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Finals Club (Dundee Medicine Master Summary Deck) > Year 3: Psychiatry > Flashcards

Year 3: Psychiatry Flashcards

Depression, BPAD, Schizophrenia, Detention Orders, Anxiety, PTSD, OCD, ADHD, ASD, LD, Personality Disorders, Eating Disorders, Addiction

1
Q

Depression is due to

A

Decreased Serotonin (5-HT)

But also due to decreased Dopamine

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2
Q

What 3 dopamine pathways are affected in depression

A

Nigrostriatal

Mesolimbic

Anterior Cingulate

Hence side effects like anhedonia etc

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3
Q

3 core symptoms of Depression

A
  • Persistent low mood (2 weeks+)
  • Anhedonia
  • Decreased energy, increased fatigue
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4
Q

F32 Criteria

(Severity of Depression)

A
  • Mild: 1/3 core features
  • Moderate: 2/3 core features + 3 additional symptoms
  • Severe: 3/3 core features + 5 additional symptoms
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5
Q

Depression immediately becomes BPAD when

A

there are any manic symptoms

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6
Q

First line treatment for depression

A

Escitalopram (SSRI)

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7
Q

An SSRI that is to be used in pregnancy, cardio patients and anxiety patients

A

Sertraline (SSRI)

“As you are certain that it’s okay in pregnancy etc”

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8
Q

Anti-depressant that increases weight gain (appetite) and is good for sleep

A

Mirtazipine (Tetracycline)

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9
Q

Anti-depressant used for resistant depression

  • Tried many drugs and they don’t work
A

Venlafaxine (SNRI)

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10
Q

Side effect of Citalopram (SSRI)

A

Can cause long QT syndrome

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11
Q

An anti-depressant with little side effects

Can be used in kids

A

Fluoxetine (SSRI)

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12
Q

Why are tricyclic anti-depressants bad in patients with suicidal risk

A

They are cardiotoxic, and so are easy to overdose on

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13
Q

Contraindications of Monoamine Oxidase Inhibitors

A

A tyramine rich diet

  • Cheese
  • Red wine
  • Cured/processed meats
  • Sauces and gravy
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14
Q

Why are tyramine rich food avoided in MAOIs

A

Can cause a hypertensive crisis

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15
Q

Contraindications with SSRIs

A

NSAIDs

Elderly (can cause hyponatraemia)

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16
Q

What is seen in Direct Self Harm?

A

Decreased activity in the pre-frontal cortex

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17
Q

Hallucinations seen in Psychotic Depression

A

Second person hallucinations

“You are fucking crazy son, kill yourself”

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18
Q

DSM-V Criteria for BPAD

(Subtypes of Bipolar Affective Disorder)

A

Type 1: More manic than depressed

Type 2: More depressed than manic

Type 3: Hypomanic due to chronic use of antidepressants

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19
Q

Examples of Type 1 BPAD

A

The “classic Bipolar person”

  • Have a manic episode lasting 1 week+
  • Has been depressed in the past
  • Flight of ideas, grandiosity, increased activity etc
  • On an absolute high

High 15% of the time

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20
Q

Examples of Type 2 BPAD

A

Most common form of BPAD

  • Hypomania lasting 4 days
  • Has been depressed in the past
  • Reckless behaviour (spending money rashly)
  • Increased libido

High 5% of the time

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21
Q

ICD-10 Criteria for BPAD shows

A

The severity of Bipolar Affective Disorder

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22
Q

ICD-10 Criteria for a hypomanic episode

A

Increased mood sustained for 4 consecutive days

Need 3/6 symptoms

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23
Q

ICD-10 Criteria for a manic episode

A

Increased mood sustained for 1 week

3/9 Symptoms

Symptoms are a bit more mental

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24
Q

If a BPAD patient is manic and on an antidepressant then

A

Take them off the antidepressant

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25
Q

1st line drug for BPAD

A

Lithium carbonate

To stabilise long term mood

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26
Q

If a patient is on lithium you should

A
  • 12-hour monitoring when first started
  • U&Es - as nephrotoxic
  • TFTs- as thyrotoxic
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27
Q

Main rule for 2nd line prescribing in BPAD

A
  • If you prescribe an antidepressant then you must also prescribe an antimanic drug
  • If you prescribe an antimanic drug you must also prescribe an antidepressant drug
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28
Q

If BPAD patient is mainly manic what is the 2nd line drug combination

A

Sodium valproate (antiepileptic) and fluoxetine (SSRI)

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29
Q

If BPAD patient is mainly depressed what is the 2nd line drug combination

A

Lamotrigine (antiepileptic) and fluoxetine (SSRI)

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30
Q

1st line for acute mania management

A

Olanzapine (atypical antipsychotic)

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31
Q

2nd line for acute mania management

A

Quetiapine (atypical antipsychotic)

Has a sedative effect

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32
Q

Risk factor for schizophrenia

A

Cannabis use

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33
Q

Pathophysiological changes in schizophrenia

A
  • Reduction in grey matter
  • Enlarged ventricles
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34
Q

Neurochemical changes in schizophrenia

A

Increase in dopamine

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35
Q

3 first rank symptoms of schizophrenia

A
  • Delusions
  • 3rd party hallucinations
  • Thought interference

Patients often have a lack of insight

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36
Q

ICD-10 Criteria states that you need

A
  • 1/3 first rank symptoms
  • 2/4 additional symptoms
  • blunting of emotion, catatonic behaviour etc
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37
Q

Bad prognosis of schizophrenia

A

Quick onset

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38
Q

Good prognosis of schizophrenia

A

If patient is depressive

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39
Q

Atypical Antipsychotics work on

A

Serotonin and dopamine

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40
Q

Typical Antipsychotics work on

A

Dopamine

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41
Q

Name some Atypical antipsychotics

A
  • Risperidone
  • Quetiapine
  • Clozapine
  • Aripiprazole
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42
Q

Name some typical antipsychotics

A
  • Chlorpromazine
  • Haloperidol
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43
Q

First line drug for schizophrenia

A

Risperidone

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44
Q

Which antipsychotic class has the least side effects

A

Atypicals

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45
Q

Side effects of atypical antipsychotics

A

Metabolic syndrome

  • HTN
  • Hyperglycaemia
  • Hypercholesterolaemia
  • Increased body fat around the waist
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46
Q

Side effects of typical antipsychotics

A

Extrapyramidal symptoms

  • Acute dystonia (muscle contraction/spasm)
  • Akathisia (motor restlessness)
  • Bradykinesia (slow movement)
  • Tremor
  • Tardive Dyskinesia (irregular jerky movements)

Basically, you give them Parkinson’s due to blocking dopamine

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47
Q

Side effect of Clozapine (atypical antipsychotic)

A

Agranulocytosis

(decreased WCC)

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48
Q

What is good about aripiprazole (atypical antipsychotic)

A

It has the least side effects

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49
Q

Patient can’t move their neck

A

Acute neck dystonia due to haloperidol

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50
Q

Risk factor for puerperal psychosis

A

BPAD

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51
Q

Mum gave birth a few weeks ago and is batshit crazy, killing baby

A

Puerperal psychosis

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52
Q

Management for puerperal psychosis

A

Admission to specialised unit

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53
Q

Olfactory hallucination is usually due to

A

epilepsy / stroke

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54
Q

Auditory hallucination is usually due to

A

Psychosis

2nd person: Depressive psychosis

“You are useless”

3rd person: Schizophrenia

“He wants to kill her”

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55
Q

Visual hallucination is usually due to

A

An organic cause:

  • Lewy Body Dementia
  • Delirium
  • Eye problems
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56
Q

Tactile hallucinations are usually due to

A
  • Schizophrenia: Skin stretched across their head
  • Parkinsonism, Ekbom’s syndrome and alcohol and cocaine use: Bugs underneath/ on skin
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57
Q

Gustatory (taste) hallucinations are usually due to

A

Epilepsy

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58
Q

Haptic hallucinations (inside of body/organs) are usually due to

A

Mood disorders

“My insides are dying”

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59
Q

What is the Common Law

A

If a psychiatric patient is going absolutely fucking mental then sedate them to fuck

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60
Q

Drugs used in common law

A

1st line: Lorazepam

  • If patient is know to be on antipsychotics then add on haloperidol

Give orally if possible

If not, then give IM, if that doesn’t work wait 30mins and go IM again

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61
Q

The 5 pillars you need to detain someone

A
  1. Danger to themselves or others
  2. There must be treatment available that works
  3. Patient can’t make their own decisions
  4. No other alternative
  5. Confirmed mental health problem (THAT IS NOT ALCOHOL/DRUG RELATED)
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62
Q

Emergency Detention Order

A

72 hours

Section 36

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63
Q

Who do you need to consent to emergency detention

A

No one to begin with

ACT FIRST THINK LATER

MHO is required to consent while detainment is happening

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64
Q

Short Term Detention Order

A

28 days

Section 44

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65
Q

Who do you need to consent to a short term detention order

A

MHO before detention begins

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66
Q

Compulsory Detention Order

A

6 months

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67
Q

Who do you need to give consent to a compulsory detention order

A

Goes to court: Tribunal

Application is needed: MHO and 2 medical reports

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68
Q

Do not detain

A

Alcoholics or drug users

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69
Q

4 types of thought interference

A
  • Insertion: “There are thoughts being put in my head”
  • Withdrawal: “They are extracting my thoughts from my head”
  • Broadcasting: “Everyone knows what I’m thinking”
  • Blocking: “I get halfway through thinking and then my thoughts vanish”
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70
Q

What to say in an OCSE to someone that is clearly nuts

A

“I think that there is evidence to suggest that you are actually unwell, and I think that for your own wellbeing you need to receive treatment, even if that means you need to be in a hospital, although I recognise that you don’t agree with this”

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71
Q

Biggest comorbidity in general anxiety disorder (GAD)

A

Depression

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72
Q

Criteria for GAD

A
  • Must feel anxious and have associated symptoms most days for 6 months
  • Loss of function/ affects daily life
  • Not controllable
  • Irrational
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73
Q

Short term treatment for GAD

A

BZD (e.g. Diazepam)

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74
Q

Long term treatment for GAD

A

Sertraline

“Because you’re certain that it works”

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75
Q

Panic disorder principles

A
  • >10mins
  • Unpredictable
76
Q

50% of panic disorders lead to

A

Agoraphobia

(avoidance of places or situations due to anxiety)

77
Q

What physiological signs are seen in panic attacks

A

Increased lactate and CO2

(Due to being so stressed)

78
Q

Gold standard treatment for Panic Disorder

A

CBT

79
Q

Treatment of phobias

A

Gradual Exposure

80
Q

Criteria of Obsessive Compulsion Disorder (OCD)

A
  • Must be debilitating
  • Obsessions over behaviours due to overwhelming compulsions
81
Q

Treatment for OCD

A

Clomipramine (Tricyclic Antidepressant)

82
Q

Two types of PTSD

A

Type 1: Single incident (RTA)

Type 2: Repetitive trauma (Abuse)

83
Q

Tonic immobility is seen in

A

Sexual Assault

84
Q

Physiological signs in PTSD

A
  • Decreased cortisol (probably due to increased sensitivity)
  • Atrophy of the hippocampus
  • Deactivated Broca’s area when reliving the event (so they literally can’t speak about it)
85
Q

DSM-V Criteria for PTSD

A

Need all within 1 month:

  • 1 x intrusive symptom (e.g. flashback)
  • 1 x avoidance symptom
  • 2 x increased arousal symptoms
  • alongside a negative mood change
86
Q

1st line treatment for PTSD

A

Eye Movement Desensitization and Reprocessing (EMDR)

87
Q

2nd line treatment for PTSD

A

CBT and Venlafaxine (SNRI)

Sometimes other drugs are used:

  • Primary care: Paroxetine (SSRI) and Mirtazapine (Tetracyclic)
  • Secondary care: Amitriptyline (Tricyclic) and Phenelzine (MAOI)
88
Q

Mammalian brain

A

Works down

89
Q

Reptilian brain

A

Works up

90
Q

Three eating disorders

A
  • Anorexia Nervosa
  • Bulimia Nervosa
  • Binge-eating Disorder
91
Q

Differentiation between eating disorders

A
  • Anorexia: Restricted eating and purging
  • Bulimia: Binge-eating and purging
  • Binge-eating disorder: Binge-eating and no purge
92
Q

DSM V Criteria for Anorexia

A
  • Persistent restriction
  • Intense fear of gaining weight
  • Persistent purging
  • Body dysmorphia
  • Lack of insight
93
Q

DSM V Criteria for Bulimia

A
  • Recurrent binge eating
  • Recurrent purging to compensate
  • Decreased body image confidence
  • Happens 1/7 for 3/12
94
Q

Binge eating criteria

A
  • Eat ridiculous amounts of food
  • No purging
  • Happens 1/7 for 3/12
  • Often over-weight
95
Q

Physiological effects on the body due to anorexia/bulimia

A

Decreased grey and white matter in the brain which leads to poor concentration etc

96
Q

Treatment for eating disorders

A

CBT and supportive therapy

97
Q

Re-feeding syndrome

A
  1. Body is used to decreased nutrients
  2. When you give a starved patient a good amount of food, their body will then think it’s fine, and use up all possible nutrients including its own stores
  3. Stores become depleted
98
Q

Prevention of re-feeding syndrome

A

Taper food and supportive therapy

Monitor nutrient levels etc

99
Q

3 major signs of anorexia and bulimia

A
  • Dental caries (due to acid reflux)
  • Russell’s sign (scratching of knuckles from front teeth)
  • Metabolic problems (e.g. bone fractures, hair thinning)
100
Q

Low-risk BMI for anorexia/bulimia

A

16-17.5

101
Q

Moderate-risk BMI for anorexia/bulimia

A

15-15.9

102
Q

High-risk BMI for anorexia/bulimia

A

13-14.9

103
Q

Very high-risk BMI for anorexia/bulimia

A

<13

104
Q

DSM V Criteria for Personality Disorders

A
  • Can be traced back into childhood
  • Remains stable and unfluctuating
  • Abnormal to social norms
  • Impairs individual’s functioning/ has an impact on their life
105
Q

3 clusters of personality disorders

A
  • Cluster A: Mad “Odd and Eccentric”
  • Cluster B: Bad “Emotional”
  • Cluster C Sad “Anxious and Avoidant”
106
Q

Subtypes of Cluster A: Mad

A
  • Paranoia “Alex Jones”
  • Schizoid “Willy Wonka”
107
Q

Subtypes of Cluster B: Bad

A
  • Antisocial: “A ned”
  • Borderline: “Unstable girl who breaks up with bf”
  • Histrionic: “Seductive lady”
108
Q

Subtypes of Cluster C: Sad

A
  • Avoidant: “Loner that lives with his mum”
  • Dependant: “Needy girlfriend”
  • Obsessive-compulsive/ Anakanistic: “Germaphobe”
109
Q

Difference between Obsessive-compulsive personality disorder and OCD

A
  • Obsessive-compulsive personality disorder is egosyntonic (in line with your own thinking)
  • OCD is egodystonic (makes you do things you don’t actually want to do)
110
Q

Treatment for Borderline Personality Disorder

A

CBT

111
Q

“Alex Jones” - conspiracy guy, government are spying on us

A

Paranoia Personality Disorder

112
Q

“Willy Wonka”- eccentric, no emotion, seclusive

A

Schizoid Personality Disorder

113
Q

“A ned” gets in fights, destroys stuff, doesn’t think about other people’s feelings

A

Antisocial Personality Disorder

114
Q

“Unstable girl” - breaks up with boyfriend, makes rash decisions

A

Borderline Personality Disorder

115
Q

“Seductive lady” trys to flirt with doctor

A

Histrionic Personality Disorder

116
Q

“Loner that lives with his mum”- doesn’t socialise

A

Avoidant Personality Disorder

117
Q

“Needy girlfriend”

A

Dependant Personality Disorder

118
Q

“Germaphobe” - repeatedly washes hands, and cleans worksurfaces to feel better

A

Obsessive-compulsive Personality Disorder

119
Q

Behavioural disorders in children

“Young Antisocial Personality Disorder”

  • Repeatedly gets in fights
  • Suspended from school
A
  • <12: Oppositional deficit disorder (ODD)
  • >12: Conduct disorder
120
Q

Treatment for anger in personality disorders, usually Borderline or Antisocial

A

Topiramate (anticonvulsant)

121
Q

Learning disabilities increase the risk of

A
  • Epilepsy
  • Psychiatric conditions
122
Q

Learning difficulty triad

A
  • Difficulty understanding new or complex information
  • Difficulty with learning new skills
  • Difficulty coping independently
123
Q

Normal IQ

A

70- 130

124
Q

Learning Difficulty definition

A

IQ <70

125
Q

Mild Learning Difficulty IQ

A

50-69

126
Q

Moderate Learning Difficulty IQ

A

35-49

Mental age of 6-12

127
Q

Severe Learning Difficulty IQ

A

20-34

Mental age of 3-6

128
Q

Profound Learning Difficulty IQ

A

<20

Mental age of < 3

129
Q

Assessment tool for Learning Difficulty

A

Wechsler Adult Intelligence Scale (WAIS)

130
Q

Attention Deficit Hyperactivity Disorder (ADHD) Triad

A
  • Inattention
  • Hyperactivity
  • Impulsivity
131
Q

Pathophysiology of ADHD

A
  • Decreased Dopamine in the frontal lobe, this is due to increased dopamine transporters that take away dopamine faster than usual
  • Decreased NorA = affects focus
  • Decreased Serotonin = affects mood
132
Q

When do you treat ADHD

A

Only in moderate to severe cases

133
Q

Management for everyone with ADHD

A

Supportive social care etc

134
Q

First line treatment for ADHD

A
  • Methylphenidate “Ritalin”
  • Dexamphetamine “Adderall” - requires monitoring
135
Q

Mechanism of action of Methylphenidate

A

Blocks dopamine transporters, so less dopamine is taken away

So increases dopamine

136
Q

Mechanism of action of Dexamphetamine

A

Blocks transporters of dopamine, NorA and serotonin

So increases Dopamine, NorA and Serotonin

137
Q

Second line treatment in ADHD

A

Atomoxetine (SNRI)

138
Q

Third line treatment in ADHD

A

Clonidine (Alpha receptor agonist)

139
Q

Fourth line treatment in ADHD

A

Imipramine (TCA) and Risperidone (Atypical antipsychotic)

140
Q

Autism Spectrum Disorder (ASD) Triad

A
  • Decreased Communication
  • Decreased Social Interaction = “Plays alone”
  • Decreased Imagination = “Repetitive behaviours, no imaginative play”
141
Q

Comorbidities in ASD

A
  • ADHD
  • Depression
  • Epilepsy
  • Dyslexia
  • OCD
  • Tourettes
142
Q

What is the spectrum

A

Mild end: Asperger’s Syndrome

Moderate: Pervasive developmental disorder, not otherwise specified (PDD-NOS)

More severe: Autistic Disorder

Severe: Childhood disintegrative disorder

143
Q

Asperger’s Syndrome

A

“High functioning”

Doctor Asperger created this syndrome during WWII to save his patients from going to Nazi Concentration camps

144
Q

Rett’s Syndrome

A

Associated with ASD due to similar symptoms, however, is not part of the spectrum

  • Small head and seizures
  • Only found in girls, as boys die early on
145
Q

Pathophysiology in ASD

A

Increased activity in Frontal lobe: explains “obsessions”

Increased activity in amygdala: explains “social anxiety”

Increased activity in cerebellum: explains “arm flapping”

146
Q

Treatment for ASD

A
  • Supportive social care
  • In aggressive patients: Risperidone (atypical antipsychotic)- decreases dopamine
147
Q

Medication to aid sleep in ASD

A

Melatonin (secreted by the pineal gland)

148
Q

Mechanism of GABA

A
  1. GABA increases the frequency of open GABA Cl- channels
  2. When GABA Cl- channels are open, more Cl- is allowed through which lowers the resting membrane potential (because it is negative)
  3. Lowered resting membrane potential makes it more difficult for a stimulus (neuron) to reach the transmission threshold to generate a transmission signal
149
Q

Increased GABA

A

“Relaxed effect”

Decreases neurons firing in the brain due to the lowered threshold

  • Calming effect
  • Sedative effect
  • Muscle relaxant
  • Anterograde amnesia (can’t make new memories)
150
Q

Decreased GABA

A

“Excited effect”

  • Insomnia
  • Anxiety
151
Q

Mechanism of action of BZDs

A

Increase GABA to cause a relaxed effect

152
Q

Withdrawal effect from BZDs

A

Excited effect

Due to neurons being used to decreased Cl - levels, that have lowered the resting membrane potential. When the resting membrane returns to normal there are over-firing of neurons

153
Q

ICD-10 Criteria for Addiction

A
  • Strong desire
  • Difficulty controlling addiction
  • Absence of stimulus causes a withdrawal state
  • Developed tolerance
  • Neglect of other pleasures
  • Persistence despite harm
154
Q

Pathophysiology of addiction

A
  • Dopamine D2 receptors become desensitized
  • Orbital frontal cortex: increased in situations of opportunity for stimulus and in cravings
  • Pre-frontal cortex: is overpowered
155
Q

Action of orbital frontal cortex

A

Motivator to act

156
Q

Action of Mesolimbic pathway

A

Responsible for incentive behaviour and is involved in normal pleasure

157
Q

Action of pre-frontal cortex

A

Rational self

158
Q

Effect on the brain of dopamine

A

Allows you to set new goals and focus on them

159
Q

Dopamine levels in ADHD

A

Decreased

As they have no new goals to concentrate on hence why they cannot concentrate on one thing at a time

160
Q

Dopamine levels in ASD

A

Increased

Which means they become too focused on one goal hence their obsessions

161
Q

Why is it easier to become addicted to something when you are younger

A

Frontal lobe areas are still developing and so your rational self is overpowered more easily, and you have more motivation to act etc

162
Q

Pathophysiology of tolerance

A
  1. Due to repeated dopamine release, D2 receptors become desensitised to dopamine
  2. This means that to get a stronger high you need to get more dopamine to elicit the same response
  3. Hence why you increase your dose to get the same high
  4. This is tolerance building
163
Q

CAGE questionnaire in addiction

A
  • “Have you been thinking about Cutting down addiction habit”
  • “Do you or other people get Annoyed at your addiction”
  • “Do you feel Guilty about your addiction”
  • “Do you use it as an Eye-opener in the morning, like coffee?”

1/4 = Raises suspicion

2/4 = indicative of abuse

164
Q

Pathophysiology of Alcohol Addiction

A
  • Alcohol increases the effect of GABA

Hence why you have less inhibition when drunk

  • Chronic effect of this causes a tolerance to GABA and to alcohol
  • Glutamate channels (NMDA) don’t work in Alcohol
165
Q

Delerium Tremens peaks at

A

2 days

166
Q

Seizures happen in Delirium Tremens within

A

24 hours of withdrawal

167
Q

Delirium Tremens resolves in

A

5-7 days

168
Q

Pathophysiology of Delirium tremens

A

Due to the tolerance of alcohol, the neurons in the brain are more used to a lowered resting membrane potential (as GABA works better in the presence of alcohol)

In a withdrawal state: this causes the resting membrane potential to be increased due to the absence of alcohol, so the neurons over fire the threshold “hyperexcitability” causing excitatory symptoms like:

  • Seizures
  • Tremor
  • Confusion- due to inhibited glutamate (used in memory)
169
Q

Treatment of Delirium Tremens

A
  • Chlordiazepoxide (BZD) or diazepam (BZD)- cause a relaxing effect
  • Thiamine (B1) supplements
170
Q

Liver function test raised in Alcoholism (liver injury)

A

GGT

171
Q

Haematological marker raised in alcoholics

A

Increased MCV

172
Q

Calculation for Alcohol units

A

1 unit = 10ml pure ethanol

units = (% x volume) / 10

173
Q

Ethanol is broken down into

A

Acetaldehyde

174
Q

Enzyme responsible for breakdown of ethanol to acetaldehyde

A

Alcohol dehydrogenase (ADH)

175
Q

Acetaldehyde is responsible for

A

Hangovers

176
Q

Acetaldehyde is broken down into

A

Acetate

177
Q

Enzyme responsible for the breakdown of acetaldehyde into acetate

A

aldehyde dehydrogenase (ALDH)

178
Q

Some Asian populations lack

A

ALDH

This causes them to have a build up of acetaldehyde which causes them to experience hangover symptoms instantly instead of the next morning

179
Q

Drugs used to prevent Alcohol addiction relapse

A
  • 1st line: Naltrexone
  • Disulfiram
  • Acamprosate
    *
180
Q

Effect of Naltrexone

A

Reduces reward from alcohol

181
Q

Effect of Disulfiram

A

Inhibits ALDH causing hangover symptoms immediately

182
Q

Effect of Acamprosate

A

Reduces alcohol cravings

183
Q

Antidote to Opiate overdose

A

Naloxone

184
Q

Predetermined person to make decisions on your behalf if you are not deemed to have capacity

A

Power of Attorney

185
Q

Court assigns a guardian to make decisions on a patient once they are incapacitated

A

Guardianship

186
Q

Doctors making the best decisions on behalf of the patient until a guardian is decided

A

Adults with Incapacity Act

187
Q

Authorises treatment of someone without capacity

A

Mental Health Act 2003 (Section 47)

Finals Club (Dundee Medicine Master Summary Deck) (8 decks)

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