to the development of a depressive illness following childbirth and may form part of a bipolar or, more usually, a unipolar illness.

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79
Q

How are postnatal mood disorders classified?

A
  1. Baby blues - seen in the majority of women in the first week or so after birth. (No treatment, reassurance/support)
  2. Postnatal depression - seen in about 1/10 women, with a peak around three months after birth.
  3. Puerperal psychosis - seen in about 1/1000 women, starting a few weeks after birth.
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80
Q

What is the epidemiology of postnatal depression?

A
  1. Affects 10-15% of women
  2. Onset usually within 4-6 weeks, can occur within 1st year
  3. More common with history of anxiety/depression
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81
Q

What is the aetiology of PN depression?

A

Combination of hormonal changes, genetic predisposition, psychosocial stressors (e.g., relationship problems, lack of support), and pre-existing mental health conditions.

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82
Q

What are the risk factors for developing PN depression?

A
  • PHx/FHx of depression or anxiety
  • Lack of social support
  • Traumatic birth experience
  • Relationship difficulties
  • Socioeconomic stressors
  • Discontinuing psychopharmacological treatments
  • Sleep deprivation
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83
Q

How is PN depression assessed?

A

Clinical:
- Edinburgh PN depression scale - score above 10/30 suggests mild to severe depression
- PHQ-9
Other tests:
- TFTs
- FBC - other causes of fatigue
- Urine drug screen

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84
Q

What are differential diagnoses for PN depression?

A

Minor mood disorder (baby blues)
Postnatal psychosis
OCD
Bipolar disorder
Thyroid dysfunction
Anaemia

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85
Q

How is PN depression managed?

A

Mild:
1st line - Self help strategies, CBT

Moderate - Severe:
1st line - SSRIs (like sertraline) +/- high intensity psychological intervention (CBT)

  • Consider admission if risk to self/or baby
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86
Q

What are potential complications of postnatal depression?

A
  1. Impaired bonding with infant
  2. Neglect of baby or infanticide
  3. Suicide
  4. Bipolar disorder
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87
Q

What are risk factors for developing postnatal psychosis?

A
  • History of bipolar disorder or schizophrenia.
  • Previous episode of postpartum psychosis.
  • Family history of psychotic disorders.
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88
Q

How does postnatal psychosis present?

A
  1. 90% of women have onset within 1 week
  2. Delusions
  3. Hallucinations
  4. Depression - catatonia or psychomotor retardation
  5. Mania
  6. Confusion
  7. Thought disorder
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89
Q

How should postnatal psychosis be managed?

A
  • Psychiatric emergency, admission to mother and baby unit.
  • Medications: antipsychotics, mood stabilizers (e.g., lithium), and possibly antidepressants.
  • Electroconvulsive therapy (ECT) may be considered in severe or treatment-resistant cases.
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90
Q

What is Post Traumatic Stress Disorder (PTSD)?

A

PTSD is a relatively common mental condition that develops following exposure to 1 or more traumatic event involving actual or threatened death, serious injury or sexual violence.

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91
Q

What is the difference between PTSD and Complex PTSD?

A

PTSD develops after a single or short term traumatic event.
Complex PTSD develops after prolonged/repeated exposure to trauma which are difficult to escape from. CPTSD has additional symptoms (emotional, interpersonal and negative self worth).

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92
Q

What is the epidemiology of PTSD?

A
  • Affects around 3-5% of adults in the UK
  • Higher prevalence in women
  • Higher frequency in conflict-affected and inner city areas
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93
Q

What is the aetiology of PTSD?

A

Triggered by exposure to traumatic events:
- War
- Physical/sexual assault
- Severe accidents (e.g RTA)
- Natural disasters

Genetic predisposition, structural brain changes and altered neurochemicals (increased noradrenaline)

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94
Q

What are the risk factors for developing PTSD?

A
  1. Increased likelihood of exposure (emergency workers, refugees, armed forces)
  2. Severity and duration of trauma
  3. Multiple traumas
  4. Female sex
  5. Younger age
  6. Hx of mental disorder
  7. Low social support
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95
Q

How is PTSD diagnosed (DSM-V + ICD 11)?

A

A. Exposure to a traumatic event
B. Intrusive (re-experiencing) - 1 or more
C. Avoidance - 1 or more
D. Negative cognitions/mood - at least 2
E. Arousal/reactivity - at least 2

B-E - duration >1 month
Causes significant distress and impairment to function
Not due to medication, substance use

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96
Q

What is the timeline of PTSD onset?

A

A.1st month defined as acute stress disorder
B.1-6 month - typical onset of PTSD
C. After 6 months - PTSD w/ delayed expression

97
Q

How is PTSD managed?

A
  1. Active monitoring in mild/subthreshold symptoms
  2. Trauma-focused CBT
  3. Eye-movement desensitisation and reprocessing
  4. Pharmacotherapy - SSRIs, venlafaxine, beta-blockers, antipsychotics (risperidone)
98
Q

What are potential complications of PTSD?

A
  • Increased distress due to exposure therapy
  • CVD
  • Dementia
  • Depression
  • Psychosis
  • Suicide
99
Q

What are the differentials for PTSD?

A
  • Acute stress disorder
  • Anxiety
  • Major depressive disorder
  • Dissociative disorder
  • Specific phobias
  • Psychosis
100
Q

What is Schizophrenia?

A

Schizophrenia is a chronic, severe mental health disorder characterised by episodes of psychosis, which involves distortions in thinking, perception, emotions and behaviour.

101
Q

What is the epidemiology of Schizophrenia?

A
  1. Affects 1% of global population
  2. Most often presents between 15-30 years
  3. Women tend to present later (late 20s)
  4. Similar sex prevalence (1.4:1 - M:F)
102
Q

Describe the aetiology/risk factors of Schizophrenia

A

Multifactorial:
1. Genetic - Highly heritable (around 60-80%)
2. Environmental - social adversity, childhood trauma, urban residence, cannabis use, migration
3. Neurodevelopmental - maternal infections, obstetric complications, preterm birth, hypoxia, low IQ

103
Q

What is the pathophysiology of Schizophrenia?

A

Not fully understood:
1. Dopamine theory - Overactive in the mesolimbic pathway (positive symptoms - hallucinations) and underactivity in the mesocortical pathway (negative symptoms - reduced motivation) are implicated.

  1. Structural brain changes - Enlarged ventricles, reduced grey matter, and abnormalities in the prefrontal cortex and temporal lobes are associated with schizophrenia.
  2. Inflammation and Immune Dysregulation: Elevated pro-neuroinflammatory markers are observed in some patients.
104
Q

What are positive symptoms in schizophrenia?

A

These are the core features of psychosis, and refer to excesses or distortions of normal functions.

  1. Hallucinations: Perceptions without external stimuli, commonly auditory (hearing voices), but can also be visual, olfactory, gustatory, or tactile.
  2. Delusions: Strongly held false beliefs that are resistant to reasoning, despite evidence. Common types include persecutory, grandiose, and referential delusions.
  3. Disorganised Speech: Incoherent or tangential speech that reflects disordered thought processes (e.g., word salad, loose associations).
  4. Disorganised or Catatonic Behavior: Unpredictable, inappropriate, or erratic behaviors. Catatonia involves motor disturbances ranging from complete immobility to excessive agitation.
105
Q

What are negative symptoms of Schizophrenia?

A

These involve a reduction or loss of normal functions. Including flattened affect, apathy, anergia, social withdrawal, alogia and anhedonia (these can be difficult to differentiate from comorbid depression).

106
Q

What is the prodromal phase in Schizophrenia?

A

The prodromal phase is characterised by subtle changes in behavior, cognition, and functioning that precede the first psychotic episode (e.g. social withdrawal, poor memory, mood swings, disturbed sleep). Identifying this early has been associated with more favourable outcomes.

107
Q

What is the criteria for a diagnosis of Schizophrenia?

A

DSM V:
2 or more of the following symptoms, each present for a significant portion of 1-month period. At least one of symptoms 1-3.
1. Delusions
2. Hallucinations
3. Disorganised speech
4. Grossly disorganised or catatonic behavior
5. ‘Negative’ symptoms

108
Q

What are differentials of Schizophrenia?

A
  1. Schizoaffective disorder - prominent mood symptoms combined with psychosis
  2. Depression w/ psychosis - mood congruent
  3. Bipolar w/ psychosis - clear presence of mania/hypomania
  4. Substance induced psychosis
  5. Munchausen’s syndrome
  6. Delusional disorder
  7. Organic psychosis (encephalitis, syphilis, b12 deficiency)
109
Q

How is an episode of acute psychosis managed?

A
  1. Ensure safety of patient and others - Mental health act 2005
  2. Oral benzodiazepine - lorazepam or midazolam
  3. Consider rapid tranquillisation if patient is aggressive/violent - IM lorazepam or promethazine + haloperidol
    Refer to specialist to start antipsychotic
110
Q

What is the long-term management for Schizophrenia?

A

Psychosocial, CBT + family interventions should be offered to all patients

1st line: Non-clozapine antipsychotic (Monitor physical health)
2nd line: Try alternative non-clozapine antipsychotic
3rd line: Clozapine (under specialist care)

111
Q

What are the complications of Schizophrenia?

A
  • Antipsychotic SEs
  • Suicidal tendencies
  • Substance use
  • Tobacco use
  • Depression
112
Q

What is the prognosis of Schizophrenia?

A
  • Good recovery following 1st episode of psychosis
  • 20% will make a full recovery, 35% have long periods of remission
  • Mean life expectancy is around 15 years lower
  • 20-30% of cases are considered treatment resistant
  • Increased suicide risk
113
Q

What factors are associated with poor prognosis of Schizophrenia?

A

Strong family history
gradual onset
low IQ
prodromal phase of social withdrawal
lack of obvious precipitant

114
Q

What is schizoaffective disorder?

A

Is characterised by a combination of schizophrenia symptoms and a prominent mood disorder (depression or mania).

115
Q

What is the criteria for diagnosis of schizoaffective disorder?

A
  1. Uninterrupted period of illness, during which there is a major depressive or manic episode concurrent with symptoms meeting criterion A for schizophrenia.
  2. Two weeks of delusions or hallucinations in the absence of prominent mood symptoms. Rules out mood disorders w/ psychotic features.
  3. Mood symptoms are present for the majority of the illness duration (during the active and residual phases).
116
Q

How can schizoaffective disorder be classified?

A
  • Bipolar type - if manic episode is present, depressive may also be present.
  • Depressive type - only major depressive episode is present.
117
Q

How is schizoaffective disorder treated?

A

CBT + general health maintenance
Consider anxiolytics (diazepam, clonazepam)
Consider lithium (manic symptoms or poor response)
Consider antidepressants (with depressive symptoms)

1st line: Atypical antipsychotics (olanzapine, risperidone, quetiapine)
2nd line: Clozapine (if 2 a. antipsychotics fail)
3rd line: Typical antipsychotic (haloperidol)
4th line: Long acting IM antipsychotic (Risperidone, olanzapine)
5th line: ECT

118
Q

What are personality disorders?

A

Refer to persistent maladaptive personality traits that adversely affect how an individual functions. Affects a person’s thought, behaviour and emotions.

119
Q

What is the epidemiology of personality disorders?

A
  • Borderline and antisocial PD are the most diagnosed
  • Onset in late childhood or early adolescence
  • Prevalence - 1/20 people
120
Q

What are the risk factors for developing a personality disorder?

A
  • Early life trauma/abuse
  • FHx of Schizophrenia
  • Negative parenting interactions
  • Disruptive disorder in childhood
121
Q

How are personality disorders classified in DSM-V criteria?

A

10 individual PDs in 3 clusters:
A - Odd or eccentric
B - Dramatic or erratic
C - Anxious or fearful

122
Q

What personality disorders are in each cluster?

A

Cluster A ‘Weird’ - Paranoid, Schizotypal, Schizoid

Cluster B ‘Wild’ - Borderline, Antisocial, Narcissistic, Histrionic

Cluster C ‘Worried’ - Obsessive compulsive, Avoidant, Dependant

123
Q

What are the clinical features of Paranoid personality disorder?

A
  1. Paranoid -
    Pervasive distrust and suspiciousness of others.
    Suspicious without reason, doubts loyalty, reluctance to confide, reads hidden/threatening meaning, persistent grudges, perceives character attack and responds angrily, recurrently suspects partner infidelity
124
Q

What are the clinical features of Schizotypal personality disorder?

A
  1. Schizotypal -
    Pervasive pattern of acute discomfort in close relationships, cognitive or perceptual distortions, and eccentric behavior.
    Includes odd beliefs, magical thinking, unusual perceptual experiences, inappropriate affect, odd thinking/speech, excess social anxiety and paranoid ideation.
125
Q

What are the clinical features of Schizoid personality disorder?

A
  1. Schizoid -
    Pervasive detachment from social relationships and a restricted range of emotional expression. Prefers solitude, lacks interest in social or sexual relationships, appears indifferent to praise or criticism, emotional coldness and few interests.
126
Q

What are the clinical features of Borderline personality disorders?

A
  1. Borderline
    Instability in relationships, self-image, and emotion with marked impulsivity.

Symptoms include fear of abandonment, unstable interpersonal relationships, identity disturbance, self-damaging and impulsive behavior, suicidal/self harming behavior, and emotional instability (intense anger, affective instability).

127
Q

What are the clinical features of Antisocial personality disorder?

A
  1. Antisocial
    Disregard for, and violation of, the rights of others. More common in men

Requires evidence of conduct disorder before age 15 and includes criteria like deceitfulness, impulsivity, aggression/violence, difficult relationships and lack of remorse.

128
Q

What are the clinical features of Narcissistic personality disorder?

A
  1. Narcissistic
    Pervasive grandiosity, need for admiration, and lack of empathy.
    Includes self-importance, fantasies of success, belief in being special, exploitative behavior, and arrogant attitudes.
129
Q

What are the clinical features of Histrionic personality disorder?

A
  1. Histrionic
    Pervasive attention-seeking behavior and excessive emotionality.
    Includes criteria like discomfort when not the center of attention, provocative/sexual behavior, shallow emotions, and exaggerated expressions.
130
Q

What are the clinical features of Obsessive compulsive personality disorder?

A
  1. Obsessive compulsive
    Preoccupation with orderliness, perfectionism, and control at the expense of flexibility, openness, and efficiency.
    Includes rigidity/inflexible about matters of morality, ethics and values, over-conscientiousness, hoarding behavior, and reluctance to delegate tasks.
131
Q

What are the clinical features of Avoidant personality disorder?

A
  1. Avoidant
    Pervasive social inhibition, feelings of inadequacy, and hypersensitivity to criticism.
    Criteria include avoiding social situations due to fears of rejection, being preoccupied with being criticised, and feelings of inferiority.
132
Q

What are the clinical features of Dependant personality disorder?

A
  1. Dependant
    Pervasive and excessive need to be taken care of, leading to submissive and clinging behavior and fears of separation.
    Includes difficulty making decisions, needing others to assume responsibility, and difficulty expressing disagreement.
133
Q

What is the treatment for personality disorders?

A

CBT/DBT for all patients. Treat comorbid depression/anxiety. Hospitalisation for self harm/suicide. Suicide prevention.

  1. Cluster A - Psychotherapy (CBT/DBT), consider low-dose antipsychotics.
  2. Cluster B - Psychotherapy (CBT/DBT), consider mood stabilisers/anticonvulsants (lithium, lamotrigine, topiramate)
  3. Cluster C - Psychotherapy (CBT/DBT), consider antidepressants (SSRI, SNRIs)
134
Q

What are complications/prognosis of personality disorders?

A
  • High risk of self harm/suicide especially BPD, ASPD.
  • Severe social impairment
  • Some symptoms may attenuate with age
135
Q

Define substance misuse/abuse

A

Repetitive harmful pattern of substance use that leads to negative consequences.

136
Q

Overview - Substance use

A
  1. Initial Use: Driven by factors such as curiosity, peer pressure, or self-medication for stress/anxiety.
  2. Reward Pathway Activation: Most substances increase dopamine release in the mesolimbic system, which includes the ventral tegmental area (VTA) and the nucleus accumbens (NAc).
  3. Positive Reinforcement: The surge in dopamine causes feelings of euphoria or pleasure, reinforcing the behavior of substance use.
  4. Conditioning: Over time, the brain starts associating environmental cues (like places, people, or emotions) with substance use, leading to cravings even when not using the substance.
137
Q

What is the pathophysiology of addiction?

A

Neuroadaptation: With repeated use, the brain adapts by reducing the natural production of dopamine and altering receptor sensitivity. Leading to tolerance and withdrawal symptoms.

Homeostatic Disruption: The brain becomes reliant on the substance to maintain normal dopamine levels, resulting in compulsive use despite negative consequences.

Broader Brain Impact: The prefrontal cortex (decision-making and impulse control) becomes impaired, reducing the ability to resist urges. The amygdala (involved in emotions) also changes, leading to increased stress and anxiety when the substance is unavailable.

Dopamine Dysregulation: The chronic activation of the mesolimbic pathway alters dopamine signaling, making natural rewards (like food or social interaction) less pleasurable compared to the substance.

138
Q

Substance-Specific Pathophysiology Variations

A

Opioids: Strongly activate the mesolimbic system by binding to opioid receptors, which also affects pain pathways and other brain regions, leading to profound euphoria and risk of severe withdrawal symptoms.
Stimulants (e.g., Cocaine, Amphetamines): Directly increase dopamine levels in the synaptic cleft by blocking dopamine reuptake (cocaine) or increasing dopamine release (amphetamines), causing intense activation of the reward pathway and rapid addiction potential.
Cannabis: Primarily acts on the endocannabinoid system by binding to CB1 receptors, which modulate dopamine release. The effect is more subtle but can still lead to changes in reward processing and long-term changes in brain function with chronic use.

139
Q

What is an opioid?

A

A natural (codeine, morphine) or semi synthetic agent (fentanyl, heroin, methadone) that stimulates opioid receptors and produces opium like effects.

140
Q

What is the epidemiology of opioid abuse?

A
  • Significant public health issue
  • Prevalence is highest in people aged 25-34 years
  • Opioid dependence is associated with a high risk of overdose, infections (HIV, hepatitis C), and social harm.
141
Q

What is the aetiology of substance abuse?

A
  • FHx of substance use genetic predisposition
  • Comorbid psychiatric conditions
  • Social/Environmental - peer influence, availability, homelessness, hx of criminal activity, social deprivation
142
Q

What are the clinical features of opioid intoxication?

A
  • Miosis (absent in synthetic opioids - fentanyl)
  • Shallow/slow respirations
  • Memory impairment
  • Disturbed consciousness, cognition, perception
  • Mood changes - euphoria/dysphoria
  • Itching/scratching
  • Sedation
  • Bradycardia
143
Q

What are the clinical features of opioid use disorder?

A
  • Needle track marks
  • Dilated pupils
  • Chronic constipation/abdominal cramps
  • Weight loss
  • Nausea/vomiting
  • Insomnia
  • Yawning
  • Rhinorrhoea/sneezing
  • Tachypnoea
  • Agitated/restless
  • Backache/muscle spasm
  • Watery eyes
144
Q

What are the risk factors for developing opioid dependancy?

A
  • Young age/ male gender
  • Hx of mental illness
  • Childhood trauma - homelessness, neglect, abuse
  • Social disadvantage
  • Genetic predisposition
  • Peer substance use/availability
145
Q

What investigations should be ordered for someone with opioid intoxication/overdose?

A

Clinical signs to suspect opioid dependancy
Initial investigations:
- Urine or saliva drug screen
- GC-MS - to detect specific opioid
- FBC - raised WBC in infections
- U&E/creatinine + LFTs - renal/hepatic impairment
- Hep/HIV serology
- beta HCG

146
Q

How do you manage opioid overdose?

A

IV or IM naloxone: has a rapid onset and relatively short duration of action

147
Q

How do you manage opioid dependance/use disorder?

A

Detoxification (4-12 weeks) or harm minimisation

Maintenance therapy:
1st line: Buprenorphine +/- Naloxone or
Methadone (for high opioid use - hard to come off)
Symptom relief

Psychosocial counselling: CBT, recovery coordinator, education

148
Q

What are the complications of opioid use disorder?

A
  1. Opioid withdrawal + Overdose
  2. Hepatitis A,B and C
  3. Scarred or vein collapse
  4. Endocarditis/Osteomyelitis
  5. Arthritis/other rheum conditions
  6. Obstetric/neonatal complications
  7. Hypogonadism/cortisolism
  8. DVT
149
Q

What is the prognosis of opioid use disorder?

A

Chronic disorder, relapse rate is >90% in untreated individuals. High % of comorbidities.

150
Q

What are the features of opioid overdose?

A
  • Miosis
  • Bradypnoea (<12 breaths/minute)
  • Altered mental status
  • Frothy pink sputum (ARD)
  • Pulmonary rales (ARD)
  • Seizures
151
Q

What is hazardous alcohol use?

A

Refers to a pattern of alcohol consumption that increases the risk of harmful consequences for the user. It does not yet cause significant physical or mental health problems but is likely to lead to them if continued.

152
Q

What is harmful alcohol use?

A

A pattern of alcohol consumption that is already causing damage to health, whether it be physical (e.g., liver disease) or mental (e.g., depression). May or may not involve alcohol dependence, but the drinking has clear and negative effects on the individual’s well-being.

153
Q

What is alcohol use-disorder/dependance?

A

Encompasses both harmful drinking and alcohol dependence characterised by craving, tolerance, a preoccupation with alcohol, and continued drinking in spite of harmful consequences.

154
Q

How do you calculate units of alcohol?

A

Volume (ml) x Alcohol Content (%) ÷ 1000 = Units of Alcohol

155
Q

What are the recommended alcohol consumption guidelines?

A

No more than 14 units of alcohol a week, spread across 3 days or more.
2 alcohol free days a week
Not more than 5 units a day

156
Q

What is the epidemiology of alcohol use disorder?

A
  • Harmful use is responsible for 5.3% of deaths globally
  • Higher prevalence in men (2:1)
  • Around 20-25% of people in the UK drink in excess
  • Alcohol use-disorder has a lifetime prevalence of 7-10% in most western countries
157
Q

What is the aetiology/risk factors for developing alcohol use-disorder?

A
  1. Genetic factors
  2. Psychosocial - Stress, trauma, mental health disorders, social influence, peer pressure
  3. Environmental - Availability, cultural attitudes, SES
  4. Chronic use - Continued exposure leads to requirement of alcohol to feel normal
158
Q

Physiology of alcohol and pathological consequences?

A

Alcohol (ethanol) is a depressant. It stimulates GABA receptors which have a relaxing effect on the brain. It also inhibits glutamate receptors (also known as NMDA receptors), causing a further relaxing effect on the electrical activity of the brain (glutamate is an excitatory neurotransmitter).

Long-term alcohol use results in the GABA system becoming down-regulated and the glutamate system becoming up-regulated to balance the effects of alcohol. The patient must continue drinking alcohol, or they will experience unpleasant, uncomfortable and potentially dangerous withdrawal symptoms.

159
Q

What are the clinical features of alcohol intoxication?

A

Symptoms range from mild to severe:
1. CNS depression - slurred speech, incoordination, unsteady gait, impaired memory, stupor/coma (severe)

  1. Behavioral - Euphoria, disinhibition, aggression, mood lability
  2. Physiological - Flushed face, tachycardia, hypotension, vomiting, hypoglycaemia, resp depression
160
Q

What are the clinical features of alcohol withdrawal?

A

Occurs after the cessation or reduction in heavy and prolonged alcohol use: Symptoms due to autonomic hyperactivity

6-12 hours: sweating, tachycardia, hypertension, tremor, anxiety, N&V.

36 hours: Withdrawal seizures

48-72 hours: Delirium Tremens - Confusion, delusions, coarse tremor, visual/auditory hallucinations, fever, tachycardia.

161
Q

What screening tools are used to identify problem drinking?

A

CAGE questionnaire - 4 questions

AUDIT - (Alcohol Use Disorders Identification Test) for initial screening to assess pattern and severity of alcohol misuse. Score of 8> indicates risk.

Severity of Alcohol Dependence Questionnaire (SADQ) can be used to assess the severity of alcohol dependence.

162
Q

How is the severity of alcohol withdrawal assessed?

A

Clinical Institute Withdrawal Assessment – Alcohol, revised (CIWA-Ar) scale.
Absent or minimal withdrawal: score 0-9
Moderate withdrawal: score 10-19
Severe withdrawal: score > 20

163
Q

What is the DSM V criteria for a diagnosis of alcohol use disorder?

A

Clinically significant impairment, defined by 2 of these criteria in the same 12 month period:

  • Alcohol Consumption (large/long periods)
  • Persistent Desire (can’t cutdown)
  • Time Spent (obtaining, using, or recovering)
  • Craving/strong desire
  • Failure to Fulfill Major Roles (work, school, or home)
  • Social or Interpersonal Problems
  • Reduction in Important Activities
  • Use in Hazardous Situations (e.g,driving, poor health)
  • Physical or Psychological Problems
  • Tolerance (more needed to be intoxicated)
  • Withdrawal symptoms

Mild: 2-3
Moderate: 4-5
Severe: 6 >

164
Q

What blood tests can show signs of alcohol excess?

A
  1. LFTs - Raised ALT, AST, GGT (especially)
  2. FBC - Raised MCV, macrocytic anaemia
  3. Carbohydrate-deficient transferrin (CDT) - Increased, very sensitive
165
Q

What is delirium tremens?

A

Medical emergency associated with alcohol withdrawal, if untreated mortality is 35%. GABA system under active and glutamate system over functions causing extreme excitability and excessive adrenergic (adrenaline-related) activity.

166
Q

When should a patient be managed in hospital for withdrawal (detox)?

A
  • Drink 30 or more units a day
  • SADQ score more than 30
  • Hx of epilepsy, DTs or withdrawal seizures
  • Concurrent withdrawal from benzos
  • Vulnerable - homeless, young etc
167
Q

What is the management of alcohol withdrawal?

A

CIWA-Ar scale above 10:
1st line - Benzodiazepine (Chlordiazepoxide or Lorazepam in hepatic failure)
Given as fixed reduced dose or PRN (symptom triggered) .
2nd line - Anticonvulsants (Carbamazepine)
3rd line - Clomethiazole - inpatient alone, very addictive.

Supportive care -
Oral/IV fluids
High-dose B vitamins (Pabrinex) - prevent/treat WE
Treat concurrent acute medical illness
Beta blockers (tachycardia, hypertension)

168
Q

What is the long term management for relapse prevention?

A

Psychosocial treatment - CBT, AA, specialist alcohol services, motivational interviewing.
Manage medical comorbidities

Medication:
Naltrexone (50mg od) - opioid receptor antagonist

Acamprosate (666mg tds) - Reduce cravings by normalising glutamate and GABA neurotransmission.

Disulfiram (200mg od) - For patients wanting to abstain.
Causes unpleasant reaction when consuming alcohol, mental anticipation prevents use.

169
Q

What are the neurological complications of chronic alcohol use?

A

Cognitive impairment (e.g., memory loss, confusion)
Peripheral neuropathy (tingling, numbness in limbs)
Wernicke-Korsakoff syndrome (due to thiamine deficiency)
Seizures (including alcohol withdrawal seizures)
Alcohol-related dementia
Subdural haematomas (more common)

170
Q

What are the psychiatric complications of chronic alcohol use?

A

Depression and anxiety disorders
Suicidality
Alcoholic hallucinosis (visual or auditory hallucinations)
Insomnia
Psychosis

171
Q

What is self harm?

A

Intentional act of 1) self injury or 2) self poisoning regardless of the motivation.

172
Q

What are the prevalence rates of self harm?

A

1) 2014 6.4% of people (16-74) reported having self harmed.
2) More common in women 1.5:1
3) More common in adolescents. Peak incidence - Females 15-19 and Males 20-24.
4) 50-100X greater suicide risk self harmers

173
Q

What are the clinical features of self harming?

A

1) Self injury (10% of cases) - Cutting, burning, slashing. Less common methods include Jumping in front of vehicles, from heights or drowning.

2) Self poisoning (90% of cases) - Paracetamol/Aspirin ingestion most common. Also anxiolytics + antidepressants. (many DSH have depression)

174
Q

What are the investigations for someone who has self poisoning?

A

Paracetamol/salicylate levels.
U&Es, LFTs, clotting
Urinalysis - toxicology
CT head/LP - Rule out head injury/infection causing symptoms

175
Q

What are important questions to be asked in the history of someone who has self harmed?

A
  1. Intentions before/during the act
  2. Suicidal ideation
  3. Current problems (life stressors)
  4. Other psychiatric disorders
  5. Collateral history
176
Q

What is the management of self harm patients?

A

Acute management - Antidotes, suturing, surgery

Suicide/repeating self harm risk assessment - crisis team or hospitilisation +/- MHA

Treat any psychiatric disorders - e.g antidepressants

Manage psychosocial needs - drug/alcohol services, financial/occupational advice etc

Managing future crisis - Follow up, limit drug supply, samaritans/mental health team

177
Q

What are the antidotes to common overdoses in self harm?

A
  1. Activated charcoal - In first hour for most drugs to reduce absorption
  2. N-acetylcysteine - paracetamol
  3. Opiates - Naloxone
  4. Benzos - Flumazenil
  5. Beta blockers - Glucagon
  6. TCAs - Sodium bicarbonate
178
Q

What is the prevalence of suicide?

A
  • Around 5000 deaths/year in the UK
  • Men are more likely to commit suicide than women
  • Highest completed suicide seen in 45-49 years both M+F
  • Increasing in young men and old men
179
Q

What are the most common methods of suicide?

A
  • Hanging, suffocation and strangulation - especially in men
  • Poisoning - more common in women
180
Q

What are the risk factors for suicide?

A

Very difficult to predict - around 50% suicides occur in ‘low risk’

Demographics - Male, Age (F -16-24, M - 25-34), LGBTQ, migrants/refugees, prisoners.

Social/environmental - Unemployed, social isolation, marital status (divorce, widow etc), low SES, alcohol/drug use, stressful life event (domestic violence, bereavement etc)

Clinical - Previous SH or suicide attempt, chronic illness (terminal), mental health disorder (depression, bipolar, schizophrenia), childhood abuse, FHx of suicide

181
Q

What are protective factors against suicide?

A

Children at home, pregnancy, strong religious convictions, social support, positive coping skills

182
Q

How do you assess suicide risk?

A

Explore:
1. Suicidal ideation
2. Suicidal intent
3. Risk factors
4. Mental state exam
5. Protective factors
6. Risk to others/from others
7. Formulate management plan

183
Q

How do you manage someone at risk of suicide?

A
  1. Ensure personal + patient safety - Regular and easily observable, remove access to objects, verbally de-escalate.
    Medical stabilisation of suicide attempt.
  2. Treat any self harm or physical illness.
  3. Determine treatment setting - Consider hospitilisation with MHA or crisis resolution and home team.
  4. Safety plan in place
  5. Psychotherapy assessment
  6. Treat underlying psychiatric illness
184
Q

What is anorexia nervosa (AN)?

A

Severe mental health disorder characterised by restriction of caloric intake leading to low body weight, an intense fear of gaining weight and distorted body image.

185
Q

What is the epidemiology of AN?

A
  • More common in females (10:1)
  • Highest incidence ages 15-19
  • Most commonly begins in adolescence and young adulthood (15-25)
  • Increased prevalence in high income countries and in groups who value thinness (athletes, models)
186
Q

What are the causes and risk factors of AN?

A
  1. Genetic - FHx of ED and mood disorders
  2. Female gender
  3. Adolescence
  4. History of trauma, stressful life events
  5. Obsessive and perfectionist traits
  6. Low self esteem
  7. Cultural/peer pressure (western media, athletes, family)
187
Q

What common behaviours are seen in patients with AN?

A
  • Feeling overweight despite evidence against
  • Restriction of energy intake causing low body weight
  • Intense fear of gaining weight
  • Binge eating and/or purging
  • Misuse of laxatives, diuretics, diet pills
  • Distorted body image
  • Preoccupation with food/cooking
  • Denial of problem
188
Q

What physiological signs may be present in a person with AN?

A

Significantly reduced BMI
Amenorrhea + loss of libido
Lanugo hair
General fatigue, weakness, poor concentration
Hypotension/Bradycardia
Nonspecific GI symptoms
Cold peripheries

189
Q

What are the complications associated with AN?

A
  1. Cardiovascular - Bradycardia, arrhythmias, hypotension
  2. Endocrine - Amenorrhea, female infertility, osteoporosis, growth delay, thyroid issues
  3. Psychological - Depression, anxiety, poor QofL, low mood, suicidal ideation
  4. Metabolic - Dehydration, refeeding syndrome, electrolyte abnormality
  5. Acute and chronic renal failure
  6. Derm - Dry skin, alopecia, chilblains, lanugo hair
  7. MSK - Reduced muscle mass, osteopenia/porosis, fractures, growth retardation

Highest rate of mortality in psychiatric conditions primarily due to complications and suicide.

190
Q

What is the diagnostic criteria for Anorexia Nervosa?

A

Criteria:
A. Restriction of energy intake relative to requirements, leading to significantly low weight for age, sex, developmental trajectory, and physical health. BMI <17.5 or less than 15% expected BW.

B. Intense fear of gaining weight or persistent behaviour that interferes with weight gain, despite being a significantly low weight.

C. Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight.

191
Q

How should a person with AN be assessed?

A

Thorough history, examination and follow-up:

  1. History
  2. Examination - BMI, vital signs, muscle strength (sit up-squat-stand)
  3. Investigations -
    FBC (anaemia, leucopenia, thrombocytopenia)
    LFTs (elevated)
    TFTs (low T3)
    ECG (bradycardia, prolonged QT, arrhythmias), Urinalysis (ketonuria)
    U&Es
    DEXA scan
    Blood glucose
192
Q

What are differentials for AN?

A

Bulimia Nervosa
Hyperthyroidism
Depression
ARFID
T1DM
OCD
Crohn’s or UC

193
Q

How should an outpatient with AN be managed?

A

Structured eating plan with oral nutrition
Psychotherapy - CBT, anorexia focused family therapy
Consider oral potassium supplements - result of purging and/or laxative use

Monitoring - Continued assessment tools, BMI, BP, blood tests

194
Q

How should an anorexia patient with medically unstable or failed outpatient control be managed?

A

Inpatient admission (+/-) oral, enteral or parenteral nutrition. Daily bloods
Psychotherapy
Consider fluid/electrolyte correction
Consider antidepressants and antipsychotic
Referral for comorbidities

195
Q

What is the prognosis of AN?

A

50% have a full recovery
20-30% have chronic illness
Mortality rates are very high

196
Q

What is refeeding syndrome?

A

During prolonged starvation, cell metabolism reduces to conserve energy and intracellular phosphate (first), potassium and magnesium shifts into the blood. During refeeding, particularly carb intake, these electrolytes and glucose shift into the cells leading to reduced electrolytes and fluid overload. This can be fatal due to arrhythmias, cardiac failures, seizures, coma.

197
Q

What is bulimia nervosa (BN)?

A

An eating disorder characterised by recurrent episodes of binge eating, followed by behaviours aimed at compensating for the binge. Including inducing vomiting, fasting, excessive exercise, laxative or diuretic use.

198
Q

What is the prevalence of BN?

A

Many people with ED don’t present to health services.
- More common in women
- Less common in children + adolescents
- Peak onset 15-25, common in women 20-35.

199
Q

What are the causes/risk factors for developing BN?

A
  • Female sex
  • Impulsivity (Hx of impulse control disorder)
  • Past obesity
  • Hx of sexual abuse
  • Depression, anxiety, low self esteem
  • Sociocultural factors - Family, athletes, etc
  • FHx of alcoholism, depression, ED
  • Early onset of puberty
200
Q

How do you screen for eating disorders?

A

SCOFF questionnaire:
S – Do you ever make yourself Sick because you feel uncomfortably full?
C – Do you worry that you have lost Control over how much you eat?
O – Have you recently lost more than One stone in a 3-month period?
F – Do you believe yourself to be Fat when others say you are too thin?
F – Would you say that Food dominates your life?

201
Q

What is the diagnostic criteria for BN?

A

DSM V:
1. Recurrent episodes of binge eating, defined by both:
a) Eating an excessive amount of food in a discrete time period.
b) A sense of lack of control during the episode.
Recurrent compensatory behaviors to prevent weight gain, such as vomiting, laxative use, or excessive exercise.

  1. Binge eating and compensatory behaviors occur at least once a week for 3 months.
  2. Self-evaluation is unduly influenced by body shape and weight.
  3. The disturbance does not occur exclusively during episodes of anorexia nervosa.
202
Q

How is bulimia nervosa classified?

A

Partial remission: full criteria for BN previously met, but now only some criteria met for sustained period.

Full remission: full criteria for bulimia nervosa were previously met, but now no criteria met for a sustained period.

Severity: Frequency of inappropriate behaviours

Mild: Average of 1-3 episodes/week.
Moderate: Average of 4-7 episodes/week.
Severe: Average of 8-13 episodes/week.
Extreme: Average of 14> episodes/week.

203
Q

What are the clinical signs/symptoms of BN?

A
  • Recurrent episodes of binge eating (discrete time period)
  • Presence of inappropriate compensatory behaviours

Physical:
- Dental erosion
- Parotid hypertrophy
- Normal/overweight BMI (often)
- Russell’s sign (scarring on dorsum of hand)
- Arrhythmias
- Abdominal pain, bloating
- Electrolyte disturbance

Psychological:
- Depression/low self esteem
- Preoccupation with body shape/weight
- Fear of weight gain

204
Q

What are complications of BN?

A

Hypovolemia
Tooth erosion
Hypomagnesaemia and kalemia
Cardiac dysrhythmia
Haematemesis
Oesophagitis/barrett’s
Hypotension/arrhythmias - electrolyte imbalances

205
Q

How do you manage someone with BN?

A

CBT-ED focus - self guided or standard. Family based therapy in children/adolescents

Plus nutrition and meal counselling

SSRI - Fluoxetine high dose

Regular monitoring of physical health, manage comorbid mental health conditions

206
Q

What investigations should be done in BN?

A

Blood tests - U&Es, LFTs, magnesium, glucose, TFTs
Venous blood gas - May show metabolic alkalosis, due to repeated vomiting of HCl from stomach.
ECG

207
Q

What are differentials for BN?

A

Anorexia nervosa - with binge eating/purging type

Binge eating disorder - No compensatory behaviour

Other specified feeding or eating disorders (OSFED) - Not all of the criteria for bulimia nervosa

Borderline personality disorder

Kleine-levin syndrome - sleep disorder in adolescent males, characterised by binge eating + hypersomnia

208
Q

What is delirium?

A

Acute and fluctuating change in mental status with inattention, disorganised thinking, and altered levels of consciousness. It is a potentially life-threatening disorder characterised by high morbidity and mortality.

209
Q

What are the risk factors for delirium?

A
  • Older age
  • Dementia or cognitive impairment
  • Visual or hearing impairment
  • Functional impairment or immobility
  • History of delirium
  • Decreased oral intake (e.g., dehydration)
  • Polypharmacy
  • Co-existing medical illness
  • Physical frailty
  • Surgery
210
Q

What are the causes of delirium?

A

HE IS NOT MAAD:
- Hypoxia (Resp failure, MI, PE)
- Endocrine (Hyper/hypo thyroid, hypoglycaemia, cushings)
- Infection (UTI, pneumonia, meningitis, encephalitis)
- Stroke/other intracranial events
- Nutritional (Low thiamine, nicotinic acid, B12)
- Other (Severe pain, sleep deprivation)
- Theatre (Anesthetics, post-op complications)
- Metabolic (Hepatic/renal impairment, electrolyte disturbance)
- Abdominal (faecal impaction, malnutrition, urinary retention, catheters)
- Alcohol (intoxication, withdrawal)
- Drugs (steroids, anti-parkinson drugs, opiates)

211
Q

What are the subtypes of delirium?

A
  1. Hypoactive (40%) - Lethargy, reduced motor activity, apathy. Underdiagnosed, confused with depression.
  2. Hyperactive (25%) - Agitation, irritability, aggression, delusions, hallucinations. May be confused with psychosis.
  3. Mixed (30%) - Both subtypes co-exist.
212
Q

What is the criteria for delirium diagnosis?

A

DSM V and ICD 11:
1. Disturbance in attention and awareness
2. Acute onset (hours to days)
3. Disturbance in cognition (memory deficit, perception change, language disturbance)
4. Evidence of a cause
5. Not explained by another neurocognitive disorder

213
Q

What are the clinical features of delirium?

A

DELIRIUM:
D - disordered thinking: slowed, irrational, incoherent thoughts
E - euphoric, depressed, apathy, fearful, angry
L - language impaired - rambling, repetitive, disruptive
I - Illusions, delusions, hallucinations
R - reversal of sleep-wake cycle
I - inattention
U - unaware/disoriented - to time, place, person
M - memory deficits

214
Q

What investigations should be done in patients with delirium?

A

Routine:
Urinalysis
Bloods - FBC, U&Es, LFTs, calcium, glucose, CRP, B12
ECG
CXR
Blood/urine culture

Specific - ABG (hypoxia), CT head, LP, EEG
Diagnostic questionnaire - AMT (Abbreviated mental test), Confusion assessment method (CAM), MMSE

215
Q

How do you treat people with delirium?

A

Treat underlying cause

Environmental - Quite, well lit room, reassure, reorientation.

Agitation/hyperactivity (last resort):
Antipsychotics - short term Haloperidol, or olanzapine. Avoid benzos unless alcohol withdrawal.

216
Q

What is the outcome for delirium?

A

Very high mortality, increased risk of long term cognitive impairment.

Dependant on rapid identification and treatment of underlying cause.

Differentials - Psychosis, dementia, depression

217
Q

What is wernicke’s encephalopathy (WE)?

A

A neurological emergency resulting from thiamine deficiency (vitamin B1) with varied neurocognitive manifestations, typically involving mental status changes and gait and oculomotor dysfunction.

218
Q

What are the causes of wernicke’s encephalopathy?

A
  • Chronic alcohol abuse: most common due to malabsorption, increased requirements, poor diets.
  • Malnutrition - prolonged fasting, anorexia
  • Severe diarrhoea
  • Hyperemesis (gravidarum)
  • HIV/AIDS
219
Q

What is the pathophysiology of WE?

A

Thiamine is essential for ATP production and stores of thiamine only last around 18 days. This deficiency results in neural cell death, especially in areas where high energy requirements are needed, such as the mammillary body, brainstem, cerebellum, thalamus. Damage to these areas is associated with the symptoms of WE.

220
Q

What are the clinical features of WE?

A

Triad:
- Confusion: Disorientation, memory impairment, cognitive dysfunction.
- Ataxia: Gait abnormalities, wide-based stance, and incoordination.
- Ocular abnormalities: Nystagmus, ophthalmoplegia (paralysis of eye muscles), and diplopia (double vision).

Other symptoms:
GI symptoms, tachycardia, apathy, agitation, hypo/hyperthermia, altered consciousness/coma

221
Q

What are the differentials for WE?

A
  • Alcohol intoxication/withdrawal
  • Hepatic encephalopathy
  • Stroke/intracranial event
  • Viral encephalitis
222
Q

What is the treatment for WE?

A

Urgent high dose IV thiamine (500mg TID for 2-3 days) followed by 250 mg daily for 5 days.

Continue with oral thiamine long term.

223
Q

What are the complications/prognosis of WE?

A

Mortality of 20% if untreated.

Korsakoff’s syndrome occurs in 80% if left untreated.

Even if treated permanent neurological damage can occur. (hearing loss, ataxia, horizontal nystagmus)

224
Q

What is Korsakoff’s syndrome?

A

A chronic and severe memory disorder resulting from untreated Wernicke’s encephalopathy. It is marked by profound memory impairment (anterograde and confabulation. Treatment with 100mg oral thiamine/day.

225
Q

What are the clinical features of Korsakoff’s syndrome.

A
  • Memory impairment (anterograde and retrograde)
  • Confabulation
  • Lack of insight
  • Apathy
226
Q

Selective Serotonin Reuptake Inhibitors (SSRIs)

A

Examples: Sertraline, Citalopram, Fluoxetine, Escitalopram, Paroxetine.

MoA: These are inhibitors of the serotonin transporter (SERT) which prevent reuptake of serotonin (5-HT) from the synaptic cleft, increasing its availability and potentiating its action. Takes 4-6 weeks for full effect.

Indications: Depression, anxiety disorders, OCD, PTSD
Contraindications: Mania

Side effects:
Common - Nausea, insomnia, sexual dysfunction, weight changes, headaches.
Serious - Increased risk of suicide in younger populations (initially), serotonin syndrome (rare).

227
Q

Serotonin-Noradrenaline Reuptake Inhibitors (SNRIs)

A

Examples: Venlafaxine, Duloxetine

MoA: Inhibit reuptake of both serotonin (5-HT) and noradrenaline (NA) in synaptic cleft

Indications: Depression, generalised anxiety disorder (GAD), neuropathic pain.
Contraindications: Conditions with high risk of arrhythmias, uncontrolled hypertension.

Side effects: Similar to SSRIs, but with additional risk of hypertension (dose-dependent).
Sweating, dry mouth, dizziness.

Important Notes:
Can be more effective in severe depression.
Monitor blood pressure regularly.

228
Q

Tricyclic Antidepressants (TCAs)

A

Examples:
More sedative: Amitriptyline, Clomipramine, Dosulepin, Less sedative: Nortriptyline, Imipramine

MoA: Block reuptake of serotonin and noradrenaline. Also antagonises various receptors (e.g., histamine, muscarinic, alpha-1 adrenergic).

Indications: Depression (second-line), chronic pain, insomnia.
Contraindications: Recent MI, arrhythmias (especially heart block), mania, severe liver disease, agranulocytosis

Side Effects:
Common: Dry mouth, constipation, urinary retention, sedation, weight gain, hyponatremia.
Serious: Cardiotoxicity (QT prolongation), arrhythmias, orthostatic hypotension.

Important Notes:
Risk of overdose can be fatal due to cardiac toxicity.
Not recommended as first-line due to side effect profile.

229
Q

Monoamine Oxidase Inhibitors (MAOIs)

A

Examples:
Irreversible: Phenelzine, isocarboxide
Reversible: Moclobemide, Tranylcypromine

MoA: Inhibits monoamine oxidase, the enzyme that breaks down serotonin, norepinephrine, and dopamine.

Indications: Refractory depression, atypical depression, social phobia
Contraindications: Acute confusional state, pheochromocytoma

Side Effects: Orthostatic hypotension, weight gain, sexual dysfunction, insomnia.
Serious: Hypertensive crisis if taken with tyramine-rich foods or certain medications.

230
Q

First-Generation (Typical) Antipsychotics

A

Examples: Haloperidol, Chlorpromazine, Fluphenazine

MoA: Block dopamine D2 receptors, primarily affecting the mesolimbic pathway.

Indications: Schizophrenia, acute psychosis, mania, delirium, psychomotor agitation.
Contraindications: Parkinson’s disease, CNS depression, severe hypotension.

Side effects: Extrapyramidal symptoms (EPS), tardive dyskinesia, neuroleptic malignant syndrome, sedation, anticholinergic effects, weight gain. Antimuscarinic: dry mouth, blurred vision, urinary retention, constipation.
Raised prolactin: galactorrhoea, impaired glucose tolerance.
Prolonged QT interval (particularly haloperidol).

Important notes: Clozapine specific side effects hypersalivation and agranulocytosis.

231
Q

What are extrapyramidal symptoms?

A
  1. Dystonia - Sudden, involuntary muscle contractions that can lead to painful, abnormal postures.
  2. Parkinsonism - Tremor, bradykinesia (slowed movements), rigidity, shuffling gait.
  3. Akathisia - A feeling of inner restlessness with a compulsion to move.
  4. Tardive Dyskinesia - Late symptom after long term use of antipsychotics. Involuntary, repetitive movements, particularly of the face and tongue. Can be irreversible.
232
Q

What is neuroleptic malignant syndrome (NMS)?

A

A rare but potentially life-threatening neurological disorder that occurs as a reaction to antipsychotic medications (dopamine antagonists). More common with 1st gen antipsychotics. Usually occurs in first 10 days of initiation/dose change.

233
Q

How does NMS present?

A

Characterised by:
Hyperthermia - >38, sometime >40 (severe)
Muscle rigidity
Altered mental status - confusion, delirium, stupor
Dysautonomia - Raised HR, RR, labile BP, sweating (greasy), urinary incontinence, pallor

234
Q

How do you investigate NMS?

A
  • Low index of suspicion in patient taking antipsychotics.
  • Characteristic features
  • Creatinine Kinase - supporting feature, high levels (at least 4X baseline, typically >1000 units/L)
235
Q

What are the differentials for NMS?

A
  • Serotonin syndrome (history
  • Malignant hyperthermia
  • Severe infections (sepsis, meningitis)
  • Recreational drug use (MDMA, cocaine)
236
Q

How is NMS managed?

A

Discontinue offending agent

Supportive care: Rehydrate, cooling, treat rhabdomyolysis.
Consider benzodiazepine - agitation, severe hyperthermia
Consider dopamine agonist (Bromocriptine)
Dantrolene - ryanodine receptor antagonist (causes skeletal muscle relaxation)

Follow up: most patients recover within 1-2 weeks. May require reinitiation of antipsychotic

237
Q

Second generation antipsychotics

A

Examples: Olanzapine, Risperidone, Quetiapine, Aripiprazole (partial agonist at D2), Clozapine

MofA: D2 receptor antagonism and 5-HT2A receptor antagonism (serotonin). The additional serotonin receptor blockade helps reduce the risk of EPS and improves efficacy for treating negative symptoms.

Indications: Schizophrenia, bipolar disorder, psychosis in Parkinson’s disease
Contraindications: Severe liver disease, cardiovascular disease.

Side effects:
Antimuscarinic: dry mouth, blurred vision, urinary retention, constipation
Sedation, weight gain
Raised prolactin: galactorrhoea, impaired glucose tolerance
Neuroleptic malignant syndrome (less common)
Reduced seizure threshold (greater with atypicals)

238
Q

Mood stabilisers

A

Examples: Lithium, Sodium valproate, Lamotrigine, carbamazepine.

Indications: Bipolar disorder (mania, maintenance), augmentation in treatment-resistant depression, schizoaffective disorder. Epilepsy for SV and L.

239
Q
A

Phase 3a (9 decks)

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