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Phase 3a Tera Pyo Edition > Psychiatry > Flashcards

Psychiatry Flashcards

1
Q

What is ADHD

A

Multifactorial (genetic, environmental, neurological factors) contributing to a triad of hyperactivity, inattention, impulsivity.

Presents in childhood and MAY continue to adulthood, but does not present as adult without childhood.

DSM-V criteria used. Symptoms must be persistent. 6 features <16, 5 features >16.

Twice as common as autism and affects boys more.

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2
Q

Diagnostic features of ADHD

A

Inattention
- Cant follow through instruction
- Reluctant to engage in mentally taxing tasks
- Difficult to sustain tasks
- Unorganised, forgetful in ADL
- Loses things

Hyperactivity/impulsivity
- Unable to sit still, or quietly
- Excessive talking
- Spontaneously leaves seat
- On the go
- Interrupts/intrusive
- Run and climb and answer questions before finishing question

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3
Q

Management of ADHD

A

Methylphenidate - first line in children (>5 only). 6 week trial, after considering non-pharm options.

  • Lisdexamfetamine, followed by dexamfetamine.

Monitor child’s height, weight, blood pressure, ECG.

Side effects: Tachycardia, hypertension, abdo pain, nausea, dyspepsia. Reduced appetite can cause stunted growth

All drugs cardiotoxic.

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4
Q

Non pharm ADHD management

A

Healthy diet
Exercise
Parental and child education
School adjustments and interventions

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5
Q

Define Psychosis, Delusions and Hallucinations

A

Psychosis - Loss of contact with reality. Affects a person’s ability to distinguish what’s real and what’s not.

Delusions - Fixed false belief, held despite clear evidence to the contrary. Typically illogical, and not shared by those within person’s social or cultural group.

Hallucinations - Sensory perceptions that appear real but are not. Occur in absence of external stimuli

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6
Q

Types of delusion

A
  • Persecutory delusions: Belief that one is being plotted against or harmed
  • Grandiose delusions: Belief in having exceptional abilities, wealth, fame
  • Delusions of reference: Belief that insignificant events or remarks are directed at the person
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7
Q

Types of hallucination

A
  • Auditory (most common in psychosis)
  • Visual hallucinations
  • Tactile, olfactory, gustatory (less common)
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8
Q

Psychotic features

A

Hallucinations
Delusions
Thought disorganisation
- Alogia (little information conveyed)
- Tangentiality
- Clanging (rhyming or similar sounds)
- Word salad (Linking real wrods incoherently)

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9
Q

Associated features with psychosis

A

Agitation/aggression
Neurocognitive impairment (memory, attention, executive function)
Depression
Self harm thoughts

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10
Q

Give some conditions that may present with psychosis

A
  • Schizophrenia (Most common)
  • Depression
  • BPD
  • Puerperal psychosis
  • Illicit drug use
  • Neurological conditions (parkinson, huntington)
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11
Q

When does first episode psychosis normally occur

A

15-30 years

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12
Q

What is schizophrenia and whats its main risk factor

A

Severe long term mental health disorder characterised by psychosis. Presents most between 15-30. Earlier in men than women. Must have symptoms for >6 months to diagnose.

Family history
- 50% if twin
- 10-15% if parent
- 10% if sibling

Black caribbean have relative risk of 5.4

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13
Q

What are 2 other types of schizophrenia

A

Schizoaffective disorder combines symptoms of schizophrenia with bipolar. Psychosis + mania + depression

Schizofphreniform disorder - Lasts less than 6 months

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14
Q

How does psychosis present

A

Psychosis normally preceded by prodrome phase. May have subtle memory loss, concentration, mood swings etc.

Key features of psychosis (positive symptoms)
- Delusions
- Hallucinations
- Thought disorder (Disorganised thoughts, causing abnormal speech and behaviour)

Lack of insight

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15
Q

How does schizophrenia present (positive symptoms)

A

Key positive symptoms
- Auditory hallucinations
- Somatic passivity (believing an external entity is controlling them)
- Thought broadcasting (believing others are overhearing their thoughts)
- Persecutory delusions (fasle belief people will harm them)
- Delusional perception (ordinary/unremarkable perception triggers delusion)

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16
Q

What are some negative symptoms of schizophrenia

A

4As
- Affective flattening (minimal emotional reactions to events)
- Alogia (Poverty of speech)
- Anhedonia (lack of interest in activities)
- Avolition (lack of motivation to complete goals)

Reduced functioning (social, productivity, selfcare) also important

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17
Q

What are patterns of schizophrenia

A

Continuous
Episodic (relapsing/remitting)
Single episode

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18
Q

Management of schizophrenia

A

Oral atypical antipsychotics first line
- Aripiprazole
- Olanzapine
- Risperidone
- Quetiapine

Offer CBT and WATCH for CVD risk factors, high rates of CVD in schizophrenia patients

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19
Q

Side effects of antipsychotics

A

Weight gain
Diabetes
Prolonged QT
Raised prolactin
Extrapyramidal
- Akathisia (psychomotor restlessness)
- Dystonia (abnormal muscle tone and postures)
- Pseudo-parkinsonism
- Tardive dyskinesia (abnormal movements)

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20
Q

Features associated with poor prognosis in schizophrenia

A
  • Family history
  • Gradual onset
  • Low IQ
  • Prodromal phase of social withdrawal
  • Lack of obvious precipitant
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21
Q

What are typical antipsychotics

A

Dopamine D2 receptor antagonists, block dopaminergic transmission in mesolimbic pathways
- Haloperidol
- Chlorpromazine

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22
Q

Side effects of typical antipsychotics

A

Hyperprolactinaemia and Extrapyramidal symptoms

  • Akathisia (psychomotor restlessness)
  • Dystonia (abnormal muscle tone and postures)
  • Pseudo-parkinsonism
  • Tardive dyskinesia (abnormal, involuntary movements “chewing and pouting of jaw”, excessive blinking)
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23
Q

What are atypical antipsychotics

A

Atypical (Second gen) created due to extrapyramidal and prolactin side effects.

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

E.g.
- Clozapine (most effective - only indicated after all else tried)
- Risperidone
- Olanzapine

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24
Q

Which antipsychotic is most likely to result in a long QT

A

Haloperidol

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25
Q

What are some other side effects of antipsychotics

A

Antimuscarinic - Dry mouth, blurred vision, urinary retention, constipation
- Sedation and weight gain
- Impaired glucose tolerance
- Reduced seizure threshold
- Neuroleptic malignant syndrome

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26
Q

What are some atypical antipsychotics and some side effects

A
  • Clozapine
  • Olanzapine (obesity and dyslipidaemia)
  • Risperidone
  • Aripiprazole (good side effect profile)

Weight gain
hyperprolactinaemia
Clozapine associated with agranulocytosis
Metabolic Syndrome!

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27
Q

What monitoring is required with antipsychotics

A
  • FBC, U&E, LFT at start of therapy and annually
  • Lipids and weight at start and 3 months
  • Fasting blood glucose and prolactin: at start of therapy, 6 months and annually
  • Baseline and frequently while titrating dose
  • ECG baseline
  • CVD risk assessment annually
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28
Q

ALCOHOL WITHDRAWAL SYMPTOMS and the hours at which they present

A

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

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29
Q

Explain difference between circumstantiality, tangentiality and derailment

A

A circle comes back around eventually (Circumstantiality)

A Tangent goes off forever in another direction (Tangentiality)

A derailed train goes off the track after a little while and needs to be nudged back on (Derailment)

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30
Q

How is acute dystonia due to haloperidol treated

A

Procyclidine (prepare dose just in case)

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31
Q

What is bipolar

A

Chronic periods of depression + episodes of mania (type 1) or hypomania (type 2)

Typically develops in late teen/early 20s

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32
Q

What is the difference between hypomania and mania, and what are some features of mania

A

Both relate to abnormally elevated mood or irritability

  • Hypo: Decreased/increased function >4 days, but less than 7
  • Mania: Significant functional impairment or psychotic symptoms for at least 7 days

Features of mania:
- Abnormally elevated mood
- Significant irritability
- Increased energy
- Decreased sleep (sometimes going days without sleeping)
- Grandiosity, ambitious plans, excessive spending and risk-taking behaviours
- Disinhibition and sexually inappropriate behaviour
- Flight of ideas (rapidly generating and jumping between ideas)
- Pressured speech (rapid and unrelenting speech)
- Psychosis (delusions and hallucinations - more suggestive of mania)

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33
Q

How is bipolar diagnosed

A

By a specialist using DSM-5 criteria

Other differentials:

Cyclothymia involves milder symptoms of hypomania and low mood.

Unipolar depression is when the person has only 1 episode of depression +- mania

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34
Q

How is bipolar managed long term

A

Lithium
- Serum lithium levels have to be taken 12 hours after most recent dose, initial target range 0.6-0.8mmol/L. Lithium toxicity if gets too high!

Alternatives: Sodium valproate, olanzapine. Dont forget that valproates proper fuckin teratogenic

Depression - Talking therapies and SSRI (Fluoxetine antidepressant of choice)

Address comorbities (2-3x risk of Diabetes, CVD, COPD)

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35
Q

How should Bipolar primary care referrals be carried out

A

Hypomania - Routine referral to community mental health(CMHT)

Mania or severe depression - Urgent referral

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36
Q

Acute episode management in bipolar

A

Manic episode
- Antipsychotic (e.g. haloperidol)
- Lithium/sodium valproate
- Taper and stop existing antidepressants

Depressive episode
- Olanzapine + Fluoxetine
- Antipsychotic (olanzapine)
- Lamotrigine

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37
Q

What are some adverse effects of lithium

A
  • Nausea/vomiting, diarrhoea
  • Benign leucocytosis
  • Fine tremor
  • Nephrotoxicity (polyuria, secondary nephrogenic diabetes insipidus)
  • Thyroid enlargement (Goitre) causing hypothyroidism
  • ECG: T wave flattening/inversion
  • Weight gain
  • Idiopathic intracranial hypertension
  • Hyperparathyroidism and hypercalcaemia!
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38
Q

How should patients on lithium be monitored

A
  • Sample taken 12 hours post dose
  • Lithium levels weekly and after each dose change until stable
  • Once on stable dose, check every 3 months
  • If dose change, check after 1 week, and weekly again until levels stable
  • Thyroid and renal function every 6 months
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39
Q

What is lithium toxicity, and how is it normally precipitated

A

Lithium has narrow therapeutic range (0.4-1 mmol/L) and long plasma half-life, primarily excreted by kidneys. Toxicity normally occurs >1.5mmol/L

  • Dehydration
  • Renal failure
  • Diuretics(thiazides), ACEi/ARB, NSAID, metronidazole
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40
Q

How does lithium toxicity present

A
  • Coarse tremor (whatever the fuck that is)
  • Hyperreflexia
  • Confusion
  • Polyuria
  • Seizure
  • Coma
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41
Q

How is lithium toxicity managed

A

Mild-Moderate: Fluid resuscitation with saline

Haemodialysis if severe

Sodium bicarbonate sometimes used, alkalinity of urine promotes lithium excretion

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42
Q

Give me the definitions of these thought disorders:
- Circumstantiality
- Tangentiality
- Neologisms
- Clang associations
- Word salad
- Knights move thinking
- Flight of ideas
- Perserveration
- Echolalia

A
  • Circumstantiality: Inability to answer without excessive, unnecessary detail. Go on massive tangent BUT do return to original point.
  • Tangentiality: Wander from topic without ever returning to point.
  • Neologisms: New word formations, maybe combining 2 words
  • Clang associations: Ideas related to each other only because they sound the same or rhyme
  • Word salad: Completely incoherent speech made up of real words that make no sense together
  • Knights move thinking: Severe loosening of associations. Unexpected and illogical leaps from one idea to another.
  • Flight of ideas: Feature of mania, leaps from one idea to another, but with discernable links between the 2. Super fast.
  • Perseveration: repetition of ideas or words, despite attempting to change subject
  • Echolalia: repeating someone else’s speech, including asked question
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43
Q

Symptoms common to both hypomania and mania

A

The following symptoms are common to both hypomania and mania

Mood
predominately elevated
irritable

Speech and thought
pressured
flight of ideas: characterised by rapid speech with frequent changes in topic based on associations, distractions or word play
poor attention

Behaviour
insomnia
loss of inhibitions: sexual promiscuity, overspending, risk-taking
increased appetite

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44
Q

Hypomania vs mania

A

Mania >7 days, psychotic symptoms, severe impairment in social or work setting, may need admission

Hypomania <7 days, 3-4 days usually, high functioning - no significant impairment, unlikely to require hospital, no psychosis

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45
Q

What is Generalised anxiety disorder, and what are some non GAD causes of anxiety

A

Excessive worry about a number of events associated with heightened tension, that significantly impact patients life. Symptoms persist most days for at least 6 months, with no other cause.

  • Hyperthyroidism
  • Cardiac disease
  • Medication (salbutamol, theophylline, corticosteroids, antidepressants, caffeine)
  • Phaeochromocytoma
  • Alcohol, benzodiazepine withdrawal
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46
Q

How does GAD present

A

Emotionally:
- Excessive, uncontrollable worrying
- Restlessness
- Difficulty relaxing and concentrating
- Easily/Hard to be tired

Physical (sympathetic nervous system overactivity):
- Muscle tension
- Palpitations
- GI symptoms
- Headaches
- Sleep disturbance
- Sweating/tremor

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47
Q

How is anxiety diagnosed

A

Clinical diagnosis (GAD-7 can help)
- 5-9 mild
- 10-14 moderate
- 15-21 severe

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48
Q

What are panic attacks and how do they present

A

Sudden onset physical/emotion symptoms of anxiety that come on quickly for a short while then gradually fade. Can be isolated events or panic disorder (diagnosed symptoms present for a month)

Physical:
- Tension
- Palpitations
- Tremor
- Sweating
- Dry mouth
- Chest pain/SOB
- Dizziness/Nausea

Emotional:
- Panic
- Fear/danger
- Depersonalisation (detached)
- Loss of control

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49
Q

What are risk factors for panic disorder

A

Living alone
Early parental loss
History of abuse
Poor educational history
Urban living
Family history

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50
Q

How is anxiety managed

A

Step-wise
1 - Education + monitoring
2 - Self referral to low intensity psych intervention
3 - High intensity intervention (CBT, applied relaxation) or drugs
- Sertraline (SSRI) first line
- Then, alternative SSRI or SNRI (duloxetine/venlafexine)
- Pregabalin if cant manage SSRI/SNRI

  • If under 30, advise increased risk of suicide/self harm ideation!
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51
Q

How is panic disorder managed

A

Stepwise again, common sense pathway really.

Then:
- CBT
- Drugs (SSRI first line, imipramine or clomipramine if not!)

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52
Q

What do benzodiazepines do and what are their side effects

A

Enhance inhibitory GABA by increasing frequency of chloride channels. Range of effects:
- Sedation, hypnosis, anxiolytic, anticonvulsant, muscle relaxant

Side effects:
- Tolerance/dependance - only prescribe for short time (2-4 weeks)
- Withdrawals, up to 3 weeks after stopping, if they come off abruptly.
- Withdrawal symptoms: insomnia, irritability, anxiety, tremors, tinnitus, perceptual disturbance, seizures

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53
Q

How are beta blockers used in anxiety

A

non selective beta blocker reduces sympathetic nervous system effects, treating physical symptoms. (Tremors, palpitations, sweating etc). Contraindication is asthma (bronchoconstriction/bronchospasms)

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54
Q

What is OCD

A

Obsessions - unwanted intrusive thought, image, urge, repeatedly entering persons mind

Compulsions - repetitive behaviours or mental acts that person feels driven to perform. Can be overt (checking a door is closed) or covert (mentally repeating a phrase)

Usually a combination of both

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55
Q

Risk factors for OCD

A
  • Family history
  • Age 10-20 at onset
  • Pregnancy/postnatal
  • History of abuse, bullying, neglect
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56
Q

What is the OCD cycle

A

Obsessions
Anxiety
Compulsion
Temporary relief

Becomes more ingrained each cycle

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57
Q

How is OCD diagnosed

A

DSM-5 and/or ICD 11 scoring

Yale-Brown Obsessive Compulsive Scale (Y-BOCS) is used to assess severity of symptoms

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58
Q

Management of OCD

A

Mild:
- Low intensity psych treatments (CBT including exposure and response prevention (ERP))

Moderate or mild ineffective:
- SSRI (Any fine but fluoxetine specifically for body dysmorphic disorder) or more intense CBT with ERP
- Clomipramine (TCA) if SSRI not wanted

Severe
- Secondary care referral with SSRI and CBT with ERP in meantime.

*ERP = Exposing patient to anxiety provoking situation without allowing compulsion.

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59
Q

2 considerations when prescribing SSRIs in OCD

A
  • Requires longer than depression (at least 12 weeks) for initial response
  • If effective, continue for at least 12 months to prevent relapse
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60
Q

What is PTSD

A

Mental health condition resulting from traumatic experiences. Affects any age, and increases risk of depression, anxiety, substance misuse, and suicide. Symptoms last longer than 1 month (DSM-5)

Can arise from witnessing or experiencing:
- Violence (domestic, sexual, abuse or physical attacks)
- Major car accidents
- Major health events
- War
- Natural disasters

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61
Q

How does PTSD present

A

Re-experiencing: flashbacks, nightmares, repetitive and disturbing intrusive thoughts/images.

Avoidance: avoiding people, situations, circumstances associated with the event

Hyperarousal: Hypervigilance for threat, exaggerated startle response, sleep problems, irritability, difficulty concentrating

Emotional numbing - lack of feeling, feeling detached, derealisation (world isnt real)

Also:
- Substance misuse
- Anger
- Depression
- Unexplained physical symptoms
- Negative beliefs and emotions

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62
Q

How is PTSD Diagnosed

A

Trauma Screening Questionnaire

Diagnosis based off:
- ICD-11 or
- DSM-5

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63
Q

Management of PTSD

A

Following a traumatic event, single session intervention probably not great.

Watchful waiting if mild/less than 4 weeks

Trauma focused CBT or eye movement desensitisation and reprocessing (EMDR)

Drug treatment SSRI or venlafaxine, but definitely not first line.

Army offers services to military personnel

64
Q

What is acute stress disorder

A

Acute stress reaction in first 4 weeks following a traumatic event. (PTSD is >4 weeks)

  • Intrusive thoughts (flashback, nightmare)
  • Dissociation
  • Negative mood
  • Avoidance
  • Arousal

Managed with CBT and Benzodiazepines sometimes used (addictive!!)

65
Q

What is mirtazapine, its MoA, use case and side effects

A

An antidepressant that works to block alpha2-adrenergic receptors, increasing release of neurotransmitters.

Fewer side effects and interactions, so good in old people, who may be on lots of meds

Two main side effects: Sedation and increased appetite, good for old people who are skinny and cant sleep.

Take in evening to sleep

66
Q

What are the 4 criteria of capacity

A

Understanding: Patient must understand the information relevant to the decision

Retention: Retain the info long enough to make the decision

Weighing: Weight up the information, consider both risks and benefits

Communicating: Communicate their decision back, verbally or non verbally.

Explain the decision, assess their understanding, check their retention sometime later, and assess their ability to weigh it up. If they can communicate all this clearly, respect their decision

67
Q

What are the main points of a mental state examination

A
  1. appearance/behaviour
  2. Speech
  3. Mood/affect
  4. Thought
  5. Perception
  6. Cognition
  7. Insight
  8. Judgement
68
Q

How can overdose to various drugs be treated acutely

A

Activated charcoal - within an hour of various substances to reduce absorption

69
Q

What can you give for overdose of these drugs:
- Paracetamol
- Opiods
- Benzodiazepines
- Beta blockers
- CCB
- Cocaine
- Cyanide
- Methanol/ethylene (solvents or fuels/antifreeze)
- Carbon monoxide

A
  • Paracetamol: N-Acetylcysteine
  • Opiods: Naloxone
  • Benzodiazepines: Flumazenil
  • Beta blockers: Glucagon (heart failure/cardiogenic shock) or atropine for bradycardia
  • CCB: Calcium chloride or gluconate
  • Cocaine: Diazepam
  • Cyanide: Dicobalt edetate
  • Methanol/ethylene (solvents or fuels/antifreeze): Fomepizole or Ethanol (alcohol)
  • Carbon monoxide: 100% Oxygen
70
Q

What is a personality disorder

A

Maladaptive personality traits that cause significant psychosocial distress and interfere with functioning.

Patterns of thought behaviour and emotion that inhibit normal relationships, QOL and physical health.

Genetic and environmental causes, including history of childhood trauma and difficult circumstances

71
Q

What are the 3 clusters of personality disorder

A

DSM-5

A - Suspicious
B - Emotional/impulsive
C - Anxious

72
Q

Give the types of Suspicious (or Odd/Eccentric) Personality Disorder

A

DSM-5

Paranoid - Difficulty trusting or revealing personal info. Hypersensitive and unforgiving.

Schizoid - Lack of interest or desire to form relationships, with the belief that this is of no benefit to them. Prefer solitary activities.

Schizotypal - Unusual beliefs, thoughts and behaviours and social anxiety that makes forming relationships hard. Odd speech, eccentric behaviour, magical thinking.

73
Q

Give the types of Emotional/Impulsive personality disorders

A

Antisocial - Reckless, harmful behaviour. Lack of concern for the consequences or impact of their behaviour. Aggression. Criminal. Men>women

Borderline - Fluctuating strong emotions and difficulty with identity and maintaining relationships. Recurrent suicidal behaviours. Chronic emptiness etc

Histrionic - Needs to be centre of attention and performing for others to maintain this. Sexual seductiveness, rapidly shifting, shallow emotions, self dramatisation.

Narcissistic - Feelings that they are special and need this to be recognised, or they get upset. Put self first. Entitled, lack empathy, chronic envy. Arrogant

74
Q

Give types of anxious personality disorders

A

Avoidant - Severe anxiety about rejection or disapproval, causing avoidance of social situations or relationships. Constantly think theyre being criticised or rejected.

Dependent - Heavy reliance on others to make decisions, very passive, cant take responsibility for own life. Need constant support and reassurance

Obsessive-Compulsive - Unrealistic expectations of how things should be done, catastrophising about what will happen if needs not met. Stingy spending, meticulous, rigid morals, ethics. Hoarding.

75
Q

According to ICD-11 how should we instead think of personality disorders

A

With trait domains

Negative affectivity
- Wide range of negative emotions, prone to mood swings, insecurity, emotional lability

Detachment
- Avoidance of interactions, relationships, emotional withdrawal. Limited pleasure

Dissociality
- Disregard for rights/feelings of others. Lack empathy, impulsive and manipulative

Disinhibition
- Impulsive, risk taking, difficulty controlling self. Struggle with planning and foresight; reckless and irresponsible

Anankastia
- Orderliness, control, perfectionism. Rigid and stubborn

Borderline pattern
- Additional qualifier for those with emotional instability, intense and unstable interpersonal relationships, fluctuating sense of identity, impulsivity.

76
Q

How is severity classified in personality disorder

A

Mild
- Some impairment, limited. Symptoms noticable, but do not cause pervasive distress. Still maintains relationships.

Moderate
- More significant impairments in multiple areas of life. Struggle with maintaining relationships, but can manage day to day

Severe
- Impairments to all aspects of life. Pervasive difficulties in interpersonal relationships, significant effect on QOL, dysfunction and distress.
- Intense and long term therapeutic intervention may be required

77
Q

Management of Personality disorders

A

CBT
Risk management (self harm, suicide, harm to others - MDT approach)
Medication not recommended long term, but may help in crisis.

Treat coexisting mental health issues

78
Q

Give me the ages and genders most likely to self harm and commit suicide

A

Self harm
- 15-24 and females (but males use more lethal methods)

Suicide
- Middle aged men highest (40-49)
- Men 3-4x more likely to die by suicide, but women attempt more, just less lethal methods usually.

79
Q

Repeating steps in the cycle of self harm

A

1 Emotional suffering
2 Emotional overload
3 Panic
4 Self harm
5 Temporary relief
6 Shame and guilt

80
Q

What are some factors protective from suicide

A
  • Social support/community
  • Sense of responsibility to others
  • Resilience, coping, problem solving skills
  • Access to mental health support
81
Q

What is the Mental Capacity Act and what are its 5 key principles

A

MCA 2005 applies to adults over 16 and sets out who can make decisions if they become incapacitated

  1. A person must be assumed to have capacity unless it is established that he lacks capacity
  2. A person is not to be treated as unable to make a decision unless all practicable steps to help him to do so have been taken without success
  3. A person is not to be treated as unable to make a decision merely because he makes an unwise decision
  4. An act done, or decision made, under this Act for or on behalf of a person who lacks capacity must be done, or made, in his best interests
  5. Before the act is done, or the decision is made, regard must be had to whether the purpose for which it is needed can be as effectively achieved in a way that is less restrictive of the person’s rights and freedom of action
82
Q

What should be considered when assessing whats in someones best interests

A
  1. Whether the person is likely to regain capacity and can the decision wait
  2. How to encourage and optimise the participation of the person in the decision
  3. The past and present wishes, feelings, beliefs, values of the person and any other relevant factors
  4. Views of other relevant people
83
Q

How does an advance decision on refusing life saving treatment need to be made

A

Written, signed, witnessed.

Other advance decisions to deny treatments can be made verbally.

84
Q

What decisions can someone with lasting power of attorney make

A
  • Property/financial affairs
  • Health and welfare decisions
  • Life-sustaining decision authority must be pre specified.
  • LPA must be registered with the Office of the Public Guardian
85
Q

Whats the Mental Health Act 1983

A

Provides legal framework for keeping patients in hospital against their will (detaining/sectioning)

If patient agrees, its called an voluntary or informal admission, doesnt involve mental health act

86
Q

What is a mental health act assessment and who can initiate it

A

Detailed evaluation into whether or not to detain someone under MHA.

Approved Mental Health Professional (AMHP) is primary person making application and organising admission. Nearest relative can do this too.

Decision needs to be recognised by 2 doctors;
- A section 12 doc (Qualified doctor who can undertake MHA assessments (usually Psych))
- Another doctor

Can result in compulsory admission under Section 2 or 3

87
Q

What are section 2 and 3 of the MHA

A

2: Compulsory admission for assessment, maximum period of 28 days. Non renewable, must discharge or go onto:

Section 3: Compulsory admission for treatment. Max period 6 months, the Responsible Clinician can renew.

88
Q

What are Section 4, Section 5(2), Section 5(4) and section 136 of the MHA

A

4 - detain patients for up to 72 hrs in urgent scenarios. Requires AMHP and a doctor.

5(2) - Used in emergency to detain patient voluntarily in hospital. Up to 72 hours, requires 1 doctor.

5(4) - Same as 5(2) but lasts 6 hours and only needs a nurse

135 - can break into a house to remove someone to Place of Safety
136 - used by police to remove someone that has a mental health disorder from public place to safe place for assessment. Lasts up to 24 hours.

ALL are followed by a Mental Health Act Assessment

89
Q

How do you calculate units of alcohol

A

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

90
Q

What is the MoA of alcohol on the brain

A

Stimulates GABA (inhibitory) receptors, having a relaxing effect on the brain. Also inhibits NMDA receptors (usually binded by glutamate - excitatory neurotransmitter), causing further relaxing effect.

Chronic alcohol results in GABA system becoming down regulated and glutamate system becoming upregulated. Patient must continue drinking or suffer severe withdrawal symptoms

91
Q

What is the recommended level of alcohol consumption in the UK, what counts as binge drinking

A

<14 units/week
<5 units/day

> 6 units for women, or >8 units for men, in a single session classify as binge drinking.

92
Q

Complications of alcohol excess

A

Alcoholic liver disease, cirrhosis, HCC, varices

Alcohol dependence/withdrawal

Wernicke-Korsakoff

Pancreatitis

Alcoholic Myopathy/cardiomyopathy

Pregnancy:
SGA
Miscarriage
Preterm delivery
Fetal alcohol syndrome

93
Q

What 2 questionnaires can be used to identify harmful alcohol use?

A

AUDIT - WHO. 10 MCQs, >8=harmful use.

CAGE
Cut down - Do you ever think you should?
Annoyed - Do you get annoyed at others commenting on your drinking?
Guilty - Do you ever feel guilty about drinking?
Eye opener - Do you ever drink in the morning to help hangover or nerves?

94
Q

Findings on examinations and blood results of alcoholism

A

Examination
- Smelling of it
- Slurred speech
- Bloodshot eyes
- Dilated capillaries on face (telangactasia)
- Tremor

Bloods
- Raised MCV
- Raised AST and ALT (AST:ALT >1.5 in particular)
- Raised GGT

95
Q

How do alcohol withdrawal symptoms present

A

6-12 hours: Tremor, sweating, headache, cravings, anxiety
12-24 hours: Hallucinations
~36 hours: Seizures
48-72 hours: Delirium tremens

96
Q

What is delirium tremens (Pathophys)

A

Medical emergency with high untreated mortality, associated with alcohol withdrawal.

Long term alcohol down regulates GABA and upregulates Glutamate systems. When removed, GABA underfunctions and glutamate overfunctions, causing extreme excitability and excessive adrenergic activity.

97
Q

How does delirium tremens present

A
  • Acute confusion
  • Coarse tremor
  • Delusions
  • Tachycardia, Hypertension, Hyperthermia
  • Ataxia
98
Q

How is alcohol withdrawal managed

A

CIWA-Ar tool to score symptoms and guide treatment

Benzodiazepine - Chlordiazepoxide or Diazepam as a reducing dose protocol, over ~7 days.*

High dose vitamin B followed by long term Thiamine (B1) to prevent Wernicke Korsakoff

*In liver disease use Lorazepam, as chlordiazepoxide is excreted through CYP450 pathway, which is impaired in cirrhosis, increasing risk of accumulation and toxicity.

Naltrexone or disulfiram or acamprosate for long term prevention of relapse

99
Q

What is Wernicke’s encephalopathy

A

Thiamine (vitamin B1) deficiency, commonly seen in alcohol excess.

Thiamine deficiency causes Wernicke’s and eventually leads to Korsakoff syndrome.

Petechial haemorrhages occur in variety of brain structures including mamillary bodies and ventricle walls.

100
Q

Features of Wernicke’s encephalopathy

A

Oculomotor dysfunction
- Nystagmus (most common)
- Ophthalmoplegia

Gait ataxia
Confusion
Disorientation
Peripheral sensory neuropathy

Triad is:
- Ophthalmoplegia and nystagmus
- Ataxia
- Encephalopathy

101
Q

Investigations and management of Wernicke’s

A
  • Decreased red cecll transketolase
  • MRI

Managed with thiamine replacement

102
Q

What can Wernicke’s lead to if untreated

A

Korsakoff syndrome, caused by continued haemorrhage and damage to mamillary bodies in hypothalamus.

Features of wernickes with added retro and anterograde amnesia, and confabulation (false memory making). Can be irreversible.

103
Q

Define tolerance and dependence

A

T - Need for increasing drug dosage to achieve same effect over time

D - Physical and psychological need to use a drug regularly to avoid withdrawals

104
Q

What is the main neurotransmitter associated with psychological addiction?

A

Dopamine, released by brain’s mesolimbic reward system

105
Q

Withdrawal symptoms from benzodiazepines

A

Anxiety
Tremor
Insomnia
Seizure

106
Q

What is Charles Bonnet syndrome

A

Persistent or recurrent complex hallucinations in clear consciousness. Must occur in absence of any other neuropsychiatric disturbance.

Associated with age related macular degeneration, glaucoma and cataracts

107
Q

What is Somatisation disorder

A

When multiple physical symptoms have existed for at least 2 years, with no organic cause and patient refuses to accept reassurance or negative results

108
Q

What is functional neurological disorder

A

AKA Conversion disorder

Sensory and motor symptoms unexplained by neurological disorders
- Gait disturbance
- Weakness
- Seizures
- Sensory loss
- Visual disturbance

Symptoms not under patients control, they are not faking nor seeking material gain

109
Q

What is hypochondriasis

A

Persistent belief in the presence of a serious underlying disease, with no accepting reassurance or negative results

110
Q

What is Factitious disorder

A

AKA Munchausen’s. Intentional production of physical or psychological symptoms

111
Q

What is malingering

A

Fraudulent simulation or exaggeration of symptoms for financial or other gain

112
Q

What is delusional parasitosis

A

Delusional belief of parasitic infection (bugs, worms, parasites, mites, bacteria, fungi)

113
Q

What is Cotard delusion

A

Delusion that they are dead or dying. Most often caused by psychiatric conditions (schizophrenia, depression) but can be due to neurological conditions, such as tumours or migraines.

114
Q

What is Capgras syndrome

A

False belief that a duplicate has replaced someone close to them, possibly causing suspicion or aggression towards them

AKA Delusional misidentification syndrome

115
Q

Whats De Clerambaults

A

AKA Erotomania

Delusion that high status or famous person is in love with them. Can lead to harassment or stalking. Usually has little/no contact with person

116
Q

Whats Todd Disorder

A

AKA Alice in Wonderland syndrome

Incorrectly perceiving size of body parts (too big/small). Also associated with changes to perception of time and symptoms of migraine (e.g. aura and headache).

Caused by migraine epilepsy brain tumours

117
Q

What is Koro syndrome

A

Belief that sex organs are retracting or shrinking and will disappear, killing the patient. Causes anxiety and panic attacks.

Mostly seen in asia, especially china and india

118
Q

What is body integrity dysphoria

A

Apotemnophilia involves a strong feeling that a body part doesn’t belong to them, causing them distress, and wanting to remove it. May have desire to be disabled.

No associations

119
Q

What is Binge eating disorder

A

Episodes where patient overeats often as an expression of distress. Typically feels a loss of control, not restrictive like anorexia or bullimia, patients likely to be overweight

  • Planned binge involving binge foods, eating quickly, unrelated to hunger, becoming uncomfortably full and eating in dazed state
120
Q

How do bloods present in Binge Eating Disorder

A
  • Anaemia
  • Leucopenia
  • Thrombocytopenia
  • Hypokalaemia

(low Hb, WCC, platelets, potassium)

Reduced bone marrow activity causes normocytic normochromic anaemia, leukopenia and thrombocytopenia

121
Q

What is refeeding syndrome

A

Occurs when someone with an extended severe nutritional deficit resumes eating. The lower the BMI, and the longer the period of malnutrition, the higher the risk.

122
Q

Pathophys of refeeding syndrome

A

During starvation, intracellular potassium, phosphate, magnesium depleted. These electrolytes move from inside cells to blood to maintain serum levels

Cell metabolism reduces to conserve energy, causing a loss of intracellular electrolytes.

During refeeding, potassium, phosphate and sodium shift into blood. Carbs cause increase in insulin which drives glucose, potassium, phosphate into cells.

Na+/K+ pump pumps K+ into cells and Na+ out. Insulin causes sodium reabsorption from kidneys.

123
Q

Overall metabolic effects of refeeding syndrome on bloods

A
  • Hypomagnesaemia
  • Hypokalaemia
  • Hypophosphataemia
  • Fluid overload
124
Q

Clinical features of refeeding syndrome

A

Hypophosphataemia
- Main cause of symptoms
- Muscle weakness (including cardiac and diaphragm) -> heart and respiratory failure

Hypomagnesaemia may cause torsades de pointes

125
Q

Clinical consequences of hypophosphataemia (as in refeeding)

A
  • Cardiac dysfunction
  • Respiratory failure
  • Confusion, seizures, coma
  • Tissue hypoxia and haemolysis
  • Rhabdomyolysis
126
Q

How is refeeding syndrome prevented

A

If patient hasnt eaten, or high risk, for more than 5 days, aim to refeed at no more than 50% of requirements for first 2 days.

High risk if
- BMI <16
- Unintentional weight loss >15% over 3-6 months
- Little nutritional intake 10+ days
- Derranged electrolytes prior to feeding

If 2 or more of:
- BMI <18.5
- Weight loss >10%
- Little intake >5days
- History of alcohol abuse, drugs, chemotherapy, diuretics, antacids, insulin

127
Q

What is metabolic syndrome

A
  • Hypercholesterolaemia
  • Hypertension
  • Impaired glucose tolerance
  • Central obesity

Caused more often by atypical antipsychotics (aripiprazole less so, has less side effects)

128
Q

When can u use ECT

A

Severe, medication resistant or psychotic depression. Course of treatments.

Involves triggering a short generalised seizure under anaesthaesia.

Side effects: Headache, muscle ache, short term memory loss

129
Q

How do SSRIs, SNRIs and TCAs work

A

SSRI - Block reuptake of serotonin by presynaptic membrane on axon terminal. Hence, more serotonin in synapses throughout CNS, boosting communication between neurones

SNRI - Blocks reuptake of serotonin and noradrenaline by presynaptic membrane

TCA - Block serotonin reuptake and noradrenaline by presynaptic membrane. Also block ACh and histamine receptors, giving them anticholinergic and sedative effects

130
Q

What are anticholinergic side effects

A

Anticholinergics block Ach, which is involved in bodily secretions, having a drying effect around the body.

Results in:
- Dry mouth
- Constipation
- Blurred vision
- Dizziness
- Cognitive impairment

“cant see pee or climb a tree”
Blurred vision, urinary retention and muscle pain/impaired coordination and balance

131
Q

Side effects of SSRIs

A
  • Sertraline - usually safe but associated with diarrhoea
  • Citalopram - Can prolong QT, which can lead to torsades de pointes. Least safe SSRI in patients with heart disease
  • Fluoxetine - Long half life (4-7 days) first line in children
  • Paroxetine causes weight gain

Other side effects:
- GI symptoms
- Headaches
- Sexual dysfunction (loss of libido, ED, orgasm difficulty)
- Increased risk of bleeding (esp when taken with NSAID, anticoagulant)
- SIADH causing hyponatraemia!

132
Q

SNRI side effects

A

Similar to SSRIs. Can increase BP so contraindicated in uncontrolled HTN.

Venlafaxine - more likely to cause discontinuation symptoms when stopped. Increased risk of death by OD

Duloxetine - Treats neuropathic pain, especially diabetic neuropathy

133
Q

TCA side effects

A

Amitriptyline - used at low dose to treat neuropathic pain

TCA - cardiotoxic!! Cause arrhythmia -> tachycardia, long QT, Bundle branch block. Dose dependent. Very dangerous in overdose, so not used in depression

Also have anticholinergic side effects.

134
Q

Vortioxetine. Tell me about it

A

Serotonin reuptake inhibitor. 3rd line after inadequate response from 2 others.

Stimulates and blocks other serotonin receptors. Good for anti-anxiety. Not many side effects, safe in heart disease.

Causes nausea for first few weeks

135
Q

Considerations when prescribing antidepressants

A

Can be initial period of agitation, anxiety, suicidal ideation, acts of suicide.

Review all patients within 2 weeks of starting (1 week in 18-25 due to high suicide risk)

Noticable response 2-4 weeks after starting.

Some can be directly switched, others need to be crosstapered. Most SSRI and SNRI are safe to switch between except fluoxetine due to long half life

136
Q

Advice for stopping antidepressants

A
  • continue for at least 6 months (2 years in recurrent) before stopping
  • Reduce slowly over 4 weeks to prevent discontinuation symptoms

Discontinuation symtpoms
- Flu like
- Electric shock sensations
- Insomnia
- Irritability
- Vivid dreams

137
Q

What drugs interact with SSRIs

A
  • NSAIDs (prescribe with PPI)
  • Warfarin/heparin (consider mirtazapine instead)
  • Aspirin
  • Triptans and MAOIs - increased risk of serotonin syndrome!
138
Q

SSRI risks in pregnancy

A

1st trimester - Small risk of congenital heart defects
3rd trimester - persistent pulmonary HTN of the baby

Paroxetine has risk of congenital malformations!

139
Q

Clozapine Side effects

A

One of the earliest atypical agents, carries risk of agranulocytosis. FBC monitoring ESSENTIAL!

  • Agranulocytosis, neutropenia
  • Constipation
  • Myocarditis
  • Hypersalivation

Dose adjustment if start/stop smoking

140
Q

What food cant you eat with a MAOI

A

Cheese because it contains tyramine whatever the fuck that is

141
Q

What is serotonin syndrome

A

Serotonin syndrome is a potentially life threatening drug reaction. Typically results from the use of serotonergic drugs.

Caused by:
- MOAI
- SSRIs (St John’s Wort and tramadol interact with SSRIs to cause serotonin syndrome)
- Ecstasy
- Amphetamines (ADHD Meds - Lisdex)
- Triptans

Usually due to interactions, doses that are too high, or a new drug is added without sufficient time to affect levels.

142
Q

Features of serotonin syndrome

A

Neuromuscular excitation
- Hyperreflexia
- Myoclonus
- Rigidity

Autonomic Nervous System excitation
- Hyperthermia
- Sweating

Altered mental state
- Confusion

143
Q

Management of serotonin syndrome

A

How is serotonin syndrome managed
- IV fluids
- Benzodiazepines
- Serotonin antagonists, cyproheptadine, chlorpromazine if severe

144
Q

What is Neuroleptic Malignant syndrome (NMS)

A

Condition caused by a sudden dopamine deficiency usually caused by overdoing

Gradual 1-3 days after starting or increasing an antipsychotic

145
Q

Symptoms of NMS

A
  • Fever
  • Muscle rigidity
  • Autonomic lability: typical features include HTN, tachycardia, tachypnoea.
  • Agitated delirium/confusion.
146
Q

Investigations of NMS

A
  • Raised Creatinine Kinase
  • AKI Secondary to Rhabdomyolysis
  • Leucocytosis
147
Q

Management of NMS

A

Stop antipsychotics
- IV Fluids
- Benzodiazepines

Severe cases -Dantrolene

148
Q

Serotonin syndrome vs NMS

A

SS
- Caused by SSRI, MAOI, ecstasy, novel psychoactive stimulants
- Faster onset (hours)
- Hyperreflexia, clonus, dilated pupils
- Severe treatment: Cyproheptadine, Chlorpromazine

NMS
- Caused by antipsychotics
- Slower onset (hours-days)
- Reduced reflexes, lead pipe rigidity, normal pupils
- Severe treatment: Dantrolene

149
Q

How is acute personality disorder crisis management

A

Acute short term antipsychotic (quetiapine), mood stabiliser (valproate/lamotrigine) if severe

150
Q

How do MAOIs work, give an example or 2

A

Serotonin and noradrenaline are metabolised by monoamine oxidase in the presynaptic cell

MAOI = Monoamine oxidase inhibitor

  • Tranylcypromine, phenelzine
151
Q

Adverse effects of MOAIs

A
  • Hypertensive reactions with tyramine containing foods (cheese, pickled herring, Bovril, Oxo, Marmite, broad beans)

Anticholinergic effects
- Dry mouth
- Blurred vision
- Constipation
- Urinary retention
- Confusion
- Tachycardia

152
Q

How should SSRIs be stopped, what can happen if not done right

A

Stop gradually over 4 weeks

Discontinuation symptoms (especially with Paroxetine, Fluoxetine can be stopped whenever)
- Increased mood change
- Restlessness
- Difficulty sleeping
- Electric shock sensations
- Unsteadiness/dizziness
- GI sx - pain, cramping, diarrhoea, vomiting
- Paraesthesia

153
Q

What is treatment resistant psychosis and how is it treated. What are some considerations of treatment

A

Uncontrolled psychosis following 2 antipsychotic drugs (right dose and timeframe)

Treated with clozapine.
48 hr rule: if missed for 48 hrs, must be retitrated.

Side effects:
- Myocarditis
- Constipation (cholinergic receptor block)
- Smoking cessation increases levels (smoking increases cytochromic b450 levels in liver)
- Increased salivation

154
Q

What medication can be given as a deterrent from alcohol and why

A

Disulfiram - causes vomiting, nausea, facial flushing

155
Q

What is an anti-craving medication from alcohol

A

Acamprostate

156
Q

Opioid addiction drug - alternative to methadone

A

Buprenephorine

157
Q

What is low and what is high in anorexia nervosa

A

G’s and C’s raised: growth hormone, glucose, salivary glands, cortisol, cholesterol, carotinaemia

Most other things low

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