Psych Flashcards

1
Q

Patients ≤ 25 years who have been started on an SSRI should be reviewed when?

A

after 1 week

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2
Q

What is flight of ideas?

A

Jumping from idea to idea with links between these

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3
Q

What is Knights move?

A

Jumping from idea to idea with no links between these

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4
Q

What is the risk of SSRI in third trimester?

A

Persistent pulmonary HTN

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5
Q

What is a C/I to triptans for migraines?

A

Patients taking SSRI

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6
Q

Patients under 25 starting an SSRI should be reviewed when?

A

After 1 week

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7
Q

When do you get alcohol withdrawal symptoms, seizures and delirium?

A

symptoms: 6-12 hours
seizures: 36 hours
delirium tremens: 72 hours

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8
Q

Management of OCD?

A
  1. SSRI
  2. Clomipramine
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9
Q

OCD vs OCPD?

A

OCD must have functional component/impact of daily life

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10
Q

Management of SSRIs before ECT?

A

Dose should be reduced but not stopped

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11
Q

When should lithium levels be checked after a change in dose?

A

One week after change and then weekly until levels are stable

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12
Q

Signs of alcohol addiction

A

Attempted and failure of abstinence, compulsion to drink, narrowing of drinking repertoire, increased tolerance to alcohol, alcohol is priority over oth e r aspects of life, physical withdrawal when alcohol is stopped

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13
Q

Why can antipsychotics cause elevated prolactin?

A

Prolactin release from lactotrophs is inhibited by dopamine released from the hypothalamus. Therefore, when this inhibition is lifted, prolactin release is increased

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14
Q

How can patients appeal against being sectioned?

A

Appeal must be applied for in writing to a mental health tribunal within 14 days o f detention

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15
Q

How does activated charcoal work?

A

Activated charcoal works by providing a large surface area to absorb a potential poison and stop it from being absorbed by the GI tract;

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16
Q

Lithium toxicity may be precipitated by what?

A

NSAIDs

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17
Q

Management of PTSD?

A
  • Trauma focused CBT
  • EMDR
  • Venlafaxine/SSRI
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18
Q

Triggers for lithium toxicity

A

Dehydration
Infection
Renal failure
ACE/ARB
NSAID
Diuretic

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19
Q

How long should symptoms be present for with PTSD?

A

4 weeks

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20
Q

What is the management of lithium toxicity?

A

Mild/Moderate: IV Fluid resus
Severe: Haemodialysis

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21
Q

Bipolar I vs Bipolar II

A

Bipolar I - mania and depression
Bipolar II - hypomania and depression

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22
Q

Purposefully causing symptoms such as hypoglycaemia?

A

Munchausen syndrome

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23
Q

Hypomania in the community?

A

Routine referral to community mental health

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24
Q

How do you define chronic insomnia?

A

Trouble falling asleep/staying asleep for 3 months or longer

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25
Q

What are risk factors for insomnia?

A
  • Increasing age
  • Female gender
  • Lower educational attainment
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26
Q

Which medications can cause insomnia?

A

Corticosteroids

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27
Q

OCD vs psychosis?

A

OCD will have a level of insight of their actions

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28
Q

What can be protective factors against completed suicide ideation?

A
  • Social support
  • Religious beliefs
  • Having children at home
  • Regretting an attempt
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29
Q

What are common PTSD symptoms?

A
  • Flashbacks/nightmares
  • Avoiding people or situations
  • Hypervigilance/Sleep problems
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30
Q

Schizoid vs schizotypal PD?

A

Schizotypical will also have unusual beliefs/magical thinking

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31
Q

How should SSRI dose be stopped?

A

Over a 4 week period

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32
Q

What ophthalmic feature is associated with Charles Bonnet?

A

Age related MD

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33
Q

Flight of idea vs tangentiality?

A

In flight of ideas, they would answer the question then jump to another idea whereas in tangentiality, they would not answer the question

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34
Q

Sweating, tremor, confusion and hyperreflexia?

A

Serotonin syndrome

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35
Q

Which medications can cause serotonin syndrome?

A
  • MAO
  • SSRIs + Tramadol/St Johns Wort
  • Ecstasy
  • Amphetamines
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36
Q

Which medications can be used as mood stabilizers?

A
  • Lithium
  • Sodium valproate
  • Carbamazepine
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37
Q

5 stages of grief

A
  • Denial
  • Anger
  • Bargaining
  • Depression
  • Acceptance
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38
Q

What is an hallucination?

A

Abnormal perception in the absence of external stimulus

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39
Q

Which deaths should be referred to coroner?

A
  • Unknown cause of death
  • Death was violent or suspicious
  • Accidental death
  • Death due to self neglect
  • Death related to employment/industrial disease
  • Death during operation
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40
Q

What are risk factors for NMS?

A
  • Use of neuroleptic medication
  • High dose medication
  • Depot
  • Previous NMS
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41
Q

Which receptor is blocked in NMS?

A

Dopamine

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42
Q

What are principles of the mental capacity act?

A
  • Assume capacity
  • Decisions made in best interests
  • Help can be provided to make decision for themselves
  • People with capacity can make unwise decisions
  • Decisions made should be with the least restrictive option
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43
Q

Who can be a representative party for patients when no relatives during mental capacity discussions?

A

Independent Mental Capacity Advocates

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44
Q

What is an advanced decision?

A

Legally bound document allowing someone to state treatment they would not want in the future if they lack capacity to make the decision

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45
Q

What is panic disorder?

A

Regular, sudden or unexpected attacks of panic or fear

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46
Q

What questionnaires can be used for anxiety?

A
  • Beck Anxiety Inventory
  • Hamilton Anxiety scale
  • General health questionnaire
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47
Q

Signs of anorexia on examination

A
  • Bradycardia
  • Lanugo hair
  • Dry skin
  • Evidence of self harm
  • Acid erosion
  • Hypotension
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48
Q

What is a community treatment order?

A

Service user has to meet certain supervised conditions in the community, if they fail to do this, they may be recalled to hospital

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49
Q

Risk of using antipsychotics in elderly?

A
  • Stroke
  • VTE
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50
Q

Recurrent vomiting can cause what?

A
  • Russell sign
  • Erosion of teeth
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51
Q

Clozapine S/E

A
  • Agranulocytosis
  • Reduced seizure threshold
  • Constipation
  • Dose must be adjusted if smoking if started/stopped
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52
Q

What assessment tools can be used for depression?

A
  • HAD scale
  • PHQ-9 scale
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53
Q

Section 2

A
  • Admission for upto 28 days
  • AMHP
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54
Q

Section 3

A

Treatment for 6 months
- 2 doctors and AMHP

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55
Q

Section 4

A
  • 72 hours order
  • GP and AMHP
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56
Q

Section 5(2)

A

Detained for 72 hours by doctor

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57
Q

Section 5(4)

A

Detained for 6 hours by nurse

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58
Q

Section 17(A)

A

Community treatment order

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59
Q

Section 135

A

Police order to retrieve someone from home to place of safety

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60
Q

Section 136

A

Police order to bring someone from public place to a place of safety

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61
Q

What is the most important prognostic indicator in paracetamol overdose?

A

Arterial PH

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62
Q

What is indication for liver transplant in paracetamol overdose?

A

pH < 7.3 more than 24 hours after transplant

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63
Q

What kind of reaction does N-acetylcysteine cause?

A

Anaphylactoid - non-IgE mediated mast cell release

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64
Q

What is high in anorexia?

A
  • Growth hormone
  • Glucose
  • Salivary glands -> parotidomegaly
  • Cortisol
  • Cholesterol
  • Carotenaemia
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65
Q

When can paracetamol overdose become high risk to develop liver failure?

A
  • Chronic alcoholic
  • HIV
  • Anorexia
  • Taking P450 inducers
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66
Q

Lead pipe rigidity is a sign of what?

A

Neuroleptic malignant syndrome

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67
Q

What is a Fregoli delusion?

A

Belief that everyone is the same person/strangers are familiar

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68
Q

What is a capgras delusion?

A

Relative/Friend has been replaced by an imposter

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69
Q

What are C/I to using anti-cholinesterase inhibitors?

A
  • prolonged QT
  • 2nd/3rd degree heart block
  • Sinus bradycardia

Use Cognitive stimulation therapy instead

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70
Q

What is logoclonia?

A

Where the patient gets stuck on a particular word and repeats it

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71
Q

What is Ekbom syndrome?

A

Believe they are infested with parasites

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72
Q

What test is used to assess muscle wasting in patients with anorexia?

A

Sit-up-squad-stand test

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73
Q

Postpartum depression has to be within when?

A

12 months after birth

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74
Q

Stopping of voluntary movement or staying still in an unusual position

A

Catatonia

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75
Q

Serotonin syndrome vs NMS

A

Serotonin: faster onset, increased reflexes, dilated pupils
NMS: slower onset, decreased reflexes, normal pupils

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76
Q

Social phobia vs agoraphobia

A

Agoraphobia - fear of open spaces + crowds / difficulty of immediate easy escape to a safe place
Social Phobia - feat of scrutiny in small groups e.g. public speaking

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77
Q

Lithium can cause a benign what?

A

Leucocytosis - raised WCC

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78
Q

Antipsychotics can increase the risk of what?

A

Stroke

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79
Q

Symptoms of aspirin overdose?

A
  • Hyperventilation
  • Tinnitus
  • Sweating
  • N+V
  • Seizures
  • Causes respiratory alkalosis then metabolic acidosis
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80
Q

Conversion disorder?

A

Neuro symptoms without any underlying cause

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81
Q

Tahycardia, HTN, CNS stimulate, GI upset?

A

Think opioid withdrawal

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82
Q

What is agnosia?

A

Inability to recognise people, objects or places which were once known

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83
Q

Confusion screen bloods

A

FBC, U&E, LFTs, CRP/ESR, Ca2+, TFTs, B12, folate, syphilis, HIV

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84
Q

ophthalmoplegia, ataxia, and confusion

A

Wernickes

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85
Q

Personality disorders

A

Cluster A - Paranoid, schizoid, schizotypal
Cluster B - Antisocial, EUPD, Histrionic, Narcissistic
Cluster C - OCPD, Avoidant, Dependent

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86
Q

Fregoli delusion

A

Different people are the same person

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87
Q

How long should treatment for SSRI be continued before thinking about switching?

A

4 weeks - younger
6 weeks - elderly

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88
Q

What is schizoaffective disorder?

A

Schizophrenia with mood disturbance e.g. depression/mania

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89
Q
A
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90
Q

What should be considered in elderly patients with new onset psychosis?

A

Organic cause -> CT head

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91
Q

Acute stress disorder?

A

acute stress reaction that occurs in 1st 4w after person has been exposed to a traumatic event eg. threatened death, serious injury (road traffic accident, sexual assault ect)

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92
Q

PTSD vs acute stress disorder?

A

Acute stress disorder= occurs in 1st 4w after exposed to traumatic event

PTSD= diagnosed after 4w

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93
Q

Features of acute stress disorder?

A

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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94
Q

Examples of intrusive thoughts in acute stress disorder?

A

flashbacks, nightmares

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95
Q

Examples of dissociation in acute stress disorder?

A

being ‘in a daze’, time slowing

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96
Q

Mx for acute stress disorder?

A

1st= trauma focused CBT

acute symptoms (eg. agitations, sleep disturbance)= benzodiazepines (should only be used with caution due to addictive potential and concerns that they may be detrimental to adaptation)

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97
Q

DSM-V defines ADHD as what?

A

condition incorporating features relating to inattention and/or hyperactivity/impulsivity that are persistent

has to be an element of developmental delay (like many paeds conditions)

=<16yrs= need 6 features
17yrs+= 5 features

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98
Q

Who is ADHD more common in?

A

males

most diagnosed 3-7yrs

possible genetic component

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99
Q

Diagnostic features of ADHD (need 6 features if =<16yrs or 5 if 17yrs+)?

A

Inattention:
- does not follow through on instructions
- reluctant to enage in mentally-intense tasks
- easily distracted
- finds it difficult to sustain tasks
- finds difficult to organise tasks/activities
- forgetful in daily activities
- often lose things
- often does not seem to listen when spoken to directly

Hyperactivity/Impulsivity:
- unable to play quietly
- talks XSly
- does not wait their turn easily
- will spontaneously leave their seat when expected to sit
- is often ‘on the go’
- interruptive or intrusive to others
- will answer prematurely before a question has been finished
- will run and climb in situations not appropriate

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100
Q

ADHD is a behavioural syndrome characterised by what?

A

hyperactivity, impulsivity and inattention

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101
Q

When does ADHD typically appear?

A

3-7yrs but may not be recognised until after 7yrs esp if hyperactivity not present

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102
Q

Assessing ADHD?

A
  • core symptoms= hyperactivity, inattention and/or impulsivity present since childhood
  • result in signif psycho, social and/or educational impairment
  • symptoms present at least 6m
  • symptoms at least in 2 settings eg. home, school, social situations
  • other causes excluded
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103
Q

Suspect ADHD if at least 5 (6 in adults) inattention symptoms and/or 6 (5 in adults) hyperactivity-impulsivity symptoms that have….

A
  • started <12yrs old
  • occurred in 2+ setting
  • present for at least 6m
  • interfered with or reduced quality of social, academic or occupational functioning
  • not explained by another disorder eg. oppositional defiant disorder or conduct disorder
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104
Q

Ix for ADHD?

A
  • formal diagnosis and Tx carried out by specialist
  • if only moderate impairment can be initially Mx in primary care with self-help, behavioural Mx or parent support programmes
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105
Q

What to do if ADHD is suspected in a child?

A

1) assess social and educational impact of their symptoms

2) if adverse effects on life then= watch and wait up to 10w with self help and behavioural Mx; parent support group

3) Refer children to CAMHS, specialist paeds or child psychiatrist if severe, watching not acceptable or problems persist

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106
Q

What to do if ADHD is suspected in a adult?

A

1) assess psych, social, educational or occupational impact of symptoms

2) refer pt without prior diagnosis for assessment by specialist
2) if previously Tx for ADHD then refer to general adult psych services for assessment

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107
Q

How to assess social and educational impact of ADHD in child?

A

School-age children= extent of impairment should be judged in the context of self-care (for example, eating, or hygiene), travelling independently, making and keeping friends, achieving in school, forming positive relationships with other family members, developing a positive self-image, avoiding criminal activity, avoiding substance misuse, maintaining emotional states free of excessive anxiety and unhappiness, and understanding and avoiding common hazards.

For adolescents, difficulties may extend to cover occupational or educational underachievement, dangerous driving, and difficulties in carrying out daily activities (such as shopping and organizing household tasks), in making and keeping friends, and intimate relationships (for example, excessive disagreement).

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108
Q

Suspected ADHD= in addition to assessing social and educational impact of their symptoms in children, primary care practitioners with appropriate training/expertise may wish to augment this assessment using what?

A

Strengths and Difficulties questionnaire or the Conners’ rating scale.

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109
Q

Mx of ADHD is initiated and coordinated by who?

A

Specialists

Depending on locally-agreed shared care arrangements, drug treatments initiated and titrated by a specialist may be continued and monitored in primary care.

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110
Q

What should be documented in pts notes if they have ADHD and on treatment?

A

1) weight= every 3m if 10yrs and younger; 3m & 6m when starting Tx and every 6m after in children >10yrs; every 6m in adults (BMI)

2) height= every 6m

3) BP and HR= before and after each dose change and every 6m

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111
Q

When to seek specialist advice for pt who has ADHD and is managed in primary care using shared care arrangement?

A

if drug treatment results in sustained resting tachycardia (>120 bpm), arrhythmia, or systolic blood pressure greater than the 95th percentile (or a clinically significant increase) measured on two occasions, or other significant adverse effects develop.

Specialist advice should also be sought if a child or young person’s height over time is significantly affected by medication (that is, they have not met the height expected for their age), as a planned break in treatment over school holidays may be required to allow ‘catch-up’ growth.

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112
Q

ADHD: what to give advice on if adult is prescribed an amfetamine eg. dexamfetamine or lisdexamfetamine) for ADHD?

A

They should not drive if they feel drowsy, dizzy, unable to concentrate or make decisions, or if they have blurred or double vision.

It is now an offence to drive if they have more than a specified amount of amfetamines in their body, whether driving is impaired or not. It may be helpful for the person to keep evidence (such as the other half of their prescription) in the car to show that they are taking the amfetamine in accordance with medical advice.

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113
Q

Diet and exercise advise for pt with ADHD?

A

normal healthy diet and regular exercise

if appears to be a link between certain food/drink advise to keep food diary; ?refer to dietician before dietary elimination considered

if weight a problem= take ADHD meds with or after food not before; additional meals/snacks in morning or late evening when drugs worn off

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114
Q

Secondary care Mx for preschool children with ADHD?

A

1st line= ADHD focused group parent-training programme

  • if still impairment after environmental modifications been implemented, advise from ADHD service specialist
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115
Q

Secondary care Mx for school aged children and young people with ADHD?

A
  • group support to pt and parents= education and info; liaison with school/uni if consent
  • individual parent-training programmes if can’t attend group or too complex for group
  • Still not improved= methylphenidate
  • if insomnia= melatonin 6-17yrs
  • if medication effective but still impairment eg. social skills, self control= CBT
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116
Q

Secondary care Mx for adults with ADHD?

A
  • environmental modifications
  • no improved= medication
  • meds effective but still impairment= structured supportive psychological intervention, regular follow up and/or CBT
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117
Q

Medication for ADHD?

A

methylphenidate

contraindicated/ineffective= Lisdexamfetamine, dexamfetamine or atomoxetine

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118
Q

Following presentation with suspected ADHD, immediate Mx?

A

watch and wait for 10w to observe if symptoms change or resolve

if persists then refer to secondary care= CAMHS or specialist paeds for tailored plan of action

holistic approach= parents attending education and training programmes; medication last resort if this fails or if severe

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119
Q

When is drug therapy used for ADHD?

A

last resort and only in pts aged 5yrs+

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120
Q

1st line drug for ADHD?

A

methylphenidate
initially 6w trial

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121
Q

MOA of methylphenidate for ADHD?

A

CNS stimulant which acts as a dopamine/norepinephrine reuptake inhibitor

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122
Q

Side effects of methylphenidate for ADHD?

A

abdo pain, nausea, dyspepsia, stunted growth in children, weight loss

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123
Q

What should be monitored every 6m if on methylphenidate for ADHD?

A

height and weight

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124
Q

What if methylphenidate not effective for ADHD Mx?

A

switch to lisdexamfetamine;

Dexamfetamine should be started in those who have benefited from lisdexamfetamine, but who can’t tolerate its side effects.

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125
Q

1st line ADHD meds in adults?

A

Methylphenidate or lisdexamfetamine are first-line options;

Switch between these drugs if no benefit is seen after a trial of the other.

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126
Q

What should be done before starting pt on ADHD drugs?

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.

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127
Q

Why is baseline ECG done before starting ADHD drugs?

A

all ADHD drugs potentially cardiotoxic

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128
Q

Autism?

A

pattern of qualitative differences and impairments in reciprocal social interaction and social communication, combined with restricted interests and rigid and repetitive behaviours, often with lifelong impact

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129
Q

When do features of autism usually present?

A

in early childhood

persistent

may not become apparent until a change in the child or young person’s life eg. transition to school

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130
Q

Difficulties in autism can affect what?

A

personal, social, educational, occupational or other functioning

usually observable in all settings

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131
Q

Autism spectrum disorder?

A

broad, heterogeneous neurodevelopmental disorder which is behaviourally defined, with different levels of severity, that encompasses autism, Asperger’s syndrome, and atypical autism.

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132
Q

Cause of autism?

A

unknown

genetic, neurobiological and environmental factors

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133
Q

Autism may be associated with range of coexisting problems such as what?

A

neurodevelopmental= learning disability, severe visual & hearing impairments, motor or co-ordination disorders, speech & language disorders, epilepsy, ADHD

Mental health= anxiety, depression, conduct disorder, Tourettes

Functional= sleep, diet, nutrition, bladder and bowel

Other= social isolation, exclusion, bullying, child exploitation and maltreatment, carer stress

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134
Q

Assessment for suspected autism in child?

A
  • developmental history and behaviour, speech, language and communication; social skills; sensory difficulties; severity and duration of features and presence in different settings; impact on the person and family/carers; family history; risk factors for autism; coexisting physical, mental health, and behavioural problems; educational history; safeguarding issues, any previous assessments and treatments.

Examination of general appearance, developmental stage, growth, eye contact, vocabulary and language skills, social interaction and communication, behaviour; neurological, vision and hearing assessment.

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135
Q

Ix/Mx for suspected autism?

A
  • referral to local team/paeds/psych depending on age, RFs, level of concern
  • if suspect genetic/chromosomal anomaly= refer to clinical genetics specialist
  • review after watchful waiting and gathering info about development and behaviour from other health, social and educational professionals if uncertain
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136
Q

Mx of child with confirmed autism?

A
  • liasise with allocated key worker and local autism team for ongoing care and support= social and communication skills, physical and mental health, behaviour that challenges, sleep, safeguarding concerns
  • info and support
  • advise about making reasonable adjustments or adaptations, structuring time and activities, carer support and future planning
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137
Q

When to suspect autism in preschool child? (features consistently present across different settings)

A
  • language delay or regression, unusual characteristics of spoken language, reduced/infrequent use of language
  • reduced or absent interaction with others
  • reduced eye contact, pointing and other gestures
  • reduced or absent imagination and variety of pretend play
  • unusual or restricted interests and/or rigid and repetitive behaviours eg. hand flapping, body rocking while standings, spinning
  • over or under reaction to sensory stimuli eg. sounds, smells, taste, textures; extreme food fads
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138
Q

When may diagnosing autism be challenging?

A
  • <24m
  • child developmental age of <18m
  • child where lack of info about early life eg. adopted
  • severe sensory impairment eg. hearing or vision or motor disorder eg. cerebral palsy
  • milder symptoms and/or average or above intelligence
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139
Q

When to suspect autism in primary school/secondary school child? (features consistently present across different settings)

A
  • unusual speech eg. limited, repetitive, monotonous
  • reduced, absent or negative response to others eg. reduced/absent response to facial expressions; reduced/no response to name but normal hearing
  • reduced or absent interaction with others
  • reduced or absent eye contact, pointing or other gestures
  • reduced or absent ideas and imagination
  • unusual or restricted interests and/or rigid and repetitive behaviours eg. strong preference for for familiar routines and dislike of change
  • over or under reaction to sensory stimuli
  • unusual profile of skills or deficits eg. skills or knowledge advanced for chronological or mental age
  • social development more immature eg. XS trusting
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140
Q

ASD?

A

autism spectrum disorder

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141
Q

Prognosis of autism?

A

no cure for ASD, early diagnosis and intensive educational and behavioural management may improve outcomes

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142
Q

Around 50% of children with ASD have what

A

intellectual disability

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143
Q

Autism: when may features present?

A

Social communication impairments and repetitive behaviours are present during early childhood (typically evident before 2-3 years of age), or maybe manifested later.

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144
Q

Clinical features of autism can be classified as what?

A
  • impaired social communication and interaction
  • repetitive behaviours, interests and activities
  • often associated with intellectual impairment or language impairment
  • may also have ADHD (35%) and epilepsy (18%)
  • associated with higher head circumference to brain volume ratio
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145
Q

What conditions are associated with autism?

A

ADHD (35%) and epilepsy (18%)

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146
Q

Clinical features of autism= examples of impaired social communication and interaction?

A

Children frequently play alone (younger children may not play alongside other children) 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.

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147
Q

Clinical features of autism= examples of repetitive behaviours, interests and activities?

A

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.

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148
Q

Mx for autism should be what?

A

initiated early, involves educational and behavioural Mx, medical therapy and family counselling

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149
Q

Goal in the Mx of autism?

A

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
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150
Q

Non-pharmacological therapy for autism?

A

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).

Family support and counselling:
- Parental education on interaction with the child and acceptance of his/her behaviour.

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151
Q

Pharmacological interventions for autism?

A

no consistent evidence

may need methylphenidate if also have ADHD

self-injury, aggression= antipsychotic drugs

anxiety, aggression, repetitive behaviours= SSRIs

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152
Q

What was bipolar previously known as?

A

manic depression

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153
Q

Bipolar?

A

serious long term mental illness, characterised by episodic depressed and elated moods, and increased activity (hypomania or mania)

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154
Q

Manic episode in bipolar according to NICE?

A

period during which there is abnormally and persistently elevated, expansive, or irritable mood lasting at least 1 week, accompanied by at least three additional symptoms, and which is severe enough to cause marked impairment in social or occupational functioning or necessitate hospitalization, or which includes psychotic features.

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155
Q

Hypomanic episode in bipolar according to NICE?

A

similar to a manic episode except that a diagnosis only requires that symptoms have lasted for 4 days, is not severe enough to cause marked impairment in social or occupational functioning or necessitate hospitalization, and there are no psychotic features.

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156
Q

Depressive episode in bipolar according to NICE?

A

period of at least 2 weeks during which there is either depressed mood or loss of interest or pleasure in nearly all activities (or irritability in children and adolescents), accompanied by at least four additional depressive symptoms.

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157
Q

What is a mixed episode in bipolar according to NICE?

A

A mixture or rapid alternation of manic and depressive symptoms, or

A period of time (at least 1 week) in which the criteria are met for either a manic or hypomanic episode and at least three symptoms of depression are present during the majority of the days of the current or most recent episode of mania or hypomania, or

A period of time (at least 2 weeks) in which the criteria for a major depressive episode are met and at least three manic or hypomanic symptoms are present during the majority of days of the current or most recent episode of depression.

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158
Q

What is rapid-cycling bipolar disorder?

A

defined as the experience of at least four depressive, manic, hypomanic, or mixed episodes within a 12-month period.

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159
Q

Most important Cx of bipolar?

A

suicide and deliberate self-harm

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160
Q

Cx of acute episodes in bipolar?

A
  • suicide and self-harm
  • Financial difficulties from overspending.
  • Traumatic injuries and accidents.
  • Sexually transmitted infections and unplanned pregnancy from disinhibition and increased libido.
  • Damage to reputation, income and occupation, and relationships.
  • Self-neglect, exhaustion, and dehydration.
  • Exploitation by others.
  • Alcohol and substance misuse.
  • Harm to others.
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161
Q

When to suspect bipolar in someone?

A

present with symptoms suggestive of mania, hypomania, depression and a history of previous episodes of possible mania or hypomania, or a mixture of both manic and depressive symptoms.

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162
Q

What to do if suspect bipolar disorder?

A
  • refer for specialist mental health assessment, Mx, follow up
  • risk assessment to determine urgency of referral
  • if considered a danger to themselves or other then arrange hospital admission

-Tx in secondary care but can be transferred to primary care for ongoing Mx once stabilised

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163
Q

Diagnostic criteria for bipolar disorder in children and young people state that…

A
  • Mania must be present.
  • Euphoria must be present on most days and for most of the time, for at least 7 days.
  • Irritability is not a core diagnostic criterion.
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164
Q

Suspect bipolar if pt has or has had any symptoms of what?

A
  • mania
  • hypomania
  • depression and history of previous episodes of mania or hypomania
  • mixture of both manic and depressive symptoms
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165
Q

List symptoms of mania in bipolar?

A
  • abnormally elevated mood, extreme irritability, aggression
  • increased activity/energy, restlessness, decreased need for sleep eg. feel rested after 3hrs sleep
  • pressure of speech or incomprehensible speech
  • flight of ideas or racing thoughts
  • distractibility, poor conc
  • increased libido, disinhibition, sexual indiscretion
  • extravagant or impractical plans eg. spending sprees
  • psychotic symptoms eg. delusions (grandiose) or hallucinations (usually voices)
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166
Q

Diagnosis of manic episode in bipolar requires symptoms of mania lasting how long?

A

at least 7 days which usually begin abruptly

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167
Q

examples of psychotic symptoms in manic episode in bipolar?

A

delusions (usually grandiose) or hallucinations (usually voices)

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168
Q

What suggests hypomania in bipolar?

A

symptoms of mania that are not severe enough to cause marked impairment and the absence of psychotic features

  • mild elevation of mood/irritability
  • increased energy & activity which may lead to increased performance at work/socially
  • feeling of well-being, physical and mental efficiency
  • increased sociability, talkativeness and over familiarity
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169
Q

Diagnosis of hypomanic episode in bipolar requires what?

A

symptoms to last at least 4d

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170
Q

Mixed episode in bipolar?

A

mixture or rapid alternation (usually within few hrs) of manic/hypomanic and depressive symptoms

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171
Q

Are symptoms of depression required to diagnose bipolar?

A

no

but at onset, most people with bipolar disorder present with a depressive episode, and a proportion of people with a diagnosis of unipolar depression will actually have bipolar disorder.

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172
Q

Symptoms and signs that may help distinguish bipolar disorder from unipolar depression include:

A

Hypersomnia, lability, and weight instability (experienced by around 90% of people with bipolar disorder and around around 50% of people with unipolar depression).

Earlier age of onset (peak age 15 to 19 years), abrupt onset (possibly triggered by stressor).

More frequent episodes of shorter duration.

Comorbid substance misuse.

Higher post-partum risk.

Psychosis, psychomotor retardation, and catatonia.

Lower likelihood of somatic symptoms.

FHx bipolar

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173
Q

When diagnosing bipolar, what is it important to do?

A

be aware of differential diagnoses to determine whether TFTs, FBC, vit D or other bloods (incl. toxicology screen) are required

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174
Q

How is bipolar diagnosed in secondary care?

A

adults= refer to specialist mental health

children= made after intensive monitoring by specialist:
<14yrs= refer to CAMHS
14-18yrs= specialist early intervention in psychosis or CAMHS

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175
Q

Differential diagnosis for autism (may be misdiagnosed or comorbid also)?

A
  • unipolar depression
  • cyclothymia
  • schizophrenia
  • mood disorders due to stroke, thyroid disease or MS
  • substance misuse
  • organic brain disease
  • iatrogenic= antidepressents, levodopa, corticosteroids, methylphenidate
  • metabolic disorders= hyperthyroidism, Cushings, Addisions, vit B12 def, end-stage kidney disease
  • personality disorders
  • anxiety disorders
  • OCD
  • PTSD
  • ADHD
  • sexual, emotional or physical abuse
  • learning difficulties
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176
Q

most common comorbidities in people with bipolar disorder include

A

anxiety disorders, alcohol and substance misuse, and personality disorders. Comorbidity occurs in two-thirds of people with bipolar disorder throughout their lifetimes.

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177
Q

Onset of mania in later life may be indicative of what?

A

underlying medical comorbidity

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178
Q

Mx of bipolar in the acute phase?

A

therapeutic trial of oral antipsychotic eg. haloperidol, olanzapine, quetiapine or risperidone

if 1st not effective, can add 2nd, if still not can add lithium

mixed episodes Tx same as mania

Tx of depression= Quetiapine alone, or
Fluoxetine combined with olanzapine

  • 4w after acute episode resolved then secondary care Mx long term
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179
Q

Chronic mental health disorder characterised by periods of mania/hypomania alongside episodes of depression

A

bipolar disorder

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180
Q

Epidemiology of bipolar?

A

typically develops in late teen years

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181
Q

2 types of bipolar disorder?

A

Type I= mania and depression (most common)

Type II= hypomania and depression

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182
Q

What is hypomania and mania?

A

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

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183
Q

Hypomania vs mania?

A

psychotic symptoms (e.g.delusions of grandeur or auditory hallucinations) suggest mania

no psychotic symptoms= hypomania

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184
Q

Mx for bioplar?

A
  • psychological interventions
  • mood stabiliser= lithium; alternative is valproate
  • Mx of mania/hypomania= consider stopping antidepressant if the patient takes one; antipsychotic therapy e.g. olanzapine or haloperidol
  • Mx of depression= talking therapies; fluoxetine antidepressant of choice
  • adress co-morbidities= 2-3 times increased risk of diabetes, cardiovascular disease and COPD
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185
Q

Mx of mania/hypomania in bipolar?

A

consider stopping antidepressant if the patient takes one; antipsychotic therapy e.g. olanzapine or haloperidol

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186
Q

Mx of depression in bipolar?

A

talking therapies; fluoxetine is the antidepressant of choice

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187
Q

Mood stabiliser of choice in bipolar?

A

lithium

valproate alternative

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188
Q

Primary care referral for bipolar?

A

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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189
Q

Pts with bipolar may have what to help with Mx of relapse?

A

advanced care plan

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190
Q

Advice to pt with bipolar to prevent relapse?

A

Encouraging compliance with treatment.
Maintaining an adequate amount of sleep.
Avoidance, if possible, of shift work, night flying and flying across time zones, or routinely working excessively long hours.
Establishing a regular routine in the morning.
Structuring the day with some activity and social contact.
Self-monitoring of symptoms (including triggers and early warning signs) and coping strategies.
Avoiding caffeinated drinks such as tea, coffee, or cola.
Smoking — advise the person to stop, or if this is not possible cut down (nicotine is a stimulant).
Avoiding alcohol and drug misuse.

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191
Q

Lithium?

A

mood stabilising drug used most commonly prophylactically in bipolar disorder but also as an adjunct in refractory depression

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192
Q

Therapeutic range and half life for lithium?

A

very narrow therapeutic range (0.4-1.0 mmol/L) and a long plasma half-life being excreted primarily by the kidneys.

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193
Q

MOA of lithium?

A

not fully understood, two theories:
- interferes with inositol triphosphate formation
- interferes with cAMP formation

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194
Q

Adverse effects of lithium?

A

nausea/vomiting, diarrhoea

fine tremor

nephrotoxicity: polyuria, secondary to nephrogenic diabetes insipidus

thyroid enlargement, may lead to hypothyroidism

ECG: T wave flattening/inversion

weight gain

idiopathic intracranial hypertension

leucocytosis

hyperparathyroidism and resultant hypercalcaemia

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195
Q

Lithium ECG changes?

A

T wave flattening/inversion

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196
Q

When to check lithium levels to monitor, when should the sample be taken?

A

12hrs post dose

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197
Q

When should lithium be monitored when starting?

A

after starting, levels should be performed weekly and after each dose change until concentrations are stable

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198
Q

When should lithium blood levels be monitored?

A

every 3m

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199
Q

When should lithium levels be checked after a change in dose?

A

1w after changing and weekly until levels are stable

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200
Q

Monitoring lithium= what should be checked every 6m?

A

thyroid and renal function

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201
Q

What should pts with bipolar be given when started on lithium?

A

info booklet, alert card and record book

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202
Q

Monitoring of lithium in bipolar?

A
  • when checking levels, take sample 12hrs post dose
  • check weekly after starting until concentrations are stable
  • check levels weekly after change in dose
  • once levels stable check levels every 3m
  • every 6m check thyroid and renal function
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203
Q

How is depression classified?

A

less severe and more severe depresson

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204
Q

‘Less severe’ depression?

A

PHQ-9 score <16

previously termed subthreshold and mild depression

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205
Q

‘More severe’ depression?

A

PHQ-9 score >=16

previously termed moderate and severe depression

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206
Q

Mx of less severe depression (in order of preference)?

A

1) guided self-help
2) group CBT
3) group behavioural activation (BA)
4) Individual CBT
5) Individual BA
6) group exercise
7) group mindfulness and meditation
8) interpersonal psychotherapy (IPT)
9) SSRIs
10) counselling
11) short-term psychodynamic psychotherapy (STPP)

(order of preference)

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207
Q

Are antidepressants offered 1st line for less severe depression?

A

no, unless that is the pts preference

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208
Q

How is Tx approached in less severe depression?

A

discuss Tx options with pts to reach shared decision; least intrusive and least resource intensive Tx 1st

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209
Q

Mx for more severe depression (in order of preference)?

A

1) combined CBT and antidepressant
2) individual CBT
3) Individual behavioural activation
4) Antidepressants= SSRI or SNRI or other
- individual problem-solving
counselling
- short-term psychodynamic psychotherapy (STPP)
- interpersonal psychotherapy (IPT)
- guided self-help
- group exercise

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210
Q

What 2 questions can be used to screen for depression?

A

‘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?’

if yes to either then more depth assessment needed

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211
Q

Name 2 tools to assess degree of depression?

A

Hospital Anxiety and Depression (HAD) scale

and

Patient Health Questionnaire (PHQ-9)

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212
Q

Assessing depression: Hospital Anxiety and Depression (HAD) scale?

A

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

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213
Q

Assessing depression: Patient Health Questionnaire (PHQ-9)?

A

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

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214
Q

How is severity of depression grouped?

A

2 groups= less severe and more severe

used to be subthreshold, mild, moderate and severe

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215
Q

Score <16 on PHQ-9?

A

less severe depression

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216
Q

Score of 16 or more on PHQ-9?

A

more severe depression

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217
Q

What provides a criteria for diagnosing major depressive disorder (MDD) aka depression?

A

DSM-5

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218
Q

How many symptoms needed to diagnose depression (major depressive disorder) according to DSM-5 criteria?

A

Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure.

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219
Q

Symptoms in the DSM-5 criteria to diagnose depression include what?

A
  • Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad, empty, hopeless) or observation made by others (e.g., appears tearful). (Note: In children and adolescents, can be irritable mood.)
  • Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation).
  • Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a month), or decrease or increase in appetite nearly every day. (Note: In children, consider failure to make expected weight gain.)
  • Insomnia or hypersomnia nearly every day.
  • Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down).
  • Fatigue or loss of energy nearly every day.
  • Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick).
  • Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others).
  • Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.
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220
Q

Depression meds= can you switch from from citalopram, escitalopram, sertraline, or paroxetine to another SSRI?

A

direct switch possible

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221
Q

Depression meds= switching between fluoxetine to another SSRI?

A

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

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222
Q

Depression meds: switching from SSRI to tricyclic antidepressant (TCA)?

A

cross-tapering is recommended (the current drug dose is reduced slowly, whilst the dose of the new drug is increased slowly)

  • an exception is fluoxetine which should be withdrawn, the leave a gap of 4-7 days prior to TCAs being started at a low dose
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223
Q

Depression meds: switching from citalopram, escitalopram, sertraline, or paroxetine to venlafaxine?

A

direct switch is possible (caution if paroxetine used)

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224
Q

Depression meds: switching from fluoxetine to venlafaxine?

A

withdraw and then start venlafaxine at a low dose 4–7 days later

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225
Q

SSRI stands for?

A

selective serotonin reuptake inhibitors

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226
Q

1st line medical Mx for depression?

A

SSRIs

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227
Q

Examples of SSRIs?

A
  • citalopram
  • sertraline
  • fluoxetine
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228
Q

What SSRI is useful post MI?

A

sertraline

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229
Q

SSRIs should be used in caution in what population?

A

children and adolescents

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230
Q

SSRI of choice when indicated in a child or adolescent with depression?

A

fluoxetine

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231
Q

Adverse effects of SSRIs?

A
  • GI symptoms (most common)
  • increased risk GI bleeding so PPI if also taking NSAIDs
  • increased anxiety after starting
  • fluoxetine and paroxetine have a higher propensity for drug interactions
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232
Q

When first starting SSRI, what should you warn pts?

A

anxiety and agitation may increase at first

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233
Q

SSRIs: citalopram and escitalopram are associated with what? So do not use in who?

A

dose-dependent QT interval prolongation

those with= congenital long QT syndrome; known pre-existing QT interval prolongation; or in combination with other medicines that prolong the QT interval

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234
Q

Citalopram max daily dose (due to dose-dependent QT interval prolongation)?

A

40 mg for adults; 20 mg for patients older than 65 years; and 20 mg for those with hepatic impairment

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235
Q

Interactions with SSRIs?

A
  • NSAIDs (do not offer SSRIs but if do then give PPI too)
  • warfarin and heparin= consider mirtazapine not SSRI
  • aspirin
  • triptans
  • monoamine oxidase inhibitors (MAOIs)
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236
Q

Why to avoid SSRIs in pts taking triptans or MAOIs?

A

increased risk of serotonin syndrome

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237
Q

When to review pt by a doctor after starting antidepressant therapy?

A

after 2w

but if <25yrs or at risk of suicide then review after 1w

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238
Q

How long should pt be on antidepressants?

A

if good response then be on at least 6m after remission (symptoms better) to reduce risk of relapse

(don’t stop as soon as feel better)

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239
Q

How to stop SSRI antidepressants?

A

the dose should be gradually reduced over a 4 week period (this is not necessary with fluoxetine). Paroxetine has a higher incidence of discontinuation symptoms.

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240
Q

SSRI discontinuation symptoms?

A

increased mood change
restlessness
difficulty sleeping
unsteadiness
sweating
gastrointestinal symptoms: pain, cramping, diarrhoea, vomiting
paraesthesia

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241
Q

SSRIs and pregnancy?

A
  • weigh up benefits and risk when deciding whether to use in pregnancy.
  • Use during the first trimester gives a small increased risk of congenital heart defects
  • Use during the third trimester can result in persistent pulmonary hypertension of the newborn
  • Paroxetine has an increased risk of congenital malformations, particularly in the first trimester
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242
Q

Risk of SSRIs in 1st trimester of pregnancy?

A

small increased risk of congenital heart defects

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243
Q

Use of SSRIs during 3rd trimester of pregnancy?

A

can result in persistent pulmonary HTN of the newborn

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244
Q

Paroxetine (SSRI) and pregnancy?

A

increased risk of congenital malformations, esp in 1st trimester

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245
Q

Features of beta-blocker overdose?

A

bradycardia
hypotension
heart failure
syncope

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246
Q

Mx of beta blocker overdose?

A
  • bradycardic= atropine
  • resistant then give glucagon

haemodialysis NOT effective

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247
Q

Drugs that can be cleared with haemodialysis in overdose?

A

BLAST

Barbiturate
Lithium
Alcohol (inc methanol, ethylene glycol)
Salicylates
Theophyllines (charcoal haemoperfusion is preferable)

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248
Q

Drugs that cannot be cleared with haemodialysis in overdose?

A

tricyclics
benzodiazepines
dextropropoxyphene (Co-proxamol)
digoxin
beta-blockers

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249
Q

Cx of iron overdose?

A
  • metabolic acidosis
  • erosion of gastric mucosa= GI bleeding
  • shock
  • hepatotoxicity and coagulopathy
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250
Q

Iron overdose= Mx is guided by what?

A

total amount of iron ingested (elemental iron/kg) and the presence/absence of symptoms (abdominal pain, diarrhoea, vomiting, lethargy)

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251
Q

Mx of iron overdose= ingested <40mg/kg elemental iron and are symptomatic?

A

observed at home

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252
Q

Mx of iron overdose= ingested >40mg/kg iron or symptomatic?

A

medical assessment with serum iron levels measured 2-4 hours post-ingestion and abdominal x-ray

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253
Q

Iron overdose= Mx for all patients presenting within 4 hours who have ingested > 60mg/kg elemental iron or have undissolved tablets on abdominal x-ray?

A

Whole bowel irrigation

if not effective or iron is adhered to gastric wall then endoscopy or surgery

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254
Q

Can you use activated charcoal in iron poisoning?

A

no

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255
Q

Drug used in iron overdose?

A

Desferrioxamine

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256
Q

When is desferrioxamine indicated in iron overdose?

A

Patients with serum iron level > 90umol/l,

Patients with serum iron level 60-90umol/l, who are symptomatic or have persistent iron on abdominal x-ray despite whole bowel irrigation

Any patient with shock, coma or metabolic acidosis

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257
Q

When is lithium used?

A

prophylactically in bipolar disorder but also as an adjunct in refractory depression

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258
Q

Half-life of lithium?

A

long plasma half-life

excreted by kidneys

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259
Q

Lithium toxicity generally occurs following concentrations of what?

A

> 1.5mmol/L

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260
Q

Lithium toxicity may be precipitated by what?

A

dehydration

renal failure

drugs: diuretics (especially thiazides), ACE inhibitors/angiotensin II receptor blockers, NSAIDs and metronidazole.

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261
Q

Features of lithium toxicity?

A

coarse tremor (a fine tremor is seen in therapeutic levels)
hyperreflexia
acute confusion
polyuria
seizure
coma

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262
Q

Mx of lithium toxicity?

A

mild-moderate= may respond to volume resuscitation with normal saline:
- IV fluids with isotonic saline, until euvolemic, then typically twice maintenance rate
- monitor serum sodium closely (every 4 hours with serial lithium concentrations) if there is a concern about lithium-induced nephrogenic diabetes insipidus

haemodialysis may be needed in severe toxicity

sodium bicarbonate is sometimes used but there is limited evidence to support this (by increasing the alkalinity of the urine it promotes lithium excretion)

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263
Q

Paracetamol overdose= minority of pts that present within 1hr may benefit from what?

A

activated charcoal to reduce absorption of the drug

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264
Q

Drug for the Mx of paracetamol overdose?

A

N-Acetylcysteine

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265
Q

When should acetylcysteine be given in paracetamol overdose?

A

the plasma paracetamol concentration is on or above a single treatment line joining points of 100 mg/L at 4 hours and 15 mg/L at 15 hours, regardless of risk factors of hepatotoxicity

there is a staggered overdose or there is doubt over the time of paracetamol ingestion, regardless of the plasma paracetamol concentration

patients who present 8-24 hours after ingestion of an acute overdose of more than 150 mg/kg of paracetamol even if the plasma-paracetamol concentration is not yet available

patients who present > 24 hours if they are clearly jaundiced or have hepatic tenderness, their ALT is above the upper limit of normal
- acetylcysteine should be continued if the paracetamol concentration or ALT remains elevated whilst seeking specialist advice

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266
Q

What rate is aceytlcysteine infused over in paracetamol overdose?

A

1hr (used to be 15mins)

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267
Q

Why in paracetamol overdose, is acetylcysteine infused over 1hr and not 15mins?

A

reduce the number of adverse effects.

Acetylcysteine commonly causes an anaphylactoid reaction (non-IgE mediated mast cell release).

Anaphylactoid reactions to IV acetylcysteine are generally treated by stopping the infusion, then restarting at a slower rate.

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268
Q

Anaphylactoid reactions to IV acetylcysteine are generally treated by

A

stopping the infusion, then restarting at a slower rate.

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269
Q

Paracetamol overdose= King’s College Hospital criteria for liver transplantation (paracetamol liver failure)?

A

Arterial pH < 7.3, 24 hours after ingestion

or all of the following:
- prothrombin time > 100 seconds
- creatinine > 300 µmol/l
- grade III or IV encephalopathy

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270
Q

When is an overdose considered as staggered?

A

if all the tablets were not taken within 1hr

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271
Q

Pathophysiology behind paracetamol overdose?

A

The liver normally conjugates paracetamol with glucuronic acid/sulphate. During an overdose the conjugation system becomes saturated leading to oxidation by P450 mixed function oxidases*. This produces a toxic metabolite (N-acetyl-B-benzoquinone imine)

Normally glutathione acts as a defence mechanism by conjugating with the toxin forming the non-toxic mercapturic acid. If glutathione stores run-out, the toxin forms covalent bonds with cell proteins, denaturing them and leading to cell death. This occurs not only in hepatocytes but also in the renal tubules

*this explains why there is a lower threshold for treating patients who take P450 inducing medications e.g. phenytoin or rifampicin

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272
Q

Pathophysiology behind paracetamol overdose= why is N-acetyl cysteine used?

A

as it is a precursor of glutathione and hence can increase hepatic glutathione production

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273
Q

The following groups of patients are at an increased risk of developing hepatotoxicity following a paracetamol overdose:

A

1) patients taking liver enzyme-inducing drugs (rifampicin, phenytoin, carbamazepine, chronic alcohol excess, St John’s Wort)

2) malnourished patients (e.g. anorexia nervosa) or patients who have not eaten for a few days

Acute alcohol intake, as opposed to chronic alcohol excess, is not associated with an increased risk of developing hepatotoxicity and may actually be protective.

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274
Q

Salicylate overdose leads to what results on ABG?

A

mixed respiratory alkalosis and metabolic acidosis.

Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis. In children metabolic acidosis tends to predominate.

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275
Q

Features of salicylate overdose?

A

hyperventilation (centrally stimulates respiration)
tinnitus
lethargy
sweating, pyrexia
nausea/vomiting
hyperglycaemia and hypoglycaemia
seizures
coma

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276
Q

Why may pt get pyrexia with salicylate overdose?

A

salicylates cause the uncoupling of oxidative phosphorylation leading to decreased adenosine triphosphate production, increased oxygen consumption and increased carbon dioxide and heat production

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277
Q

Tx for salicylate overdose?

A

general (ABC, charcoal)

urinary alkalinization with intravenous sodium bicarbonate - enhances elimination of aspirin in the urine

haemodialysis

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278
Q

Indications for haemodialysis in salicylate overdose?

A

serum concentration > 700mg/L

metabolic acidosis resistant to treatment

acute renal failure

pulmonary oedema

seizures

coma

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279
Q

Causes of serotonin syndrome?

A

monoamine oxidase inhibitors

SSRIs
- St John’s Wort, often taken over the counter for depression, can interact with SSRIs to cause serotonin syndrome
- tramadol may also interact with SSRIs

ecstasy

amphetamines

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280
Q

Features of serotonin syndrome?

A

neuromuscular excitation= hyperreflexia, myoclonus, rigidity

autonomic nervous system excitation= hyperthermia, sweating

altered mental state= confusion

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281
Q

Mx of serotonin syndrome?

A

supportive including IV fluids

benzodiazepines

more severe cases are managed using serotonin antagonists such as cyproheptadine and chlorpromazine

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282
Q

Serotonin syndrome vs Neuroleptic maligant syndrome?

A

SS= caused by SSRIs, MAOIs, ecstasy/novel psychoactive stimulants; faster onset (hrs); increased reflexes, clonus, dilated pupils; Mx of severe= cyproheptadine, chlorpromazine

NMS= caused by antipsychotics; slower onset (hrs-d); decreased reflexes, ‘lead pipe’ rigidity, normal pupils; Mx of severe= dantrolene

Both= drug reactions often in young pts; tachycardia, HTN; pyrexia, diaphoresis; rigidity; increased CK (more in NMS); IV fluids, benzodiazepines

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283
Q

Serotonin syndrome or neuromalignant syndrome= increased reflexes, clonus , rigidity and dilated pupils?

A

Serotonin syndrome

NMS= decreased reflexes, lead pipe rigidity, normal pupils

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284
Q

What tricyclics are particularly dangerous in overdose?

A

amitriptyline and dosulepin (dothiepin)

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285
Q

Early features of tricyclic overdose?

A

anticholingeric= dry mouth, dilated pupils, agitation, sinus tachy and blurred vision

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286
Q

Features of severe tricyclic overdose?

A

arrhythmias
seizures
metabolic acidosis
coma

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287
Q

ECG changes in tricyclic overdose?

A

sinus tachycardia
widening of QRS
prolongation of QT interval

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288
Q

Tricyclic overdose= widening of QRS and prolonged QT means what?

A

Widening of QRS > 100ms is associated with an increased risk of seizures whilst QRS > 160ms is associated with ventricular arrhythmias

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289
Q

Mx for tricyclic overdose?

A
  • IV bicarbonate= first-line therapy for hypotension or arrhythmias; indications include widening of the QRS interval >100 msec or a ventricular arrhythmia
  • other drugs for arrhythmias
  • correction of acidosis is the first line in the management of tricyclic-induced arrhythmias
  • intravenous lipid emulsion is increasingly used to bind free drug and reduce toxicity
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290
Q

What is ineffective in tricyclic overdose?

A

dialysis

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291
Q

What is contraindicated in tricyclic overdose?

A

+ class 1a (e.g. quinidine) and class Ic antiarrhythmics (e.g. Flecainide) are contraindicated as they prolong depolarisation

class III drugs such as amiodarone should also be avoided as they prolong the QT interval

response to lignocaine is variable and it should be emphasized that correction of acidosis is the first line in the management of tricyclic-induced arrhythmias

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292
Q

Antidotes can be given in overdose why?

A

to prevent the poison from working or reverse the effects of the poison

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293
Q

Antidote for paracetamol overdose?

A

acetylcysteine

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294
Q

Antidote for digoxin overdose?

A

Digoxin-specific antibody fragments

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295
Q

Antidote for benzodiazepine overdose?

A

Flumazenil injection

reverses the central nervous system and respiratory depression.

if the person has also taken a tricyclic antidepressant or has epilepsy, there must be caution, as flumazenil can cause seizures and arrhythmias.

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296
Q

Antidote for insulin, BB or CCB overdose?

A

Glucagon injection

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297
Q

Antidote for morphine, heroin or opiate overdose?

A

naloxone injection

In people with reduced consciousness due to suspected opioid poisoning, administration which leads to significant improvement in the person’s condition within 1-2 minutes is highly suggestive of opioid poisoning.

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298
Q

Antidote for iron overdose?

A

Desferrioxamine mesilate

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299
Q

Antidote for ethylene glycol or methanol overdose?

A

fomepizole

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300
Q

Most common cause of admission to child and adolescent psychiatric wards?

A

anorexia nervosa

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301
Q

Epidemiology of anorexia nervosa?

A

90% female

teens and young-adults mainly

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302
Q

Diagnosis of anorexia nervosa based on what criteria?

A

DSM-5 (BMI and amenorrhoea no longer specifically mentioned)

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303
Q

DSM-5 criteria for diagnosis of anorexia nervosa?

A
  1. Restriction of energy intake relative to requirements leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health.
  2. Intense fear of gaining weight or becoming fat, even though underweight.
  3. Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or denial of the seriousness of the current low body weight.
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304
Q

Mx of anorexia nervosa?

A

one of:
individual eating-disorder-focused cognitive behavioural therapy (CBT-ED)

Maudsley Anorexia Nervosa Treatment for Adults (MANTRA)

specialist supportive clinical management (SSCM).

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305
Q

1st line Mx of anorexia nervosa in children and young people?

A

‘anorexia focused family therapy’

The second-line treatment is cognitive behavioural therapy.

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306
Q

Prognosis of anorexia?

A

poor

Up to 10% of patients will eventually die because of the disorder.

307
Q

Features of anorexia nervosa?

A

reduced body mass index
bradycardia
hypotension
enlarged salivary glands

308
Q

Physiological abnormalities in anorexia?

A

hypokalaemia

low FSH, LH, oestrogens and testosterone

raised cortisol and growth hormone

impaired glucose tolerance

hypercholesterolaemia

hypercarotinaemia

low T3

309
Q

Mx of binge eating disorder?

A

‘binge-eating-disorder-focused’ guided self-help programme

if guided self-help is unacceptable, contraindicated, or ineffective after 4 weeks, NICE recommend that we offer group eating-disorder-focused cognitive behavioural therapy (CBT-ED)

310
Q

Bulimia nervosa?

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.

311
Q

DSM-5 diagnostic criteria for bulimia nervosa?

A

1) 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)

2) a sense of lack of control over eating during the episode

3) 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

4) the binge eating and compensatory behaviours both occur, on average, at least once a week for three months.

5) self-evaluation is unduly influenced by body shape and weight.

6) the disturbance does not occur exclusively during episodes of anorexia nervosa.

312
Q

Pt with bulimia nervosa may have what physical signs?

A

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

313
Q

Mx for bulimia nervosa?

A

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)

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

314
Q

Eating disorders?

A

complex mental health conditions characterised by abnormal eating habits that negatively affect an individual’s physical and psychological well-being.

315
Q

Types of eating disorder?

A

anorexia nervosa, bulimia nervosa, and binge eating disorder, though there are other specified and unspecified feeding or eating disorders (OSFED/UFED)

316
Q

Aetiology of eating disorders?

A

multifactorial, encompassing biological, psychological, and sociocultural factors.

317
Q

Criteria for anorexia nervosa (AN)?

A

Restriction of food intake leading to a weight that is significantly below that which is expected.

Intense fear of gaining weight or persistent behaviour to avoid it.

Disturbance in the perception of body weight or shape, undue influence of body weight on self-worth, or persistent denial of the seriousness of the current low body weight.

318
Q

Criteria for bulimia nervosa (BN)?

A

Recurrent episodes of binge eating: consuming an abnormally large amount of food in a short time frame with a sense of lack of control.

Recurrent inappropriate compensatory behaviours to prevent weight gain.

Binge eating and compensatory behaviours both occur, on average, at least once a week for three months.

Self-worth is overly influenced by body shape and weight.

319
Q

Binge eating disorder (BED)?

A

Binge eating disorder is similar to bulimia nervosa in terms of the binge eating episodes, but differs in that individuals with BED do not consistently engage in inappropriate compensatory behaviours.

320
Q

Binge eating disorder (BED) criteria?

A

Recurrent episodes of binge eating.

Binge eating episodes are associated with at least three of the following: eating more rapidly than normal, eating until feeling uncomfortably full, eating large amounts when not feeling physically hungry, eating alone due to embarrassment, and feeling disgusted, depressed, or guilty after the episode.

Marked distress regarding binge eating.

Binge eating occurs, on average, at least once a week for three months.

321
Q

Diagnosis of eating disorders?

A

Diagnosis of eating disorders is based on clinical evaluation, which should consider medical history, physical examination, and diagnostic criteria. It is essential to rule out other medical conditions or psychiatric disorders.

322
Q

Mx of eating disorders?

A

Early detection and multidisciplinary intervention, encompassing medical, psychological, and nutritional support, are crucial for optimal outcomes.

323
Q

Cx of eating disorders?

A

Untreated eating disorders can lead to severe physical and psychological complications, including cardiac arrhythmias, electrolyte imbalances, osteoporosis, and increased risk of mortality.

Psychological complications might include depression, anxiety, and an increased risk of self-harm or suicide.

324
Q

Atypical eating disorders?

A

closely resemble anorexia nervosa, bulimia nervosa, and/or binge eating but do not meet the precise diagnostic criteria.

325
Q

Most common eating disorders?

A

Atypical eating disorders are most common, followed by binge eating disorders, then bulimia nervosa. Anorexia nervosa is the least common.

326
Q

Anorexia nervosa definition?

A

low body weight due to restriction of food intake or persistent behaviour which interferes with weight gain and intense fear of gaining weight.

327
Q

Bulimia nervosa definition?

A

recurrent episodes of uncontrolled eating of an abnormally large amount of food over a short time period (binge eating) followed by compensatory behaviour such as self-induced vomiting, laxative abuse, or excessive exercise.

328
Q

Binge eating disorder definition?

A

recurrent episodes of binge eating in the absence of compensatory behaviours. Episodes are marked by feelings of lack of control.

329
Q

When to consider emergency admission for eating disorders?

A

Severely compromised physical health — BMI or body weight below a safe range, cardiovascular instability, hypothermia, reduced muscle power, concurrent infection, overall ill health or abnormal blood tests.

Risk of refeeding syndrome.

Lack of support at home.

Acute mental health risk — risk of suicide attempt or serious self-harm.

330
Q

What to do if suspect pt has eating disorder?

A

Referral of all people with a suspected eating disorder to an age-appropriate eating disorder service.

While awaiting assessment by the eating disorder team:
- Arranging regular reviews to monitor the level of physical and mental health risk.
- Seeking advice from an appropriate specialist for people with co-morbidities (such as diabetes) and pregnant women.
- Considering the impact of malnutrition and compensatory behaviour on medication effectiveness and risk of side effects.

331
Q

Mx of confirmed eating disorder involves what?

A

Ensuring there is a clear agreement between primary and secondary care about responsibility for monitoring a person with an eating disorder.

Monitoring ongoing levels of risk to the person’s mental and physical health and managing complications — specialist input may be indicated.

Placing an alert in the person’s prescribing record to highlight the potential risk of adverse drug effects.

Giving advice on contraceptive use and pregnancy to women with eating disorders.

Ensuring the person and their family/carers have access to information and support.

332
Q

Central feature of anxiety?

A

‘excessive worry about a number of different events associated with heightened tension.’

333
Q

When considering a psychiatric diagnosis, always consider what?

A

a potential physical cause

334
Q

What physical causes is it important to eliminate before diagnosing generalised anxiety disorder?

A

hyperthyroidism, cardiac disease and medication-induced anxiety

335
Q

What meds might trigger anxiety?

A

salbutamol, theophylline, corticosteroids, antidepressants and caffeine

336
Q

GAD?

A

generalised anxiety disorder

337
Q

Mx of GAD?

A

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.

step 4: highly specialist input e.g. Multi agency teams

regular follow up

338
Q

Drug Tx for GAD?

A

1st line= sertraline (SSRI)
2nd= alternative SSRI or SNRI eg. duloxetine
3rd= pregabalin

339
Q

Pts under 30 starting SSRI for anxiety, warn them of what?

A

warn patients of the increased risk of suicidal thinking and self-harm. Weekly follow-up is recommended for the first month

340
Q

Mx of panic disorder?

A

step 1: recognition and diagnosis

step 2: treatment in primary care

step 3: review and consideration of alternative treatments

step 4: review and referral to specialist mental health services

step 5: care in specialist mental health services

341
Q

Tx of panic disorder in primary care?

A

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

342
Q

Criteria for GAD?

A

excessive worry about every day issues that is disproportionate to any inherent risk.

At least three of the following symptoms are present most of the time= restlessness or nervousness, being easily fatigued, poor concentration, irritability, muscle tension, or sleep disturbance.

Symptoms are present for at least 6 months and cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

343
Q

Prognosis of GAD?

A

chronic condition that may fluctuate in severity, with low rates of remission over the short- and medium-term.

344
Q

GAD is defined, and its severity categorized, by one of two main classification systems:

A

American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR), or the World Health Organization (WHO) International Classification of Diseases (ICD-11).

345
Q

Most common psychiatric disorder?

A

anxiety disorders

346
Q

RFs for GAD?

A

Female sex.
Comorbid anxiety disorders.
Family history of anxiety disorders.
Childhood adversity.
History of sexual or emotional trauma.
Sociodemographic factors.

347
Q

Cx of GAD?

A

Distress, substantial disability, and impaired quality of life.
Impaired social and occupational functioning.
Comorbidities.
Suicidal ideation and attempts.

348
Q

Suspect GAD in who?

A

person who reports chronic, excessive worry which is not related to particular circumstances, and symptoms of physiological arousal such as restlessness, insomnia, and muscle tension.

Attend primary care frequently and=
- Have a chronic physical health problem.
- Do not have a physical health problem, but are seeking reassurance about somatic symptoms (particularly older people and people from minority ethnic groups).
- Are repeatedly worrying about a wide range of different issues.

349
Q

How to assess/determine the severity of GAD?

A

GAD-2 or GAD-7 questionnaires

350
Q

Referral for specialist Tx for GAD in who?

A

if GAD is complex, if the person has treatment-refractory GAD, if there is very marked functional impairment, or a if there is a high risk of self-harm.

351
Q

What does OCD stand for?

A

Obsessive-compulsive disorder

352
Q

OCD?

A

characterised by the presence of either obsessions or compulsions, but commonly both. The symptoms can cause significant functional impairment and/ or distress.

353
Q

Obsession definition?

A

an unwanted intrusive thought, image or urge that repeatedly enters the person’s mind

354
Q

Compulsions definition?

A

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.

355
Q

RFs for OCD?

A

family history
age: peak onset is between 10-20 years
pregnancy/postnatal period
history of abuse, bullying, neglect

356
Q

How to classify OCD?

A

classigy impairment into mild, moderate or severe
they recommend the use of the Y-BOCS scale

an example of ‘severe’ OCD would be someone who spends > 3 hours a day on their obsessions/compulsions, has severe interference/distress and has very little control/resistance

357
Q

Mx of OCD if functional impairment is mild?

A

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 a choice of either a course of an SSRI or more intensive CBT (including ERP)

358
Q

Mx of OCD if moderate functional impairment?

A

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)

consider clomipramine (as an alternative first-line drug treatment to an SSRI) if the person prefers clomipramine or has had a previous good response to it, or if an SSRI is contraindicated

359
Q

Mx of OCD if severe functional impairment?

A

refer to the secondary care mental health team for assessment

whilst awaiting assessment - offer combined treatment with an SSRI and CBT (including ERP) or consider clomipramine as an alternative as above

360
Q

OCD Mx= what is ERP?

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).

helps them confront their anxiety and the habituation leads to the eventual extinction of the response

361
Q

OCD= what if Tx with SSRI is effective?

A

continue for at least 12 months to prevent relapse and allow time for improvement

362
Q

OCD= SSRI use in OCD compared to depression?

A

SSRI usually requires a higher dose and a longer duration of treatment (at least 12 weeks) for an initial response in OCD

363
Q

Why is OCD undertreated?

A

People with OCD often fear stigmatization and fail to disclose their symptoms spontaneously, leading to low rates of recognition and, consequently, undertreatment.

364
Q

Diagnosis of OCD?

A

Screening people with symptoms of depression, anxiety, alcohol or substance misuse, body dysmorphic disorder, or an eating disorder.

Excluding other conditions including body dysmorphic disorder, illness anxiety disorder, and autism.

Assessing the severity of functional impairment as mild, moderate, or severe.

Assessing the risk of self-harm and suicide and the impact of compulsive behaviours on others.

365
Q

Mx of OCD?

A

depends on the level of functional impairment and includes:

  • Cognitive-behavioural therapy, ideally including exposure and response prevention.
  • SSRI or clomipramine. SSRIs should only be prescribed to people under 18 years of age following assessment and diagnosis by a child and adolescent psychiatrist.
  • Specialist referral (depending on factors including the person’s age, severity of symptoms, and previous treatment failures).
366
Q

OCD= when to refer for urgent psychiatric assessment?

A

people with a suspected high risk of self-harm or suicide.

367
Q

Personality disorders (PD)?

A

group of mental health conditions characterised by persistent patterns of thinking, feeling, and behaving that are significantly different from cultural expectations. These patterns can lead to distress or problems in personal, social, and occupational functioning

368
Q

How are people with personality disorder diagnosed?

A

For many years patients were diagnosed with a specific ‘named’ personality disorder, such as narcissistic or paranoid.

This approach was changed significantly with the introduction of the ICD-11 classification which marked a shift towards a more dimensional model, such as severity and specific problems.

This allows for a more flexible and comprehensive understanding of personality pathology.

369
Q

Most pts with personality disorders will be…

A

‘labelled’ using the previous classification system rather than the more modern way that just focuses on severity and specific problems

370
Q

4 Key features of personality disorder (ICD-11)?

A

1) Persistent Pattern: The individual’s patterns of cognition, emotional experience, behaviour, and interpersonal functioning deviate from cultural expectations. These patterns are stable over time and span across various personal and social situations.

2) Impairment: The deviation results in significant problems or dysfunctions in the person’s life, especially in relationships, work, or social functioning.

3) Duration: These characteristics are stable over time, beginning in adolescence or early adulthood, and are not transient.

4) Distress or Dysfunction: The impairment may result in distress to the individual or others. These patterns are not explained by another mental disorder, a medical condition, or substance misuse.

371
Q

In the ICD-11 personality disorders are classified how? This provides a broader and more flexible approach.

A

Mild
Moderate
Severe

Also trait domains

372
Q

Mild personality disorder?

A

Some impairments in functioning, often limited to specific areas of life (e.g., intimate relationships or work).

Symptoms may be noticeable to others but do not cause pervasive distress or dysfunction.

The individual may still maintain relatively stable relationships and occupational roles.

373
Q

Moderate personality disorder?

A

More significant impairments in multiple areas of life (personal, social, and work).

The individual may struggle with maintaining close relationships, and there may be greater interpersonal difficulties.

More distressing symptoms are present, but the individual can manage day-to-day functioning with some effort or support.

374
Q

Severe personality disorder?

A

Profound impairments in all areas of life.

Individuals may experience pervasive difficulties in interpersonal relationships, self-identity, and coping mechanisms.

Significant distress, dysfunction, and reduced quality of life are common.

Individuals may require intensive and long-term therapeutic interventions.

375
Q

Key features of personality disorder (ICD-11)= persistent pattern?

A

The individual’s patterns of cognition, emotional experience, behaviour, and interpersonal functioning deviate from cultural expectations. These patterns are stable over time and span across various personal and social situations.

376
Q

Key features of personality disorder (ICD-11)= impairment?

A

The deviation results in significant problems or dysfunctions in the person’s life, especially in relationships, work, or social functioning.

377
Q

Key features of personality disorder (ICD-11)= duration?

A

These characteristics are stable over time, beginning in adolescence or early adulthood, and are not transient.

378
Q

Key features of personality disorder (ICD-11)= distress or dysfunction?

A

The impairment may result in distress to the individual or others. These patterns are not explained by another mental disorder, a medical condition, or substance misuse.

379
Q

In addition to severity, ICD-11 also characterises personality disorders how?

A

trait domains that represent the predominant problematic areas in the individual’s personality

380
Q

Name the Personality Disorder Trait Domains?

A

1) Negative Affectivity
2) Detachment
3) Dissociality
4) Disinhibition
5) Anankastia
6) Borderline Pattern

381
Q

Personality Disorder trait domains= negative affectivity?

A

Tendency to experience a wide range of negative emotions such as anxiety, depression, guilt, and anger.

Individuals may be prone to mood swings, insecurity, and emotional lability.

382
Q

Personality Disorder trait domains= Disinhibition?

A

Impulsiveness, risk-taking, and difficulty controlling behaviours.

Individuals may struggle with planning and foresight, leading to reckless or irresponsible actions.

382
Q

Personality Disorder trait domains= Detachment?

A

Avoidance of social interactions, emotional withdrawal, and limited pleasure from relationships.

Individuals may appear cold, aloof, and isolated.

382
Q

Personality Disorder trait domains= Dissociality?

A

Disregard for the rights and feelings of others, lack of empathy, and difficulty forming prosocial relationships.

Impulsivity and manipulative behaviours are common traits.

383
Q

Personality Disorder trait domains= Anankastia?

A

Preoccupation with orderliness, control, and perfectionism.

Individuals may be rigid, stubborn, and excessively focused on rules and details.

384
Q

Personality Disorder trait domains= Borderline Pattern?

A

An additional qualifier for those showing emotional instability, intense and unstable interpersonal relationships, a fluctuating sense of identity, and impulsivity.

This pattern is akin to borderline personality disorder as recognised in ICD-10 and DSM-5.

385
Q

Previous classification of personality disorders= used to be categorised how?

A

as 3 clusters:

Cluster A= odd or eccentric

Cluster B= dramatic, emotional or erratic

Cluster C= anxious and fearful

386
Q

Previous classification of personality disorders= Cluster A?

A

Odd or Eccentric

  • Paranoid
  • Schizoid
  • Schizotypal
387
Q

Previous classification of personality disorders= Cluster B?

A

Dramatic, emotional or erratic

  • antisocial
  • borderline (emotionally unstable)
  • histrionic
  • narcissistic
388
Q

Previous classification of personality disorders= Cluster C?

A

anxious and fearful

  • obsessive-compulsive
  • avoidant
  • dependent
389
Q

Previous classification of personality disorders= Cluster A (odd or eccentric)- Paranoid?

A

Hypersensitivity and an unforgiving attitude when insulted

Unwarranted tendency to questions the loyalty of friends

Reluctance to confide in others

Preoccupation with conspirational beliefs and hidden meaning

Unwarranted tendency to perceive attacks on their character

390
Q

Previous classification of personality disorders= Cluster A (odd or eccentric)- Schizoid?

A

Indifference to praise and criticism

Preference for solitary activities

Lack of interest in sexual interactions

Lack of desire for companionship

Emotional coldness

Few interests

Few friends or confidants other than family

391
Q

Previous classification of personality disorders= Cluster A (odd or eccentric)- Schizotypal?

A

Ideas of reference (differ from delusions in that some insight is retained)

Odd beliefs and magical thinking

Unusual perceptual disturbances

Paranoid ideation and suspiciousness

Odd, eccentric behaviour

Lack of close friends other than family members

Inappropriate affect

Odd speech without being incoherent

392
Q

Previous classification of personality disorders= Cluster B (dramatic, emotional or erratic)- Antisocial?

A

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

393
Q

Previous classification of personality disorders= Cluster B (dramatic, emotional or erratic)- Borderline (Emotionally Unstable)?

A

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

394
Q

Previous classification of personality disorders= Cluster B (dramatic, emotional or erratic)- Histrionic?

A

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

395
Q

Previous classification of personality disorders= Cluster B (dramatic, emotional or erratic)- Narcissistic?

A

Grandiose sense of self importance

Preoccupation with fantasies of unlimited success, power, or beauty

Sense of entitlement

Taking advantage of others to achieve own needs

Lack of empathy

Excessive need for
admiration

Chronic envy

Arrogant and haughty attitude

396
Q

Previous classification of personality disorders= Cluster C (anxious and fearful)- Obsessive-compulsive?

A

Is occupied with details, rules, lists, order, organization, or agenda to the point that the key part of the activity is gone

Demonstrates perfectionism that hampers with completing tasks

Is extremely dedicated to work and efficiency to the elimination of spare time activities

Is meticulous, scrupulous, and rigid about etiquettes of morality, ethics, or values

Is not capable of disposing worn out or insignificant things even when they have no sentimental meaning

Is unwilling to pass on tasks or work with others except if they surrender to exactly their way of doing things

Takes on a stingy spending style towards self and others; and shows stiffness and stubbornness

397
Q

Previous classification of personality disorders= Cluster C (anxious and fearful)- Avoidant?

A

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

398
Q

Previous classification of personality disorders= Cluster C (anxious and fearful)- Dependent?

A

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

399
Q

Mx of personality disorders?

A

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

400
Q

PTSD stands for what?

A

post-traumatic stress disorder

401
Q

PTSD can develop in who?

A

people of any age following a traumatic event eg. major disaster or childhood sexual abuse

402
Q

‘shell shock’ in WW1?

A

PTSD

403
Q

For PTSD diagnosis, how long should symptoms have lasted?

A

more than 1 month

404
Q

Features of PTSD?

A

re-experiencing: flashbacks, nightmares, repetitive and distressing intrusive images

avoidance: avoiding people, situations or circumstances resembling or associated with the event

hyperarousal: hypervigilance for threat, exaggerated startle response, sleep problems, irritability and difficulty concentrating

emotional numbing - lack of ability to experience feelings, feeling detached

405
Q

Features of PSTD= from other people?

A

depression

drug or alcohol misuse

anger

unexplained physical symptoms

406
Q

Mx of PTSD?

A

following a traumatic event single-session interventions (often referred to as debriefing) are not recommended

watchful waiting may be used for mild symptoms lasting less than 4 weeks
military personnel have access to treatment provided by the armed forces

trauma-focused cognitive behavioural therapy (CBT) or eye movement desensitisation and reprocessing (EMDR) therapy may be used in more severe cases

drug Tx not 1st line but can be used

407
Q

Mx of PTSD: if drug Tx is used then what should they be used?

A

venlafaxine or SSRI eg. sertraline

severe= risperidone

408
Q

PTSD= ICD-11 describes a major traumatic event as what?

A

‘a stressful event or situation of an exceptionally threatening or catastrophic nature, which is likely to cause pervasive distress in almost anyone’.

409
Q

PTSD= DSM-5 describes major traumatic event as what?

A

‘exposure to actual or threatened death, serious injury, or sexual violence’

410
Q

PTSD= prognosis in adults?

A

In around two-thirds of people, symptoms resolve naturally, although this may take several months.

For around a third of people, symptoms are longer lasting, and for many, these are severe and enduring.

411
Q

PTSD= when do the symptoms typically occur?

A

usually in the first month after the traumatic event. In a minority of people, symptoms can be delayed by months or years.

412
Q

Complex PTSD?

A

may develop after extreme prolonged or repeated trauma (such as repeated childhood sexual abuse or prolonged captivity involving torture).

413
Q

When to suspect PTSD?

A

Re-experiencing symptoms — which may occur in the daytime when the person is awake (flashbacks or intrusive images or thoughts) or as nightmares when asleep. This is the most characteristic symptom.

Avoidance of people or places that remind the person of the event.

Emotional numbing/negative thoughts, where the person expresses a lack of ability to experience feelings or feels detached from other people, or has negative thoughts about themselves.

Hyperarousal/hyperreactivity, where the person is on guard all the time, looking for danger (hypervigilance), or the person has irritable behaviour or angry outbursts with little or no provocation.

414
Q

PTSD= pt with sub-clinical PTSD symptoms?

A

consider a period of watchful waiting and arrange regular review

415
Q

PTSD= adults with clinically important PTSD symptoms of any duration, offer?

A

referral to a specialist mental health service for trauma-based psychological therapies and/or drug treatment. The need for emergency medical or psychiatric referral should be assessed by looking for the presence and severity of secondary psychological disorders.

416
Q

PTSD= For children and young people aged 18 years and under with clinically important PTSD symptoms…?

A

If the symptoms have persisted for more than one month, offer referral to a specialist mental health service.

If the trauma occurred within the last month, use clinical judgement to determine whether watchful waiting or specialist referral are appropriate.

417
Q

Mild PTSD?

A

distress caused by the symptoms is manageable, and the person’s social and occupational functioning are not significantly impaired.

418
Q

Moderate PTSD?

A

distress and impact on functioning lie somewhere between mild and severe, and there is not considered to be a significant risk of suicide, harm to self, or harm to others.

419
Q

Severe PTSD?

A

istress caused by the symptoms is felt to be unmanageable, and/or there is significant impairment in social and/or occupational functioning, and/or there is considered to be a significant risk of suicide, harm to self, or harm to others.

420
Q

Clinically important symptoms of PTSD can be defined as what?

A

those causing at least moderate functional impairment and/or those scoring above a clinical threshold on a validated scale (where this has been assessed). Where symptoms are deemed to be ‘moderate’, use clinical judgement to determine the need for intervention.

421
Q

Summarise PTSD Mx?

A

1) Trauma focused psychological Tx= CBT (12 sessions typically), exposure therapy or cognitive therapy

2) Eye movement desensitisation and reprocessing (EMDR)= up to 12 sessions, more if severe

3) Antidepressants= venlafaxine or SSRI; risperidone if severe

422
Q

EMDR for PTSD?

A

EMDR uses bilateral stimulation (eye movements, taps, and tones) while the person focuses on memories and associations. This is thought to help the brain process flashbacks and make sense of the traumatic experience.

423
Q

Trauma focused CBT for PTSD?

A

combination of exposure therapy and trauma-focused cognitive therapy. More complex presentations are likely to require longer treatment. If a child/young person is being treated, trauma-focused CBT should be adapted to their age and development and involve parents or carers as appropriate.

424
Q

Exposure therapy in PTSD?

A

the person confronts traumatic memories (usually by recounting the event) and is repeatedly exposed to situations which they have been avoiding that elicit fear.

425
Q

Trauma focused cognitive therapy for PTSD?

A

identifies and modifies misrepresentations of the trauma and its aftermath that lead the person to overestimate the threat. For example, rape victims may blame themselves, war veterans may feel that it was their fault a friend was killed, and people who survive accidents may feel that they are in danger of having another accident.

426
Q

Antipsychotics?

A

used in Mx of schizophrenia and other forms of psychosis, mania and agitation

427
Q

Antipsychotics= divided into what types?

A

typical (1st generation) and atypical antipsychotics (2nd generation)

428
Q

Why were atypical antipsychotics developed?

A

due to the problematic extrapyramidal side-effects which are associated with the first generation of typical antipsychotics

429
Q

Typical antipsychotics= mechanism of action?

A

Dopamine D2 receptor antagonists, blocking dopaminergic transmission in the mesolimbic pathways

430
Q

Typical antipsychotics= adverse effects?

A

Extrapyramidal side-effects and hyperprolactinaemia common

431
Q

Typical antipsychotics= examples?

A

Haloperidol
Chlorpromazine

432
Q

Atypical antipsychotics= mechanism of action?

A

Act on a variety of receptors (D2, D3, D4, 5-HT)

433
Q

Atypical antipsychotics= adverse effects?

A

Extrapyramidal side-effects and hyperprolactinaemia less common

Metabolic effects

434
Q

Atypical antipsychotics= examples?

A

Clozapine
Risperidone
Olanzapine

435
Q

Extrapyramidal side effects and hyperprolactinaemia more common in what type of antipsychotics?

A

typical

436
Q

Haloperidol and chlorpromazine are examples of what?

A

typical antipsychotics

437
Q

Closzapine, risperidone and olanzapine are examples of what?

A

atypical antipsychotics

438
Q

Examples of extrapyramidal side effects (EPSEs) eg. from typical antipsychotics?

A
  • parkinsonism
  • acute dystonia
  • akathisia
  • tardive dyskinesia (late onset)
439
Q

Acute dystonia?

A

sustained muscle contraction (e.g. torticollis, oculogyric crisis)

may be managed with procyclidine

440
Q

Acute dystonia may be managed with what?

A

procyclidine

441
Q

Akathisia?

A

severe restlessness

442
Q

Tardive dyskinesia?

A

late onset of choreoathetoid movements, abnormal, involuntary, may occur in 40% of patients on typical antipsychotics, may be irreversible, most common is chewing and pouting of jawq

443
Q

Pt on long term typical antipsychotics= get involuntary chewing and pouting of jaw movements?

A

tardive dyskinesia

444
Q

When antipsychotics are used in elderly pts, there is an increased risk of what?

A

stroke and VTE

445
Q

Anticholinergic (antimuscarinic- type of anticholinergic drug but similar effects) side effects?

A

dry mouth, blurred vision, urinary retention, constipation

446
Q

dry mouth, blurred vision, urinary retention, constipation side effects are examples what what?

A

antimuscarinic (anticholinergic) side effects

447
Q

Anticholinergic vs antimuscarinic?

A

Anticholinergics are a class of drugs that block acetylcholine, while antimuscarinics are a subtype of anticholinergic drugs that block muscarinic receptors.

448
Q

Other side effects of antipsychotics?

A
  • antimuscarinic (anticholinergic)= dry mouth, blurred vision, urinary retention, constipation
  • sedation, weight gain
  • raised prolactin
  • impaired glucose tolerance
  • neuroleptic malignant syndrome: pyrexia, muscle stiffness
  • reduced seizure threshold (greater with atypicals)
  • prolonged QT interval (particularly haloperidol)
449
Q

Side effects of antipsychotics= raised prolactin which may result in what?

A

galactorrhoea

due to inhibition of dopaminergic tuberoinfundibular pathway

450
Q

Side effects of antipsychotics= symptoms of neuroleptic malignant syndrome?

A

pyrexia, muscle stiffness

451
Q

Side effects of antipsychotics= reduced seizure threshold particularly with what type?

A

atypicals

452
Q

Side effects of antipsychotics= prolonged QT interval particularly with what?

A

haloperidol

453
Q

Strongest risk factor for developing a psychotic disorder?

A

family history

454
Q

Having a parent with schizophrenia leads to a relative risk (RR) of what?

A

7.5

455
Q

Risk of developing schizophrenia if monozygotic twin has schizophrenia?

A

50%

456
Q

Risk of developing schizophrenia if parent has schizophrenia?

A

10-15%

457
Q

Risk of developing schizophrenia if sibling has schizophrenia?

A

10%

458
Q

Risk of developing schizophrenia if no relative has schizophrenia?

A

1%

459
Q

RFs for psychiatric disorders?

A
  • FHx
  • black Caribbean ethnicity
  • migration
  • urban environment
  • cannabis use
460
Q

Schizophrenia features= Schneider’s first rank symptoms may be divided into?

A

auditory hallucinations, thought disorders, passivity phenomena and delusional perceptions

461
Q

Schizophrenia features?

A

Schneider’s first rank symptoms:
- auditory hallucinations
- thought disorders
- passivity phenomena
- delusional perceptions

462
Q

Schizophrenia features= Schneider’s first rank symptoms- auditory hallucinations?

A

specific type:
- two or more voices discussing the patient in the third person
- thought echo
- voices commenting on the patient’s behaviour

463
Q

Schizophrenia features= Schneider’s first rank symptoms- thought disorders?

A
  • thought insertion
  • thought withdrawl
  • thought broadcasting
464
Q

Schizophrenia features= Schneider’s first rank symptoms- passivity phenomena?

A

bodily sensations being controlled by external influence

actions/impulses/feelings - experiences which are imposed on the individual or influenced by others

465
Q

Schizophrenia features= Schneider’s first rank symptoms- delusional perceptions?

A

(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’.

466
Q

Schizophrenia features?

A
  • Schneider’s first rank symptoms= auditory hallucinations, thought disorders, passivity phenomena, delusional perceptions
  • impaired insight
  • negative symptoms
  • neologisms
  • catatonia
467
Q

Schizophrenia features= negative symptoms?

A
  • incongruity/blunting of affect
  • anhedonia (inability to derive pleasure)
  • alogia (poverty of speech)
  • avolition (poor motivation)
  • social withdrawal
468
Q

Schizophrenia features= negative symptoms: anhedonia?

A

inability to derive pleasure

469
Q

Schizophrenia features= negative symptoms: alogia?

A

poverty of speech

470
Q

Alogia?

A

poverty of speech

471
Q

Schizophrenia features= negative symptoms: avolition?

A

poor motivation

472
Q

Avolition?

A

poor motivation

473
Q

Anhedonia?

A

inability to derive pleasure

474
Q

Schizophrenia features= neologisms?

A

made up words

475
Q

Neologisms?

A

made up words

476
Q

Mx for schizophrenia summary?

A

oral atypical antipsychotics 1st line

+ CBT 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 and high smoking rates)

477
Q

Factors associated with poor prognosis in schizophrenia?

A
  • strong family history
  • gradual onset
  • low IQ
  • prodromal phase of social withdrawal
  • lack of obvious precipitant
478
Q

Psychosis?

A

encompasses a number of symptoms associated with significant alternations to a person’s perception, thoughts, mood, and behaviou

479
Q

Positive signs and symptoms?

A

disorganised behaviour, speech, and/or thoughts (thought disturbance), delusions (fixed or falsely-held beliefs), and/or hallucinations (perceptions in the absence of stimulus).

480
Q

Negative signs and symptoms?

A

emotional blunting, reduced speech, loss of motivation, self-neglect, social withdrawal.

481
Q

Psychotic signs and symptoms?

A

cardinal features of psychotic disorders, the most common of which is schizophrenia, but may also be caused acutely by certain medicines, substance misuse, and some medical conditions such as sepsis.

482
Q

With Tx, psychotic signs and symptoms may…

A

resolve fully, recur intermittently with periods of remission between, or persist

483
Q

Cx of psychotic disorders?

A

An increased risk of premature death due to higher rates of suicide, cardiovascular disease, and type 2 diabetes.
Difficulties in social functioning.
Substance misuse.

484
Q

What may be precede the development of a psychotic disorder?

A

prodromal period of emotional disturbance

485
Q

Pt may be in prodromal period before development of psychotic disorder if they exhibit what?

A

distress and/or a deterioration in social functioning, and has:

  • Transient (short duration) or attenuated (low intensity) psychotic symptoms, or
  • Other experiences or behaviour suggestive of possible psychosis (for example, suspicion, mistrust, or perceptual changes), or
  • A first-degree relative with a psychotic disorder.
486
Q

?psychotic disorder- high risk of harm?

A

same-day mental health assessment by the early intervention in psychosis service should ideally be arranged. If this service is not available, is unable to provide urgent intervention, or the level of risk exceeds the management capacity of the early intervention in psychosis service, the person should be referred to a crisis resolution and home treatment team.

487
Q

?psychotic disorder- not high risk of harm?

A

referred without delay to the early intervention in psychosis service. If the service cannot provide urgent intervention, the person should be referred to the crisis resolution and home treatment team.

488
Q

Pt is in prodromal phase of psychosis and is not judged to be high risk of harm?

A

eferred without delay to the early intervention in psychosis service (if available) or a specialist mental health service. A consultant psychiatrist or a trained specialist with experience in at-risk mental states should carry out an assessment.

489
Q

Whilst awaiting specialist assessment in suspected psychotic disorder, what should you NOT do?

A

DO NOT give antipsychotic unless under advice from consultant psychiatrist

490
Q

For people who are at risk of developing a psychotic disorder, what will be offered?

A

specialist mental health services will usually offer treatment with individual cognitive behavioural therapy (CBT) with or without family intervention.

491
Q

Pt with diagnosed psychotic disorder, specialist mental health services will usually offer what?

A

therapeutic trial of an oral antipsychotic in conjunction with family intervention, individual CBT, or art therapy.

492
Q

For people with an established diagnosis of a psychotic disorder who relapse, a risk assessment of harm to the person or others should be carried out:

A

A person with a treatment care plan should be managed according to the plan.

A person without a care plan who is judged to be at immediate risk of harm should be referred for same-day specialist assessment to the local crisis resolution and home treatment team.

A person without a care plan not judged not to be at immediate risk of harm should be referred to the community mental health service.

493
Q

Who is responsible for monitoring pts physical health and effects of any antipsychotic meds?

A

secondary care team for the 1st 12m of Tx or until the person’s condition has stabilised (whichever is the longest).

After this, the responsibility for monitoring may be transferred to primary care, depending on locally agreed shared care guidelines or the person’s care plan.

494
Q

When to suspect frank psychosis?

A

person with positive symptoms such as hallucinations and delusions, and negative symptoms such as affective flattening (lack of spontaneity or reactivity of mood), avolition (lack of drive), anhedonia (lack of pleasure), attention deficit, or impoverishment of speech and language.

495
Q

Psychosis may be preceded by what?

A

prodromal period that can last from a few days to around 18 months

496
Q

Why is it crucial to identify the prodromal stage of psychosis?

A

offers a critical treatment window to delay or prevent the person’s transition to frank psychosis.

497
Q

Prodromal period of psychosis is characterised by?

A

increasing distress and a decline in personal, cognitive and social functioning.

498
Q

Prodromal period of psychosis= specific symptoms may include:

A

Transient, low-intensity psychotic symptoms — intermittent, self-limiting episodes, typically lasting less than a week. May include hallucinations/unusual perceptual experiences, unusual thoughts (including new preoccupation with mystical or religious themes, concerns about being under surveillance) and may manifest as unusual or uncharacteristic behaviour.

Reduced interest in daily activities — may manifest as poor personal hygiene and/or reduced performance at school or work.

Problems with mood, sleep, memory, concentration, communication, affect, and motivation.

Anxiety, irritability, or depressive features.
Incoherent or illogical speech — suggestive of thought disturbance.

499
Q

Psychosis= positive symptoms may not be readily disclosed by the person so may be necessary to do what?

A

directly ask them whether they are experiencing hallucinations (‘feeling, seeing, or hearing things that other people cannot’) or experiencing delusional thoughts (‘feeling that you are being talked about, watched, or given a hard time for no reason, suspecting you are being externally controlled, or having thoughts inserted or removed from your mind, or others being aware of your thoughts’).

500
Q

Differential diagnosis of psychosis?

A
  • severe affective (mood) disorders with psych symptoms eg. severe depression or bipolar
  • drug induced psychosis eg. cannabis, corticosteroids, opioids, cocaine, amphetamines
  • sepsis
  • underlying med condition eg. cerebral tumours, temporal lobe epilepsy, cerebrovascular disease
  • PTSD
  • OCD
  • ASD or communication disorders
501
Q

People diagnosed with a psychotic disorder are likely to be offered the following secondary care management:

A

1) A therapeutic trial of an oral antipsychotic (first- or second-gen) in conjunction with any or all of the following:
- Family intervention; 10 planned sessions over 3 months to 1 year.
- Individual CBT — at least 16 planned sessions.
- Arts therapies may be offered, particularly to help with negative symptoms.

2) Monitoring at least 12 or until stabilised

3) During maintenance treatment, antipsychotic doses should not be reduced below the standard dose range recommended for acute stabilisation because reducing the dose further is associated with an increased risk of both relapse and all-cause discontinuation.

4_ Care plan= crisis plan, advance statement and key clinical contacts in case of emergency

502
Q

People who do not have a clear diagnosis of a psychotic disorder should ideally be monitored in secondary care for up to

A

3yrs

o ensure early diagnosis if a psychotic disorder develops.

However, if this is not possible, monitor the person in primary care and refer back to secondary care if there are any emerging symptoms.

The frequency and duration of monitoring will depend upon the severity and frequency of symptoms, the level of impairment or distress, and the degree of family disruption or concern.

If the person is being monitored in secondary care and asks to be discharged, ensure they are offered follow-up appointments in primary care and the option to self-refer back in the future.

503
Q

Psychosis: what may be helpful for managing symptoms of psychosis or preventing relapse?

A

Digital health technologies

504
Q

What to consider for pts with complex psychosis?

A

rehabilitation

for people with complex psychosis, who have treatment-resistant psychosis, who have frequent admissions or long stays, or who have a 24-hour staffed placement that is breaking down

505
Q

When to suspect relapse in psychosis?

A

if a person with an established diagnosis of a psychotic disorder presents with increased psychotic symptoms or a significant increase in the use of alcohol or other substances

506
Q

How to screen psychotic symptoms eg. hallucinations and delusions?

A

Do you hear voices when nobody is around?

Do you ever think that people are talking or gossiping about you, maybe even thinking about trying to get you?

Do you ever think that somehow people can pick up on what you are thinking or can manipulate what you are thinking?

507
Q

Psychosis: how to review adherence to Tx and ask about symptoms that may be due to adverse effects eg. sedation, extrapyramidal symptoms?

A

Arrange specialist review if adherence with medication is poor, symptoms are poorly controlled, or adverse effects are poorly tolerated.

Ask about symptoms of raised prolactin (such as low libido, sexual dysfunction, menstrual abnormalities [amenorrhoea or oligomenorrhoea], gynaecomastia, and galactorrhoea) particularly if the person is taking a first-generation antipsychotic or risperidone.

Clozapine — people taking clozapine are managed exclusively in secondary care. Clozapine can cause neutropenia or agranulocytosis, and frequent monitoring of the full blood count is required (weekly for 18 weeks after starting treatment, then every 2 weeks for the next 18 weeks, and then every 4 weeks thereafter). This is carried out by the specialist clozapine monitoring service.

508
Q

Why are pts taking clozapine managed exclusively in secondary care?

A

can cause neutropenia or agranulocytosis, and frequent monitoring of the full blood count is required (weekly for 18 weeks after starting treatment, then every 2 weeks for the next 18 weeks, and then every 4 weeks thereafter). This is carried out by the specialist clozapine monitoring service.

509
Q

Pts taking what antipsychotic drug are managed and monitored exclusively in secondary care?

A

clozapine

510
Q

Clozapine can cause what?

A

neutropenia or agranulocytosis

511
Q

Monitoring of clozapine?

A

frequent monitoring of the full blood count is required (weekly for 18 weeks after starting treatment, then every 2 weeks for the next 18 weeks, and then every 4 weeks thereafter)

512
Q

What to monitor in pts taking antipsychotics?

A

pulse, BP= CVD risk

Fasting glucose, HbA1c.
Lipid profile.
Urea and electrolytes.
Full blood count.
Liver function tests.
Prolactin (annual prolactin measurement is not required if the person is taking aripiprazole, clozapine, quetiapine, or olanzapine).

513
Q

When to do an ECG if pt is taking antipsychotics?

A

haloperidol, pimozide or sertindole if they have had a previous ECG abnormality, or if they have an additional risk factor for QT prolongation (for example taking another medication that can increase the QT interval such as erythromycin, co-trimoxazole, or pregabalin). These drugs have been associated with QTc prolongation.

A QT interval of >450 milliseconds may be cause for concern, while a QT interval > 500 milliseconds should prompt the seeking of specialist advice.

514
Q

How to manage a women with psychosis or schizophrenia who is pregnant or planning pregnancy?

A

do not alter drug Tx without seeking specialist advice: isks to the mother of under-treatment (relapse), the potential benefits of a particular treatment, and the (largely hypothetical) risks to the fetus that may be associated with any drug treatment

may be offered the following options:
- Remaining on current drug treatment throughout conception, pregnancy, and birth — commonly advised when a woman’s condition is well-controlled.
- Switching to another drug treatment.
- Stopping or reducing the dose of her medication.

515
Q

Can pt breastfeed if taking antipsychotic?

A

yes unless on clozapine

Infants exposed via breastmilk to antipsychotics should, as a precaution, be monitored for adverse effects, particularly if at high risk (e.g. preterm or low birth weight infants). These may include drowsiness, irritability, motor abnormalities and poor feeding.

516
Q

RFs associated with increased risk of suicide?

A

male sex

history of deliberate self-harm

alcohol or drug misuse

history of mental illness:
- depression
- schizophrenia: NICE estimates that 10% of people with schizophrenia will complete suicide

history of chronic disease

advancing age

unemployment or social isolation/living alone

being unmarried, divorced or widowed

517
Q

If a patient has actually attempted suicide, there are a number of factors associated with an increased risk of completed suicide at a future date:

A

efforts to avoid discovery
planning
leaving a written note
final acts such as sorting out finances
violent method

518
Q

Protective factors which reduce the risk of a pt committing suicide?

A

family support
having children at home
religious belief

519
Q

Somatisation disorder?

A

multiple physical SYMPTOMS present for at least 2yrs

pt refuses to accept reassurance or negative test results

520
Q

Illness anxiety disorder (hypochondriasis)?

A

persistent belief in the presence of an underlying serious DISEASE, e.g. cancer

patient refuses to accept reassurance or negative test results

521
Q

Conversion disorder aka

A

functional neurological disorder

522
Q

Functional neurological disorder (conversion disorder)?

A

typically involves loss of motor or sensory function

the patient doesn’t consciously feign the symptoms (factitious disorder) or seek material gain (malingering)

523
Q

Dissociative disorder?

A

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

524
Q

Factitious disorder?

A

aka Munchausen’s syndrome

the intentional production of physical or psychological symptoms

525
Q

Malingering?

A

fraudulent simulation or exaggeration of symptoms with the intention of financial or other gain

526
Q

Examples of disorders where no organic cause can be found?

A
  • somatisation disorder
  • hypochondriasis (illness anxiety disorder)
  • functional neuro disorder (conversion disorder)
  • dissociative disorder
  • factitious disorder
  • malingering
527
Q

Functional neurological disorder (FND)?

A

condition in which a person experiences neurological symptoms caused by a disorder of neurological system functioning, rather than a structural disorder. It can be considered a disorder of ‘brain network functioning’.

528
Q

FND?

A

functional neurological disorder

529
Q

When is the term FND used?

A

when these symptoms (not caused by a structural disorder and more disorder of brain network functioning) reach a threshold at which they are causing significant morbidity. More minor symptoms may be termed ‘functional neurological symptoms’.

FND may affect any part of the nervous system. It can cause a variety of symptoms, including motor, sensory, balance, and speech symptoms; and functional seizures.

530
Q

RFs that may increase likelihood of, trigger or maintain FND?

A
  • anxiety, chronic pain, depression, fatigue, IBS, migraine, neuro conditions
  • child or adult stressful life event
  • physical trauma
  • neurodivergence
531
Q

FND accounted for what % of neuro outpt appointments?

A

6%

532
Q

Cx of FND?

A

reduced quality of life, psychological comorbidity, social stigma, and healthcare costs.

poor long-term physical and psychosocial outcomes.

533
Q

Diagnosis for FND?

A

‘rule-in’ diagnosis made by identifying positive signs of FND in association with symptoms consistent with the disorder, eg:
- Motor symptoms such as tremor, jerks, or weakness.

  • Sensory symptoms such as tingling, numbness, and loss of vision.
  • Other cognitive or dizziness symptoms.
  • Composite symptoms such as gait impairment due to weakness, and loss of sensation and coordination.
  • Functional seizures (usually dissociative).
  • Positive signs
534
Q

Diagnosis of FND: positive signs?

A

demonstration of internal inconsistency, or signs incongruent with recognized neuroanatomical pathways, such as sensory change having variable boundaries on repeat examination or not following a known anatomical distribution; weakness varying with redirection of attention; ad weakness present with voluntary but not involuntary movement.

535
Q

Assessment for pt with possible FND should include what?

A

Asking about symptoms including onset and course, duration, frequency, and variability; any triggers; impact on functioning; psychological and other comorbidities; family history and social support; and previous investigation(s) and treatment(s).

Examination for positive signs of FND and evidence of neurological deficit suggesting an alternative or coexisting diagnosis.

536
Q

Suspected FND?

A

Neurology referral should be arranged for specialist assessment and confirmation of the diagnosis

537
Q

Management of a person with confirmed FND in primary care includes?

A

Explaining the diagnosis and advising about sources of information and support.

Offering individualized multidisciplinary treatment, including physiotherapy, occupational therapy, speech and language therapy, and psychological support, depending on the person’s needs and wishes.

Managing any coexisting conditions.

Arranging re-referral to a neurologist or other specialist if there is diagnostic uncertainty; severe, complex, or refractory symptoms; or new neurological symptoms suggesting a coexisting condition.

Reviewing symptoms; reinforcing attentional redirection and self-help techniques; and agreeing a self-management plan for symptom exacerbation and relapse prevention.

538
Q

Useful phrases which may help to explain the possible mechanisms of functional neurological disorder (FND)= rule in diagnosis?

A

‘We think you have typical symptoms and signs of FND for the following reasons: a, b and c.’

539
Q

Useful phrases which may help to explain the possible mechanisms of functional neurological disorder (FND)= general?

A

‘FND is a problem with the functioning of the nervous system rather than damage. A potentially reversible problem with the software rather than the hardware of the nervous system. The brain has got stuck with a faulty (movement) programme.’

‘We think FND arises from a problem with how the brain and nervous system sends and receives signals, rather than an identifiable disease process.’

‘FND is a brain network disorder, meaning different parts of the brain are not communicating as they should be.’

‘As we think FND is a brain signalling problem and not a disease process, positive outcomes can be achieved with treatments that ‘retrain the brain’.’

540
Q

Useful phrases which may help to explain the possible mechanisms of functional neurological disorder (FND)= limb weakness/movements?

A

‘Did you see how your leg/other body part returned briefly to normal when I did that test? That shows us that there is a problem with the way your brain is sending the signal to your leg (voluntary movement), but the automatic movements are still okay.’

‘The leg/vision/sensation is there but the brain thinks it isn’t anymore. The map of that part of the body in the brain has gone wrong.’

‘Functional brain scans have shown that the brain is working too hard in FND. Normally we shouldn’t have to think about how to move our arms our legs. As soon as our brains start to work on this too hard it goes wrong. It’s similar to thinking about your feet when you are climbing upstairs, or trying too hard to fall asleep at night.’

541
Q

Useful phrases which may help to explain the possible mechanisms of functional neurological disorder (FND)= dystonia?

A

‘Your brain thinks that the foot is straight even though it’s turned inwards. That’s why it’s hard for you to keep it in a straight position.’

542
Q

Useful phrases which may help to explain the possible mechanisms of functional neurological disorder (FND)= seizures?

A

‘Functional seizures are when the brain goes into a trance-like state called ‘dissociation’ suddenly, all by itself. This is the medical word for being cut off or distant from your surroundings. That’s a bit like the feeling you have just before your seizures sometimes. We think it does this as a ‘reflex’ response - sometimes to get rid of a horrible feeling that many people report just before. After a while, it will often happen for no reason and when people are most relaxed.’

‘Functional seizures are a red alert state which the brain has learnt to switch off automatically by going into a trance-like state’

543
Q

Useful phrases which may help to explain the possible mechanisms of functional neurological disorder (FND)= chronic pain?

A

‘Chronic pain is usually due to an increased volume knob in the pain pathways throughout the nervous system, but especially the brain. This is called ‘central sensitization’ and, like FND, is also a problem with abnormal nervous system functioning.’

544
Q

Useful phrases which may help to explain the possible mechanisms of functional neurological disorder (FND)= associated psychological symptoms/stress?

A

‘If you have been feeling stressed/low/worried that will often make the symptoms even worse’

‘It’s common in FND for people to have problems like anxiety and depression. This can be a consequence of having the symptoms but, in many, it is already there for other reasons. FND symptoms make people fearful of falling and being injured and of being embarrassed. For some, there are things that have happened which may explain why your brain is vulnerable to going wrong in this way and could be worth exploring further. What do you think?’

545
Q

Mechanism of alcohol withdrawl?

A

chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors

alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)

546
Q

Features of alcohol withdrawl?

A

symptoms start at 6-12hrs= tremor, sweating, tachycardia, anxiety

36hrs= peak incidence of seizures

48-72hrs= peak incidence of delirium tremens- coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia

547
Q

Features of alcohol withdrawl= tremor, sweating, tachycardia and anxiety when/

A

6-12hrs

548
Q

Features of alcohol withdrawl= seizures when?

A

36hrs

549
Q

Features of alcohol withdrawl= peak incidence of delirium tremens : coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia. When?

A

48-72hrs

550
Q

Features of alcohol withdrawl= delirium tremens?

A

coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia

551
Q

patients with a history of complex withdrawals from alcohol (i.e. delirium tremens, seizures, blackouts) should be

A

admitted to hospital for monitoring until withdrawals stabilised

552
Q

Phenytoin is not as affective in Tx of what?

A

alcohol withdrawl seizures

553
Q

Mx of alcohol withdrawl?

A

1st line= long acting benzos eg. chlordiazepoxide or diazepam

Hepatic failure (liver cirrhosis)= lorazepam

typically given as part of reducing dose protocol

554
Q

Mx of alcohol withdrawl in pt with liver cirrhosis?

A

lorazepam

555
Q

Why is lorazepam used in alcohol withdrawl if pt has liver cirrhosis?

A

Lorazepam is metabolised through glucuronidation, which is less affected by liver function. Even in patients with significant liver impairment, glucuronidation tends to remain intact, making lorazepam a safer choice

chlordiazepoxide, on the other hand, undergoes hepatic oxidation via the cytochrome P450 system, which is significantly impaired in cirrhosis. This can lead to prolonged drug accumulation and an increased risk of toxicity, including sedation and hepatic encephalopathy.

556
Q

Problem alcohol use is defined as

A

exceeding low-risk drinking guidelines

557
Q

Recommended alcohol intake ‘low risk drinking guidelines’?

A

It is safest not to drink more than 14 units a week on a regular basis.

People who drink as much as 14 units per week should spread this evenly over 3 days or more.

During pregnancy, the safest approach is to avoid drinking alcohol.

558
Q

Hazardous (increasing risk) drinking is a pattern of alcohol consumption that increases a person’s risk of harm; what is this?

A

Drinking more than 14 units of alcohol a week, but less than 35 units a week for women.

Drinking more than 14 units of alcohol a week, but less than 50 units a week for men.

559
Q

Alcohol-use disorder (AUD)?

A

Harmful (higher-risk) drinking — a pattern of alcohol consumption causing health problems directly related to alcohol.

and

Alcohol dependence — characterized by craving, tolerance, a preoccupation with alcohol, and continued drinking in spite of harmful consequences.

560
Q

Routine alcohol screening should be an integral part of practice in primary care. For example, when:

A

Registering a new patient.
Screening for other conditions.
Managing a chronic disease (for example, diabetes, hypertension, or chronic heart disease).
Carrying out a medication review.
Promoting sexual health.
Seeing someone for an antenatal appointment.
Treating minor injuries.

561
Q

What questionnaire should be used to assess the nature and severity of alcohol misuse?

A

AUDIT (Alcohol Use Disorders Identification Test)

If time is limited, an abbreviated version, such as AUDIT PC or AUDIT-C, can be used. This should be followed up with the full questionnaire if problem drinking is indicated.

562
Q

…. used to test for alcohol use disorder in adults. It is not used to diagnose the disease but only to show whether a problem might exist.

A

CAGE questionnaire

563
Q

CAGE questionnaire= questions?

A

Have you ever felt you needed to Cut down on your drinking?

Have people Annoyed you by criticizing your drinking?

Have you ever felt Guilty about drinking?

Have you ever felt you needed a drink first thing in the morning (Eye-opener) to steady your nerves or to get rid of a hangover?

564
Q

Blood tests should not be used routinely to detect whether a person has been misusing alcohol. However, they may help identify

A

physical health needs relating to alcohol use.

565
Q

People in acute alcohol withdrawal, or who are assessed to be at high risk of developing alcohol withdrawal seizures or delirium tremens, should be offered

A

admission to hospital for immediate medically assisted alcohol withdrawal.

566
Q

People with clinical features of Wernicke’s encephalopathy should be

A

urgently admitted for treatment with parenteral thiamine.

567
Q

Primary care management of people misusing alcohol should include:

A

Offering a session of structured brief advice on alcohol consumption — where possible, a recognized, evidence-based resource that is based on FRAMES principles should be used.
Offering an extended brief intervention if the person has not responded to structured brief advice.
Offering a psychological intervention for harmful drinkers and people with mild dependence.
Offering prophylactic oral thiamine to harmful or dependent drinkers.
Providing appropriate information and advice.
Arranging a follow-up.

568
Q

FRAMES principles when giving brief advice on alcohol?

A

Feedback — on the person’s risk of having alcohol problems.

Responsibility — change is the person’s responsibility.

Advice — provision of clear advice when requested.

Menu — what are the options for change?

Empathy — an approach that is warm, reflective, and understanding.

Self-efficacy — optimism about the person’s ability to change their own behaviour.

569
Q

Features of cannabinoid toxicity (cannabis)?

A

CNS: agitation, tremor, anxiety, confusion, somnolence, syncope, hallucinations, changes in perception, acute psychosis, nystagmus, convulsions and coma.

Cardiac: tachycardia, hypertension, chest pain, palpitations, ECG changes.

Renal: acute kidney injury.

Muscular: hypertonia, myoclonus, muscle jerking and myalgia.

Other: cold extremities, dry mouth, dyspnoea, mydriasis, vomiting and hypokalaemia

570
Q

What is cocaine?

A

an alkaloid derived from the coca plant.

It is widely used as a recreational stimulant.

The price of cocaine has fallen sharply in the past decade resulting in cocaine toxicity becoming a much more frequent clinical problem.

571
Q

Mechanism of action of cocaine?

A

cocaine blocks the uptake of dopamine, noradrenaline and serotonin

572
Q

Cocaine adverse effects?

A

cardiovascular=
coronary artery spasm → myocardial ischaemia/infarction; both tachycardia and bradycardia may occur; hypertension; QRS widening and QT prolongation; aortic dissection

neurological= seizures; mydriasis; hypertonia; hyperreflexia

psychiatric effects=
agitation; psychosis; hallucinations

others=
ischaemic colitis is recognised in patients following cocaine ingestion. This should be considered if patients complain of abdominal pain or rectal bleeding; hyperthermia; metabolic acidosis; rhabdomyolysis

573
Q

Cardiovascular effects of cocaine?

A

coronary artery spasm → myocardial ischaemia/infarction

both tachycardia and bradycardia may occur

hypertension

QRS widening and QT prolongation

aortic dissection

574
Q

Suspect what in pt who has took cocaine and has abdo pain or rectal bleeding?

A

ischaemic colitis

575
Q

Mx of cocaine toxicity?

A

chest pain=
benzodiazepines + glyceryl trinitrate

if myocardial infarction develops then PCI

hypertension= benzodiazepines + sodium nitroprusside

alternative= beta blockers

576
Q

Ecstasy?

A

(MDMA, 3,4-Methylenedioxymethamphetamine) use became popular in the 1990’s during the emergence of dance music culture.

577
Q

CP of ecstasy (MDMA) poisoning?

A

neurological= agitation, anxiety, confusion, ataxia

cardiovascular= tachycardia, hypertension

hyponatraemia= this may result from either syndrome of inappropriate ADH secretion or excessive water consumption whilst taking MDMA

hyperthermia

rhabdomyolysis

578
Q

Mx for ecstasy poisoning?

A

supportive

dantrolene may be used for hyperthermia if simple measures fail

579
Q

LSD?

A

Lysergic acid diethylamide (LSD) is the first synthetic hallucinogen.

Its psychedelic effects usually involve heightening or distortion of sensory stimuli and enhancement of feelings and introspection. It is one of the most potent psychoactive compounds known.

580
Q

Pts with LSD toxicity typically present following what?

A

acute panic reactions (known as bad trips), massive ingestions or unintentional ingestions

581
Q

LSD intoxication= psychoactive symptoms?

A

Variable subjective experiences

Impaired judgements which can lead to injury

Amplification of current mood which leads to euphoria or dysphoria

Agitation, appearing withdrawn - especially in inexperienced users

Drug-induced psychosis

582
Q

Somatic symptoms of LSD intoxication?

A

Nausea
Headache
Palpitations
Dry mouth
Drowsiness
Tremors

583
Q

Signs of of LSD intoxication?

A

Tachycardia
Hypertension
Mydriasis
Paresthesia
Hyperreflexia
Pyrexia

584
Q

LSD intoxication: Manifestations such as tachycardia, hypertension, pupillary dilation, tremor, and hyperpyrexia can occur when?

A

within minutes following oral administration of 0.5-2 µg/kg.

585
Q

Massive overdoses of LSD can lead to the following complications:

A

Respiratory arrest
Coma
Hyperthermia
Autonomic dysfunction
Bleeding disorders

586
Q

LSD toxicity: Ix?

A

The diagnosis of LSD toxicity is mainly based on history and examination.

Most urine drug screens do not pick up LSD.

587
Q

Mx of LSD intoxication?

A

depends on specific behavioural manifestation elicited by the drug.

Agitation, e.g. from a ‘bad trip’= supportive reassurance in a calm, stress-free environment. If ineffective, benzodiazepines are the medication of choice.

LSD-induced psychosis= may require antipsychotics.

Massive ingestions of LSD should be treated with supportive care, including respiratory support and endotracheal intubation if needed.

Hypertension, tachycardia, and hyperthermia should be treated symptomatically. Hypotension should be treated initially with fluids and subsequently with vasopressors if required.

Because LSD is rapidly absorbed through the gastrointestinal tract, activated charcoal administration and gastric emptying are of little clinical value by the time a patient presents to the emergency department.

588
Q

Nitrous oxide?

A

(N‚‚O), colloquially known as ‘laughing gas’, is a colourless, sweet-smelling gas that has found utility in medical, dental, and recreational domains. It possesses legitimate clinical uses, primarily as an anaesthetic and analgesic agent. However, recreational misuse has become increasingly prevalent.

589
Q

Nitric oxide misuse= mechanism of action?

A

when inhaled, nitrous oxide acts as a dissociative anaesthetic, blocking the NMDA receptors, thus impairing the perception of pain and inducing a state of euphoria and relaxation

it also causes the release of endogenous opioids and dopamine, contributing to its addictive potential.

590
Q

Clinical presentation of nitrous oxide misuse?

A

psychological symptoms=
euphoria; altered perception of reality, hallucinations, anxiety, paranoia

neurological symptoms=
dizziness, headache, incoordination, numbness, tremors

physiological effects=
hypoxia
hypothermia
elevated heart rate and blood pressure

591
Q

Long term effects of nitrous oxide misuse?

A

vitamin B12 deficiency
- chronic exposure to nitrous oxide can oxidise and inactivate vitamin B12, leading to deficiency
- persistent misuse can lead to subacute combined degeneration of the spinal cord, resulting in irreversible neurological impairments.

psychological Issues: Chronic users may develop psychological dependencies, leading to mood disorders, anxiety, and other psychiatric conditions.

physical harm: The act of inhaling gas from containers or balloons poses a risk of lung damage, barotrauma, and frostbite.

592
Q

Novel psychoactive substances?

A

medical term for the many new substances which are chemically related to established recreational drugs such as MDMA and cannabis. They are often referred to as ‘legal highs’ although this is a misnomer in the UK, as their distribution and sale have been illegal since 2016.

593
Q

Examples of novel psychoactive substances?

A
  • stimulants
  • cannabinoids
  • hallucinogenics
  • depressant
  • others
594
Q

Novel psychoactive substances= others?

A

Gamma-hydroxybutyric acid (GHB) and gamma-butyrolactone (GBL): ‘G’, ‘Geebs’ or ‘Liquid Ecstasy’

GHB causes respiratory depression. When taken with other respiratory depressants, most commonly alcohol, this can be potentially life threatening

Nitrous oxide: ‘Hippie crack’

595
Q

Novel psychoactive substances= stimulants?

A

similar to MDMA, amphetamines and cocaine, resulting in increased levels of serotonin, dopamine and noradrenaline, resulting in a ‘high’ and feeling of euphoria

a common example is a stimulant NPS is mephedrone (‘bath salts’,’M-CAT’.’meow meow’). It is a cathinone and structurally similar to khat, a plant found in East Africa

another example is benzylpiperazine (‘Exodus’, ‘Legal X’, ‘Legal E’)

typically swallowed as a pill/powder (‘bombing’) or snorted

adverse effect profile similar to MDMA/cocaine, with the risk of serotonin syndrome

596
Q

Novel psychoactive substances= cannabinoids?

A

termed synthetic cannabinoid receptor agonists

commonly referred to as ‘spice’

typically sprayed on to herbal mixtures which are then smoked. Also available in liquid form which is then inhaled using e-cigarettes

similar adverse effects to cannabis

597
Q

Novel psychoactive substances= hallucinogenics?

A

can be either dissociatives and psychedelics

dissociatives produce a similar effect to ketamine, with a sense of not being connected to the physical body or time. A common dissociative NPS is methoxetamine (‘mexxy’)

psychedelics have a similar effect to LSD although NPS versions may also be a stimulant

598
Q

Novel psychoactive substances= depressant?

A

can be either opioid or benzodiazepine-based

usually taken as a pill or a powder

often structurally very similar to the original drug class, hence the adverse effects are similar

benzodiazepine NPS often have a significantly longer half-life

599
Q

Opioids?

A

substances which bind to opioid receptors. This includes both naturally occurring opiates such as morphine and synthetic opioids such as buprenorphine and methadone.

600
Q

Features of opioid misuse?

A

rhinorrhoea
needle track marks
pinpoint pupils
drowsiness
watering eyes
yawning

601
Q

pinpoint pupils
drowsiness
watering eyes
yawning

A

opioid misuse

602
Q

Cx of opioid misuse?

A

viral infection secondary to sharing needles: HIV, hepatitis B & C

bacterial infection secondary to injection: infective endocarditis, septic arthritis, septicaemia, necrotising fasciitis

venous thromboembolism

overdose may lead to respiratory depression and death

psychological problems: craving

social problems: crime, prostitution, homelessness

603
Q

Emergency Mx of opioid overdose?

A

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

604
Q

Opioid misuse harm reduction interventions?

A

needle exchange

offering testing for HIV, hepatitis B & C

605
Q

Mx of opioid dependence?

A

methadone or buprenorphine as the first-line treatment in opioid detoxification

usually managed by specialist drug dependence clinics although some GPs with a specialist interest offer similar services

patients may be offered maintenance therapy or detoxification

compliance is monitored using urinalysis

detoxification should normally last up to 4 weeks in an inpatient/residential setting and up to 12 weeks in the community

606
Q

Mx of opioid dependence= methadone?

A

full agonist of the mu-opioid receptor - binds to these receptors in the brain and fully activates them. This action can relieve withdrawal symptoms and cravings. Has a long half-life

607
Q

Mx of opioid dependence= buprenorphine?

A

partial agonist of the mu-opioid receptor and an antagonist of the kappa-opioid. It binds to the mu-opioid receptors in the brain but only partially activates them. This partial activation is enough to alleviate cravings and withdrawal symptoms in individuals with opioid dependence.

Furthermore, the binding of buprenorphine to the mu-opioid receptor is very strong, or ‘high affinity,’ meaning it can displace other opioids from these receptors and prevent them from exerting their effects.

As a kappa-opioid receptor antagonist, buprenorphine may contribute to its ability to reduce symptoms of opioid withdrawal and potentially reduce depressive and dysphoric states.

608
Q

Poison may be what?

A

drug, household product, industrial chemical, or plant or animal derivative.

609
Q

Overdose= Emergency transfer to hospital should be arranged for people if they have had a seizure, or if any of the following features are present?

A

Unconscious, or reduced level of consciousness.
Reduced respiratory rate or oxygen saturation is reduced.
Hypotension.
Tachycardia or bradycardia or an irregular pulse.
Hypothermia or hyperthermia.
Any other concerning clinical features are present, or the person’s condition is deteriorating.

610
Q

clinical situations where poisoning is a possibility include….

A

Acute confusional states, for example from the use of illegal drugs.

Hypoglycaemia, for example from sulfonylurea or meglitinide overdose
.
Abnormal liver function tests. Paracetamol overdose needs to be excluded if there are raised transaminases in combination with a prolonged prothrombin time.

Unexplained seizures, which can be caused by drug toxicity from tricyclic antidepressants or cocaine.

Abnormal bleeding, for example due to anticoagulants.

Several people presenting with similar symptoms. Symptoms such as headache and confusion affecting members of the same household can be due to carbon monoxide poisoning.

Recurrent or chronic unexplained symptoms in children. Deliberate poisoning (as a form of Munchausen syndrome by proxy or fictitious disorder)

611
Q

CP of paracetamol poisoning?

A

frequently asymptomatic. People who are suspected of taking a paracetamol overdose should be urgently admitted to hospital.

Nausea and vomiting usually settle within 24 hours. If these continue, often with the development of right subcostal pain and tenderness, this suggests the development of hepatic necrosis. Liver damage is maximal after 3-4 days and may lead to liver failure, hypoglycaemia, encephalopathy, coma, and death.

People may also present with coma, a reduced level of consciousness, or respiratory depression, if they have taken paracetamol with a drug that reduces the level of consciousness, such as opioids (for example a combined paracetamol/opioid preparation) or alcohol.

612
Q

CP of aspirin poisoning?

A

Hyperventilation, tinnitus, deafness, vasodilatation, and sweating. Coma if very severe poisoning.

613
Q

CP of Tricyclic and related antidepressants poisoning?

A

Dry mouth, seizures, coma, cardiac conduction defects, and arrhythmias, hypothermia, hypotension, hyperreflexia, extensor plantar response, convulsions, and respiratory failure. There may be dilated pupils and urinary retention.

614
Q

CP of SSRI poisoning?

A

Nausea, vomiting, agitation, tremor, nystagmus, drowsiness, sinus tachycardia. There may be convulsions. Rarely, severe poisonings may result in serotonin syndrome with marked neuropsychiatric effects, autonomic instability and neuromuscular hyperactivity. There may be hyperthermia, rhabdomyolysis, renal failure, and coagulation deficiencies.

615
Q

CP of beta-blocker poisoning?

A

Bradycardia, hypotension, syncope, conduction abnormalities and heart failure. Other features may include drowsiness, confusion, convulsions, hallucinations, and in severe cases coma. Effects vary depending on the beta-blocker.

616
Q

CP of calcium channel blocker poisoning?

A

Nausea, vomiting, agitation, confusion, dizziness, and coma. Metabolic acidosis and hyperglycaemia may occur. Dihydropyridine calcium-channel blockers cause profound peripheral vasodilatation and severe hypotension. Verapamil and diltiazem can cause arrhythmias including complete heart block and asystole.

617
Q

CP of iron salts poisoning?

A

Nausea, vomiting, diarrhoea, abdominal pain, haematemesis, and rectal bleeding. Hypotension and hepatocellular necrosis can occur later. If severe poisoning: coma, shock and metabolic acidosis.

618
Q

CP of lithium poisoning?

A

Most cases of toxicity occur in people who are on long-term treatment with lithium, and whose excretion of lithium is reduced for example due to dehydration or infection. There is a delayed onset of symptoms in deliberate overdose (12 hours or more). Initially, apathy and restlessness followed by vomiting, diarrhoea, ataxia, tremor, weakness, dysarthria, and muscle twitching. If severe poisoning: electrolyte imbalance, dehydration, convulsions, renal failure, hypotension, and coma.

619
Q

Initially, apathy and restlessness followed by vomiting, diarrhoea, ataxia, tremor, weakness, dysarthria, and muscle twitching. If severe poisoning: electrolyte imbalance, dehydration, convulsions, renal failure, hypotension, and coma.

A

lithium toxicity

620
Q

CP of benzodiazepines poisoning?

A

Drowsiness, dysarthria, ataxia, and nystagmus. Respiratory depression and coma can also occur.

621
Q

CP of Antimalarials (quinine, chloroquine, hydroxychloroquine) poisoning?

A

Rapid onset of life-threatening arrhythmias and intractable convulsions.

Note: overdose with these is extremely dangerous and difficult to treat. The person should be referred to hospital urgently.

622
Q

CP of Phenothiazines and related drugs poisoning?

A

Sinus tachycardia, arrhythmias, hypothermia, hypotension, reduced consciousness, and respiratory depression. Dystonic reactions may be seen with therapeutic doses. Seizures in severe cases.

623
Q

CP of Second-generation antipsychotic drugs poisoning?

A

Drowsiness, hypotension, extrapyramidal symptoms, convulsions, ECG abnormalities such as QT prolongation.

624
Q

CP of Amphetamines poisoning?

A

Initially excessive activity, wakefulness, hallucinations, paranoia, and hypertension. Later there may be convulsions, hyperthermia, exhaustion and coma.

625
Q

CP of cocaine poisoning?

A

Agitation, hypertension, tachycardia, dilated pupils, hallucinations, hyperthermia, hypertonia, and hyperreflexia and cardiac effects such as chest pain, arrhythmias, myocardial infarction.

626
Q

CP of opioid poisoning?

A

Drowsiness, coma, respiratory depression, pinpoint pupils.

627
Q

Overdose= pinpoint vs dilated pupils?

A

pinpoint= opioid

dilated= cocaine

628
Q

CP of Methylenedioxymethamfetamine (MDMA, ecstasy) poisoning?

A

Delirium, coma, hyperthermia, rhabdomyolysis, acute renal failure, acute hepatitis, disseminated intravascular coagulation, adult respiratory distress syndrome, hyperreflexia, hypotension and intracerebral haemorrhage; hyponatraemia, convulsions, ventricular arrhythmias, delirium, coma.

629
Q

Anticholinergics= common agents?

A

Antihistamines, tricyclic antidepressants, carbamazepine, phenothiazines.

630
Q

Anticholinergics (Antihistamines, tricyclic antidepressants, carbamazepine, phenothiazines) CP of toxicity?

A

Tachycardia, hyperthermia, mydriasis, warm and dry skin, urinary retention, loss of sweating, agitation/delirium, seizures.

631
Q

Cholinergic agents in poisoning?

A

Carbamates and organophosphate insecticides, some mushrooms.

632
Q

cholinergic (Carbamates and organophosphate insecticides, some mushrooms) CP of toxicity?

A

Salivation, lacrimation, miosis, urination, diarrhoea, bronchorrhoea, bronchospasm, bradycardia, hypotension, vomiting, muscle weakness.

633
Q

Hallucinogenic agents?

A

Amphetamines, cocaine, MDMA.

634
Q

Hallucinogenics (Amphetamines, cocaine, MDMA) CP of toxicity?

A

Hallucinations, panic, seizures, hypertension, tachycardia, tachypnoea.

635
Q

Opioid agents?

A

Morphine, heroin, codeine, methadone.

636
Q

Opioids (Morphine, heroin, codeine, methadone) CP of toxicity?

A

Hypoventilation, hypotension, miosis, sedation, bradycardia.

637
Q

Sedative/hypnotic agents?

A

Anticonvulsants, benzodiazepines, ethanol.

638
Q

Sedative/hypnotics (Anticonvulsants, benzodiazepines, ethanol) CP of toxicity?

A

Ataxia, blurred vision, sedation, hallucinations, slurred speech, hypotonia, hyporeflexia, hypotension, nystagmus.

639
Q

Serotonergic drugs (serotonin)?

A

(for example citalopram, tramadol, ecstasy)

640
Q

Serotonergic drugs (for example citalopram, tramadol, ecstasy) CP of toxicity?

A

Agitation, confusion, myoclonus, hyperreflexia, sweating, tremor, diarrhoea, incoordination/ataxia, fever.

641
Q

Sympathomimetic agents?

A

Amphetamines, cocaine, MDMA.

642
Q

Sympathomimetics (Amphetamines, cocaine, MDMA) CP of toxicity?

A

Tachycardia, hypertension, tachypnoea, mydriasis, agitation, seizures, hyperthermia, tremor, sweating.

643
Q

Overdose= A neurological examination)=
Abnormal movements?

A

acute dystonic movements (which can occur after exposure to antidopaminergics, such as antipsychotics), hypertonia, hyperreflexia, and extensor plantar response (which can occur after tricyclic antidepressant poisoning).

644
Q

Overdose= A neurological examination)= pupil size and reaction?

A

widely dilated pupils that react poorly to light be due to agents with anticholinergic activity (for example tricyclic antidepressants), or sympathomimetic activity (for example, amfetamines). Pinpoint pupils (miosis) occur after exposure to opioids or agents with cholinergic activity (for example, pesticides).

645
Q

Overdose= A neurological examination)= eye movements?

A

strabismus, internuclear ophthalmoplegia, dysconjugate roving eye movements and total external ophthalmoplegia may be seen in poisoning with tricyclic antidepressants, barbiturates, phenothiazines and anticonvulsants such as phenytoin and carbamazepine

646
Q

Overdose= A neurological examination)= visual acuity and fields?

A

blurring, loss of vision and tunnel vision may occur with some drugs (for example, quinine poisoning).

647
Q

For people who have ingested a considerable quantity of a low toxicity substance, or if the person has symptoms other than mild gastrointestinal upset following ingestion of a low toxicity substance, follow advice from

A

TOXBASE

648
Q

For people who have accidentally taken an additional tablet of their own medication — hospital assessment is not usually indicated.
Consider:

A

The indications, maximum daily doses, toxic doses, adverse effects and interactions of the medicine.
The person’s past medical history (especially renal and liver impairment) and medication history.
The person’s age and social circumstances.

649
Q

The Mental Capacity Act (2005) has five key principles:

A

Presumption of capacity — adults should always be presumed to have the capacity to make a decision unless the healthcare professional can prove otherwise.

Maximizing decision-making capacity — the person must be given all practical support before it can be decided that they lack capacity. Support may involve extra time for assessment, repeating the assessment if capacity fluctuates, or using an interpreter or sign language.

The freedom to make seemingly unwise decisions — if the person makes a seemingly unwise decision, this in itself is not proof of incapacity. Proof of incapacity depends on the process by which the decision is made, not the decision itself.

Best interests — any decision or action taken on behalf of the person must be in their best interests. If the decision can be delayed until the person regains capacity, then it should be. A decision taken on another’s behalf should take account of their wishes, including those expressed in an advance decision, and their beliefs and values. The decision-making process should involve, when appropriate, family, carers, and significant others.

The least restrictive alternative — when a decision is made on the person’s behalf, the healthcare professional must choose the alternative that interferes least with the person’s rights and freedoms while still achieving the necessary goal.

650
Q

The Mental Health Act (1983, amended 2007)

The Mental Health Act (1983) allows compulsory admission of people who:

A

Have a mental disorder of a nature and degree that warrant assessment or treatment in hospital, and

Need to be admitted in the interests of their own health or safety, or for the protection of other people.

651
Q

Compulsory admission is arranged using the appropriate section of the Mental Health Act:

A

Section 2 allows compulsory admission for up to 28 days for assessment.

Section 3 allows compulsory admission for up to 6 months for treatment.

652
Q

Sections 2 and 3 require an application from an

A

Approved Mental Health Professional (AMHP), or the person’s nearest relative, and recommendations from two doctors; one of whom is section 12-approved (usually a psychiatrist) and one who has previous acquaintance with the person (usually the person’s GP if at all practicable). Ideally, the person should be examined jointly by the two doctors with the AMHP also present. Where this is not possible, each doctor may carry out a separate examination. If the AMHP is not present, it is essential that at least one of the doctors discusses the person with the AMHP.

653
Q

Section 4?

A

used in exceptional cases to permit compulsory admission for up to 72 hours if there is urgent necessity, and undesirable delay would occur while trying to arrange admission under section 2.

It requires an application from an AMHP (or, rarely, the person’s nearest relative) and just one medical recommendation, preferably from a doctor with a previous acquaintance (usually the person’s GP).

654
Q

Section 136?

A

may be used by police to take people from a public place to a place of safety and enable examination by a registered medical practitioner and interview by an AMHP. The person’s GP, where known, may be informed.

655
Q

Prevention of absorption in overdose?

A

Activated charcoal can bind to the poison and prevent absorption. The sooner it is given the more effective, but it may still be effective up to 1 hour after ingestion, or longer for modified release preparations or medicines with antimuscarinic properties. An important use is to prevent the absorption of medicines which are toxic in small amounts, such as antidepressants.

In children this is only used if a potentially toxic amount of a drug that adsorbs to charcoal has been taken, the child has presented within 1 hour of ingestion, in the absence of contraindications, and after a risk-benefit analysis when this is being considered.

656
Q

Overdose= active elimination?

A

suitable for a limited number of drugs:

Repeated doses of activated charcoal enhance the elimination of some drugs even after they have been absorbed, such as carbamazepine, phenobarbital, quinine, theophylline, and dapsone.

Alkalinisation of the urine for salicylate poisoning.

Haemodialysis for ethylene glycol, lithium, methanol, phenobarbital, salicylates, and sodium valproate.

657
Q

Overdose= removal from GI tract?

A

Gastric lavage is rarely required — it is indicated only if a life-threatening amount has been ingested within the previous hour, and the poison cannot be removed using other methods. It may be useful for drugs such as lithium and iron that are not absorbed by charcoal. Lavage should never be done if a petroleum distillate or a corrosive substance has been ingested.

Whole bowel irrigation may be used if there has been poisoning with certain sustained-release or enteric-coated medicines, or in severe poisoning with iron or lithium salts. This should only be performed following discussion with the NPIS.

658
Q

Overdose antidotes= paracetamol?

A

acetylcysteine

659
Q

Overdose antidotes= digoxin?

A

digoxin-specific antibody fragments

660
Q

Overdose antidotes= benzodiazepines?

A

Flumazenil injection

This reverses the central nervous system and respiratory depression. However, if the person has also taken a tricyclic antidepressant or has epilepsy, there must be caution, as flumazenil can cause seizures and arrhythmias.

661
Q

Overdose antidotes= insulin, beta blockers and calcium channel blockers?

A

glucagon injection

662
Q

Overdose antidotes= morphine, heroin, opiates?

A

naloxone injection

In people with reduced consciousness due to suspected opioid poisoning, administration which leads to significant improvement in the person’s condition within 1-2 minutes is highly suggestive of opioid poisoning.

663
Q

Overdose antidotes= iron salts?

A

desferrioxamine mesilate

664
Q

Overdose antidotes= ethylene glycol or methanol?

A

Fomepizole

665
Q

Charles-Bonnet syndrome (CBS)?

A

persistent or recurrent complex hallucinations (usually visual or auditory), occurring in clear consciousness.

This is generally against a background of visual impairment (although visual impairment is not mandatory for a diagnosis).

Insight is usually preserved.

This must occur in the absence of any other significant neuropsychiatric disturbance.

666
Q

RFs for Charles-Bonnet syndrome?

A

Advanced age
Peripheral visual impairment
Social isolation
Sensory deprivation
Early cognitive impairment

667
Q

Most common ophthalmological condition associated with Charles-Bonnet syndrome?

A

age-related macular degeneration, followed by glaucoma and cataract.

668
Q

Hallucinations in Charles-Bonnet syndrome?

A

Well-formed complex visual hallucinations are thought to occur in 10-30 per cent of individuals with severe visual impairment. Prevalence of CBS in visually impaired people is thought to be between 11 and 15 per cent.

Around a third find the hallucinations themselves an unpleasant or disturbing experience.

669
Q

Prognosis of Charles-Bonnet syndrome?

A

In a large study published in the British Journal of Ophthalmology, 88% had CBS for 2 years or more, resolving in only 25% at 9 years (thus it is not generally a transient experience).

670
Q

ICD10 definition of hallucinations?

A

false sensory perception in the absence of an external stimulus. Maybe organic, drug-induced or associated with mental disorder.

671
Q

Definition of pseudohallucinations?

A

false sensory perception in the absence of external stimuli when the affected is aware that they are hallucinating.

no mention of pseudohallucinations in either the ICD10 nor the DSM-5

672
Q

Many specialists feel that it is more appropriate to think about pseudohallucinations how?

A

on a spectrum from mild sensory disturbance to hallucinations to prevent symptoms from being mistreated or misdiagnosed.

673
Q

Example of pseudohallucinations?

A

hypnagogic hallucination which occurs when transitioning from wakefulness to sleep. These are experienced vivid auditory or visual hallucinations which are fleeting in duration and may occur in anyone. These are pseudohallucinations as the affected person is able to determine that the hallucination was not real.

674
Q

The relevance of pseudohallucinations in practice?

A

patients may need reassurance that these experiences are normal and do not mean that they will develop a mental illness

675
Q

Psuedohallucinations commonly occur in people who are….?

A

grieving

676
Q

Monitoring of antipsychotics?

A

FBC, U&E, LFT= at start, annually; clozapine requires more frequent FBC (initially weekly)

Lipids and weight= at start, 3m, annually

Fasting blood glucose, prolactin= at start, 6m, annually

BP= baseline and frequently during dose titration

ECG= baseline

Cardiovascular risk assessment= annually

677
Q

Type of antipsychotics used 1st line in schizophrenia?

A

atypical

678
Q

main advantage of the atypical antipsychotics?

A

significant reduction in extrapyramidal side-effects

679
Q

Adverse effects of atypical antipsychotics?

A

weight gain

clozapine is associated with agranulocytosis

hyperprolactinaemia

680
Q

Risks when antipsychotics are used in elderly pts?

A

increased risk of stroke and VTE

681
Q

Examples of atypical antipsychotics?

A

clozapine= angranulocytosis

olanzapine: higher risk of dyslipidemia and obesity

risperidone

quetiapine

amisulpride

aripiprazole: generally good side-effect profile, particularly for prolactin elevation

682
Q

GABAA drugs?

A

benzodiazipines increase the frequency of chloride channels

barbiturates increase the duration of chloride channel opening

Frequently Bend - During Barbeque

…or…

Barbidurates increase duration & Frendodiazepines increase frequency

683
Q

Benzodiazepines MOA?

A

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

684
Q

Benzodiazepines are used for what?

A

sedation
hypnotic
anxiolytic
anticonvulsant
muscle relaxant

685
Q

How long to prescribe benzodiazepines for and why?

A

short period eg. 2-4w as pts commonly develop a tolerance and dependence

686
Q

How to withdraw a benzodiazepine?

A

The dose should be withdrawn in steps of about 1/8 (range 1/10 to 1/4) of the daily dose every fortnight. A suggested protocol for patients experiencing difficulty is given:

  • switch patients to the equivalent dose of diazepam
  • reduce dose of diazepam every 2-3 weeks in steps of 2 or 2.5 mg
  • time needed for withdrawal can vary from 4 weeks to a year or more
687
Q

If patients withdraw too quickly from benzodiazepines they may experience

A

benzodiazepine withdrawal syndrome, a condition very similar to alcohol withdrawal syndrome. This may occur up to 3 weeks after stopping a long-acting drug

688
Q

benzodiazepine withdrawal syndrome features?

A

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

689
Q

Clozapine is what?

A

atypical antipsychotic

690
Q

Risks of using clozapine (atypical antipsychotic)?

A

angranulocytosis so monitor FBC

only use is resistant to other antipsychotics

691
Q

What to monitor in pt on clozapine?

A

FBC as risk of agranulocytosis

692
Q

When to use clozapine?

A

if schizophrenia is not controlled despite the sequential use of two or more antipsychotic drugs (one of which should be a second-generation antipsychotic drug), each for at least 6-8 weeks.

693
Q

Adverse effects of clozapine?

A

agranulocytosis (1%), neutropaenia (3%)

reduced seizure threshold - can induce seizures in up to 3% of patients

constipation

myocarditis: a baseline ECG should be taken before starting treatment

hypersalivation

694
Q

Dose adjustment of clozapine may be needed when?

A

if smoking is started or stopped during Tx

695
Q

Electroconvulsive therapy?

A

useful treatment option for patients with severe depression refractory to medication (e.g. catatonia) those with psychotic symptoms.

696
Q

Absolute contraindication to electroconvulsive therapy?

A

raised ICP

697
Q

Side effects of electroconvulsive therapy?

A

Short-term side-effects:
headache
nausea
short term memory impairment
memory loss of events prior to ECT
cardiac arrhythmia

Long-term side-effects:
some patients report impaired memory

698
Q

5 stages of grief?

A

1) Denial: this may include a feeling of numbness and also pseudohallucinations of the deceased, both auditory and visual. Occasionally people may focus on physical objects that remind them of their loved one or even prepare meals for them

2) Anger: this is commonly directed against other family members and medical professionals

3) Bargaining

4) Depression

5) Acceptance

699
Q

Does everyone go through all 5 stages of grief?

A

no

700
Q

Abnormal, or atypical, grief reactions are more likely to occur in who?

A

women and if the death is sudden and unexpected. Other risk factors include a problematic relationship before death or if the patient has not much social support.

701
Q

Features of atypical grief reaction?

A

delayed grief: sometimes said to occur when more than 2 weeks passes before grieving begins

prolonged grief: difficult to define. Normal grief reactions may take up to and beyond 12 months

702
Q

Delayed grief?

A

sometimes said to occur when more than 2 weeks passes before grieving begins

703
Q

Prolonged grief?

A

difficult to define. Normal grief reactions may take up to and beyond 12 months

704
Q

Korsakoff’s syndrome?

A

marked memory disorder often seen in alcoholics

thiamine deficiency causes damage and haemorrhage to the mammillary bodies of the hypothalamus and the medial thalamus

in often follows on from untreated Wernicke’s encephalopathy

705
Q

Features of Korsakoff’s syndrome?

A

anterograde amnesia: inability to acquire new memories

retrograde amnesia

confabulation

706
Q

Mirtazapine?

A

antidepressant that works by blocking alpha2-adrenergic receptors, which increases the release of neurotransmitters.

707
Q

When may mirtazapine be useful?

A

fewer side effects and interactions than many other antidepressants and so is useful in older people who may be affected more or be taking other medications. Two side effects of mirtazapine, sedation and an increased appetite, can be beneficial in older people that are suffering from insomnia and poor appetite.

708
Q

When is mirtazapine usually taken?

A

in the evening as it can be sedative

709
Q

serotonin and noradrenaline are metabolised by

A

monoamine oxidase in the presynaptic cell

710
Q

Non-selective monoamine oxidase inhibitors?

A

e.g. tranylcypromine, phenelzine

used in the treatment of atypical depression (e.g. hyperphagia) and other psychiatric disorder

not used frequently due to side-effects

711
Q

Adverse effects of non-selective monoamine oxidase inhibitors?

A

hypertensive reactions with tyramine containing foods e.g. cheese, pickled herring, Bovril, Oxo, Marmite, broad beans

anticholinergic effects

712
Q

Othello’s syndrome?

A

pathological jealousy where a person is convinced their partner is cheating on them without any real proof. This is accompanied by socially unacceptable behaviour linked to these claims.

713
Q

For Panic disorder to be diagnosed symptoms have to be present for at least

A

1m

714
Q

Mx of panic disorder?

A

SSRIs and CBT

715
Q

RFs for panic disorder?

A

Living alone, early parental loss, a history of abuse, poor educational history and urban living are risk factors for developing panic disorder. There is a 40% prevalence seen in 1st degree relatives of those with panic disorder and it generally follows a chronic, mild and stable course in 50% of patients.

716
Q

When is post-concussion syndrome seen?

A

even after minor head trauma

717
Q

Typical features of post-concussion syndrome?

A

headache
fatigue
anxiety/depression
dizziness

718
Q

Seasonal affective disorder (SAD)?

A

depression which occurs predominately around the winter months.

719
Q

Seasonal affective disorder (SAD) Mx?

A

should be treated the same way as depression, therefore as per the NICE guidelines for mild depression, you would begin with psychological therapies and follow up with the patient in 2 weeks to ensure that there has been no deterioration. Following this an SSRI can be given if needed. In seasonal affective disorder, you should not give the patient sleeping tablets as this can make the symptoms worse. Finally, the evidence for light therapy is limited and as such it is not routinely recommended.

720
Q

When is sectioning under the Mental Health Act done?

A

This is used for someone who will not be admitted voluntarily. Patients who are under the influence of alcohol or drugs are specifically excluded

721
Q

Mental Health Act= Section 2?

A

admission for assessment for up to 28 days, not renewable

an Approved Mental Health Professional (AMHP) or rarely the nearest relative (NR) makes the application on the recommendation of 2 doctors

one of the doctors should be ‘approved’ under Section 12(2) of the Mental Health Act (usually a consultant psychiatrist)

treatment can be given against a patient’s wishes

722
Q

Mental Health Act= Section 3?

A

admission for treatment for up to 6 months, can be renewed

AMHP along with 2 doctors, both of which must have seen the patient within the past 24 hours

treatment can be given against a patient’s wishes

723
Q

Mental Health Act= Section 4?

A

72 hour assessment order
used as an emergency, when a section 2 would involve an unacceptable delay

a GP and an AMHP or NR

often changed to a section 2 upon arrival at hospital

724
Q

Mental Health Act= Section 5(2)?

A

a patient who is a voluntary patient in hospital can be legally detained by a doctor for 72 hours

725
Q

Mental Health Act= Section 5(4)?

A

similar to section 5(2), allows a nurse to detain a patient who is voluntarily in hospital for 6 hours

726
Q

Mental Health Act= Section 17a?

A

Supervised Community Treatment (Community Treatment Order)

can be used to recall a patient to hospital for treatment if they do not comply with conditions of the order in the community, such as complying with medication

727
Q

Mental Health Act= Section 135?

A

a court order can be obtained to allow the police to break into a property to remove a person to a Place of Safety

728
Q

Mental Health Act= Section 136?

A

someone found in a public place who appears to have a mental disorder can be taken by the police to a Place of Safety

can only be used for up to 24 hours, whilst a Mental Health Act assessment is arranged

729
Q

Sections in the mental health act?

A

2
3
4
5(2)
5(4)
17a
135
136

730
Q

Serotonin and noradrenaline reuptake inhibitor (SNRI’s) MOA?

A

class of relatively new antidepressants.

Inhibiting the reuptake increases the concentrations of serotonin and noradrenaline in the synaptic cleft leading to the effects.

731
Q

Serotonin and noradrenaline reuptake inhibitor (SNRI’s) examples?

A

venlafaxine and duloxetine

732
Q

Serotonin and noradrenaline reuptake inhibitor (SNRI’s) indications?

A

major depressive disorders, generalised anxiety disorder, social anxiety disorder and panic disorder and menopausal symptoms

733
Q

Sleep paralysis?

A

common condition characterized by transient paralysis of skeletal muscles which occurs when awakening from sleep or less often while falling asleep. It is thought to be related to the paralysis that occurs as a natural part of REM (rapid eye movement) sleep. Sleep paralysis is recognised in a wide variety of cultures

734
Q

Sleep paralysis features?

A

paralysis - this occurs after waking up or shortly before falling asleep

hallucinations - images or speaking that appear during the paralysis

735
Q

Sleep paralysis Mx?

A

if troublesome clonazepam may be used

736
Q

Adverse effects of SSRI?

A

gastrointestinal symptoms are the most common side-effect

there is an increased risk of gastrointestinal bleeding in patients taking SSRIs. A proton pump inhibitor should be prescribed if a patient is also taking a NSAID

hyponatraemia
patients should be counselled to be vigilant for increased anxiety and agitation after starting a SSRI

fluoxetine and paroxetine have a higher propensity for drug interactions

737
Q

Citalopram adverse effect?

A

citalopram and escitalopram are associated with dose-dependent QT interval prolongation and should not be used in those with: congenital long QT syndrome; known pre-existing QT interval prolongation; or in combination with other medicines that prolong the QT interval

the maximum daily dose is now 40 mg for adults; 20 mg for patients older than 65 years; and 20 mg for those with hepatic impairment

738
Q

SSRIs= interactions?

A

NSAIDs: NICE guidelines advise ‘do not normally offer SSRIs’, but if given co-prescribe a proton pump inhibitor

warfarin / heparin: NICE guidelines recommend avoiding SSRIs and considering mirtazapine

aspirin: see above

triptans: avoid SSRIs

739
Q

Following the initiation of antidepressant therapy patients should normally be reviewed by a doctor after…

A

1 week if =<25 or increased risk of suicide

2 weeks others

If a patient makes a good response to antidepressant therapy they should continue on treatment for at least 6 months after remission as this reduces the risk of relapse.

740
Q

Stopping SSRIs?

A

When stopping a SSRI the dose should be gradually reduced over a 4 week period (this is not necessary with fluoxetine). Paroxetine has a higher incidence of discontinuation symptoms.

741
Q

SSRI Discontinuation symptoms?

A

increased mood change
restlessness
difficulty sleeping
unsteadiness
sweating
gastrointestinal symptoms: pain, cramping, diarrhoea, vomiting
paraesthesia

742
Q

Why are Tricyclic antidepressants (TCAs) less commonly used for depression?

A

due to their side-effects and toxicity in overdose. They are however used widely in the treatment of neuropathic pain, where smaller doses are typically required.

743
Q

The primary mechanism by which TCAs exert their antidepressant effects is…

A

through the inhibition of the reuptake of neurotransmitters:

  • Serotonin (5-HT): This neurotransmitter has a pivotal role in mood regulation. Inhibition of its reuptake leads to increased concentrations in the synaptic cleft, enhancing serotonergic neurotransmission.
  • Noradrenaline (NA): Similar to 5-HT, blocking the reuptake of NA increases its synaptic cleft concentration, intensifying noradrenergic neurotransmission.
744
Q

As well as 5-HT and NA, tricyclics interact with number of other receptors that contribute to their side-effect profile….

A

antagonism of histamine receptors= drowsiness

antagonism of muscarinic receptors= dry mouth, blurred vision, constipation, urinary retention

antagonism of adrenergic receptors=
postural hypotension

lengthening of QT interval

745
Q

Choice of tricyclic?

A

low-dose amitriptyline is commonly used in the management of neuropathic pain and the prophylaxis of headache (both tension and migraine)

lofepramine has a lower incidence of toxicity in overdose

amitriptyline and dosulepin (dothiepin) are considered the most dangerous in overdose

746
Q

Tricyclic antidepressants
examples?

A

More sedative:
- Amitriptyline
- Clomipramine
- Dosulepin
- Trazodone (technically a ‘tricyclic-related antidepressant’)

Less sedative:
- Imipramine
- Lofepramine
- Nortriptyline

747
Q

Z drugs MOA?

A

similar effects to benzodiazepines but are different structurally. They act on the α2-subunit of the GABA receptor.

748
Q

Z drugs can be divided into what 3 groups?

A

Imidazopyridines: e.g. zolpidem

Cyclopyrrolones: e.g. zopiclone

Pyrazolopyrimidines: e.g. zaleplon

749
Q

Adverse effects of Z drugs?

A

similar to benzodiazepines

increase the risk of falls in the elderly

750
Q

Prader-Willi syndrome genetics?

A

an example of genetic imprinting where the phenotype depends on whether the deletion occurs on a gene inherited from the mother or father:

  • Prader-Willi syndrome if gene deleted from father
  • Angelman syndrome if gene deleted from mother
751
Q

Prader-Willi syndrome cause?

A

associated with the absence of the active Prader-Willi gene on the long arm of chromosome 15. This may be due to:
- microdeletion of paternal 15q11-13 (70% of cases)
- maternal uniparental disomy of chromosome 15

752
Q

Features of Prader-Willi syndrome?

A

hypotonia during infancy

dysmorphic features

short stature

hypogonadism and infertility

learning difficulties

childhood obesity

behavioural problems in adolescence

753
Q

Refeeding syndrome?

A

metabolic abnormalities which occur on feeding a person following a period of starvation. It occurs when an extended period of catabolism ends abruptly with switching to carbohydrate metabolism.

754
Q

Refeeding syndrome metabolic consequences?

A

hypophosphataemia

hypokalaemia

hypomagnesaemia

abnormal fluid balance

755
Q

What in refeeding syndrome may predispose to torsades de pointes?

A

hypomagnesaemia

756
Q

Hallmark symptom of refeeding syndrome?

A

hypophosphataemia

may result in significant muscle weakness, including myocardial muscle (→ cardiac failure) and the diaphragm (→ respiratory failure)

757
Q

Pathophysiology of Hypophosphatemia in refeeding syndrome?

A

Shift from Fat to Carbohydrate Metabolism: In refeeding syndrome, the reintroduction of carbohydrates leads to a shift from fat to carbohydrate metabolism. This switch activates insulin secretion, which in turn increases cellular uptake of glucose.

Intracellular Movement of Phosphate: Insulin and increased glucose uptake stimulate the intracellular movement of phosphate, which is used in the synthesis of ATP and 2,3-diphosphoglycerate in erythrocytes. This intracellular shift reduces serum phosphate levels.

Decreased Phosphate Stores: Patients with chronic malnutrition often have depleted phosphate stores, although their serum phosphate levels may initially be normal. When refeeding starts, the sudden demand for phosphate in anabolic processes exceeds the supply, leading to hypophosphatemia.

758
Q

Clinical Consequences of Hypophosphatemia in refeeding syndrome?

A

Cardiac Dysfunction: Hypophosphatemia can impair myocardial contractility, leading to heart failure. It may also cause arrhythmias due to its role in maintaining normal cellular electrophysiology.

Respiratory Failure: Phosphate is essential for ATP production, necessary for respiratory muscle function. Severe hypophosphatemia can lead to muscle weakness, including the diaphragm and intercostal muscles, potentially resulting in acute respiratory failure.

Neurological Complications: These can range from confusion and seizures to coma, attributable to disturbed ATP metabolism in the central nervous system.

Haematological Effects: Reduced 2,3-diphosphoglycerate levels in erythrocytes affect oxygen release from haemoglobin, leading to tissue hypoxia. Hypophosphatemia can also result in hemolysis.

Rhabdomyolysis: Phosphate depletion impairs ATP production in muscles, which can lead to muscle breakdown and rhabdomyolysis.

759
Q

How to avoid refeeding syndrome?

A

identifying patients at a high-risk of developing refeeding syndrome

760
Q

What pts are considered high risk for refeeding syndrome?

A

one or more of the following=
- BMI < 16 kg/m2
- unintentional weight loss >15% over 3-6 months
- little nutritional intake > 10 days
- hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high)

If two or more of the following=
- BMI < 18.5 kg/m2
- unintentional weight loss > 10% over 3-6 months
- little nutritional intake > 5 days
- history of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids

761
Q

Refeeding syndrome prevention= NICE recommend that if a patient hasn’t eaten for > 5 days, aim to re-feed at no more than?

A

50% of requirements for the first 2 days.

762
Q
A