Mental Health Conditions MLA Flashcards

1
Q

What is acute stress reaction?

A

Acute stress disorder is defined as an acute stress reaction that occurs in the first 4 weeks after a person has been exposed to a traumatic event (threatened death, serious injury e.g. road traffic accident, sexual assault etc). This is in contrast to post-traumatic stress disorder (PTSD) which is diagnosed after 4 weeks.

A transient disorder that develops in an individual with no other apparent mental disorder in response to exceptional physical and/or mental stress; usually subsides within hours or days. It should last no more than one month.

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2
Q

What are the features of acute stress reaction?

A

Features include:

  • intrusive thoughts e.g. flashbacks, nightmares
  • dissociation e.g. ‘being in a daze’, time slowing
  • negative mood
  • avoidance
  • arousal e.g. hypervigilance, sleep disturbance
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3
Q

What is the management of acute stress reaction?

A

Management:

  • trauma-focused cognitive-behavioural therapy (CBT) is usually used in first line
  • benzodiazepines
    • sometimes used for acute symptoms e.g. agitation, sleep disturbance
    • should only be used with caution due to addictive potential and concerns that they may be detrimental to adaptation
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4
Q

What are differentials for acute stress reaction?

A
  • Differentials for this condition can include adjustment disorder. The key difference between these conditions is that an acute stress reaction will typically follow a highly stressful event, whereas with adjustment disorder, the stressor need not be severe or outside the “normal” human experience. For example, the difference between seeing a fatal car accident vs being made redundant.
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5
Q

Explain alcoholic liver disease

A

Alcoholic liver disease covers a spectrum of conditions:

  • alcoholic fatty liver disease
  • alcoholic hepatitis
  • cirrhosis
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6
Q

Patient symptoms and signs with alcoholic hepatitis?

A

Patients look like: (symptoms)

  • Malaise, high TPR (temperature, pulse, respiratory rate)
  • Anorexia
  • D&V (diarrhoea and vomiting)
  • Tender hepatomegaly +/- jaundice
  • Bleeding
  • Ascites

Selected investigation findings: (signs)

  • gamma-GT is characteristically elevated
  • the ratio of AST:ALT is normally > 2, a ratio of > 3 is strongly suggestive of acute alcoholic hepatitis
  • High WCC
  • Low platelets
  • High INR
  • High AST
  • High MCV
  • High urea
  • Jaundice, encephalopathy or coagulopathy = SEVERE hepatitis
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7
Q

What is the management for alcoholic hepatitis?

A

Selected management notes for alcoholic hepatitis:

  • glucocorticoids (e.g. prednisolone 40mg/d for 5 days) are often used during acute episodes of alcoholic hepatitis
    • Maddrey’s discriminant function (DF) is often used during acute episodes to determine who would benefit from glucocorticoid therapy
    • it is calculated by a formula using prothrombin time and bilirubin concentration
  • pentoxyphylline is also sometimes used
    • the STOPAH study (see reference) compared the two common treatments for alcoholic hepatitis, pentoxyphylline and prednisolone. It showed that prednisolone improved survival at 28 days and that pentoxyphylline did not improve outcomes
  • Vitamins
    • Vitamin K -> 10mg/d IV for 3 days
    • Thiamine -> 100mg/d PO (high dose can be given by IV this is Pabrinex)
  • Optimise nutrition 35-40kcal/kg/d (use ideal body weight for calculations)
  • Don’t use low-protein diets as prevents sepsis, encephalopathy, death
  • Daily: weight, LFT, U&Es, INR
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8
Q

What is the prognosis of alcoholic hepatitis?

A

Prognosis

  • Mild episodes hardly affect mortality if severe mortality is roughly 50% at 30 days
  • 1 year after admission for alcoholic hepatitis -> 40% are dead
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9
Q

What is anxiety disorder: generalised (GAD)? (& epidemiology)

A

Anxiety is a common disorder that can present in multiple ways. NICE define the central feature as an ‘excessive worry about a number of different events associated with heightened tension.’

Always look for a potential physical cause when considering a psychiatric diagnosis. In anxiety disorders, important alternative causes include hyperthyroidism, cardiac disease and medication-induced anxiety (NICE). Medications that may trigger anxiety include salbutamol, theophylline, corticosteroids, antidepressants and caffeine.

ICD-10 Criteria

Generalized and persistent ‘free floating’ anxiety symptoms involving elements of:

  • 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)

Epidemiology

  • 1.6% suffering from GAD at any one point
  • Very rarely begins after 35
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10
Q

What is the management of anxiety disorder: generalised (GAD)?

A

Management of GAD

NICE suggest a stepwise approach:

  • step 1: education about GAD + active monitoring
  • step 2: low-intensity psychological interventions (individual non-facilitated self-help or individual guided self-help or psychoeducational groups)
  • step 3: high-intensity psychological interventions (cognitive behavioural therapy or applied relaxation) or drug treatment. See drug treatment below for more information
  • step 4: highly specialist input e.g. Multi-agency teams

Drug treatment

  • NICE suggest sertraline should be considered the first-line SSRI
  • if sertraline is ineffective, offer an alternative SSRI or a serotonin–noradrenaline reuptake inhibitor (SNRI)
    • examples of SNRIs include duloxetine and venlafaxine
  • If the person cannot tolerate SSRIs or SNRIs, consider offering pregabalin
  • interestingly for patients under the age of 30 years NICE recommend you warn patients of the increased risk of suicidal thinking and self-harm. Weekly follow-up is recommended for the first month

QUESMED

General Management

  • Most can be treated in primary care setting
  • Advice and reassurance can help early or mild problems from worsening (psycho-education)
  • Counselling alone may be very effective – addresses patients worries (reassure about somatic symptoms)
  • Self help materials
  • CBT has good evidence
  • Other therapies: anxiety management training, relaxation techniques, autogenic training (self-monitoring anxiety and applying relaxation techniques), brief focal psychotherapy, marital or familial therapy

Note on sedatives

  • Benzodiazapines should not be prescribed for more than 10 days due to risk of dependency and sedation. Use only to overcome symptoms so severe they obstruct initiation of more appropriate psychological treatment
  • Diazepam preferred due to longer half life (less risk of withdrawal symptoms with neurotic symptoms, neurological symptoms like ataxia, paraesthesia, hyperacusis and other major symptoms such as hallucinations, psychosis and epilepsy)

Drug Therapy

  • First line drug is an SSRI or SNRI
  • SSRI combined with CBT may be superior to either alone
  • Also, Busipirone (5HT1A¬ agonist) is suitable for short term management
    • Delayed onset of action
    • Diminished efficacy in previous benzo users
    • Side effects: dizziness, headache and nausea
    • Minimal sedation
  • B-blockers effective in patients with somatic anxiety symptoms (CI in asthma and heart block)
  • Low-dose antipsychotics can also be used
  • Pregabalin may also be of use
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11
Q

What is anxiety disorder: post-common stress disorder?

A

Anxiety is a common disorder that can present in multiple ways. NICE define the central feature as an ‘excessive worry about a number of different events associated with heightened tension.’

Always look for a potential physical cause when considering a psychiatric diagnosis. In anxiety disorders, important alternative causes include hyperthyroidism, cardiac disease and medication-induced anxiety (NICE). Medications that may trigger anxiety include salbutamol, theophylline, corticosteroids, antidepressants and caffeine.

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12
Q

What is the management of anxiety disorder: post-traumatic stress disorder?

A

Management

Again a stepwise approach:

  • step 1: recognition and diagnosis
  • step 2: treatment in primary care - see below
  • step 3: review and consideration of alternative treatments
  • step 4: review and referral to specialist mental health services
  • rstep 5: care in specialist mental health services

Treatment in primary care

  • NICE recommend either cognitive behavioural therapy or drug treatment
  • SSRIs are first line. If contraindicated or no response after 12 weeks then imipramine or clomipramine should be offered
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13
Q

What are the clinical features of GAD?

A

Clinical features

  • Depersonalization (altered or lost sense of personal reality or identity) and derealisation (surroundings feel unreal). Note this is also seen in depression, schizo, alcohol, drugs, epilepsy
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14
Q

What are the differential diagnosis’ of general anxiety disorder (GAD)?

A

Differential Diagnosis

  • Hyperthyroidism (look for goitre, tremor, tachycardia, weight loss, arrhythmia, exophthalmos)
  • Substance misuse (intoxication – amphetamines; withdrawal – benzo, alcohol)
  • Excess caffeine
  • Depression: anxiety common feature of depression and likewise. Which came first and which is currently more prominent are useful clues. If both, diagnose mixed anxiety and depressive disorder
  • Anxious (avoidant) personality disorder: patient describes themselves as an anxious person with no recent major increase in anxiety levels. (note this disorder can predispose)
  • Dementia (early)
  • Schizophrenia (early)
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15
Q

What is the prognosis of GAD?

A

Prognosis

  • The more chronic the condition, the worse the prognosis
  • Stable premorbid personality good prognostic sign
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16
Q

What are the features of panic disorder (& epidemiology & ICD-10)

A

Features of Panic Disorder

  • Breathing difficulties
  • Chest discomfort
  • Palpitations
  • Tingling or numbness in hands, feet or around the mouth: Hyperventilation blows off CO2, raising pH, Calcium binds to albumin leads to hypocalcaemia. If extreme, carpopedal spasm (curling of fingers and toes can occur)
  • Shaking, sweating, dizziness
  • Depersonalization/ derealisation
  • Can lead to fear of situation where panic attacks occur or agoraphobia
  • Conditioned fear of fear pattern develops

ICD-10 criteria

  • Recurrent attacks of severe anxiety not restricted to any particular situation or set of circumstances and therefore unpredictable
  • Secondary fears of dying, losing control or going mad
  • Attacks usually last for minutes; often there is a crescendo of fear and autonomic symptoms
  • Comparative freedom from anxiety symptoms between attacks (but anticipatory anxiety is common)

Epidemiology of Panic Disorder

  • 1-2% in general population
  • 2-3x more common in females
  • Bimodal: peaks at 20yo and 50yo
  • Agoraphobia occurs in 30-50%
  • Risk of attempted suicide is raised when comorbid depression, alcohol misuse or substance misuse
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17
Q

What are the differential diagnosis for panic disorder?

A

Differential Diagnosis for Panic Disorder

  • Other anxiety disorders: GAD and agoraphobia
  • Depression (if depression precedes or criteria for depression fulfilled, it takes precedence)
  • Alcohol or drug withdrawal
  • Organic causes: CVS or respiratory disease. Others: hypoglycaemia, hyperthyroidism. Rarely: pheochromocytoma.
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18
Q

What is the psychological management of panic disorder?

A

Psychological Management of Panic Disorder

  • Reassurance
  • CBT effective in 80-100%
  • CBT is first line
  • Initial education about nature of panic attacks and fear of fear cycles
  • Cognitive restructuring; detecting flaws in logic
  • Interoceptive exposure techniques such as controlled exposure to somatic symptoms(breathing in CO2 and physical exercise)
  • Secondary agoraphobic avoidance: treat by situational exposure and anxiety management techniques
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19
Q

What is the drug management of panic disorders?

A

Drug management of Panic Disorder

  • SSRIs are first line drug treatment (but 2nd line to CBT)
  • Also, clomipramine (tricyclic with similar action on serotonin) is effective Prognosis
  • 50-60% remit with medication; 80-100% with CBT
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20
Q

What are the features of mixed anxiety and depressive disorder?

A

Features of Mixed Anxiety and Depressive Disorder

  • ICD-10 criteria: symptoms of anxiety and depression are both present but neither clearly predominates
  • Treat with counselling, cognitive therapy or psychotherapy, especially interpersonal therapy
  • Treating the depression usually relieves anxiety symptoms (SSRIs are best)
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21
Q

What are the features of specific/isolated phobias?

A

Features of Specific/isolated phobias

  • ICD-10 criteria: restricted to highly specific situations such as proximity to particular animals, heights, thunder, flying, blood etc
  • Often clear in early adulthood
  • Result in avoidance
  • Phobias of blood and bodily injury lead to bradycardia and hypotension upon exposure
  • Severity depends on effect on quality of life ( pilots afraid of flying)
  • Always exclude co-morbid depression
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22
Q

What are features of agoraphobia?

A

Features of Agoraphobia

  • ICD-10 criteria: Fear not only open spaces but also of related aspects, such as the presence of crowds and difficulty of immediate easy escape back to a safe place, usually home (may occur with or without panic disorder)
  • Commonly in 20s or mid-thirties
  • May be gradual or precipitated by a sudden panic attack
  • Comorbid depression is common (be wary of drugs and alcohol to overcome)
  • Also higher incidence of sexual problems
  • Differentials:
    • Depression
    • Social phobia
    • Obsessive Compulsive Disorder
    • Schizophrenia (may stay because of social withdrawal or as a way of avoiding perceived persecutors)
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23
Q

What are features of social phobia?

A

Features of Social Phobia

  • Most common anxiety disorder
  • ICD-10 criteria: Fear of scrutiny by other people in comparatively small groups (as opposed to crowds), leading to avoidance of social situations
  • Comparatively small = around 5-6 people (Usually 1-2 is fine)
  • May be specific (public speaking) or generalized (any social setting)
  • Physical symptoms: blushing, fear of vomiting
  • Symptoms include blushing (characteristic), palpitations, trembling, sweating
  • Can be precipitated by stressful or humiliating experiences, death of a parent, separation, chronic stress
  • Genetic vulnerability
  • May abuse alcohol or drugs (perpetuating problem)
  • Mental state examination: may appear relaxed as phobic object or situation not present
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24
Q

What are the differentials for phobias?

A

Differentials for Phobias

  • Shyness (in social phobia, there is fear)
  • Agoraphobia
  • Anxious personality disorder
  • Poor social skills/autistic spectrum disorders (will not show good skills when relaxed)
  • Benign essential tremor (familial, worse in social situations, responds to benzo and alcohol)
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25
Q

What are investigations for phobias?

A

Investigations of Phobias

  • History and Examination
  • m
  • Social and occupational assessments for effect on quality of life
  • Collateral History
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26
Q

What is the management for phobias?

A

Management of Phobias

Behavioural therapy is treatment of choice,

Exposure techniques most widely used aiming to reach systematic desensitization (using a graded hierarchy approach for e.g.)

  • Flooding (taking someone with fear of heights to a tower),
  • Modelling (individual observes therapist engaging with phobic stimulus)
  • Agoraphobia and panic disorders: CBT treatment of choice
  • Social phobia: CBT is the treatment of choice Drug management
  • SSRIs and MAOIs (phenelzine) most useful in agoraphobia and social phobia
  • Tricyclic antidepressants best for those with depressive component
  • Agoraphobia + panic disorder: CBT first line and SSRI 2nd line
  • Benzodiazepines can be used before a phobic situation
  • B-blockers are effective if somatic symptoms predominate Prognosis
  • Animal phobias have the best outcome
  • Agoraphobias do worse

Early diagnosis and treatment are essential (shorter à better

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27
Q

What is OCD?

A

OCD

Obsessive-compulsive disorder (OCD) is characterised by the presence of either obsessions or compulsions, but commonly both. The symptoms can cause significant functional impairment and/ or distress.

An obsession is defined as an unwanted intrusive thought, image or urge that repeatedly enters the person’s mind. Compulsions are repetitive behaviours or mental acts that the person feels driven to perform. A compulsion can either be overt and observable by others, such as checking that a door is locked, or a covert mental act that cannot be observed, such as repeating a certain phrase in one’s mind.

It is thought that 1 to 2% of the population have OCD, although some studies have estimated 2 to 3%.

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28
Q

What is the aetiology behind OCD?

A

s

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29
Q

What are some associations with OCD?

A

Associations

  • depression (30%)
  • schizophrenia (3%)
  • Sydenham’s chorea
  • Tourette’s syndrome
  • anorexia nervosa
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30
Q

What is the management of OCD?

A

Management

  • If functional impairment is mild
    • low-intensity psychological treatments: cognitive behavioural therapy (CBT) including exposure and response prevention (ERP)
    • If this is insufficient or can’t engage in psychological therapy, then offer choice of either a course of an SSRI or more intensive CBT (including ERP)
  • If moderate functional impairment
    • offer a choice of either a course of an SSRI (any SSRI for OCD but fluoxetine specifically for body dysmorphic disorder) or more intensive CBT (including ERP)
  • If severe functional impairment
    • offer combined treatment with an SSRI and CBT (including ERP)

Notes on treatments

  • ERP is a psychological method which involves exposing a patient to an anxiety provoking situation (e.g. for someone with OCD, having dirty hands) and then stopping them engaging in their usual safety behaviour (e.g. washing their hands). This helps them confront their anxiety and the habituation leads to the eventual extinction of the response
  • if treatment with SSRI is effective then continue for at least 12 months to prevent relapse and allow time for improvement
  • If SSRI ineffective or not tolerated try either another SSRI
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31
Q

What is anxiety?

A

Definition

Anxiety disorders include Generalized Anxiety disorder, phobias, panic disorder, Obsessive Compulsive Disorder and Post-traumatic Stress Disorder

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32
Q

What is the concept of neuroses? (anxiety)

A

Concept of neuroses

  • Symptoms that are both understandable and with which one can empathize
  • Insight is maintained
  • This is as opposed to delusions which are not understandable or cannot be empathised with
  • Neuroses are quantitively but not qualitatively different from normal
  • Neuroses different to ‘neurotic’ individuals who often suffer from lifelong personality difficulties
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33
Q

What is the epidemiology behind anxiety?

A

Epidemiology

  • Most predominantly female
  • Affects up to 10% of all individuals
  • Comorbidity with depression, substance misuse and personality disorder is common
  • If individual presents after age 35-40 years, it is more likely due to depressive disorder or organic disease
  • Associated Factors: Lower social class, unemployment, divorced, renting rather than owning, no educational qualifications, urban living Aetiology
  • Genetics: family history often seen, people with high neuroticism scores more likely
  • Early experiences and life events:
    • Childhood adversity predispose
    • Life events (WW1 trenches most extreme example)
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34
Q

What are some symptoms of anxiety?

A

Symptoms of Anxiety

  • Psychological: Fears, worries, poor concentration, irritability, depersonalization, derealisation, insomnia (can’t fall asleep), night terrors
  • Motor symptoms: Restlessness, fidgeting, feeling on edge
  • Neuromuscular: tremor, tension headache, muscle ache, dizziness, tinnitus
  • GI: Dry mouth, can’t swallow, nausea, indigestion, butterflies, flatulence, frequent or loose motions
  • CVS: Chest discomfort, palpitation
  • Respiratory: Difficulty inhaling, Tight/constricted chest
  • GI: Urinary frequency, erectile dysfunction, Amenorrhoea
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35
Q

What is attention deficit hyperactivity disorder? (ADHD)

A

Attention deficit hyperactivity disorder

March 2018 saw NICE issue new guidance around recognising and managing attention deficit hyperactivity disorder (ADHD). This condition can inflict significant morbidity on a child’s life and thus has consequences into adulthood, making good diagnosis and treatment vital.

DSM-V defines ADHD as a condition incorporating features relating to inattention and/or hyperactivity/impulsivity that are persistent. Like many paediatric conditions, developmental delay has to be an element. Six of these features have to be present for children up to the age of 16 years; in those aged 17 or over, the threshold is five features (Table below).

QUESMED
Attention deficit hyperactivity disorder (ADHD) is a condition where children under the age of 12 years old have hyperactive behaviour and problems paying attention that have a significant impact in more than one setting (for example, home and school).

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36
Q

What is the management of ADHD?

A

Management
NICE stipulates a holistic approach to treating ADHD that isn’t entirely reliant on therapeutics. Following presentation, a ten-week ‘watch and wait’ period should follow to observe whether symptoms change or resolve. If they persist then referral to secondary care is required. This is normally to a paediatrician with a special interest in behavioural disorders, or to the local Child and Adolescent Mental Health Service (CAMHS). Here, the needs and wants of the patient, as well as how their condition affects their lives should be taken into account, to offer a tailored plan of action.

Drug therapy should be seen as a last resort and is only available to those aged 5 years or more. Patients with mild/moderate symptoms can usually benefit from their parents attending education and training programmes. For those who fail to respond, or whose symptoms are severe, pharmacotherapy can be considered:

  • Methylphenidate is first line in children and should initially be given on a six-week trial basis. It is a CNS stimulant which primarily acts as a dopamine/norepinephrine reuptake inhibitor. Side-effects include abdominal pain, nausea and dyspepsia. In children, weight and height should be monitored every 6 months
  • If there is inadequate response, switch to lisdexamfetamine;
  • Dexamfetamine should be started in those who have benefited from lisdexamfetamine, but who can’t tolerate its side effects.

In adults:

  • Methylphenidate or lisdexamfetamine are first-line options;
  • Switch between these drugs if no benefit is seen after a trial of the other.

All of these drugs are potentially cardiotoxic. Perform a baseline ECG before starting treatment, and refer to a cardiologist if there is any significant past medical history or family history, or any doubt or ambiguity.

Like most psychiatric conditions, whether adult or paediatric, a thorough history and clinical examination are key, especially given the overlap of ADHD with many other psychiatric and physical conditions.

QUESMED

Management

  • Conservative:
    • Behavioural techniques
    • Extra support at school. However, ADHD does not generally affect intellectual ability.
  • Medical:
    • Stimulant medication such as methylphenidate. These medicines have some activity in the frontal lobe thus increasing executive function, attention, and reducing impulsivity.
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37
Q

What is aetiology behind ADHD?

A

Aetiology

  • ADHD is associated with reduced activity in the frontal lobe, resulting in problems with executive function. This impairs the ability to focus on different tasks and inhibit impulsive behaviours.
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38
Q

What is the prognosis of ADHD?

A

Prognosis

  • About 50% of children with ADHD continue to have significant problems with behaviour, or, more commonly, attention, into adulthood.
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39
Q

What is autism spectrum disorder?

A

Autism spectrum disorder

Autism is a neurodevelopmental condition characterized by qualitative impairment in social interaction and communication as well as repetitive stereotyped behaviour, interests, and activities. Symptoms are usually present during early childhood, but may be manifested later. Autism spectrum disorder (ASD) may occur in association with any level of general intellectual/learning ability, and manifestations range from subtle problems of understanding and impaired social function to severe disabilities. Although there is no cure for ASD, early diagnosis and intensive educational and behavioural management may improve outcomes.

QUESMED

Autistic spectrum disorders (ASDs) are characterised by a spectrum of social, language and behavioural deficits. Socially, children with autism do not enjoy or seek comfort from the company of other people. They lack ‘theory of mind’; they are not able to imagine the perspective of other people.

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40
Q

What is the epidemiology of autism spectrum ddisorder?

A

Epidemiology
The prevalence of ASD has increased over time, primarily as a result of changes in definitions and increased awareness.

  • Recent estimates suggest a prevalence of 1-2%.
  • ASD is three to four times more common in boys than girls.
  • Around 50% of children with ASD have an intellectual disability.
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41
Q

What are the clinical features of autism spectrum disorder?

A

Clinical features
Children or adults with autism may exhibit a broad range of clinical manifestations. Social communication impairments and repetitive behaviours are present during early childhood (typically evident before 2–3 years of age), or maybe manifested later. The clinical features can be classified as:

  • Impaired social communication and interaction:
    • Children frequently play alone and maybe relatively uninterested in being with other children.
    • They may fail to regulate social interaction with nonverbal cues like eye gaze, facial expression, and gestures.
    • Fail to form and maintain appropriate relationships and become socially isolated.
  • Repetitive behaviours, interests, and activities:
    • Stereotyped and repetitive motor mannerisms, inflexible adherence to nonfunctional routines or rituals are often seen.
    • Children are noted to have particular ways of going about everyday activities.
  • ASD is often associated with intellectual impairment or language impairment.
  • Attention deficit hyperactivity disorder (35%) and epilepsy (18%) are also commonly seen in children with ASD.
  • ASD is also associated with a higher head circumference to the brain volume ratio.

QUESMED

Presentation

  • As the name suggests children with autism can present with a spectrum of severities. In its most severe form:
    • Children with autism are not able to understand that other people have thoughts and feelings, prefer to play alone and avoid eye contact.
    • Children with autism have speech and language delay, monotonous tones of voice with limited expression and problems using pronouns (confuse ‘I’, ‘you’, ‘she’ etc.). They also interpret speech literally, and so have problems with the use of idiom (e.g. ‘it’s raining cats and dogs’).
    • In terms of behaviour, children with ASD commonly have narrow interests (e.g. trains), ritualistic behaviours that rely heavily on routine, and stereotyped movements (e.g. rocking, flapping hand movements).
  • Autistic spectrum disorders are commonly associated with learning difficulties.
  • About 25% of children with autism may also have seizures.
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42
Q

What is the management of autism spectrum disorder?

A

Management
Autism spectrum disorder (ASD) is a chronic condition that requires a comprehensive treatment approach. Although there is no cure for ASD, early diagnosis and early intensive treatment have the potential to affect outcomes. Treatment, which should be initiated early, involves educational and behavioural management, medical therapy, and family counselling.

The goal is to increase functional independence and quality of life through

  • Learning and development, improved social skills, and improved communication
  • Decreased disability and comorbidity
  • Aid to families

Non-Pharmacological Therapy:

  • Early educational and behavioural interventions:
    • Applied behavioural analysis (ABA).
    • ASD preschool program.
    • Treatment and Education of Autistic and Communication related handicapped CHildren (TEACCH)/Structured Teaching method.
    • Early Start Denver Model (ESDM).
    • Joint Attention Symbolic Play Engagement and Regulation (JASPER).
  • Pharmacologic interventions: no consistent evidence demonstrating medication-mediated improvements in social communication
    • SSRIs: helpful to reduce symptoms like repetitive stereotyped behaviour, anxiety, and aggression
    • Antipsychotic drugs: useful to reduce symptoms like aggression, self-injury.
    • Methylphenidate: for attention deficit hyperactivity disorder (ADHD).
  • Family support and counselling:
    • Parental education on interaction with the child and acceptance of his/her behaviour.

QUESMED

Management

  • Management of autistic spectrum disorders is complex, with the need for multidisciplinary team management and extra support for the family.
  • Applied behavioural analysis is one technique that can be of benefit, whereby positive behaviours are encouraged and negative behaviours are ignored.
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43
Q

What is the prognosis of autism spectrum disorder?

A

Prognosis

  • Autistic spectrum disorders require a huge amount of support, as less than 10% of children with ASD will be able to live independently as adults.
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44
Q

What is bipolar affective disorder?

A

Bipolar affective disorder

Bipolar disorder is a chronic mental health disorder characterised by periods of mania/hypomania alongside episodes of depression.

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45
Q

What is the epidemiology behind bipolar?

A

Epidemiology

  • typically develops in the late teen years
  • lifetime prevalence: 2%
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46
Q

What are the types of bipolar affective disorder?

A

Two types of bipolar disorder are recognised:

  • type I disorder: mania and depression (most common)
  • type II disorder: hypomania and depression
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47
Q

What is mania/hypomania?

A

What is mania/hypomania?

  • both terms relate to abnormally elevated mood or irritability
  • with mania, there is severe functional impairment or psychotic symptoms for 7 days or more
  • hypomania describes decreased or increased function for 4 days or more
  • from an exam point of view the key differentiation is psychotic symptoms (e.g.delusions of grandeur or auditory hallucinations) which suggest mania
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48
Q

What is the management of bipolar affective disorder?

A

Management

  • psychological interventions specifically designed for bipolar disorder may be helpful
  • lithium remains the mood stabilizer of choice. An alternative is valproate
  • management of mania/hypomania
    • consider stopping antidepressant if the patient takes one; antipsychotic therapy e.g. olanzapine or haloperidol
  • management of depression
    • talking therapies (see above); fluoxetine is the antidepressant of choice
  • address co-morbidities
    • there is a 2-3 times increased risk of diabetes, cardiovascular disease and COPD
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49
Q

Explain a primary care referral of bipolar affective disorder

A

Primary care referral

  • if symptoms suggest hypomania then NICE recommend routine referral to the community mental health team (CMHT)
  • if there are features of mania or severe depression then an urgent referral to the CMHT should be made
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50
Q

What is the aetiology behind bipolar affective disorder?

A

Aetiology

The aetiology of Bipolar Affective Disorder is not fully understood, but there is clear evidence to suggest that there is a genetic component and it can be inherited. Triggers for manic episodes can include stressful life events, physical illness or illicit substance misuse. A ‘manic switch’ can sometimes be induced by someone with Bipolar Affective Disorder taking antidepressants to treat a depressive episode.

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51
Q

What are the clinical features of bipolar affective disorder?

A

Clinical features

During periods of depression the patient may become withdrawn and tearful, with low mood, poor sleep and anhedonia. They may experience suicidal thoughts or make attempts.

Manic episodes are characterised by elevated mood or irritability. They may make impulsive and dangerous decisions with little thought for consequences. The need for sleep is often reduced. Mood congruent delusions may be present. They often have pressured speech and exhibit flight of ideas.

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52
Q

Explain the diagnostic criteria of bipolar affective disorder (DSM)?

A

Diagnostic criteria

The full DSM criteria for the diagnosis of bipolar disorder are as follows:

Bipolar disorder is diagnosed when a person has at least one episode of a manic or a hypomanic state, and one major depressive episode.

Mania

The DSM defines mania as a “distinct period of abnormally and persistently elevated, expansive, or irritable mood.” The episode must last at least a week. The mood must have at least three of the following symptoms:

  • Elevated self-esteem
  • Reduced need for sleep
  • Increased rate of speech
  • Flight of ideas
  • Easily distracted
  • An increased interest in goals or activities
  • Psychomotor agitation (pacing, hand wringing etc.)
  • Increased pursuit of activities with a high risk of danger

Hypomania

Additionally, the DSM states that in hypomania “the episode (should not be) severe enough to cause marked impairment in social or occupational functioning, or to necessitate hospitalisation, and there are no psychotic features”

Depression

The DSM states that a major depressive episode must have at least four of the following symptoms. They should be new or suddenly worse, and must last for at least two weeks:

  • Changes in appetite or weight, sleep, or psychomotor activity
  • Decreased energy
  • Feelings of worthlessness or guilt
  • Trouble thinking, concentrating, or making decisions
  • Thoughts of death or suicidal plans or attempts
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53
Q

What is the acute management of bipolar affective disorder?

A

Acute management of bipolar disorder

Bipolar disorder may be seen as an acute presentation of either mania or depression. The management of these are as follows:

Acute mania with agitation: patients will typically require IM therapy, either a neuroleptic or a benzodiazepine. They may need urgent admission to a secure unit.

Acute mania without agitation: oral monotherapy can be attempted with an antipsychotic. Sedation and a mood stabilizer such as lithium can be added if necessary.

Acute depression: mood stabilizer and/or atypical antipsychotic and/or antidepressant with appropriate psychosocial support.

All of these patients will require long-term follow up and maintenance therapy.

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54
Q

What is the chronic management of bipolar affective disorder?

A

Chronic management of bipolar disorder

Patients with bipolar disorder are at high risk of relapse into either depression or mania. As such, they require careful follow-up and ongoing maintenance treatment.

Lithium is the gold standard medication for bipolar disorder and acts as a mood stabiliser. Valproate is a suitable second line alternative. Anti-psychotics and anti-convulsants may also be used in treatment resistant cases.

Additionally, NICE recommends that all patients with bipolar disorder have access to psychological therapies. These should be targeted towards bipolar disorder specifically, and should be high intensity in nature. This can include CBT, interpersonal therapy or couples/family therapy.

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55
Q

What are the factors favouring delirium over dementia?

A

Factors favouring delirium over dementia

  • impairment of consciousness
  • fluctuation of symptoms: worse at night, periods of normality
  • abnormal perception (e.g. illusions and hallucinations)
  • agitation, fear
  • delusions
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56
Q

What are some factors suggesting depression over dementia?

A

Factors suggesting diagnosis of depression over dementia

  • short history, rapid onset
  • biological symptoms e.g. weight loss, sleep disturbance
  • patient worried about poor memory
  • reluctant to take tests, disappointed with results
  • mini-mental test score: variable
  • global memory loss (dementia characteristically causes recent memory loss)
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57
Q

What is delirium?

A

Delirium or acute confusional state is a common condition affecting predominantly elderly people. It is seen in up to 30% of elderly inpatients.

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58
Q

What are some clinical features of delirium?

A

Clinical features

It can present in a number of different ways, including:

  • Disorientation
  • Hallucinations
  • Inattention
  • Memory problems
  • Change in mood or personality
  • Disturbed sleep

Patients may be very agitated or very sedated and hypo-active.

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59
Q

What is the aetiology behind delirium?

A

Causes (Mnemonic: DELIRIUMS)

Common causes of delirium can be remembered using the mnemonic DELIRIUMS:

  • D - Drugs and Alcohol (Anti-cholinergics, opiates, anti-convulsants, recreational)
  • E - Eyes, ears and emotional
  • L - Low Output state (MI, ARDS, PE, CHF, COPD)
  • I - Infection
  • R - Retention (of urine or stool)
  • I - Ictal
  • U - Under-hydration/Under-nutrition
  • M - Metabolic (Electrolyte imbalance, thyroid, wernickes
  • (S) - Subdural, Sleep deprivation
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60
Q

What are the investigations for delirium?

A

Investigations

A full physical examination and infection screen should be carried out in these patients.

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61
Q

What is the management of delirium?

A

Management

Management of delirium is predominantly to treat the underlying cause. Maintaining an environment with good lighting and frequent reassurance is helpful. In extremely agitated patients small doses of haloperidol or olanzapine may be considered.

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62
Q

What is dementia?

A

Dementia

Dementia is thought to affect over 700,000 people in the UK and accounts for a large amount of health and social care spending. The most common cause of dementia in the UK is Alzheimer’s disease followed by vascular and Lewy body dementia. These conditions may coexist.

QUESMED

Definition

According to ICD-10, dementia is a syndrome, usually of chronic or progressive nature, which involves impairment of multiple higher cortical functions, such as memory, thinking, orientation, comprehension and language.

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63
Q

What are the features of dementia?

A

Features

  • diagnosis can be difficult and is often delayed
  • assessment tools recommended by NICE for the non-specialist setting include: 10-point cognitive screener (10-CS), 6-Item cognitive impairment test (6CIT)
  • assessment tools not recommended by NICE for the non-specialist setting include the abbreviated mental test score (AMTS), General practitioner assessment of cognition (GPCOG) and the mini-mental state examination (MMSE) have been widely used. A MMSE score of 24 or less out of 30 suggests dementia
  • Consciousness is not affected in the early stages (in comparison with delirium which will be)
  • Identify a decline in memory and thinking which impairs activities of daily living
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64
Q

What is the management of dementia?

A

Management

  • in primary care, a blood screen is usually sent to exclude reversible causes (e.g. Hypothyroidism). NICE recommend the following tests: FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12 and folate levels. Patients are now commonly referred on to old-age psychiatrists (sometimes working in ‘memory clinics’).
  • in secondary care, neuroimaging is performed* to exclude other reversible conditions (e.g. Subdural haematoma, normal pressure hydrocephalus) and help provide information on aetiology to guide prognosis and management

*in the 2011 NICE guidelines structural imaging was said to be essential in the investigation of dementia

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65
Q

What is the aetiology behind dementia?

A

Common causes

  • Alzheimer’s disease
  • cerebrovascular disease: multi-infarct dementia (c. 10-20%)
  • Lewy body dementia (c. 10-20%)

Rarer causes (c. 5% of cases)

  • Huntington’s
  • CJD
  • Pick’s disease (atrophy of frontal and temporal lobes)
  • HIV (50% of AIDS patients)
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66
Q

What are the important differentials behind dementia?

A

Important differentials, potentially treatable

  • hypothyroidism, Addison’s
  • B12/folate/thiamine deficiency
  • syphilis
  • brain tumour
  • normal pressure hydrocephalus
  • subdural haematoma
  • depression
  • chronic drug use e.g. Alcohol, barbiturates
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67
Q

What us Alzheimer’s disease?

A

Alzheimer’s disease

The most common cause of dementia is Alzheimer’s disease, a chronic and progressive form of dementia, which is caused by characteristic neuropathological features such as amyloid plaques and tau proteins. Alzheimer’s disease is caused by a build up of amyloid protein deposits around brain cells and tau protein tangles within brain cells.

Definition

Alzheimer’s disease is degenerative condition of the brain that leads to memory loss and ultimately global impairment of brain function.

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68
Q

What are the clinical features of Alzheimer’s disease?

A

Clinical Features

A useful mnemonic to remember the features of Alzheimer;s is the ‘4As’:

  • Amnesia (recent memories lost first)
  • Aphasia (word-finding problems, speech muddled and disjointed)
  • Agnosia (recognition problems)
  • Apraxia (inability to carry out skilled tasks despite normal motor function)
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69
Q

What is Lewy Body dementia?

A

Lewy Body Dementia

In Lewy Body Dementia, abnormal protein deposits called Lewy Bodies cause cognitive decline associated with parkinsonism (rigidity, tremor, bradykinesia).

Dementia with Lewy bodies (DLB) is a progressive, complex and challenging condition which is thought to account for 10-15% of all those with dementia. It is caused by deposits of an abnormal protein called Lewy bodies inside brain cells.

These Lewy bodies (alpha-synuclein cytoplasmic inclusions) are found in the substantia nigra, paralimbic and neocortical areas.

The relationship between Parkinson’s disease and Lewy body dementia is complicated, particularly as dementia is often seen in Parkinson’s disease. Also, up to 40% of patients with Alzheimer’s have Lewy bodies.

70
Q

What is the epidemiology of Lewy Body dementia?

A

Epidemiology

DLB is the third most common type of dementia. For every 100 people with dementia, around 10-15 will have DLB.

71
Q

What are the clinical features of Lewy Body dementia?

A

Clinical features

  • Accounts for around 20% of cases of dementia
  • Characterised by alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.
  • Associated with Parkinson’s disease - patients are also highly sensitive to neuroleptics, which causes a deterioration in parkinsonism
  • Three core features: fluctuating cognition, parkinsonism and visual hallucinations
  • Progressive cognitive impairment seen
    • In Alzeihmers is early impairments in attention and execution function rather than memory loss
  • Diagnosis is usually clinical but dopamine uptake scanning may be used
72
Q

What is fronto-temporal dementia?

A

Fronto-temporal Dementia

Fronto-temporal dementia presents with cognitive impairment, personality change and disinbition, in keeping with the frontal area of the brain which is affected. Atrophy of the frontal and temporal lobes is seen.

73
Q

What is the aetiology behind fronto-temporal dementia?

A

Aetiology

  • Frontotemporal dementia is caused by atrophy of the frontal and temporal lobes.
  • Pick’s disease
74
Q

What are the clinical features behind fronto-temporal dementia?

A

Clinical features

  • Classically presents at a younger age than other forms of dementia
  • Patients exhibit early personality change and frequently become disinhibited
  • Language can also be affected early on
  • Often misdiagnosed, and neuroimaging may need to be used. Genetic tests can also be used if an inherited form is suspected (i.e. a strong family history)
75
Q

What is Pick’s disease?

A

Pick’s disease

One specific cause of Frontotemporal Dementia is Pick’s disease.

This is diagnosed on post-mortem where “Pick’s bodies” (accumulations of TAU protein that stain with silver) are found in the neurons.

These are histologically distinct from those TAU protein collections seen in Alzheimer’s as they stain differently and are found preferentially in other areas of the brain (preferentially damaging the frontal and temporal lobes).

76
Q

What is vascular dementia?

A

Vascular Dementia

Vascular dementia, a result of multiple infarcts in the brain tends to present with sudden onset cognitive decline and stepwise deterioration in someone with previous cardiovascular illness or events, as a result of the developing infarcts.

  • Second most common cause of dementia (after Alzeihmers)
  • Caused by impaired blood flow to areas of the brain due to vascular damage
    • Mechanisms that cause ischaemia/haemorrhage secondary to cerebrovascular disease
  • Can have a ‘step-wise’ progression due to progressive infarcts over time
  • Usually a clinical diagnosis, Neuro-imaging can show evidence of significant small vessel disease
  • Treatment involves managing underlying vascular risk factors
77
Q

What is Wernicke’s encephalopathy?

A

Wernicke’s encephalopathy

Wernicke’s encephalopathy presents with the classic tetrad of ataxia, opthalmoplegia, nystagmus and acute confusional state and is associated with lesions in the mamillary bodies.

78
Q

Explain Wernicke’s encephalopathy and Korskaoff’s syndrome (and the link between them)?

A

Wernicke’s encephalopathy and Korsakoff’s syndrome

Vitamin B1 deficiency may cause Wernicke’s encephalopathy. Wernicke’s encephalopathy is the triad of: confusion + ataxia + ophthalmoplegia/nystagmus.

Untreated, Wernicke’s encephalopathy can progress to Korsakoff’s syndrome.Korsakoff’s syndrome presents as profound anterograde amnesia with limited retrograde amnesia. Patients may therefore confabulate ().

Note that both disorders can co-exist as ‘Wernicke-Korsakoff syndrome’ if elements from both exist simultaneously.

The most common cause of Wernicke’s encephalopathy is chronic alcohol abuse. It is therefore important to prescribe thiamine (vitamin B1) to prevent this from happening.

Korsakoff’s syndrome is thought to be a result of degeneration of the mammillary bodies. The mammillary bodies are part of the circuit of Papez which plays a role in memory formation.

79
Q

What is the epidemiology of vascular dementia?

A

Epidemiology

  • VD is thought to account for around 17% of dementia in the UK
  • Prevalence of dementia following a first stroke varies depending on location and size of the infarct, definition of dementia, interval after stroke and age among other variables. Overall, stroke doubles the risk of developing dementia.
  • Incidence increases with age
80
Q

What are the main subtypes of vascular dementia?

A

The main subtypes of VD:

  • Stroke-related VD – multi-infarct or single-infarct dementia
  • Subcortical VD – caused by small vessel disease
  • Mixed dementia – the presence of both VD and Alzheimer’s disease
81
Q

What are the risk factors of vascular dementia?

A

Risk factors

  • History of stroke or transient ischaemic attack (TIA)
  • Atrial fibrillation
  • Hypertension
  • Diabetes mellitus
  • Hyperlipidaemia
  • Smoking
  • Obesity
  • Coronary heart disease
  • A family history of stroke or cardiovascular

Rarely, VD can be inherited as in the case of CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.)

82
Q

What do patients with vascular dementia often present with? & main symptoms

A

Patients with VD typically presents with

  • Several months or several years of a history of a sudden or stepwise deterioration of cognitive function.

Symptoms and the speed of progression vary but may include:

  • Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms
  • The difficulty with attention and concentration
  • Seizures
  • Memory disturbance
  • Gait disturbance
  • Speech disturbance
  • Emotional disturbance
83
Q

What is diagnosis of vascular dementia mainly based on?

A

Diagnosis is made based on:

  • A comprehensive history and physical examination
  • Formal screen for cognitive impairment
  • Medical review to exclude medication cause of cognitive decline
  • MRI scan – may show infarcts and extensive white matter changes

National Institute for health and care excellence (NICE) recommends that diagnosis be made using the NINDS-AIREN criteria for probable vascular dementia

Presence of cognitive decline that interferes with activities of daily living, not due to secondary effects of the cerebrovascular event

  • established using clinical examination and neuropsychological testing

Cerebrovascular disease

  • defined by neurological signs and/or brain imaging

A relationship between the above two disorders inferred by:

  • the onset of dementia within three months following a recognised stroke
  • an abrupt deterioration in cognitive functions
  • fluctuating, stepwise progression of cognitive deficits

Presence of cognitive decline that interferes with activities of daily living, not due to secondary effects of the cerebrovascular event

  • established using clinical examination and neuropsychological testing

Cerebrovascular disease

  • defined by neurological signs and/or brain imaging

A relationship between the above two disorders inferred by:

  • the onset of dementia within three months following a recognised stroke
  • an abrupt deterioration in cognitive functions
  • fluctuating, stepwise progression of cognitive deficits
84
Q

What is the general management of vascular dementia?

A

General management

  • Treatment is mainly symptomatic with the aim to address individual problems and provide support to the patient and carers
  • Important to detect and address cardiovascular risk factors – for slowing down the progression
85
Q

What is the non-phamacological management of vascular dementia?

A

Non-pharmacological management

  • Tailored to the individual
  • Include: cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy
  • Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication
86
Q

What is the pharmacological management of vascular dementia?

A

Pharmacological management

  • There is no specific pharmacological treatment approved for cognitive symptoms
  • Only consider AChE inhibitors or memantine for people with vascular dementia if they have suspected comorbid Alzheimer’s disease, Parkinson’s disease dementia or dementia with Lewy bodies.
  • There is no evidence that aspirin is effective in treating patients with a diagnosis of vascular dementia.
  • No randomized trials found evaluating statins for vascular dementia
87
Q

How to diagnose Lewy Body Dementia?

A

Diagnosis

  • usually clinical (cognition problems, visual hallucinations and parkinsonism
  • single-photon emission computed tomography (SPECT) is increasingly used. It is currently commercially known as a DaTscan. Dopaminergic iodine-123-radiolabelled 2-carbomethoxy-3-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (123-I FP-CIT) is used as the radioisotope. The sensitivity of SPECT in diagnosing Lewy body dementia is around 90% with a specificity of 100%
88
Q

What is the management of Lewy Body Dementia?

A

Management

  • both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s. NICE have made detailed recommendations about what drugs to use at what stages. Please see the link for more details
  • neuroleptics*** should be ***avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism. Questions may give a history of a patient who has deteriorated following the introduction of an antipsychotic agent
89
Q

How to screen for depression?

A

Screening
The following two questions can be used to screen for depression

  • ‘During the last month, have you often been bothered by feeling down, depressed or hopeless?’
  • ‘During the last month, have you often been bothered by having little interest or pleasure in doing things?’

A ‘yes’ answer to either of the above should prompt a more in depth assessment.

90
Q

What assessments can you use for depression to find the severity?

A

Assessment
There are many tools to assess the degree of depression including the Hospital Anxiety and Depression (HAD) scale and the Patient Health Questionnaire (PHQ-9).

Hospital Anxiety and Depression (HAD) scale

  • consists of 14 questions, 7 for anxiety and 7 for depression
  • each item is scored from 0-3
  • produces a score out of 21 for both anxiety and depression
  • severity: 0-7 normal, 8-10 borderline, 11+ case
  • patients should be encouraged to answer the questions quickly

Patient Health Questionnaire (PHQ-9)

  • asks patients ‘over the last 2 weeks, how often have you been bothered by any of the following problems?’
  • 9 items which can then be scored 0-3
  • includes items asking about thoughts of self-harm
  • depression severity: 0-4 none, 5-9 mild, 10-14 moderate, 15-19 moderately severe, 20-27 severe

NICE use the DSM-IV criteria to grade depression:

    1. Depressed mood most of the day, nearly every day
    1. Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day
    1. Significant weight loss or weight gain when not dieting or decrease or increase in appetite nearly every day
    1. Insomnia or hypersomnia nearly every day
    1. Psychomotor agitation or retardation nearly every day
    1. Fatigue or loss of energy nearly every day
    1. Feelings of worthlessness or excessive or inappropriate guilt nearly every day
    1. Diminished ability to think or concentrate, or indecisiveness nearly every day
    1. Recurrent thoughts of death, recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide
91
Q

Explain the HAD scale in depression

A

Hospital Anxiety and Depression (HAD) scale

  • consists of 14 questions, 7 for anxiety and 7 for depression
  • each item is scored from 0-3
  • produces a score out of 21 for both anxiety and depression
  • severity: 0-7 normal, 8-10 borderline, 11+ case
  • patients should be encouraged to answer the questions quickly
92
Q

Explain the PHQ-9 questionnaire in depression

A

Patient Health Questionnaire (PHQ-9)

  • asks patients ‘over the last 2 weeks, how often have you been bothered by any of the following problems?’
  • 9 items which can then be scored 0-3
  • includes items asking about thoughts of self-harm
  • depression severity: 0-4 none, 5-9 mild, 10-14 moderate, 15-19 moderately severe, 20-27 severe
93
Q

What criteria is used in practise to grade depression?

A

NICE use the DSM-IV criteria to grade depression:

    1. Depressed mood most of the day, nearly every day
    1. Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day
    1. Significant weight loss or weight gain when not dieting or decrease or increase in appetite nearly every day
    1. Insomnia or hypersomnia nearly every day
    1. Psychomotor agitation or retardation nearly every day
    1. Fatigue or loss of energy nearly every day
    1. Feelings of worthlessness or excessive or inappropriate guilt nearly every day
    1. Diminished ability to think or concentrate, or indecisiveness nearly every day
    1. Recurrent thoughts of death, recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide
94
Q

Management of depression (various stages and methods)

For mild to moderate depression

A

Persistent subthreshold depressive symptoms or mild to moderate depression
General measures

  • sleep hygiene
  • active monitoring for people who do want an intervention

Drug treatment

  • do not use antidepressants routinely but consider them for people with:
    • a past history of moderate or severe depression or
    • initial presentation of subthreshold depressive symptoms that have been present for a long period (typically at least 2 years) or
    • subthreshold depressive symptoms or mild depression that persist(s) after other interventions
    • if a patient has a chronic physical health problem and mild depression complicates the care of the physical health problem

The following ‘low-intensity psychosocial interventions’ may be useful:

BELOW IN THE TABLE

An alternative is group-based CBT

  • be based on a model such as ‘Coping with depression’
  • be delivered by two trained and competent practitioners
  • consist of 10-12 meetings of 8-10 participants
  • typically take place over 12-16 weeks, including follow-up

For patients with chronic physical health problems NICE also recommend considering a group-based peer support programme:

  • focus on sharing experiences and feelings associated with having a chronic physical health problem
  • consist typically of 1 session per week over 8-12 weeks
95
Q

Explain switching antidepressants in depression (which ones)

A

Depression: Switching antidepressants

The following is based on the Clinical Knowledge Summaries depression guidelines, which in turn are based on the Maudsley hospital guidelines.

Switching from citalopram, escitalopram, sertraline, or paroxetine to another SSRI

  • the first SSRI should be withdrawn* before the alternative SSRI is started

Switching from fluoxetine to another SSRI

  • withdraw then leave a gap of 4-7 days (as it has a long half-life) before starting a low-dose of the alternative SSRI

Switching from a SSRI to a tricyclic antidepressant (TCA)

  • cross-tapering is recommend (the current drug dose is reduced slowly, whilst the dose of the new drug is increased slowly)
  • an exceptions is fluoxetine which should be withdrawn prior to TCAs being started

Switching from citalopram, escitalopram, sertraline, or paroxetine to venlafaxine

  • cross-taper cautiously. Start venlafaxine 37.5 mg daily and increase very slowly

Switching from fluoxetine to venlafaxine

  • withdraw and then start venlafaxine at 37.5 mg each day and increase very slowly

*this means gradually reduce the dose then stop

96
Q

Management of moderate and severe depression

A

Depression: management of unresponsive, moderate and severe depression

NICE produced updated guidelines in 2009 on the management of depression in primary and secondary care. Patients are classified according to the severity of the depression and whether they have an underlying chronic physical health problem.

Please note that due to the length of the ‘quick’ reference guide the following is a summary and we would advise you follow the link for more detail.

Persistent subthreshold depressive symptoms or mild to moderate depression with inadequate response to initial interventions and moderate and severe depression
For these patients NICE recommends an antidepressant (normally a selective serotonin reuptake inhibitor, SSRI)

The following ‘high-intensity psychological interventions’ may be useful:

TABLE BELOW

For people who decline the options above, consider:

  • counselling for people with persistent subthreshold depressive symptoms or mild to moderate depression; offer 6-10 sessions over 8-12 weeks
  • short-term psychodynamic psychotherapy for people with mild to moderate depression; offer 16-20 sessions over 4-6 months

For patients with chronic physical health problems the following should be offered:

  • group-based CBT
  • individual CBT
97
Q

What is the epidemiology of depression?

A

Epidemiology

Depression is a very common mental health disorder.

Depression is the third most common reason for consulting a GP in the UK.

98
Q

What is the diagnostic criteria for depression?

A

Diagnostic criteria

It has a number of key features that are used in diagnosis. DSM-5 uses the following diagnostic criteria:

  1. Depressed mood or irritable most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad or empty) or observation made by others (e.g., appears tearful).
  2. Decreased interest or pleasure (anhedonia) in most activities, most of each day
  3. Significant weight change (5%) or change in appetite
  4. Change in sleep: Insomnia or hypersomnia
  5. Change in activity: Psychomotor agitation or retardation
  6. Fatigue or loss of energy
  7. Guilt/worthlessness: Feelings of worthlessness or excessive or inappropriate guilt
  8. Concentration: diminished ability to think or concentrate, or more indecisiveness
  9. Suicidality: Thoughts of death or suicide, or has suicide plan

If 5 of these 9 features are seen, and are present nearly every day for 2 weeks or longer, then a diagnosis of depression can be made.

99
Q

What are the risk factors of depression?

A

Risk factors

  • Female gender
  • Past history of depression
  • Significant physical illness
  • Other mental health problems
  • Social issues (divorce, unemployment, poverty)
100
Q

What investigations should be made when some has ?depression?

A

Investigations

A careful history and appropriate screening questionnaires can help to rule other conditions out.

Low mood and depression can also occur as a result of organic diseases. It is important to always consider the possibility of an underlying organic disease before diagnosing depression, and further tests may be required (e.g. thyroid function tests, full blood count, metabolic panel and brain imaging).

101
Q

What are Organic differential diagnosis of depression/low mood?

A

Differentials

Organic diseases causing low mood include:

  • Neurological disease such as Parkinson’s disease, dementia and multiple sclerosis
  • Endocrine disorder, particularly thyroid dysfunction and hypo/hyperadrenalism (e.g. Cushing’s and Addison’s disease)
  • Drugs (e.g. steroids, isotretinoin (roaccutane), alcohol, beta-blockers, benzodiazepines and methyldopa
  • Chronic conditions such as diabetes and obstructive sleep apnoea. Additionally, long standing infections such as mononucleosis
  • Neoplasms and cancers - pancreatic cancer is a notable example. However, low mood can theoretically be a presenting complaint in any cancer. It may be as a result of pro-inflammatory cytokines and immune system modulation.
102
Q

What are psychiatric differentials of low mood/depression?

A

Psychiatric differential diagnoses include:

  • Bipolar disorder
  • Schizophrenia
  • Dementia
  • Seasonal affective disorder
  • Bereavement
  • Anxiety
103
Q

Initial management of depression

A

Initial management of depression

NICE guidelines suggest a stepped care model for the treatment of depression, depending on the severity of the presentation, comorbidity with chronic physical health problems or personal preference.

First-line, low intensity psychological interventions or group-based CBT may be offered, before moving on to either pharmacological therapy or a high intensity psychological intervention such as Cognitive Behavioural Therapy or Interpersonal Therapy. For those with moderate or severe depressive episodes, psychological therapies may be offered in conjunction with medication.

Pharmacological therapy should start with a selective serotonin reuptake inhibitor, such as Sertraline.

Patients who have benefitted from antidepressants should be continued for at least six months after remission to reduce the risk of relapse. When stopping antidepressants, doses should be reduced gradually over a four week period.

Urgent referral may be necessary if a patient is actively suicidal. It is therefore essential to screen for this during the initial consultation.

104
Q

What is the management of severe depression?

A

Management of severe depression

Severe depressive episodes can be managed in a number of ways, one of which will usually include pharmacological therapy. Antidepressants should be initiated in a typical step-wise manner, one of which should be a Selective Serotonin Reuptake Inhibitor, such as Sertraline. Psychological therapy should be offered in combination with pharmacological therapy.

If antidepressants alone do not work, they can be augmented with Lithium.

For severe depressive episodes that are life-threatening or require a rapid response, NICE guidelines recommend Electroconvulsive Therapy (ECT).

It is not known exactly how ECT works but there is evidence to suggest that the induced seizure has more of a treatment effect than ‘placebo’ ECT or ‘sham’ ECT. Short-term side effects of ECT can include headache, muscle aches or pains, nausea, temporary memory loss, confusion.

Long-term side effects of ECT can include persistent memory loss.

Due to the induced seizure, there is a risk of damage to the teeth or mouth, and due to the general anaesthetic, there is a small risk of death.

105
Q

Management of depression in children

A

Depression in children

  • Mild depression can be managed with wathcful waiting and advice about healthy habits
  • Consider referral to CAMHS for children with moderate to severe depression. Treatment options include:
    • Full assessment
    • Psychological therapy (first line)
    • Fluoxetine (first line antidepressant in children; followed by Sertraline and Citalopram)
    • Admission may be required if there is high risk of self harm, suicide or self-neglect
106
Q

What is bulimia nervosa?

A

Bulimia nervosa

Bulimia nervosa is a type of eating disorder characterised by episodes of binge eating followed by intentional vomiting or other purgative behaviours such as the use of laxatives or diuretics or exercising. Unlike anorexia nervosa they may have a normal BMI

107
Q

What are the clinical features of bulimia nervosa? & physical features

A

Clinical features

It is characterized by:

  • Binge eating: Loss of control, eating enormous amounts with thousands of calories, often in sense of urgency and compulsion
  • Purging: binges causes feelings of shame and guilt leading to attempts to ‘undo damage’ vomiting, laxatives, diuretics, can also be exercise
  • Body image distortion: feeling fat, often hate their body
  • BMI > 17.5 (usually normal or slightly increased weight and periods usually present)

Physical features

Physical features of bulimia nervosa include:

  • Dental erosion
  • Parotid gland swelling
  • Russell’s sign (scarring on fingers from induced vomiting)
108
Q

What is the management of bulimia?

A

Management

  • referral for specialist care is appropriate in all cases
  • NICE recommend bulimia-nervosa-focused guided self-help for adults
  • If bulimia-nervosa-focused guided self-help is unacceptable, contraindicated, or ineffective after 4 weeks of treatment, NICE recommend that we consider individual eating-disorder-focused cognitive behavioural therapy (CBT-ED)
    • CBT is first line
  • children should be offered bulimia-nervosa-focused family therapy (FT-BN)
  • pharmacological treatments have a limited role - a trial of high-dose fluoxetine is currently licensed for bulimia but long-term data is lacking
109
Q

What is the DMS5 criteria of bulimia nervosa?

A

DSM 5 diagnostic criteria for a diagnosis of bulimia nervosa:

  • recurrent episodes of binge eating (eating an amount of food that is definitely larger than most people would eat during a similar period of time and circumstances)
  • a sense of lack of control over eating during the episode
  • recurrent inappropriate compensatory behaviour in order to prevent weight gain, such as self-induced vomiting, misuse of laxatives, diuretics, or other medications, fasting, or excessive exercise.
    • recurrent vomiting may lead to erosion of teeth and Russell’s sign - calluses on the knuckles or back of the hand due to repeated self-induced vomiting
  • the binge eating and compensatory behaviours both occur, on average, at least once a week for three months.
  • self-evaluation is unduly influenced by body shape and weight.
  • the disturbance does not occur exclusively during episodes of anorexia nervosa.
110
Q

What is a personality disorder?

A

Personality disorder

Personality disorders may be defined as a series of maladaptive personality traits that interfere with normal function in life. It is thought that around 1 in 20 people have a personality disorder. They are typically categorised as belonging to one of three clusters:

111
Q

What are the clusters of personality disorders?

A
112
Q

Explain paranoid personality disorder

A

Cluster A: ‘Odd or Eccentric’
Paranoid

  • Hypersensitivity and an unforgiving attitude when insulted
  • Unwarranted tendency to questions the loyalty of friends
  • Reluctance to confide in others
  • Preoccupation with conspirational beliefs and hidden meaning
  • Unwarranted tendency to perceive attacks on their character
113
Q

Explain schizoid personality disorder

A

Schizoid

  • Indifference to praise and criticism
  • Preference for solitary activities
  • Lack of interest in sexual interactions
  • Lack of desire for companionship
  • Emotional coldness
  • Few interests
  • Few friends or confidants other than family
114
Q

Explain schizotypal personality disorder

A

Schizotypal

  • Ideas of reference (differ from delusions in that some insight is retained)
  • Odd beliefs and magical thinking
  • Unusual perceptual disturbances
  • Paranoid ideation and suspiciousness
  • Odd, eccentric behaviour
  • Lack of close friends other than family members
  • Inappropriate affect
  • Odd speech without being incoherent
115
Q

Explain antisocial personality disorder

A

Cluster B: ‘Dramatic, emotional or erratic’
Antisocial

  • Failure to conform to social norms with respect to lawful behaviours as indicated by repeatedly performing acts that are grounds for arrest;
  • More common in men;
  • Deception, as indicated by repeatedly lying, use of aliases, or conning others for personal profit or pleasure;
  • Impulsiveness or failure to plan ahead;
  • Irritability and aggressiveness, as indicated by repeated physical fights or assaults;
  • Reckless disregard for the safety of self or others;
  • Consistent irresponsibility, as indicated by repeated failure to sustain consistent work behaviour or honour financial obligations;
  • Lack of remorse, as indicated by being indifferent to or rationalizing having hurt, mistreated, or stolen from another
116
Q

Explain borderline personality disorder

A

Borderline - also known as Emotionally Unstable

  • Efforts to avoid real or imagined abandonment
  • Unstable interpersonal relationships which alternate between idealization and devaluation
  • Unstable self image
  • Impulsivity in potentially self damaging area (e.g. Spending, sex, substance abuse)
  • Recurrent suicidal behaviour
  • Affective instability
  • Chronic feelings of emptiness
  • Difficulty controlling temper
  • Quasi psychotic thoughts
117
Q

Explain histrionic personality disorder

A

Histrionic

  • Inappropriate sexual seductiveness
  • Need to be the centre of attention
  • Rapidly shifting and shallow expression of emotions
  • Suggestibility
  • Physical appearance used for attention seeking purposes
  • Impressionistic speech lacking detail
  • Self dramatization
  • Relationships considered to be more intimate than they are
118
Q

Explain narcissistic personality disorder

A

Narcissistic

  • Grandiose sense of self importance
  • Preoccupation with fantasies of unlimited success, power, or beauty
  • Sense of entitlement
  • Taking advantage of others to achieve own needs
  • Lack of empathy
  • Excessive need for admiration
  • Chronic envy
  • Arrogant and haughty attitude
119
Q

Explain obsessive-compulsive personality disorder

A

Cluster C: ‘Anxious and Fearful’
Obsessive-compulsive

  • Is occupied with details, rules, lists, order, organization, or agenda to the point that the key part of the activity is gone
  • Demonstrates perfectionism that hampers with completing tasks
  • Is extremely dedicated to work and efficiency to the elimination of spare time activities
  • Is meticulous, scrupulous, and rigid about etiquettes of morality, ethics, or values
  • Is not capable of disposing worn out or insignificant things even when they have no sentimental meaning
  • Is unwilling to pass on tasks or work with others except if they surrender to exactly their way of doing things
  • Takes on a stingy spending style towards self and others; and shows stiffness and stubbornness
120
Q

Explain avoidant personality disorder

A

Avoidant

  • Avoidance of occupational activities which involve significant interpersonal contact due to fears of criticism, or rejection.
  • Unwillingness to be involved unless certain of being liked
  • Preoccupied with ideas that they are being criticised or rejected in social situations
  • Restraint in intimate relationships due to the fear of being ridiculed
  • Reluctance to take personal risks due to fears of embarrassment
  • Views self as inept and inferior to others
  • Social isolation accompanied by a craving for social contact
121
Q

Explain dependent personality disorder

A

Dependent

  • Difficulty making everyday decisions without excessive reassurance from others
  • Need for others to assume responsibility for major areas of their life
  • Difficulty in expressing disagreement with others due to fears of losing support
  • Lack of initiative
  • Unrealistic fears of being left to care for themselves
  • Urgent search for another relationship as a source of care and support when a close relationship ends
  • Extensive efforts to obtain support from others
  • Unrealistic feelings that they cannot care for themselves
122
Q

Explain the management of personality disorders

A

Management
Personality disorders are difficult to treat and in the past have been considered ‘untreatable’ by definition.. However, a number of approaches have been shown to help patients, including:

  • psychological therapies: dialectical behaviour therapy
  • treatment of any coexisting psychiatric conditions
123
Q

What is the epidemiology of schizophrenia?

A

Schizophrenia

Epidemiology

The strongest risk factor for developing a psychotic disorder (including schizophrenia) is family history. Having a parent with schizophrenia leads to a relative risk (RR) of 7.5.

124
Q

What is the risk of developing schizophrenia?

A

Risk of developing schizophrenia

  • monozygotic twin has schizophrenia = 50%
  • 50% if both parents affected
  • parent has schizophrenia = 10-15%
  • sibling has schizophrenia = 10%
  • no relatives with schizophrenia = 1%

Other selected risk factors for psychotic disorders include:

  • Black Caribbean ethnicity - RR 5.4
  • Migration - RR 2.9
  • Urban environment- RR 2.4
  • Cannabis use - RR 1.4
  • Traumatic event in childhood
  • Birth trauma (hypoxia and blood loss in particular)
  • Maternal poor health (including malnutrition and infections such as rubella and cytomegalovirus)
125
Q

What are the clinical features of schizophrenia?

A

Features

Schneider’s first rank symptoms may be divided into auditory hallucinations, thought disorders, passivity phenomena and delusional perceptions:

Auditory hallucinations of a specific type:

  • two or more voices discussing the patient in the third person
  • thought echo
  • voices commenting on the patient’s behaviour

Thought disorder*:

  • thought insertion
  • thought withdrawal
  • thought broadcasting

Passivity phenomena:

  • bodily sensations being controlled by external influence
  • actions/impulses/feelings - experiences which are imposed on the individual or influenced by others

Delusional perceptions

  • a two stage process) where first a normal object is perceived then secondly there is a sudden intense delusional insight into the objects meaning for the patient e.g. ‘The traffic light is green therefore I am the King’.
  • Other features of schizophrenia include*
  • impaired insight
  • incongruity/blunting of affect (inappropriate emotion for circumstances)
  • decreased speech
  • neologisms: made-up words
  • catatonia
  • negative symptoms: incongruity/blunting of affect, anhedonia (inability to derive pleasure), alogia (poverty of speech), avolition (poor motivation)

*occasionally referred to as thought alienation

126
Q

What are prognostic indicators of schizophrenia?

A

Prognostic indicators

Factors associated with poor prognosis

  • strong family history
  • gradual onset
  • low IQ
  • prodromal phase of social withdrawal
  • lack of obvious precipitant
  • Poor social network
  • Negative symptoms predominant

Prognosis of schizophrenia (rule of quarters)

Generally speaking, the prognosis of schizophrenia can be thought of as “the rule of quarters”. 25% never have another episode, 25% improve substantially on treatment, 25% have some improvement and 25% are resistant to treatment.

127
Q

What is the management of schizophrenia?

A

Management

NICE published guidelines on the management of schizophrenia in 2009.

  • oral atypical antipsychotics are first-line (e.g. risperidone preferred to typical antipsychotics like haloperidol)
  • cognitive behavioural therapy should be offered to all patients
  • close attention should be paid to cardiovascular risk-factor modification due to the high rates of cardiovascular disease in schizophrenic patients (linked to antipsychotic medication like clozapine (used 3rd but, is most affective → risk of agranulocytosis) and high smoking rates)
  • sedative drugs e.g. lorazepam may be used in acute behaviour disturbance e.g. paranoid schizophrenia but, will not improve psychotic symptoms
  • NICE recommends Clozapine for children and young people whose schizophrenia has not responded to adequate doses of at least two different antipsychotics used sequentially for 6-8 weeks.
128
Q

What is schizophrenia?

A

Definition

Schizophrenia is a form of psychosis that can be chronic or relapsing and remitting.

129
Q

Explain the diagnosis of schizophrenia

A

Diagnosis

The ICD-10 diagnosis of paranoid schizophrenia requires at least one symptom of:

  • Thought echo, insertion, withdrawal or broadcasting
  • Delusions of control, influence or passivity
  • Hallucinatory voices giving a running commentary on the patient’s behaviour, or discussing the patient among themselves
  • Persistent delusions of other kinds that are culturally inappropriate and completely impossible

or at least two symptoms of:

  • Persistent hallucinations in any modality, when accompanied by fleeting delusions or over-valued ideas
  • Breaks in the train of thought
  • Catatonic behaviour
  • ‘Negative’ symptoms such as marked apathy, paucity of speech and blunting or incongruity of emotional responses
  • Significant and consistent change in the overall quality of personal behaviour

These symptoms should have been present for most of the time during a period of at least one month.

130
Q

What are the investigations in schizophrenia?

A

Investigations in schizophrenia

Schizophrenia is a clinical diagnosis based on diagnostic criteria, however there are a number of tests that can be considered based on the history and examination:

  • CT/MRI head
  • HIV and syphilis screen
  • Drug testing
  • Routine bloods including FBC and TFTs
131
Q

Differentials in schizophrenia

A

Differentials of schizophrenia

There are a number of conditions that can mimic schizophrenia:

  • Substance-induced psychotic disorder (commonly drugs of abuse, but can be iatrogenic e.g. steroids)
  • Organic psychosis caused by infection, brain injury and CNS diseases such as Wilson’s disease
  • Metabolic disorder such as hyperthyroidism and hyperparathyroidism
  • Dementia and depression can also co-occur with psychosis
132
Q

Differentials in schizophrenia

A

Differentials of schizophrenia

There are a number of conditions that can mimic schizophrenia:

  • Substance induced psychotic disorder (commonly drugs of abuse, but can be iatrogenic e.g. steroids)
  • Organic psychosis caused by infection, brain injury and CNS diseases such as Wilson’s disease
  • Metabolic disorder such as hyperthyroidism and hyperparathyroidism
  • Dementia and depression can also co-occur with psychosis
133
Q

What is somatisation?

A

Somatisation disorder

  • multiple physical SYMPTOMS present for at least 2 years
  • patient refuses to accept reassurance or negative test results
134
Q

What is illness anxiety disorder? (Hypochondriasis)

A

Illness anxiety disorder (hypochondriasis)

  • persistent belief in the presence of an underlying serious DISEASE, e.g. cancer
  • patient again refuses to accept reassurance or negative test results
135
Q

What is conversion disorder?

A

Conversion disorder

  • typically involves loss of motor or sensory function
  • the patient doesn’t consciously feign the symptoms (factitious disorder) or seek material gain (malingering)
  • patients may be indifferent to their apparent disorder - la belle indifference - although this has not been backed up by some studies
136
Q

What is dissociative disorder?

A

Dissociative disorder

  • dissociation is a process of ‘separating off’ certain memories from normal consciousness
  • in contrast to conversion disorder involves psychiatric symptoms e.g. Amnesia, fugue, stupor
  • dissociative identity disorder (DID) is the new term for multiple personality disorder as is the most severe form of dissociative disorder
137
Q

What is factitious disorder?

A

Factitious disorder

  • also known as Munchausen’s syndrome
  • the intentional production of physical or psychological symptoms
138
Q

What is malingering?

A
  • Malingering*
  • fraudulent simulation or exaggeration of symptoms with the intention of financial or other gain
139
Q

What is the definition of substance use disorder? (illicit substance misuse)

A

Definition

Illicit substances may be associated with wide range of harmful effects, either immediate, short-term or long-term.

According to ICD-10, mental and behavioural disorders secondary to substance misuse may be categorised in seven ways: acute intoxication, harmful use (damage to health, either physical or mental), dependence syndrome, withdrawal state, withdrawal state with delirium, psychotic disorder, amnesic syndrome or residual and late-onset psychotic disorder.

Use of illicit substances can present with a wide range of symptoms, depending on the substance taken and the route used. There are certain hallmarks of the most commonly used illicit substances which may give an indication of the class of substance misused.

140
Q

What are clinical features of opiate intoxication?

A

Clinical features of Opiate Intoxication

Common symptoms of opiate intoxication include:

  • Drowsiness
  • Confusion
  • Decreased respiratory rate
  • Decreased heart rate
  • Constricted pupils

If the substance, such as 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.

141
Q

What are the clinical features of cannabis intoxication?

A

Clinical features of Cannabis Intoxication

Common symptoms of cannabis intoxication include drowsiness, impaired memory, slowed reflexes and motor skills, bloodshot eyes, increased appetite, dry mouth, increased heart rate and paranoia. Cannabis acts at cannabinoid receptors.

142
Q

What are the clinical features of LSD intoxication?

A

Clinical features of LSD Intoxication

Common symptoms of LSD (Lysergic Acid Dethylamide) intoxication include:

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

LSD primarily acts at dopamine receptors.

143
Q

What are clinical features of stimulant intoxication?

A

Clinical features of Stimulant Intoxication

Common symptoms of stimulant intoxication include:

  • Euphoria
  • Increased blood pressure
  • Increased heart rate
  • Increased temperature

Stimulants such as cocaine or methamphetamine 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.

144
Q

What are clinical features of opiate withdrawal?

A

Opiate Withdrawal features

Withdrawal from opiates, such as heroin, may include the following symptoms:

  • Agitation
  • Anxiety
  • Muscle aches or cramps
  • Chills
  • Runny eyes
  • Runny 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.

145
Q

What is a tension headache?

A

Tension headache

Tension-type headache is form of episodic primary headache.

Recurrent, non-disabling, bilateral headache, often described as a ‘tight-band’
Not aggravated by routine activities of daily living

146
Q

What are the characteristic features of tension headaches?

A

Characteristic features

  • often described as a ‘tight band’ around the head or a pressure sensation. Symptoms tend to be bilateral, where as migraine is typically unilateral
  • tends to be of a lower intensity than migraine
  • not associated with aura, nausea/vomiting or aggravated by routine physical activity
  • may be related to stress
  • may co-exist with migraine
147
Q

What is a chronic tension-type headache?

A

Chronic tension-type headache is defined as a tension headache occur on 15 or more days per month.

148
Q

What is the management of tension-type headaches?

A

NICE produced guidelines on the management of tension-type headache in 2012:

  • acute treatment: aspirin, paracetamol or an NSAID are first-line
  • prophylaxis: NICE recommend ‘up to 10 sessions of acupuncture over 5-8 weeks’
  • low-dose amitriptyline is widely used in the UK for prophylaxis against tension-type headache. The 2012 NICE guidelines do not however support this approach ‘…there was not enough evidence to recommend pharmacological prophylactic treatment for tension type headaches. The GDG considered that pure tension type headache requiring prophylaxis is rare. Assessment is likely to uncover coexisting migraine symptomatology with a possible diagnosis of chronic migraine.’
149
Q

What is the epidemiology of tension headaches?

A

Tension headaches

Epidemiology

Tension headaches are the most common cause of chronic recurring head pain, they are more likely to affect woman than men. They have an overall lifetime prevalence of 30-70%.

150
Q

What are the symptoms of tension headaches?

A

Symptoms

Bilateral, non-pulsatile headaches. They feel tight, like a band around the head. They may be associated with tenderness of the scalp muscles, as their contraction is the primary source of the pain.

151
Q

What are the types of headaches

A
152
Q

What are causes of acute single epidsodes?

A

Acute single episode

  • meningitis
  • encephalitis
  • subarachnoid haemorrhage
  • head injury
  • sinusitis
  • glaucoma (acute closed-angle)
  • tropical illness e.g. Malaria
153
Q

What are the causes of chronic headaches?

A

Chronic headache

  • chronically raised ICP
  • Paget’s disease
  • psychological
154
Q

What is Wernicke’s encephalopathy?

A

Wernicke’s encephalopathy

Wernicke’s encephalopathy is a neuropsychiatric disorder caused by thiamine deficiency which is most commonly seen in alcoholics. Rarer causes include: persistent vomiting, stomach cancer, dietary deficiency. A classic triad of ophthalmoplegia/nystagmus, ataxia and confusion may occur. In Wernicke’s encephalopathy petechial haemorrhages occur in a variety of structures in the brain including the mamillary bodies and ventricle walls.

  • May be caused by vitamin B1 deficiency (common cause is chronic alcohol abuse)
155
Q

What are the clinical features of Wernicke’s encephalopathy?

A

Features

  • nystagmus (the most common ocular sign)
  • ophthalmoplegia
  • ataxia
  • confusion, altered GCS
  • peripheral sensory neuropathy
156
Q

What are the investigations into Wernicke’s encephalopathy?

A

Investigations

  • decreased red cell transketolase
  • MRI
157
Q

What is the management of Wernicke’s encephalopathy?

A

Treatment is with urgent replacement of thiamine which is usually given as Pabrinex IV

158
Q

What is the relationship of Wernicke’s encephalopathy and Korsakoff syndrome?

A

If not treated Korsakoff’s syndrome may develop as well. This is termed Wernicke-Korsakoff syndrome and is characterised by the addition of antero- (most) and retrograde (limited) amnesia and confabulation in addition to the above symptoms.

159
Q

What is Korsakoff’s syndrome?

A

Korsakoff’s syndrome is thought to be a result of degeneration of the mammillary bodies. The mammillary bodies are part of the circuit of Papez which plays a role in memory formation.

160
Q

How to treat heroin overdose?

A

Naloxone

161
Q

How to treat paracetamol overdose?

A

N-acetylcysteine

162
Q

How to treat benzodiazepines?

A

Flumazenil

163
Q

How to treat cocaine overdose?

A
164
Q

How to treat ketamine overdose?

A
165
Q

How to treat alcohol overdose?

A
166
Q

How to treat beta-blockers overdose?

A
  • Try atropine 3mg IV
  • Give glucagon 2-10mg IV bolus and 5% glucose if atropine fails
167
Q

How to treat cyanide overdose?

A

Has high affinity to Fe3+, inhibits cytochrome system, decrease in aerobic respiration

  • 100% o2 and GI decontamination
168
Q

How to treat carbon monoxide poisoning?

A

100% O2

169
Q

How to treat anticoagulant overdose?

A

Major bleed = vitamin K and prothrombin complex

170
Q

How to treat ecstasy overdose?

A

There is no antidote the treatment is supportive