Psychiatry Flashcards

1
Q

What is the definition of ADHD?

A

Attention Deficit Hyperactivity Disorder

Is a neuro-developmental disorder characterised by persistent patterns of inattention, impulsivity, and hyperactivity that are inappropriate for the individual’s developmental level.

The symptoms significantly affect daily functioning in more than one setting, such as at home and school or work.

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2
Q

What is the epidemiology of ADHD?

A

It is most common in children, although a significant proportion (50%) continue to have problems with behaviour or attention in adult life.

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3
Q

What is the cause of ADHD?

A

Exact cause is unknown.

But it is associated with reduced activity in the frontal lobe leading to impaired executive functioning.

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4
Q

What criteria needs to be met for a diagnosis of ADHD to be made? (According to DSM-5)

A

Inattention:

  • Six or more symptoms of inattention for children up to age 16 years, or five or more for adolescents age 17 years and older and adults
  • Symptoms of inattention have been present for at least 6 months, and they are inappropriate for developmental level

Hyperactivity and impulsivity:

  • Six or more symptoms of hyperactivity-impulsivity for children up to age 16 years, or five or more for adolescents age 17 years and older and adults
  • Symptoms of hyperactivity-impulsivity have been present for at least 6 months to an extent that is disruptive and inappropriate for the person’s developmental level

Additional criteria:

  • Several inattentive or hyperactive-impulsive symptoms present before the age of 12 years
  • Several symptoms are present in two or more settings (e.g., at home, school, or work)
  • There is clear evidence that the symptoms interfere with, or reduce the quality of, social, school, or work functioning.
  • The symptoms are not better explained by another mental disorder
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5
Q

What are some differentials for ADHD?

A

Learning Disabilities:
Characterised by difficulties in reading, writing, mathematics or other learning skills, often with normal attention span.

Conduct Disorder:
Presents with persistent pattern of antisocial behaviour, such as aggression or destructiveness.

Autism Spectrum Disorder:

Mood Disorders:
E.g. depression and bipolar disorder, can cause concentration problems and impulsivity

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6
Q

What investigations are done for ADHD?

A

Diagnosis is done primarily done using the DSM-5 criteria. But the following can also help:

  • Comprehensive history and physical examination
  • Observation of the individual’s behaviour
  • Teacher and parent reports or rating scales
  • Neuropsychological testing
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7
Q

What is the management of ADHD?

A

Non-Pharmacological

  • Behavioural techniques
    E.g. cognitive behavioural therapy (CBT), behavioural therapy, psychoeducation, and social skills training.
  • Extra support at school

Pharmacological

  • Stimulant medications:
    E.g. methylphenidate or amphetamines. These have some activity in the frontal lobe, thus increasing executive function, attention, and reducing impulsivity.
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8
Q

What is the definition of Depression?

A

It’s a common mental health disorder typified by low mood, anhedonia, significant weight change, sleep and activity changes, fatigue, feelings of guilt or worthlessness, poor concentration and suicidality.

It is defined by the DSM as the presence of 5 out of these 9 symptoms (almost every day) for at least 2 weeks.

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9
Q

What is the epidemiology of depression?

A

Increased prevalence in Females

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10
Q

What causes depression?

A

Depression results from a complex interplay of genetic and environmental factors. The following all contribute:

  • Personal or family history of depression
  • Personal history of mental health issues
  • Physical illnesses
  • Social challenges like divorce, poverty, and unemployment
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11
Q

What are the clinical features of depression?

A

Depressed mood or irritability for most of the day, indicated by either subjective report (feels sad or empty) or observation by others (appears tearful).

Anhedonia: Decreased interest or pleasure in most activities, most of the day.

Significant weight change (5%) or change in appetite.

Sleep alterations: Insomnia or hypersomnia.

Activity changes: Psychomotor agitation or retardation.

Fatigue or loss of energy

Guilt or feelings of worthlessness: Excessive or inappropriate guilt or feelings of worthlessness.

Cognitive issues: Diminished ability to think or concentrate, or increased indecisiveness.

Suicidality: Thoughts of death or suicide, or formulation of a suicide plan.

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12
Q

What are the main differentials for depression?

A

Bipolar Disorder

Anxiety Disorders

Substance/Medication-Induced Mood Disorder
Mood disturbance associated with intoxication or withdrawal from substances or side effects of medications.

Adjustment Disorders
Development of emotional or behavioural symptoms in response to identifiable stressors.

Various organic causes also need to be considered:

Neurological disorders
E.g. Parkinson’s disease, dementia, and multiple sclerosis.

Endocrine disorders especially thyroid dysfunction and hypo/hyperadrenalism (e.g., Cushing’s and Addison’s disease).

Substance use or medication side effects
e.g. steroids, isotretinoin, alcohol, beta-blockers, benzodiazepines, and methyldopa.

Chronic conditions
like diabetes and obstructive sleep apnea.

Long-standing infections

Neoplasms and cancers
low mood can theoretically be a presenting complaint in any cancer, with pancreatic cancer being a notable example.

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13
Q

What investigations are done for Depression?

A

Depression is primarily a clinical diagnosis, with patients fulfilling the diagnostic criteria outlined above. Other investigations that are done can be:

  • Patient Health Questionaire - 9 (PHQ-9)
  • FBC
  • TFTs
  • U+Es
  • LFTs
  • Blood glucose
  • B12/Folate Levels
  • Cortisol levels
  • Toxicology Screen
  • CNS Imaging
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14
Q

What is the Non-Pharmacological Management of Depression?

A

Initial treatment Involves low-intensity psychological interventions or group-based Cognitive Behavioral Therapy (CBT).

For moderate to severe depression, higher-intensity CBT/interpersonal therapy combined with pharmacological therapy is typically employed.

Mild cases may respond to CBT alone.

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15
Q

What is the Pharmacological management of depression?

A

First-line pharmacological treatment:
Selective Serotonin Reuptake Inhibitor (SSRI) such as sertraline.

Continuation of antidepressants for at least six months post-remission is recommended to mitigate relapse risk.

Tapering should be done gradually over a four-week period when discontinuing antidepressants.

2nd line pharmacological treatment
Tricyclic Antidepressants (TCAs) e.g. amitriptyline

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16
Q

What is the definition of Refractory Depression?

A

Its defined as a failure to demonstrate an adequate response to an adequate treatment trial

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17
Q

How is Refractory Depression Managed?

A

Lithium or Electroconvulsive Therapy (ECT) (After all other approaches have been tried).

Short-term side effects of ECT include headache, muscle aches, nausea, temporary memory loss, and confusion, while long-term side effects can include persistent memory loss.

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18
Q

What is the definition of Austistic Spectrum Disorders (ASDs)?

A

ASDs are a set of complex neuro-developmental disorders, characterised by a spectrum of social, language, and behavioural deficits.

They span a wide range of symptoms, skills, and levels of disability. ASDs are persistent and impact everyday living.

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19
Q

What is the epidemiology of Autistic Spectrum Disorders?

A

Higher prevalence in Males

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20
Q

What are some risk factors for developing an ASD?

A
  • Male Sex
  • Advanced parental age at the time of conception
  • Certain genetic mutations
  • Maternal exposure to specific drugs or infections during pregnancy
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21
Q

What deficits in social interaction might someone with Autism show?

A
  • Lack of eye contact
  • Delay in smiling
  • Avoids physical contact
  • Unable to read non-verbal cues
  • Difficulty establishing friendships
  • Not displaying a desire to share attention (i.e. not playing with others)
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22
Q

What deficits in communication might someone with Autism show?

A
  • Delay, absence or regression in language development
  • Lack of appropriate non-verbal communication such as smiling, eye contact, responding to others and sharing interest
  • Difficulty with imaginative or imitative behaviour
  • Repetitive use of words or phrases
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23
Q

What behavioural traits may someone with Autism show?

A
  • Greater interest in objects, numbers or patterns than people
  • Stereotypical repetitive movements. There may be self-stimulating movements that are used to comfort
    themselves, such as hand-flapping or rocking.
  • Intensive and deep interests that are persistent and rigid
  • Repetitive behaviour and fixed routines
  • Anxiety and distress with experiences outside their normal routine
  • Extremely restricted food preferences
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24
Q

What are some differentials for ASDs?

A

Intellectual Disability
Characterised by generalised deficits in intellectual functioning and adaptive behaviour, typically lacking the social deficits seen in ASD.

Attention Deficit Hyperactivity Disorder (ADHD)
Exhibits symptoms of inattention, hyperactivity, and impulsivity, but does not exhibit significant social or language communication deficits as seen in ASD.

Specific Language Impairment
Characterised by difficulties in language acquisition in the absence of cognitive impairment. Unlike ASD, social interaction is not typically affected.

Childhood Schizophrenia
Characterised by hallucinations, delusions, and disorganised speech or behaviour, which are not typical in ASD.

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25
Q

How is an ASD diagnosed?

A

Diagnosis should be made through a multidisciplinary assessment completed by a specialist in autism.

This can involve:
* Psychological evaluation
* Speech and language assessment
* Cognitive assessment
* Thorough review of the child’s behaviour in different settings (home, school, etc.).

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26
Q

How are Autistic Spectrum Disorders Managed?

A

Autism cannot be cured

Management requires a multidisciplinary approach:

Behavioural Management
Applied Behavioural Analysis is a widely used technique, whereby positive behaviours are encouraged and negative behaviours are largely ignored.

Family Support
Due to the chronic nature of the disorder and its pervasive impact on family life, significant extra support for the family is often required.

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27
Q

What is the definition of Bipolar Affective Disorder?

A

Bipolar disorder is a mental health disorder marked by alternating periods of:

Depression
Characterised by low mood, feelings of worthlessness, decreased energy, and potential suicidality.

Elevated mood (mania or hypomania)
Characterised by persistently elevated, expansive, or irritable mood, inflated self-esteem, decreased need for sleep, and potential for reckless behaviour.

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28
Q

What are the risk factors for developing Bipolar Disorder?

A
  • Having a first-degree relative, such as a parent or sibling, with bipolar disorder.
  • Periods of high stress, such as the death of a loved one or other traumatic event.
  • Drug or alcohol abuse.
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29
Q

What is the clinical presentation of Bipolar Disorder?

A

It depends on the phase of the disorder:

Depressive Phase

  • Withdrawal
  • Tearfulness
  • Low mood
  • Poor sleep
  • Anhedonia
  • Potential suicidal ideation or attempts.

Manic Phase

  • Elevated mood
  • Irritability
  • Impulsivity
  • Reduced need for sleep
  • Mood congruent delusions
  • Pressured speech
  • Flight of ideas.
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30
Q

What are some differentials for Bipolar Disorder?

A

Major Depressive Disorder
Characterised by low mood, loss of interest or pleasure, feelings of worthlessness, impaired concentration, and possible suicidality.

Schizoaffective Disorder
Presents with hallucinations, delusions, disorganised speech, disorganised behaviour, and symptoms of depression or mania.

Generalised Anxiety Disorder
Chronic and excessive worry, restlessness, fatigue, impaired concentration, and sleep disturbance.

Substance-Induced Mood Disorder
Mood disturbances caused by substance misuse or withdrawal.

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31
Q

How is Bipolar Disorder diagnosed?

A

Diagnosis is based on the DSM-5 criteria:

Mania: Requires at least one episode lasting at least a week with at least three associated symptoms (e.g. inflated self-esteem, decreased need for sleep).

Hypomania: Similar to mania but less severe, not causing marked impairment in social or occupational functioning, and lacking psychotic features.

Depression: Requires at least one major depressive episode lasting at least two weeks with at least four associated symptoms (e.g. changes in appetite or sleep, feelings of worthlessness).

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32
Q

What is the acute management for Bipolar Disorder?

A

Acute Mania with Agitation
IM therapy (neuroleptic or benzodiazepine) and potential secure unit admission.

Acute Mania without Agitation
Oral antipsychotic monotherapy, potential addition of sedatives or mood stabilisers.

Acute Depression
Mood stabiliser, atypical antipsychotic, or antidepressant with psychosocial support.

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33
Q

What is the chronic management for Bipolar Disorder?

A

Long-term maintenance therapy is crucial due to high relapse risk:

Mood stabilisers
(e.g., Lithium or Valproate) are the cornerstone of treatment.

Atypical antipsychotics and anticonvulsants
May be used in treatment-resistant cases.

High-intensity psychological therapies
e.g. CBT, interpersonal therapy, or couples/family therapy

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34
Q

What is the definition of a Generalised Anxiety Disorder (GAD)?

A

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

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35
Q

What is the epidemiology of GAD?

A

Higher prevalence in Females

Higher prevalence in younger age groups (age of onset after 35 is more indicative of depressive disorder or organic disease).

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36
Q

What are some risk factors for GAD?

A
  • Female sex
  • Comorbid anxiety disorder e.g. panic disorder or social phobia.
  • Family history of anxiety disorders, depression, or other psychiatric disorders.
  • Childhood adversity such as:
    Maltreatment (e.g. sexual or physical abuse), neglect.
    Maternal depression, family disruption (e.g. divorce).
    Domestic violence, parental alcoholism, or drug use.
  • History of physical, sexual, or emotional trauma , such as:
    Physical or sexual abuse or assault.
    Motor vehicle accident.
    Sudden bereavement.
  • Sociodemographic factors, such as:
    Separated, widowed, divorced.
    Unemployment.
    Low socioeconomic status.
    Low education levels.
    Substance dependence or exposure to organic solvents
  • Chronic physical condition e.g. cardiovascular disease, cancer, etc…
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37
Q

How is a GAD disorder diagnosed?

A

According to the DSM-5-TR criteria, 3 of the following 6 key symptoms are required for a diagnosis (only 1 in kids):

  • Restlessness or nervousness
  • Being easily fatigued
  • Poor concentration
  • Irritability
  • Muscle tension
  • Sleep disturbance

Its partly a diagnosis of exclusion, with physical health conditions, other mental health disorders, and medications or other substances being ruled out as a primary cause

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38
Q

What is the clinical presentation of GAD?

A

At least 3 of the 6 key symptoms:

  • Restlessness or nervousness
  • Being easily fatigued
  • Poor concentration
  • Irritability
  • Muscle tension
  • Sleep disturbance

Other features:
* Apprehension (worries about future misfortunes, feeling on edge, difficulty in concentrating)
* Motor tension (restless fidgeting, tension headaches, trembling, inability to relax)
* Autonomic overactivity (light-headedness, sweating, tachycardia, epigastric discomfort, dizziness, etc.)
* Depersonalization (altered or lost sense of personal reality or identity) and derealization (surroundings feel unreal).

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39
Q

What are some differentials for GAD?

A

Hyperthyroidism

Substance misuse (intoxication – amphetamines; withdrawal – benzodiazepines, alcohol)

Excessive caffeine intake

Depression
Anxiety is a common feature of depression and vice versa. Identifying which condition appeared first and which is currently more prominent provides useful diagnostic cues. If both conditions are present, a diagnosis of mixed anxiety and depressive disorder is made.

Anxious (avoidant) personality disorder
The patient describes themselves as an anxious person without a recent significant increase in anxiety levels. (Note, this disorder can predispose the individual to anxiety disorders.)

Early-stage dementia

Early-stage schizophrenia

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40
Q

How is GAD managed?

A

Mild anxiety can be managed with watchful waiting and advice about self-help strategies (e.g. meditation), diet, exercise and avoiding alcohol, caffeine and drugs.

Moderate to severe anxiety can be referred to CAMHS services to initiate:
* Counselling
* Cognitive behavioural therapy
* Medical management. Usually an SSRI such as sertraline is considered.

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41
Q

What is the definition of Obsessive Compulsive Disorder (OCD)?

A

Obsessive-compulsive disorder (OCD) is a mental health disorder characterised by the presence of persistent obsessions and/or compulsions.

These are time consuming (i.e. take more than 1 hour per day) and/or cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

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42
Q

What are Obsessions?

A

Obsessions are unwanted and uncontrolled thoughts and intrusive images that the person finds it very difficult to ignore.

E.g. an overwhelming fear of contamination with dirt or germs; or violent or explicit images that keep appearing in their mind.

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43
Q

What are Compulsions?

A

Compulsions are repetitive actions the person feels they must do, generating anxiety if they are not done. Often these compulsions are a way for the person to handle the obsessions.

E.g. checking that all electrical equipment is turned off to settle the anxiety of obsessing about the house burning down.

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44
Q

Describe the cycle of anxiety seen in OCD?

A

Obsessions lead to anxiety, which leads to the compulsive behaviour, which leads to a temporary improvement in the anxiety.

Shortly after the temporary improvement in anxiety the obsession reappears, leading to further anxiety, further compulsive behaviour with a temporary relief.

This cycle continues and each time gets more engrained in the person’s behaviour. Without doing the compulsions, the person feels they cannot get relief from their anxiety.

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45
Q

What is the epidemiology of OCD?

A

It affects Males and Females equally (although presents earlier and more severely in males)

More common in pregnant and post-partum women

Bimodal age of onset, peaking at 10 and 21 years

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46
Q

What are the risk factors for developing OCD?

A
  • Family history of OCD
  • Personal history of co-morbid psychiatric conditions e.g. anxiety disorders, depression and other mood disorders, eating disorders, etc…)
  • Pregnant/Post-Partum women
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47
Q

What is the diagnostic criteria for OCD?

A

OCD is a clinical diagnosis and according to ICD-11:

  • Either obsessions or compulsions (or both) are time-consuming and must be present for at least one hour per day.
  • They are acknowledged as originating in the mind of the patient and are not imposed by outside persons or influences.
  • They are repetitive and unpleasant and at least one obsession or compulsion must
    be present that is acknowledged as excessive or unreasonable.
  • The subject tries to resist them (but if very long-standing, resistance to some obsessions or compulsions may be minimal). At least one obsession or compulsion must be present which is unsuccessfully resisted.
  • Carrying out the obsessive thought or compulsive act is not in itself pleasurable.
  • The obsessions or compulsions cause distress or interfere with the subject’s social or individual functioning, usually by wasting time.
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48
Q

What scale is used to assess the severity of OCD symptoms?

A

Yale-Brown Obsessive Compulsive Scale

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49
Q

What is the management for OCD?

A

Mild OCD may be managed with education and self help resources.

More significant OCD may require:

  • Referral to CAMHS
  • Patient and carer education
  • Cognitive behavioural therapy
  • SSRIs medications
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50
Q

What is the definition of Postpartum depression?

A

It’s a significant mood disorder that can develop at any time up to one year after the birth of a baby.

This condition represents a considerable aspect of maternal mental health and extends beyond the common “baby blues”.

Typically presenting with persistent depressive symptoms that may interfere with daily functioning and parenting.

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51
Q

What causes Postpartum depression?

A

Development of postpartum depression is multifactorial with a combination of Biological, Psychological, and Social factors all contributing.

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52
Q

What biological factors contribute to the development of postpartum Depression?

A
  • Hormonal fluctuations post-delivery, including sudden drops in progesterone, estrogen, and thyroid hormones.
  • Alterations in melatonin and cortisol rhythms and immune-inflammatory processes
  • Genetic predispositions
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53
Q

What Psychological factors contribute to the development of postpartum Depression?

A
  • A history of mood or anxiety disorders
  • Previous episodes of postpartum depression
  • Certain personality traits such as neuroticism
  • Psychological stress from the transition to parenthood
  • Unrealistic expectations of motherhood
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54
Q

What Social Factors contribute to the development of postpartum depression?

A
  • Lack of social support
  • Relationship issues,
  • Life stressors
  • Low socioeconomic status
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55
Q

What are the signs and symptoms of postpartum depression?

A
  • Persistent lowering of mood and reduced enjoyment or interest in activities.
  • Lowering of energy levels.
  • Biological symptoms of depression like poor appetite and disturbed sleep patterns (not associated with normal disturbed sleep patterns with a baby)
  • Concerns related to bonding with the baby, caring for the baby, and in extreme circumstances, thoughts about harming oneself or the baby.
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56
Q

What are some differentials for postpartum depression?

A

Baby blues
Characterised by mild mood swings, irritability, anxiety, and tearfulness. However, these symptoms usually present within the first two weeks after birth and resolve spontaneously.

Postpartum Psychosis

Adjustment disorders
These disorders may develop in response to a major life change or stressor, such as having a baby, but the emotional or behavioural symptoms are less severe than in depression.

Generalized Anxiety Disorder (GAD)

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57
Q

What is the main screening tool for Postpartum depression?

A

Edinburgh Postnatal Depression Scale (EPDS)

A cutoff score of over 10 is used as a positive result.

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58
Q

What is the management of postpartum depression?

A

First-line treatments:

  • Self-help strategies and psychological therapies e.g. Cognitive Behavioural Therapy (CBT) or Interpersonal Therapy (IPT).

Pharmacological treatments

  • Antidepressants considered in high risk cases

In severe cases admission to a mother and baby inpatient mental health unit might also be necessary.

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59
Q

What is the definition of Postpartum Psychosis?

A

It’s a serious psychiatric disorder that typically develops within the first two weeks following childbirth.

It is characterised by a range of psychological symptoms, including paranoia, delusions, hallucinations, mania, depression, and confusion.

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60
Q

What are the risk factors for Postpartum Psychosis?

A
  • Prior history of severe mental illnesses such as schizophrenia or bipolar affective disorder
  • Family history of postpartum psychosis
  • Previous episode of postpartum psychosis
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61
Q

What is the clinical presentation of Postpartum Psychosis?

A

Paranoia
Delusions
Hallucinations
Manic episodes
Depressive episodes
Confusion

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62
Q

What is the main differential for Postpartum Psychosis?

A

Postpartum depression with psychotic features

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63
Q

How is Postpartum depression diagnosed?

A

Diagnosis is predominantly clinical, based on the presenting signs and symptoms.

It requires a thorough psychiatric evaluation.

Consideration should be given to other medical conditions that may cause similar symptoms, such as thyroid disorders or sepsis.

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64
Q

How is Postpartum psychosis managed?

A

Pharmacotherapy with:

  • Antipsychotic medications
  • Mood stabilisers in some instances

Potential referral to a specialist mother and baby inpatient mental health unit in very severe cases (when the mother experiences command hallucinations, thoughts of self-harm or suicide, or delusional beliefs regarding the baby’s role or identity).

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65
Q

What needs to be considered when prescribing medications for Postpartum Psychosis?

A

The mother’s breastfeeding status and the potential for the transfer of drugs to the nursing infant.

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66
Q

What is the definition of Post Traumatic Stress Disorder (PTSD)?

A

It’s a condition that may develop following exposure to 1 or more traumatic events involving actual or threatened death, serious injury, or sexual violence.

Exposure can be through directly experiencing the traumatic event, witnessing the event as it occurred to others or learning that the event occurred to a family member or a close friend.

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67
Q

What does the ICD-11 state PTSD is characterised by?

A
  • Re-experiencing the traumatic event in the present in the form of vivid intrusive memories, flashbacks, or nightmares. This is typically accompanied by strong or overwhelming emotions, particularly fear or horror, and strong physical sensations.
  • Avoidance of thoughts and memories of the event or events, or avoidance of activities, situations, or people reminiscent of the event.
  • Persistent perceptions of heightened current threat E.g. hypervigilance or an enhanced startle reaction to stimuli such as unexpected noises.
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68
Q

What is the definition of Complex PTSD?

A

A disorder that may develop following exposure to an event or series of events of an extremely threatening or horrific nature, most commonly prolonged or repetitive events from which escape is difficult or impossible (e.g. torture, slavery, etc…)

In addition to all the diagnostic criteria being met for PTSD; complex PTSD is characterised by severe and persistent:

  • Problems in affect regulation.
  • Beliefs about oneself as diminished, defeated or worthless, accompanied by feelings of shame, guilt or failure related to the traumatic event.
  • Difficulties in sustaining relationships and in feeling close to others.
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69
Q

What are some Risk Factors for PTSD?

A
  • Refugees and Asylum Seekers
  • First Responders
  • Combat Exposure
  • Poor Social Support
  • History of previous psychiatric disorders
  • Giving birth
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70
Q

What is the clinical presentation of PTSD?

A
  • Re-experiencing.
  • Avoidance.
  • Hyperarousal (including hypervigilance, anger and irritability).
  • Negative alterations in mood and thinking.
  • Emotional numbing.
  • Dissociation.
  • Emotional dysregulation.
  • Interpersonal difficulties or problems in relationships.
  • Negative self-perception
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71
Q

When is usually the time of onset for PTSD?

A

PTSD tends to develop soon after the event. It may be delayed, but delayed onset greater than a year post-trauma is very rare.

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72
Q

What are some differentials for PTSD?

A

Prolonged grief disorder
A disturbance in which, following the death of a person close to the bereaved, there is persistent and pervasive grief response characterised by longing for (or a persistent preoccupation with) the deceased, accompanied by intense emotional pain.

Depression

Adjustment disorders

Enduring personality change after catastrophic experience

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73
Q

What screening questionnaires are there for PTSD (1st line investigations)

A

DSM-5 PTSD Checklist
A 20 item checklist assessing the symptoms of PTSD according to DSM-5.

Trauma Screening Questionnaire (TSQ)
A set of 10 items covering re-experiencing and arousal symptoms.

Post traumatic Diagnostic Scale (PDS-5)
A 24-item self report measure assessing PTSD symptom severity in the last month.

  • International Trauma Questionnaire (ITQ)
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74
Q

What are the Non-Pharmacological managements of PTSD?

A

Cognitive Behavioural therapy
Narrative/Prolonged exposure therapy

In patients who have been diagnosed with PTSD, or in patients who present with symptoms of PTSD one or more months after a traumatic event.

Eye movement desensitisation and reprocessing (EMDR) should be offered to patients who have presented more than three months after a non-combat-related trauma

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75
Q

What is the Pharmacological management of PTSD?

A

First line:

  • Venlafaxine
  • Or an SSRI (e.g. sertraline)

In serious cases that haven’t responded to previous drug or psychological therapies:

  • Antipsychotics (like risperidone) in addition to psychological therapies
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76
Q

Define the term Learning Disability

A

It’s a general umbrella term encompassing a range of different conditions that affect the ability of the child to develop new skills.

Examples include:

  • Dyslexia
  • Dysgraphia refers to a specific difficulty in writing.
  • Dyspraxia
  • Auditory processing disorder
  • Non-verbal learning disability
  • Profound and multiple learning disability

They can vary from very mild to severe

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77
Q

What is the definition of Dyslexia?

A

It refers to a specific difficulty in reading, writing and spelling.

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78
Q

What is the definition of Dysgraphia?

A

It refers to a specific difficulty in writing.

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79
Q

What is the definition of Dyspraxia?

A

Also known as developmental co-ordination disorder.

It refers to a specific type of difficulty in physical co-ordination.

More common in boys.

It presents with delayed gross and fine motor skills and a child that appears clumsy.

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80
Q

What is the definition of Auditory processing disorder?

A

It refers to a specific difficulty in processing auditory information.

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81
Q

What is the definition of a Non-verbal learning disability?

A

It refers to a specific difficulty in processing non-verbal information, such as body language and facial expressions.

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82
Q

What is the definition of a Profound and multiple learning disability?

A

It refers to severe difficulties across multiple areas, often requiring help with all aspects of daily life.

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83
Q

How are Learning disabilities classified?

A

The severity of the learning disability is based on the IQ (intelligence quotient):

55 – 70: Mild
40 – 55: Moderate
25 – 40: Severe
Under 25: Profound

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84
Q

What are the risk factors for Learning Disabilities?

A
  • Family history of learning disability
  • Abuse
  • Neglect
  • Psychological trauma
  • Toxins
  • Certain conditions
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85
Q

What conditions are associated with learning disabilities?

A
  • Genetic disorders such as Downs syndrome
  • Antenatal problems, such as foetal alcohol syndrome and maternal chickenpox
  • Problems at birth, such as prematurity and hypoxic
  • ischaemic encephalopathy
  • Problems in early childhood, such as meningitis
  • Autism
  • Epilepsy
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86
Q

What does the management of learning disabilities involve?

A

The key is a multidisciplinary approach to support the parents and child:

Health visitors
Social workers
Schools
Educational psychologists
Paediatricians, GPs and nurses
Occupational therapists
Speech and language therapists

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87
Q

Define Psychosis

A

Its a syndrome associated with dysregulation of the neurotransmitters dopamine and serotonin, and abnormal functioning of key brain circuits (particularly involving frontal, temporal, and mesostriatal brain regions.)

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88
Q

What are the 2 main causes of Phychosis?

A

Psychosis can be due to:

  • Primary (“non-organic”) psychiatric disorders
  • Secondary to substance use or specific medical (“organic”) aetiologies
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89
Q

Give some examples of primary psychotic disorders

A

Schizophrenia

Delusional disorder

Schizoaffective disorder

Schizophreniform disorder

Brief psychotic disorder

They may also accompany other psychiatric conditions like major depressive disorder and bipolar disorder.

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90
Q

How does psychosis associated with primary psychotic disorders present?

A
  • Hallucinations (mostly auditory)
  • Delusions
  • Disorganised thought process
  • But are usually oriented and have minimal overt cognitive deficits.
  • Have normal Vital Signs
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91
Q

How does psychosis secondary to drug use or medical causes present?

A
  • Altered vital signs
  • Visual hallucinations
  • Severe cognitive impairment, including confusion or disorientation.
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92
Q

How is Psychosis investigated?

A
  • Physical examination
    (detailed neurological examination and a complete mental status examination)
  • Complete psychiatric and medical history
    (review of head injury, seizures, cerebrovascular disease, sexually transmitted infections, and new or worsening headaches)
  • Laboratory work-up
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93
Q

What lab work should be done for a Psychosis investigation?

A

FBC
Comprehensive metabolic profile
TFTs
Urine toxicology
Parathyroid hormone
calcium
vitamin B12
folate
niacin​

Based on clinical suspicion, testing for HIV infection and hepatitis C,

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94
Q

What is the management of psychosis?

A

It depends on the underlying cause.

If Schizophrenia:

1st line is (2nd gen) atypical antipsychotics e.g. Risperidone or Olanzapine

Haloperidol is also still used

95
Q

What is the definition of Schizophrenia?

A

It’s a severe mental disorder characterised by chronic or relapsing episodes of psychosis.

It involves altered perceptions of reality, disordered thinking, and social dysfunction.

96
Q

What are the risk factors for Schizophrenia?

A
  • Family History
    10% if either a parent or sibling is affected
    50% if both parents or an identical twin
  • Childhood trauma, like poor maternal bonding, poverty, or exposure to natural disasters
  • Heavy cannabis use in childhood
  • Maternal health issues, including malnutrition and infections like rubella and cytomegalovirus
  • Birth trauma, particularly hypoxia and blood loss
  • Urban living and immigration to more developed countries
97
Q

What is the clinical presentation of Schizophrenia?

A

Schneider’s first rank symptoms :

  • Audible thoughts (thought echo)
  • Voices arguing or commenting on one’s actions
  • Somatic passivity, thought withdrawal, thought insertion, and thought broadcasting
  • Made feelings, impulses, and volitional acts
  • Delusional perception

Negative Symptoms:

  • Alogia
  • Anhedonia
  • Affective incongruity or blunting
  • Avolition

ICD-10 states these should be present most of the time during a period of at least one month

98
Q

What are some differentials for Schizophrenia?

A

Substance-induced psychotic disorder
Associated with hallucinations and delusions; typically precipitated by drug use or withdrawal

Organic psychosis
Typically accompanied by neurological symptoms or changes in mental status; conditions such as infections, brain injuries, or CNS diseases like Wilson’s disease or encephalitis can lead to organic psychosis

Metabolic disorders
Hyperthyroidism and hyperparathyroidism can present with agitation, restlessness, and altered mental status

Depression and dementia
May present with psychotic symptoms alongside cognitive decline and mood symptoms

Autoimmune encephalitis
May present with subacute psychosis alongside focal neurological deficits or seizures

99
Q

How is Schizophrenia investigated?

A

It’s primarily a clinical diagnosis based on history and examination. But investigations need to be done to rule out organic causes:

  • Brain imaging (CT/MRI) to rule out structural abnormalities
  • Blood tests to exclude infectious (e.g.,HIV, syphilis) or metabolic causes (e.g., thyroid function tests)
  • Drug screening to identify substance misuse
100
Q

What is the management of Schizophrenia?

A

1st Line: Second-generation (atypical) antipsychotics e.g. Risperidone

In acute episodes: Sedatives (e.g. lorazepam, promethazine, or haloperidol) to manage dangerous behaviour.

Clozapine is considered when schizophrenia is resistant to other antipsychotics. (Due to its potential lethal side effects, it requires intensive monitoring.)

Psychotherapy, such as cognitive-behavioural therapy, is also an essential part of management.

101
Q

What is the definition of Schizoaffective disorder?

A

Schizoaffective disorder is an illness defined by a course that combines significant affective and psychotic symptoms.

Diagnosis requires the presence of schizophrenia symptoms concurrent with mood symptoms (depression or mania), lasting for a considerable part of a 1-month period.

A Schizoaffective episode is diagnosed only when the patient does not meet criteria for either schizophrenia or a depressive or manic episode.

102
Q

Define Somatisation Disorder

A

Also known as Somatic symptom disorder is diagnosed when a patient has a significant focus on physical symptoms, such as pain, weakness or shortness of breath, to a level that results in major distress and/or problems functioning.

The patient demonstrates excessive thoughts, feelings and behaviours relating to these physical symptoms.

103
Q

What are the risk factors for Somatisation Disorders?

A
  • History of IBS
  • History of PTSD
  • History of sexual or physical abuse
104
Q

What is the typical presentation of Somatic Syndrome?

A

Symptoms that are generally severe enough to affect work and relationships and lead the person to consult a doctor and take medication.

A lifelong history of ‘sickliness’ is often present:

Stress often worsens the symptoms.

Examples include:
* Cardiac (SOB, Palpitations, Chest Pain)

  • GI (Vomiting, Abdominal pain, nausea, diarrhoea)
  • MSK ( Back pain, Joint pain)
  • Neurological (Headaches, dizziness, amnesia, vision changes, paralysis or muscle weakness)
  • Urogenital (Pain during urination, low libido, dyspareunia, impotence).
105
Q

How is Somatic Syndrome Diagnosed?

A

Somatisation is often a diagnosis of exclusion but it’s much more effective to pursue a positive diagnosis when the patient presents with typical features:

  • multiple symptoms, often occurring in different organ systems.
  • Symptoms are vague or that exceed objective findings.
  • Chronic course.
  • Presence of a psychiatric disorder.
  • History of extensive diagnostic testing.
  • Rejection of previous physicians.
106
Q

What is the management of Somatic Syndrome?

A

1st Line treatment is Psychotherapy, and Cognitive behavioural therapy shows the best outcomes

Pharmacological interventions show little effect on the disease although psychiatric disorders associated with somatisation like anxiety and depression can be treated with antidepressants which will often improve somatic symptoms.

107
Q

What are some examples of atypical antipsychotics?

A

Clozapine
Risperidone
Olanzapine

108
Q

What are the side effects of atypical antipsychotics?

A

Weight gain
Drowsiness
Increased appetite
Dyslipidaemia
Galactorrhoea

109
Q

Why is Clozapine a high risk medication?

A

It can cause agranulocytosis and result in severe infections.

It can only be started after two other antipsychotics have been trialled.

110
Q

What are the side effects relevant to all anti-psychotics?

A
  • Sedation
  • Hyperprolactinaemia
  • Sexual dysfunction
  • Cardiac Arrhythmias
  • Reduction of seizure threshold
  • Increased risk of stroke death in the elderly (when used in demenatia-related psychosis)
  • Increased risk of stroke in the elderly
111
Q

What is the most common first generation antipsychotic and what are its side effects?

A

Haloperidol

There is a higher risk of extra-pyramidal side effects including:
* Akathisia
* Dystonia
* Parkinsonism
* Tardive Dyskinesia

112
Q

What is the definition of Delusions?

A

Delusions are fixed, false beliefs that are maintained despite contradictory evidence. They are a prominent feature of numerous psychiatric conditions
E.g.
Schizophrenia, bipolar disorder, and psychotic depression.

113
Q

What are some specific types of Delusions?

A

Nihilistic delusions
Negative delusions typically congruent with the individual’s depressed mood. Patients may believe that they are dead or that the world has ended.

Delusions of grandeur
Patients believe they possess extraordinary traits or powers. Common in manic phases of bipolar disorder.

Delusions of control
The individual experiences a sensation that an external entity is controlling their thoughts or actions. Frequently observed in psychotic conditions.

Capgras Delusions
Misidentification syndrome characterised by the belief by the patient that the close person is replaced by an imposter who looks physically the same

Persecutory delusions
The patient believes they are being persecuted or conspired against. Common in conditions like paranoid schizophrenia.

Somatic delusions
Patients are convinced they have a physical, medical, or biological problem despite no medical evidence supporting their claim. These delusions can manifest as a wide range of physical symptoms.

114
Q

How are delusions classified?

A

Bizarre Vs non-bizarre
(very strange or highly unusual) Vs (plausible but incorrect)

Mood-congruent (consistent with the individual’s emotional state) Vs mood-neutral

115
Q

What are some differentials for Delusions?

A

Mood disorders with psychotic features
Delusions often mood-congruent. In depressive episodes, these might be nihilistic delusions; in manic episodes, they might be grandiose.

Neurocognitive disorders
Delusions can occur in conditions such as Alzheimer’s disease or Parkinson’s disease dementia. The delusions often involve theft or persecution.

Substance-induced psychotic disorder
Delusions might be part of a broader psychotic syndrome due to intoxication or withdrawal from substances such as alcohol, hallucinogens, or amphetamines.

116
Q

What investigations are done for delusions?

A

Clinical interview
Comprehensive psychiatric history, including onset, duration, and the impact of symptoms on functioning.

Mental state examination (MSE)
Evaluation of appearance, behaviour, speech, mood, affect, thought process, thought content, perception, cognition, insight, and judgment.

Neuropsychological assessment
To rule out neurocognitive disorders or to assess for any cognitive impairment.

117
Q

What is the management of delusions?

A

Pharmacological
Antipsychotic medication is the mainstay of treatment. The choice of medication depends on the underlying disorder.

Psychotherapy
Cognitive behavioral therapy (CBT) can be beneficial.

Psychoeducation
Providing information to the patient and their family about the nature and management of the disorder.

118
Q

Define Personality Disorder

A

Personality disorder (PD) is an umbrella term that covers a number of variations of maladaptive personality traits that cause significant psychosocial distress and interfere with everyday functioning.

It is characterised by patterns of thought, behaviour and emotions that differ from what is normally expected by society.

119
Q

What are the 3 Categories of personality disorders?

A

Suspicious (Class A)

Emotional or impulsive (Class B)

Anxious (Class C)

120
Q

What are the different suspicious personality disorders?

A

Paranoid personality disorder
Features difficulty in trusting or revealing personal information to others.

Schizoid personality disorder
Features a lack of interest or desire to form relationships with others and feelings that this is of no benefit to them.

Schizotypal personality disorder
Features unusual beliefs, thoughts and behaviours, as well as social anxiety that makes forming relationships difficult.

121
Q

What are the different Emotional / Impulsive personality disorders?

A

Borderline personality disorder
Features fluctuating strong emotions and difficulties with identity and maintaining healthy relationships.

Histrionic personality disorder
Features the need to be at the centre of attention and having to perform for others to maintain that attention.

Narcissistic personality disorder
Features feelings that they are special and need others to recognise this or else they get upset. They put themselves first.

122
Q

What are the different Anxious personality disorders?

A

Avoidant personality disorder
Features severe anxiety about rejection or disapproval and avoidance of social situations or relationships.

Dependent personality disorder
Features heavy reliance on others to make decisions and take responsibility for their lives, taking a very passive approach.

Obsessive compulsive personality disorder Features unrealistic expectations of how things should be done by themselves and others, and catastrophising about what will happen if these expectations are not met.

123
Q

What are the risk factors for personality disorders?

A
  • History of abuse
  • Family history of schizophrenia
  • Negative parenting interactions
  • Emotional/disruptive disorder in childhood
124
Q

What is the 1st line investigation for personality disorders?

A

Clinical Interview

Diagnosis of personality disorders is often difficult as as these patients don’t come to the doctor for help with their personality difficulties, and may have little or no insight into their personality issues.

Diagnosis will be based on symptoms detected in talks with the patient or present in their history, whether obtained from the patient him/herself or from others who know the patient (collateral sources).

125
Q

What is the management of personality disorders?

A

Cognitive behavioural therapy (CBT) and psychotherapy is the key management option of choice.

There are no medical treatments recommended for personality disorders. Although, they can co-exist with other conditions that can be treated with drugs.

126
Q

What are the side effects of SSRIs?

A
  • GI upset
  • Anxiety and agitation
  • QT interval prolongation (especially associated with citalopram)
  • Sexual dysfunction
  • Hyponatraemia
  • Gastric Ulcer

They should be omitted in mania and not given to children.

127
Q

What are the side effects of TCAs?

A

They are strongly associated with anti-cholinergic activity:

Urinary retention
Drowsiness
Blurred vision
Constipation
Dry mouth

128
Q

What conditions are TCAs contraindicated in?

A
  • Those with previous heart disease
  • Can exacerbate schizophrenia
  • May exacerbate long QT syndrome
  • May alter blood sugar in T1 and T2 diabetes mellitus
  • May precipitate urinary retention, so avoid in men with enlarged prostates
  • Those on CP450 medications or those with liver damage (as it uses the CP450 metabolic pathway)
129
Q

What conditions are SNRIs (Serotonin and norepinephrine re-uptake inhibitors) contraindicated in?

A

Those with a history of heart disease and high blood pressure

130
Q

What is the mechanism of action of Selective Serotonin Re-uptake Inhibitors?

A

SSRIs selectively inhibit the reuptake of serotonin (5-HT) at the presynaptic neuronal membrane, thus increasing serotonergic activity by allowing serotonin to remain in the synaptic cleft and restimulate post-synaptic receptors.

131
Q

What is the mechanism of action of Tricyclic Antidepressants?

A

Tricyclic antidepressants (TCAs) inhibit a membrane pump mechanism responsible for the re-uptake of transmitter amines (e.g noradrenaline/serotonin) into the presynaptic cleft.

Thus, their concentration at the synaptic clefts is increased, and they restimulate post-synaptic receptors.

Noradrenaline and serotonin are important in regulating mood, and their increased concentration in the synaptic cleft helps to reduce depressive symptoms.

132
Q

What is the mechanism of action of Atypical Antipsychotics?

A

Atypical antipsychotics antagonise dopamine receptors (D1, D2, D3, D4), serotonin receptors (5HT2A, 5HT2C, 5HT3, 5HT6), alpha-1 adrenergic receptors, histamine receptors (H1) and muscarinic receptors in the brain.

Antagonising dopamine D2 receptors in the mesolimbic pathway blocks dopamine from acting at post-synaptic receptors. The binding is dissociable so some dopamine neurotransmission still takes place.

Action on the serotonin 5HT2A receptors in the frontal cortex decreases adverse effects (compared to typical antipsychotics).

133
Q

What are some examples of typical antipsychotics?

A

Haloperidol

Chlorpromazine

134
Q

What is the mechanism of action of typical Antipsychotics?

A

Typical antipsychotics are dopamine (D2) receptor antagonists which block dopaminergic transmission in the mesolimbic pathways, leading to a reduction in psychotic/manic symptoms.

However, dopaminergic transmission is also blocked in other pathways such as the tuberoinfundibular and nigrostriatal pathways, leading to a range of side effects.

135
Q

What is Electroconvulsive Therapy (ECT)?

A

It is a extreme treatment method that induces a generalised seizure.

136
Q

What conditions is Electroconvulsive Therapy indicated for?

A

Its indicated for:

  • Severe depressive illness or refractory depression.
  • Catatonia.
  • A prolonged or severe episode of mania that does not respond to other treatments
137
Q

What does Electroconvulsive Therapy involve?

A
  • Electrodes are placed on the skull. Either on both side or only one side.
  • Patients are given a general anaesthetic and a muscle relaxant.
  • Subsequently, an electrical current is delivered to induce a generalised seizure.
  • The patient has about 6-12 sessions (twice a week). If the patient responds, then sessions are stopped.
138
Q

What are the possible complications of Electroconvulsive Therapy?

A

Immediate:

  • Cardiovascular instability - eg, arrhythmias and hypotension.
  • Status epilepticus.
  • Laryngospasm.
  • Peripheral nerve palsies.
  • Headache.
  • Nausea.

Long term

Possible issues with short and long term memory

139
Q

What is the definition of Phobias?

A

Phobias represent a cluster of anxiety disorders characterised by excessive and irrational fears

They encompass specific phobia, social anxiety disorder (SAD), and agoraphobia.

ICD-11 Criteria: Phobias are restricted to highly specific situations such as proximity to particular animals, heights, thunder, flying, exposure to blood, etc.

140
Q

What are the general features of Phobias?

A
  • Usually apparent in early adulthood.
  • Leads to avoidance behaviour.
  • Phobias of blood and bodily injury can result in bradycardia and hypotension upon exposure.
  • Severity is dependent on the effect on quality of life (e.g., pilots afraid of flying).
  • Always rule out comorbid depression.
141
Q

What is the definition of Agoraphobia?

A

Fear of open spaces and associated factors like the presence of crowds or the perceived difficulty of immediate easy escape to a safe place, usually home (may occur with or without panic disorder).

Typically begins in 20s or mid-thirties.
Onset may be gradual or precipitated by a sudden panic attack.
Comorbid depression is common (beware of reliance on drugs and alcohol for coping).

142
Q

What is the definition of Social Phobia / Social Anxiety Disorder?

A

Fear of scrutiny by others in relatively small groups (as opposed to crowds), resulting in the avoidance of social situations.

143
Q

What are the symptoms of Social Phobia / Social Anxiety Disorder?

A
  • Blushing
  • Fear of vomiting
  • Palpitations
  • Trembling
  • Sweating.
144
Q

What other features of Social Phobia are there?

A

It can be specific (public speaking) or generalised (any social setting)

Can be precipitated by stressful or humiliating experiences, parental death, separation, chronic stress.

May lead to alcohol or drug abuse (perpetuating the problem).

Mental state examination: may appear relaxed as the phobic object or situation is not present.

145
Q

What is the management of Phobias

A

1st Line
Cognitive Behavioural Therapy** for all Phobias:

  • Exposure techniques are the most widely used, aiming for systematic desensitization
  • Flooding (exposing someone with a fear of heights to a tower)
  • Modelling (individual observes therapist interacting with phobic stimulus).

If ineffective/severe functional impairment
SSRIs are first-line medical management

146
Q

What is the definition of Substance Misuse?

A

Also known as drug misuse, is the use of alcohol, illegal drugs, or over-the-counter or prescription medications in a way that they are not meant to be used and could be harmful to you or others around you

147
Q

What is the definition of Substance Abuse?

A

Also known as drug abuse is the patterned use of a drug in which the user consumes the substance in amounts or with methods which are harmful to themselves or others.

148
Q

What is the difference between Drug Abuse and Drug Misuse?

A

The key difference between a person who misuses drugs and a person who abuses drugs is their intent.

Someone who misuses a drug, takes the drug to treat a specific ailment.

Whereas the latter uses a drug to elicit certain feelings.

149
Q

What are the clinical features of opiate intoxication?

A

Drowsiness
Confusion
Decreased respiratory rate
Decreased heart rate
Constricted pupils

If the substance (e.g. heroin) has been injected, there may be evidence of needle marks (often referred to as ‘track marks’), abscesses or vein collapse at injection sites.

Opiates such as heroin act at opioid receptors.

150
Q

What are the clinical features of cannabis intoxication?

A

Drowsiness
Impaired memory
Slowed reflexes and motor skills
Bloodshot eyes
Increased appetite
Dry mouth
Increased heart rate
Paranoia

Cannabis acts at cannabinoid receptors.

151
Q

What are the clinical features of LSD intoxication?

(Lysergic Acid Dethylamide)

A

Labile mood
Hallucinations
Increased blood pressure
Increased heart rate
Increased temperature
Sweating
Insomnia
Dry mouth

LSD primarily acts at dopamine receptors.

152
Q

What are the clinical features of stimulant intoxication (e.g. Cocaine)?

A

Euphoria
Increased blood pressure
Increased heart rate
Increased temperature

Stimulants such as cocaine or methamphetamines can, in low doses, produce a feeling of increased concentration and focus.

Cocaine acts at dopamine receptors.
Methamphetamine acts at TAAR1 (Trace Amine-Associated Receptor 1) receptors.

Both increase the available amount of dopamine in the brain, producing the associated pleasurable effects of the drugs.

153
Q

What are the clinical features of opiate withdrawal?

A

Agitation
Anxiety
Muscle aches or cramps
Chills
Runny eyes and nose
Sweating
Yawning
Insomnia

Gastrointestinal disturbance such as abdominal cramps, nausea, diarrhoea and vomiting

Dilated pupils
‘Goose bump’ skin
Increased heart rate and blood pressure

Symptoms usually occur within 12 hours of stopping the drug. The withdrawal syndrome is unpleasant but not life-threatening.

Withdrawal from opiates will resolve spontaneously, but can also be pharmacologically supported by detoxification with methadone or buprenorphine.

154
Q

What is the management for cannabis, hallucinogen and stimulant abuse (including cocaine)?

A

Psychosocial Interventions are the main treatment.

These can include:
Counselling
Cognitive behavioural therapy
Supportive help (for example with housing and benefits).

155
Q

What is the management for opioid, alcohol and polydrug misuse?

A

Psychosocial Interventions combined with drug treatment:

Methadone and buprenorphine are both effective as maintenance treatment

156
Q

What are the risk factors for substance abuse/misuse?

A
  • History of alcohol or other drug misuse
  • History of mental illness
  • Male Sex
  • Family history of addiction
157
Q

What investigations are done for substance abuse/misuse?

A
  • Comprehensive history to establish the extent of the drug abuse problem / dependence.
  • Urine Toxicology
  • Blood tests - FBC, LFTs, U+Es, etc…
158
Q

What is the definition of an opioid overdose?

A

An overdose occurs when larger quantities than physically tolerated are taken.

This results in central nervous system and respiratory depression, miosis, and apnoea, which can be fatal if not treated rapidly.

159
Q

What are is the clinical presentation of an opioid overdose?

A
  • Central nervous system depression
  • Respiratory depression
  • Miosis
  • Decreased gastrointestinal motility
  • Relative bradycardia

Fresh needle marks / old track marks on the arms or legs can also suggest a possible diagnosis.

160
Q

What investigations are done for an opioid overdose?

A

1st Line:

  • Therapeutic Trial of Naloxone (Overdose patients will show improvement of symptoms)
  • ECG (can show things like QRS prolongation and evidence of myocardial ischaemia)
161
Q

What are some differentials for opioid overdose?

A

GHB or GBL overdose
Very closely mimic an opioid overdose, but will show little / no responce to naloxone.

Clonidine/Imidazolines overdose
Presents with more profound bradycardia and hypotension than opioid overdose. And will also show only limited responce to naloxone.

Antipsychotic Overdose
Presents with hypotension and tachycardia, but will not have the profound bradypnoea seen in opioid overdose. No response to naloxone.

162
Q

What is the management of an opioid overdose?

A

Ventilatory Support
Is the most important intervention, and must be done as fast as possible.

Admission of Naloxone
Usually done IV
If needed, repeated doses of Naloxone can be done every 2-3 mins

163
Q

What is the definition of harmful drinking?

A

It’s defined as a pattern of alcohol consumption causing health problems directly related to alcohol.

This could include psychological problems such as depression, alcohol-related accidents or physical illness such as acute pancreatitis.

164
Q

What is the definition of Alcohol Dependence?

A

It’s characterised by craving, tolerance, a preoccupation with alcohol and continued drinking in spite of harmful consequences (for example, liver disease or depression caused by drinking).

165
Q

What is the definition of an Alcohol use disorder?

A

It’s defined as clinically significant impairment or psychosocial stress in the previous 12 months as a direct result from alcohol?

This term encompasses both harmful drinking and alcohol dependence.

166
Q

What are the risk factors for developing an alcohol use disorder?

A
  • Family history of alcohol-use disorder
  • Antisocial behaviour (pre-morbid)
  • High trait anxiety level
  • Low responce to the effects of alcohol
167
Q

How is an alcohol use disorder diagnosed?

A

It is diagnosed by the presence of at least 2 or more of the 11 DSM-5 screening criteria over a 12 month period.

168
Q

When do Alcohol Withdrawal Symptoms typically present?

A

6-12 hours after the last drin

169
Q

What is the clinical presentation of Alcohol Withdrawl?

A

Simple Withdrawal

Insomnia
Tremors
Anxiety
Agitation
Nausea and vomiting
Sweating
Palpitations

170
Q

What is Alcohol Hallucinosis and when does it present?

A

It’s a rare complication of alcohol withdrawal characterised predominantly by auditory hallucinations

It typically presents 12-24 hours post drink

171
Q

What is the presentation of Delerium Tremens?

A

Is another rare complication of alcohol withdrawal and typically presents 72 hours post drink

Delusions
Confusion
Seizures
Tachycardia
Hypertension
Hyperthermia

172
Q

What are some differentials of alcohol withdrawal?

A

Benzodiazepine withdrawal
Similar symptoms to alcohol withdrawal, but may also include perceptual changes, depersonalization, derealization, hypersensitivity to light and sound, and numbness/tingling in extremities.

Drug-induced delirium
Characterised by fluctuating mental status, inattention, and a disturbed sleep-wake cycle.

Other conditions causing delirium

173
Q

What are the indications for inpatient withdrawal treatment?

A
  • Patients drinking >30 units per day
  • Scoring over 30 on the SADQ score
  • High risk of alcohol withdrawal seizures (previous alcohol withdrawal seizures or delirium tremens, or history of epilepsy)
  • Concurrent withdrawal from benzodiazepines
  • Significant medical or psychiatric comorbidity
  • Vulnerable patients
  • Patients under 18
174
Q

What investigations are done for alcohol withdrawal / chronic alcoholism?

A
  • AUDIT and SADQ questionnaires to assess the severity of alcohol misuse.
  • Blood tests to assess liver function and electrolyte balance.
  • Neuroimaging may be considered in cases of persistent confusion or seizures.
175
Q

What is the management for Alcohol Withdrawal?

A

Non-Pharmacological

  • Assisted alcohol withdrawal for patients drinking over 15 units per day or scoring over 20 on the AUDIT questionnaire.
  • Following assisted withdrawal an intensive psychosocial support programme and appropriate medication should be initiated.
  • For patients with mild alcohol dependence medically-assisted withdrawal may not be required. Psychological interventions (such as cognitive behavioural therapy) should be offered first line.

Pharmacological

  • Prescription of chlordiazepoxide in a reducing regimen, guided by the CIWA score.
  • Rapid-acting benzodiazepines (such as intravenous lorazepam) for patients with alcohol-withdrawal seizures.
  • Pabrinex (1 pair of ampoules once daily) to prevent Wernicke’s encephalopathy. In the presence of Wernicke’s encephalopathy symptoms, two pairs of ampoules TDS should be prescribed.
176
Q

What is the management for Delerium Tremens?

A

Oral lorazepam as the first-line treatment for delirium tremens.

With parenteral lorazepam offered if oral treatment is declined or symptoms persist.

177
Q

What is the definition of Self-Harm?

A

Self-harm refers to an intentional act of self-poisoning or self-injury, irrespective of the motivation or apparent purpose of the act.

It is an expression of emotional distress

Deliberate self-harm is not an attempt at suicide in most cases. It is usually an attempt to maintain control in very stressful situations

178
Q

What different types of Self-Harm are there?

A
  • A behaviour (eg, self-cutting) intended to cause self-harm.
  • Ingesting a substance in excess of the prescribed or generally recognised therapeutic dose.
  • Ingesting a recreational or illicit drug that was an act that the person regarded as self-harm.
  • Ingesting a non-ingestible substance or object.
179
Q

What is the epidemiology of Self-Harm?

A

It’s most common among younger people, especially younger / teenage girls.

Self-harm increases the likelihood that the person will eventually die by suicide by between 50- and 100-fold.

180
Q

What are the risk factors for self-harm?

A
  • Younger age
  • Psychiatric problems like borderline personality disorder, depression, bipolar disorder, schizophrenia, eating disorders, drug misuse and alcohol abuse
  • Domestic violence
  • Socio-economic disadvantage
181
Q

What is the initial management of Self-Harm?

A

Urgent referral to the emergency department if required.

For drugs taken in overdose / poisoning; Activated charcoal is the first line management (preferably within one hour of ingestion).

182
Q

What further interventions should be offered to those who self-harm?

A

Assessment of needs
Includes an evaluation of the social, psychological and motivational factors specific to the act of self-harm, current suicidal intent and hopelessness, as well as a full mental health and social needs assessment.

Suicide Risk Assessment

Psychological Intervention
NICE recommends 3-12 sessions specifically structured for self-harm

Dialectical behaviour therapy (DBT)
It’s based on cognitive behavioural therapy (CBT), but is specially adapted for people who feel emotions very intensely.

183
Q

What is the epidemiology of a paracetamol overdose?

A

Paracetamol is the most common agent for intentional self-harm in the UK.

Paracetamol overdose accounts for 44% of all adult self-poisoning cases in the UK.

184
Q

What is the pathophysiology of a paracetamol overdose?

A

A paracetamol overdose involves the buildup of a toxic substance called NAPQI (N-acetyl-p-benzoquinone-imine).

Normally, NAPQI is inactivated by glutathione, but during an overdose, glutathione stores are rapidly depleted, leaving NAPQI unmetabolised and resulting in liver and kidney damage.

185
Q

What are the clinical features of a paracetamol overdose?

A

No symptoms
Nausea and vomiting
Loin pain
Haematuria and proteinuria
Jaundice
Abdominal pain
Coma
Severe metabolic acidosis

186
Q

What are some differentials of a paracetamol overdose?

A

Acute gastritis/gastroenteritis

Renal colic

Liver diseases

Metabolic acidosis

187
Q

What investigations are done for a paracetamol overdose?

A

Paracetamol level
Full Blood Count (FBC)
Urea and Electrolytes
Clotting Screen
Liver Function Tests
Venous Blood Gas

Decisions on treatment are guided by a nomogram which plots paracetamol levels.

188
Q

What is the management of a paracetamol overdose for Ingestion less than 1 hour ago + dose >150mg/kg?

A

Administer activated charcoal

189
Q

What is the management of a paracetamol overdose for Ingestion <4 hours ago?

A

Wait until 4 hours to take a level and treat with N-acetylcysteine based on level

190
Q

What is the management of a paracetamol overdose for Ingestion within 4-8 hours + dose >150mg/kg?

A

Start N-acetylcysteine immediately if there is going to be a delay of ≥8 hours in obtaining the paracetamol level

191
Q

What is the management of a paracetamol overdose for Ingestion within 8-24 hours + dose >150mg/kg?

A

Start N-acetylcysteine immediately

192
Q

What is the definition of Suicide?

A

It can be described as a fatal act of self-harm initiated with the intention of ending one’s own life

193
Q

What are some factors that increase the risk of someone attempting suicide?

A
  • Male sex
  • History of deliberate self-harm
  • History of alcohol or drug misuse
  • History of mental illness
  • Depression
  • Schizophrenia: NICE estimates that 10% of people with schizophrenia will complete suicide
  • History of chronic disease
  • Advancing age
  • Unemployment or social isolation/living alone
  • Being unmarried, divorced or widowed
194
Q

What are the factors that increase the risk of someone completing a suicide attempt in the future (if they have already attempted it once?)

A
  • Efforts to avoid discovery
  • Planning
  • Leaving a written note
  • Final acts such as sorting out finances
  • Violent method
195
Q

What are some protective factors for Suicide?

A
  • A strong religious faith.
  • Family support to find alternative solutions to their problems.
  • Having children at home.
  • A sense of responsibility for others.
  • Problem-solving skills.
196
Q

What is the best way of establishing whether a patient has suicidal intent?

A

A comprehensive clinical interview

(NICE recommends that no score systems should be used)

197
Q

What does a suicide risk assessment involve?

A

Introduction
Establish rapport, develop a trusting relationship.
Establish current anxieties or problems.
Observe behaviour and be alert to any mismatch between words and behaviour. Suicidal intent be denied.

Assess Risk Factors

Assess Current Plans and Intent
‘Red flags’ to consider may include a sense of hopelessness, a feeling of entrapment, well-formed plans, perception of no social support, distressing psychotic phenomena and significant pain/physical chronic illness.

Assess Needs
Social problems.
Untreated mental health disorders.
Physical symptoms and disorders.
Coping strategies.
Skills, strengths and assets.
Psychosocial and occupational functioning.
Personal and financial difficulties.
Needs of dependants.

198
Q

What does the management of suicidal patients involve?

A

Once a risk assessment has been performed, subsequent action will depend on the level of risk believed to be present.

Formulate a Care Plan (including a risk management and crisis plan)

Specific treatment e.g.
Medication
Counselling
Cognitive behavioural therapy (CBT)
Dialectical behaviour therapy (DBT)

Provide follow up at regular intervals

199
Q

What is the risk of prescribing an anti-depressant to someone who is suicidal?

A

As in the early stage of being on an antidepressant, it can increase the risk of suicide

200
Q

What is the 1983 Mental Health Act (MHA)?

A

It provides legal structures to define and manage procedures associated with the treatment and rights of people with mental health disorders.

201
Q

What is the definition of ‘Involuntary Commitment’ or Sectioning?

A

It is a legal process through which an individual who is deemed by a qualified agent to have symptoms of severe mental disorder is detained in a psychiatric hospital where they can be treated involuntarily.

202
Q

What is in Section 2 of the MHA?

A

Allows for admission for mental health assessment for up to 28 days, non-renewable.

203
Q

What is in Section 3 of the MHA?

A

Permits admission for treatment lasting up to 6 months, with the provision for renewal.

204
Q

What is in Section 4 of the MHA?

A

Designed for emergencies when applying Section 2 would cause an unnecessary delay.

205
Q

What is in Section 5(2) of the MHA?

A

Enables a doctor to legally detain a voluntary patient in the hospital for a period of 72 hours.

206
Q

What is in Section 5(4) of the MHA?

A

Section 5(4) is comparable to a Section 5(2) but is enacted by registered nurses and has a duration of 6 hours.

207
Q

What is in Section 17 of the MHA?

A

Allows for a Supervised Community Treatment (also known as a Community Treatment Order).

208
Q

What is in Section 135 of the MHA?

A

Court order enabling the police to enter a property to escort a person to a Place of Safety (either the police station or, more commonly, an Accident and Emergency Department (A&E)).

209
Q

What is in Section 136 of the MHA?

A

Provides police officers the authority to take an individual, who seems to be suffering from a mental disorder and is in a public place, to a Place of Safety.

210
Q

What is the definition of Wernicke’s encephalopathy?

A

Wernicke’s encephalopathy is an acute neurological syndrome resulting from a deficiency in thiamine (vitamin B1)

211
Q

What is the classic Triad of Wernicke’s encephalopathy?

A

Mental status changes (confusion)
Ataxia
Ophthalmoplegia/nystagmus

All 3 signs aren’t always present

212
Q

What is the cause of Wernicke’s encephalopathy?

A

Thiamine (vitamin B1) deficiency, most commonly due to chronic alcohol abuse.

Thiamine is critical for brain cell function, and deficiency can lead to neuronal death.

213
Q

What are some differentials for Wernicke’s encephalopathy?

A

Alcohol withdrawal syndrome

Hepatic encephalopathy

Stroke

Cerebellar disorders

214
Q

What are the first line Investigations for Wernicke’s encephalopathy?

A

Its almost always diagnosed clinically but investigations can support the diagnosis:

  • Serum Thiamine
  • Blood tests: FBC, Urea and Electrolytes, Liver Profile, Clotting, Bone Profile, Magnesium
  • Neuroimaging (MRI can show typical changes in specific regions of the brain).
215
Q

What is the management of Wernicke’s encephalopathy?

A

Urgent administration of parenteral (not oral) thiamine for a minimum of 5 days.

Oral treatment should follow parenteral treatment.

216
Q

What is the risk of giving glucose to those suspected of having Wernicke’s encephalopathy?

A

As Glucose metabolism requires thiamine and such metabolisis will further reduce thiamine levels.

Thiamine must be administered before or concurrently with any glucose administration.

217
Q

What is the definition of Korsakoff’s Syndrome?

A

It’s a chronic memory disorder, often occurring as a late complication of untreated Wernicke’s encephalopathy.

It is characterised by profound anterograde amnesia, limited retrograde amnesia, and confabulation

218
Q

Who is most likely to suffer from Korsakoff’s Syndrome?

A

Chronic alcoholics

Can also occur in non-alcoholics with severe malnutrition or malabsorption conditions leading to thiamine deficiency.

219
Q

What causes Korsakoff’s Syndrome?

A

It is the result of degeneration of the mammillary bodies and other areas within the brain due to prolonged thiamine deficiency.

The mammillary bodies are part of the circuit of Papez which plays a role in memory formation.

220
Q

What is the clinical presentation of Korsakoff’s Syndrome?

A

Profound anterograde amnesia

Limited retrograde amnesia

Confabulation (patients fabricate memories to mask their memory deficit)

221
Q

What does the management of Korsakoff’s Syndrome involve?

A

Ongoing thiamine supplementation: To replenish the body’s stores and prevent further neuronal damage.

Cognitive rehabilitation: To improve residual cognitive function and adapt to the memory loss.

Careful management of the patient’s environment: To reduce confusion and disorientation.

Treatment of underlying causes, like alcoholism: This includes counselling and support to cease alcohol consumption.

Korsakoff Syndrome causes permanent neurological damage due to its chronic nature, therefore patients rarely recover

222
Q

What are the most common causes of cognitive impairment?

A

Common

Alzheimer’s disease
Depression

Infrequent

Vascular dementia
Fibromyalgia
Lewy body dementia
Chronic fatigue syndrome
Normal pressure hydrocephalus

Rare

Frontotemporal lobar degeneration
Huntington’s disease
Creutzfeldt-Jakob disease
Duchenne muscular dystrophy
Wilson’s disease

223
Q

What is Cognitive Behavioural Therapy?

A

CBT is a term that has come to be used to refer to behavioural therapy, cognitive therapy and therapy that combines both of these approaches.

224
Q

What is the definition of Behavioural Therapy?

A

It is a treatment approach based on clinically applying theories of behaviour that have been extensively researched over many years.

225
Q

What is the definition of Cognitive Therapy?

A

Is a treatment focussing on the role of cognitions in the development of emotional disorders.

226
Q

What conditions can be treated with CBT?

A

Depression

Generalised anxiety disorder (GAD) and panic disorder

OCD

Body dysmorphic disorder (BDD)

Post-traumatic stress disorder (PTSD)

227
Q

What does Cognitive Behavioural Therapy Involve?

A

The therapy is focused on the present rather than the past; it is orientated towards solving the client’s current problems and initiating behavioural change so that the client can function better in the future, and solve their problems using their won resources.

Typically, sessions usually last about an hour and are once a week. A course of 10-15 sessions is the average.

228
Q

What are Hypnotic Drugs?

A

Hypnotics are a class of drugs that will sedate the patient when given during the day.

229
Q

What are anxiolytic (‘sedatives) Drugs?

A

Anxiolytics are drugs that will induce sleep when given at night.

230
Q

What is the most common anxiolytic/hypnotic drug?

A

Benzodiazepines

Fall into the category of both anxiolytic and hypnotic drugs

231
Q

What is the mode of action of Benzodiazepines?

A

Benzodiazepines enhance the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) by increasing the frequency of chloride channels.

232
Q

How long can Benzodiazepines be prescribed for?

A

2-4 weeks

This is because patients commonly develop a tolerance and dependence to benzodiazepines.

233
Q

What are the clinical symptoms of Benzodiazepine Withdrawal Syndrome?

A

It presents very similarly to Alcohol Withdrawal syndrome

insomnia
irritability
anxiety
tremor
loss of appetite
tinnitus
perspiration
perceptual disturbances
seizures

234
Q
A