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Psychiatry > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Type 1 trauma

A

Single incident trauma - sudden, unexpected

– Assault, robbery, rape

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2
Q

Type 2 trauma (complex trauma)

A

Repetitive trauma
– ongoing abuse, hostage taking, genocide
– betrayal of trust in primary care-giving relationship
– developmental trauma - issues about attachment /attunement

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3
Q

Importance of Trauma

A
  1. Individuals with chronic depression - a history of early life trauma predicts the need for psychotherapy as an adjunct to pharmacotherapy.
  2. 50% of patients with bipolar disorder have a history of childhood deprivation or abuse
  3. high rates of trauma exposure in the population, and among psychiatric inpatients
  4. non-recording of significant trauma common
  5. effects upon physical health
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4
Q

Psychological reactions after trauma

A
  1. Acute Stress Disorder/ Reactions
  2. Post-traumatic Stress Disorder (PTSD)
  3. Depression
  4. Grief Reactions
  5. Panic Attacks +/- agoraphobia
  6. Alcohol/Drug Dependence
  7. Brief Hypomania • Specific Phobias (e.g., travel)
  8. Complex reactions – CPTSD, Dissociative disorder
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5
Q

Normal acute reactions to trauma

A 
>	numbness, shock, denial
>	fear
>	depression or elation
>	anger, irritability
>	guilt
>	impaired sleep
>	hopelessness, helplessness
>	perceptual changes
>	avoidance
>	intrusive experiences (e.g., flashbacks)
>	hyperarousal, hypervigilance
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6
Q

Acute stress disorder

A

Defined as an acute stress reaction that occurs in the first 4 weeks after a person has been exposed to a traumatic event.

This is in contrast to post-traumatic stress disorder (PTSD) which is diagnosed after 4 weeks.

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7
Q

Post-traumatic stress disorder

A

Develop in people of any age following a traumatic event. One of the DSM-IV diagnostic criteria is that symptoms have been present for more than one month.

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8
Q

Features of PTSD

A
  1. re-experiencing: flashbacks, nightmares, repetitive and distressing intrusive images
  2. avoidance: avoiding people, situations or circumstances resembling or associated with the event
  3. hyperarousal: hypervigilance for threat, exaggerated startle response, sleep problems, irritability and difficulty concentrating
  4. emotional numbing - lack of ability to experience feelings, feeling detached
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9
Q

Management of PTSD

A
  1. watchful waiting may be used for mild symptoms lasting less than 4 weeks
  2. trauma-focused cognitive behavioural therapy (CBT) or eye movement desensitisation and reprocessing (EMDR) therapy may be used in more severe cases
  3. drug treatments should not be used as a routine first-line treatment for adults. If drug treatment is used then venlafaxine or a SSRI, such as sertraline should be tried.
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10
Q

DSM-V Criteria for diagnosis of PTSD

A
  1. Traumatic event(s)
  2. Intrusive symptoms: >1 (of 5)
    > recurrent distressing recollections, nightmares, flashbacks, distress accompanying reminders, physiological reactions
  3. Avoidance symptoms: 1 or both (of 2)
    > avoidance of thoughts or feelings about the event
    > avoidance of external reminders
  4. Negative alterations in cognitions & mood:
    ? amnesia for important aspect(s) of trauma, loss of interest in activities, negative affect (fear, horror, anger, guilt or shame), overly negative thoughts & assumptions about self/ world, exaggerated blame (self or others) for causing traumatic event(s), feeling isolated / detached, difficulty experiencing positive emotion (incl. numbing
  5. Increased arousal & reactivity: > 2 (of 6)
    > sleep disturbance, irritability / aggression, concentration difficulties, hypervigilance, exaggerated startle response, risky & destructive behaviour
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11
Q

Complex PTSD

A

Diagnosis consists of core PTSD symptoms PLUS

  1. Negative self-concept - low self-esteem, self-blame, hopelessness, helplessness, pre-occupation with threat, pervasive shame or guilt
  2. Emotional dysregulation – violent or emotional outbursts, reckless or self-destructive behaviour, dissociation. Including tension reduction activities - binge-purging, self-mutilation, substance misuse etc.
  3. Chronic interpersonal difficulties – issues with trust, maintaining relationships etc
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12
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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13
Q

Management of Acute Stress Disorder

A
  1. trauma-focused cognitive-behavioural therapy (CBT) is usually used first-line
  2. benzodiazepines
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14
Q

Generalised anxiety disorder (GAD)

A

A pervasive uncontrolled anxiety, that may be chronic and affect normal life. It can result in severe impairment of normal functionality, and the risk of suicidal ideation, self-harm and self-neglect is increased.

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15
Q

GAD risk factors

A 
o	Female sex
o	Family history
o	Childhood abuse and neglect
o	Environmental stress (e.g. redundancy, divorce)
o	Emotional trauma
o	Substance abuse
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16
Q

Non-pharmacological management for GAD

A
  1. step 1: education about GAD + active monitoring
  2. step 2: low-intensity psychological interventions
  3. step 3: high-intensity psychological interventions (cognitive behavioural therapy or applied relaxation) or drug treatment.
  4. step 4: highly specialist input e.g. Multi agency teams
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17
Q

Pharmacological management for GAD

A

NICE suggest sertraline should be considered the first-line SSRI

If sertraline is ineffective, offer an alternative SSRI or a (SNRI)

If the person cannot tolerate SSRIs or SNRIs, consider offering pregabalin

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18
Q

Panic disorder management

A

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

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19
Q

Panic disorder management in Primary care

A

NICE recommend either cognitive behavioural therapy or drug treatment

SSRIs are first-line. If contraindicated or no response after 12 weeks then imipramine or clomipramine should be offered

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20
Q

Panic disorder features

A
  1. may occur with, or without, agoraphobia
  2. Agoraphobia is a type of anxiety disorder in which you fear and avoid places or situations that might cause you to panic and make you feel trapped, helpless or embarrassed. You fear an actual or anticipated situation, such as using public transportation, being in open or enclosed spaces, standing in line, or being in a crowd.
  3. not due to the direct physiological effects of a substance (drug) or general medical condition
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21
Q

Agoraphobia

A

A disorder in which you fear and avoid places or situations that might cause you to panic and make you feel trapped, helpless or embarrassed - Avoidance of the phobic situation is often prominent, and some people with agoraphobia experience little anxiety because they are able to avoid their phobic situations.

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22
Q

Social phobia

A

A persistent fear of one or more social or performance situations in which the person is exposed to unfamiliar people or to possible scrutiny by others.

Individual fears that he or she will act in a way (or show anxiety symptoms) that will be embarrassing and humiliating.

Exposure to the feared situation almost invariably provokes anxiety, which may take the form of a situationally bound panic attack.

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23
Q

Treatment of Social Phobia

A
  1. CBT
  2. SSRIs / SNRIs
  3. Benzodiazepines (short term only)
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24
Q

Specific phobia (aka simple phobia)

A

A marked and persistent fear that is excessive or unreasonable, cued by the presence or anticipation of a specific object or situation:

Exposure to the phobic stimulus almost invariably provokes an immediate anxiety response, akin to a panic attack

The person recognizes that the fear is excessive or unreasonable

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25
Q

Treatment of specific phobias

A
  1. Behavioural Therapy – exposure
  2. Graded exposure / systematic desensitisation
  3. Add in CBT if necessary
  4. SSRIs / SNRIs if required
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26
Q

Obsessive-compulsive disorder (OCD)

A

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

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27
Q

Obsession

A

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

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28
Q

Compulsions

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.

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29
Q

Diagnosis of OCD

A

Obsessional symptoms or compulsive acts must be present most days for at least 2 weeks AND be a source of distress and interference with activities

  1. Obsessions must be individuals own thoughts
  2. Resistance must be present
  3. Rituals are not pleasant
  4. Obsessional thoughts/images/impulses repetitive
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30
Q

Disorders associated with OCD

A
  1. depression (30%)
  2. schizophrenia (3%)
  3. Sydenham’s chorea
  4. Tourette’s syndrome
  5. anorexia nervosa
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31
Q

Management of OCD with mild functional impairment

A

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

If this is insufficient or can’t engage in psychological therapy, then offer choice of either a course of an SSRI or more intensive CBT (including ERP)

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32
Q

Management of OCD with 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)

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33
Q

Management of OCD with severe functional impairment

A

offer combined treatment with an SSRI and CBT (including ERP)

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34
Q

ERP

A

A psychological method which involves exposing a patient to an anxiety provoking situation (e.g. for someone with OCD, having dirty hands) and then stopping them engaging in their usual safety behaviour (e.g. washing their hands). This helps them confront their anxiety and the habituation leads to the eventual extinction of the response

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35
Q

Amygdala-Centred Circuit is involved in

A

> 

Fear
Panic
Phobia
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36
Q

Cortico-Striatal-Thalamic-Cortical Circuit is involved in:

A
  1. Worry
  2. Anxiety
  3. Apprehension
  4. Obsessions
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37
Q

Neurotransmitters Involved in Amygdala Centred Circuits

A
  1. 5HT (Serotonin)
  2. GABA (Gamma-aminobutyric acid)
  3. Glutamate
  4. CRF (Corticotrophin releasing factor)
  5. NE (Norepinephrine)
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38
Q

Mechanism of Action SSRIs

A

Serotonin transporter transports neurotransmitter out of the synaptic cleft into the neuron that released them

SSRI inhibit the reuptake of serotonin leading to increased serotonin in the synaptic cleft

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39
Q

Main inhibitory transmitter in the brain

A

GABA

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40
Q

Benzodiazepines Mechanism of action

A

Enhance GABA action
o Main receptors – GABA-A, GABA-B & GABA-C
o GABA-A – target of benzodiazepines, barbiturates & alcohol

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41
Q

Pharmacology of benzodiazepines

A

Benzodiazepines bind at a separate site to GABA

Increases the likelihood that GABA binding will activate the receptor and/or increases the effect that GABA has when it binds to the receptor

Positive Allosteric Modulator – act as agonists at the allosteric modulatory site but have no action on their own

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42
Q

Pharmacological Effects of Benzodiazepines

A 
o	Reduce anxiety and aggression
o	Hypnosis/sedation
o	Muscle relaxation
o	Anticonvulsant effect
o	Anterograde amnesia
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43
Q

Clinical uses of Benzodiazepines

A

o Acute treatment of extreme anxiety, Hypnosis,
o Alcohol withdrawal
o Mania, Delirium, Rapid tranquillization
o Premedication before surgery or during minor procedures
o Status epilepticus

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44
Q

Examples of benzodiazepines

A

Midazolam, Lorazepam, Loprazolam
Oxazepam, Temazepam, Alprazolam
Nitrazepam, Diazepam, Chlordiazepoxide, Flurazepam

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45
Q

Side effects of benzodiazepines

A

o Fairly safe in overdose as alone are unlikely to cause respiratory depression (Antagonist – Flumazenil)
o Paradoxical aggression
o Anterograde amnesia & impaired coordination
o Tolerance and dependence

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46
Q

Neuroadaptation of the GABA response with benzodiazepines

A
  • Chronic treatment with benzodiazepines ↓ response to GABA

* Withdrawal results in anxiety/convulsions possibly due to ↓ density of benzodiazepine receptors

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47
Q

Functional disorders

A

A medical condition that impairs normal functioning of bodily processes that remains largely undetected under examination, dissection or even under a microscope. At the exterior, there is no appearance of abnormality.

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48
Q

Symptoms of functional disorders

A
  1. Weakness or paralysis., Abnormal movement, such as tremors or difficulty walking.
  2. Loss of balance., Difficulty swallowing or feeling “a lump in the throat”
  3. Seizures or episodes of shaking and apparent loss of consciousness (nonepileptic seizures)
  4. Episodes of unresponsiveness.
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49
Q

Examples of neurological functional disorders

A

Functional weakness, non-epileptic attacks, hemisensory symptoms

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50
Q

Examples of gastrointestinal functional disorders

A

IBS, non-ulcer dyspepsia, chronic abdominal pain

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51
Q

Examples of gynecological functional disorders

A

Chronic pelvic pain, premenstrual syndrome,

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52
Q

Examples of ENT functional disorders

A

Functional dysphonia, globus pharynges,

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53
Q

Examples of Cardiac functional disorders

A

Atypical chest pain, unexplained palpitations

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54
Q

Examples of rheumatological functional disorders

A

Fibromyalgia

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55
Q

Conversion Disorder

A

It refers to an idea that patients are ‘converting’ their mental distress into physical symptoms. Conversion disorder refers to symptoms of weakness, movement disorder, sensory symptoms and non-epileptic attacks.

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56
Q

Psychogenic

A

originating in the mind or in mental or emotional conflict

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57
Q

Somatisation

A

Suggests that the person has physical symptoms because of mental distress. The arguments here are the same as those for ‘conversion disorder’.

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58
Q

Hysteria

A

In the 18th and 19th century it was used to describe any physical symptom not explained by disease. In the 20th century its use was narrowed more specifically to neurological symptoms and is now used more rarely.

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59
Q

Dissociation

A

– detachment from reality

60
Q

Depersonalisation

A

A feeling that your body doesn’t quite belong to you or is disconnected from you

61
Q

Derealisation

A

A feeling that you are disconnected from the world around you or “spaced out”

62
Q

Hoover’s test

A

Is for of functional leg weakness – the patient may have difficulty pushing their “bad” leg down (hip extension), but when they are asked to lift up their “good” leg, movement in the “bad” leg returns transiently to normal.

63
Q

The tremor entrainment test

A

Test for functional tremor – this is when the shaking of an arm or leg becomes momentarily better when the person concentrates on copying a movement that the examiner makes.

64
Q

Dissociative (non-epileptic) seizures test

A

Can often be recognised by a trained health professional using a combination of typical features such as: an episode of violent limb thrashing in which the eyes remain closed, side-to-side head movements, or an event lasting longer than 5 minutes where the eyes are closed, hyperventilation during a shaking attack or tearfulness on recovery.

65
Q

ICD-10 criteria of dependence

A
  • A strong desire to take the substance
  • Difficulties in controlling substance use
  • A physiological withdrawal state
  • Tolerance
  • Neglect of alternative pleasures
  • Persistence despite evidence of harm
66
Q

Alcohol intake guidelines

A
  1. men and women should drink no more than 14 units of alcohol per week
  2. they advise ‘if you do drink as much as 14 units per week, it is best to spread this evenly over 3 days or more’
  3. pregnant women should not drink.
67
Q

Tools for Screening for Alcohol Use disorders

A

FAST - FAST alcohol screening(A&E)
AUDIT - Alcohol Use Disorders Identification Test
CAGE - screening for dependence

68
Q

What does FRAMES stand for?

A

> 

Feedback -  review problems experienced because of alcohol.
Responsibility – patient is responsible for change.
Advice – advise reduction or abstinence.
Menu – provide options for changing behaviour.
Empathy – use empathic approach.
Self-efficacy –encourage optimism about changing behaviour
69
Q

What is FRAMES?

A

Brief intervention: Patient-centred discussion that employs Motivational Interviewing concepts to raise an individual’s awareness of his/her substance use and enhancing his/her motivation towards behavioural change. Brief interventions are typically performed in 3-15 minutes and should occur in the same session as the initial screening. Repeated sessions are more effective than a one-time intervention.

70
Q

Alcohol withdrawal pathophysiology

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)

71
Q

Features of alcohol withdrawal

A
  1. symptoms start at 6-12 hours: tremor, sweating, tachycardia, anxiety
  2. peak incidence of seizures at 36 hours
  3. peak incidence of delirium tremens is at 48-72 hours: coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia
72
Q

Alcohol dependence diagnosis

A

Three or more of the following have been present together at some time during the previous year:

  1. Strong desire or sense of compulsion to take drug
  2. Difficulty in controlling use of substance in terms of onset, termination or level of use
  3. Physiological withdrawal state
  4. Evidence of tolerance
  5. Progressive neglect of other pleasures/ interests because of use/ effects of substance
  6. Persistence with use despite clear evidence of harmful consequences
73
Q

Management of alcohol withdrawal

A

History of complex withdrawals from alcohol (i.e. delirium tremens, seizures, blackouts) should be admitted to hospital for monitoring until withdrawals stabilised

First-line: long-acting benzodiazepines e.g. chlordiazepoxide or diazepam. Lorazepam may be preferable in patients with hepatic failure.

74
Q

Pathos score

A

Mainly used in adolescents (age 13-18) who present with an overdose.

75
Q

Questions in Pathos

A

> 

P – Problems – have you had problems for more than 1 month?
A – Alone – were you alone at the time?
T – Time – have you planned it for more than 3 hours?
Ho – Hopeless – are you feeling hopeless about the future
S – Sad – were you feeling sad for most of the time before the overdose?
76
Q

Delirium

A

An acute and fluctuating disturbance in level of consciousness, attention and global cognition. Delirium is an acute, transient and reversible state of confusion, usually the result of other organic processes (infection, drugs, dehydration).

77
Q

Two main states of delirium

A

‘hyperactive‘ and ‘hypoactive‘ delirium.

78
Q

Who does delirium usually affect?

A

Delirium occurs most commonly in the elderly and very young.

79
Q

Symptoms of delirium

A 
o	Reduced level of consciousness.
o	Disorientation (time/place/person);
o	Inattention
o	Illusions/hallucinations.
o	Altered personality.
o	Mood disorders.
o	Speech disorders
o	Lacking insight.
80
Q

Clinical features of hyperactive delirium include:

A
  1. Agitation
  2. Delusions
  3. Hallucinations
  4. Wandering
  5. Aggression
81
Q

Clinical features of hypoactive delirium include:

A
  1. Lethargy
  2. Slowness with everyday tasks
  3. Excessive sleeping
  4. Inattention
82
Q

What drugs cause delirium?

A

Anticholinergics, antiemetics, antipsychotics, corticosteroids, digoxin, levodopa, TCAs, opioids, alcohol

83
Q

What infections cause delirium?

A

Encephalitis, meningitis, pneumonia, sepsis, UTI, burns, hypothermia

84
Q

What endocrine disorders cause delirium?

A

Hyperparathyroidism, hyper/hypothyroidism

85
Q

What metabolic disorders cause delirium?

A

Acid-base disturbance, hepatic encephalopathy, uraemia, hypo/hyperglycaemia, electrolyte abnormalities, thiamine/vitamin B12 deficiency

86
Q

Main features of delirium

A

Sudden onset and fluctuating course over days – weeks
Variation in level of consciousness
Impaired attention
Psychomotor changes

87
Q

Main features of dementia

A

Gradual onset, slowly progressive over months – years
Consciousness unimpaired
Attention preserved
Often normal

88
Q

Blood tests for delirium

A

> 

FBC (e.g. infection, anaemia, malignancy)
U&Es (e.g. hyponatraemia, hypernatremia)
Coagulation/INR (e.g. intracranial bleeding)
TFTs (e.g. hypothyroidism)
Calcium (e.g. hypercalcaemia)
B12 + folate/haematinics (e.g. B12/folate deficiency)
Glucose (e.g. hypoglycaemia/hyperglycaemia)
Blood cultures (e.g. sepsis)
 LFTs (e.g. liver failure with secondary encephalopathy)
89
Q

Most common cause of delirium in the elderly

A

UTI

90
Q

Imaging in delirium

A

CT head: if there is concern about intracranial pathology (bleeding, ischaemic stroke, abscess)

Chest X-ray: may be performed if there is concern about lung pathology (e.g. pneumonia, pulmonary oedema)

91
Q

Advantages of MMSE

A
  • Relatively quick and easy to perform
  • Requires no additional equipment
  • Can provide a method of monitoring deterioration over time
92
Q

Disadvantages of MMSE

A
  • Biased against people with poor education due to elements of language and mathematical testing
  • Bias against visually impaired
  • Limited examination of visuospatial cognitive ability
  • Poor sensitivity at detected mild/early dementia
93
Q

Cognitive function tests in dementia

A
  1. Mini Mental State Exam (MMSE)
  2. CLOX test
  3. Montreal Cognitive Assessment (MoCA)
  4. Hopkins Verbal Learning Test
94
Q

Montreal Cognitive Assessment (MoCA)

A

A brief 30-question test that takes around 10 to 12 minutes to complete and helps assess people for dementia.

95
Q

Investigations in dementia

A
  1. Thyroid function tests
  2. B12
  3. Blood glucose
  4. Urea and electrolytes
  5. Liver function tests
  6. Metabolic causes in liver dysfunction
  7. Infective screen
  8. Autoimmune screen
  9. CT brain
  10. MRI
96
Q

Mechanism of action of Typical antipsychotics

A

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

97
Q

Mechanism of action of atypical antipsychotics

A

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

98
Q

Side effects of typical antipsychotics

A 
Extrapyramidal side-effects (EPSEs): 
Parkinsonism
acute dystonia
akathisia (severe restlessness)
tardive dyskinesia
99
Q

Other side effects of typical anti-psychotics other than extra-pyramidal ones

A

> antimuscarinic:
sedation, weight gain
raised prolactin - may result in galactorrhoea
impaired glucose tolerance
neuroleptic malignant syndrome
reduced seizure threshold (greater with atypicals)
prolonged QT interval (particularly haloperidol)

100
Q

Charles-Bonnet syndrome (CBS)

A

Characterised by 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).

101
Q

Risk factors for Charles-Bonnet syndrome (CBS)

A 
Advanced age
Peripheral visual impairment
Social isolation
Sensory deprivation
Early cognitive impairment
102
Q

Most common ophthalmological conditions associated with Charles-Bonnet syndrome (CBS)

A

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

103
Q

Cotard syndrome

A

A rare mental disorder where the affected patient believes that they (or in some cases just a part of their body) is either dead or non-existent.

104
Q

De Clerambault’s syndrome

A

A form of paranoia

The patient, often a single woman, believes that a famous person is in love with her.

105
Q

Delusional parasitosis

A

A relatively rare condition where a patient has a fixed, false belief (delusion) that they are infested by ‘bugs’ e.g. worms, parasites, mites, bacteria, fungus.

106
Q

Factors suggesting diagnosis of depression over dementia

A
  1. short history, rapid onset
  2. biological symptoms e.g. weight loss,
  3. patient worried about poor memory
  4. reluctant to take tests, disappointed with results
  5. mini-mental test score: variable
  6. global memory loss
107
Q

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

A

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

108
Q

Switching from 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

109
Q

Switching from a SSRI to a tricyclic antidepressant (TCA)

A

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

110
Q

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

A

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

111
Q

Switching from fluoxetine to venlafaxine

A

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

112
Q

Absolute contraindication to Electroconvulsive therapy

A

Raised intracranial pressure.

113
Q

Short term effects of Electroconvulsive therapy

A

headache
nausea
short term memory impairment
cardiac arrhythmia

114
Q

The 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
  3. Bargaining
  4. Depression
  5. Acceptance
115
Q

Features of atypical grief reactions

A
  1. delayed grief: sometimes said to occur when more than 2 weeks passes before grieving begins
  2. prolonged grief: difficult to define. Normal grief reactions may take up to and beyond 12 months
116
Q

Acute insomnia

A

Is more typically related to a life event and resolves without treatment.

117
Q

Chronic insomnia

A

May be diagnosed if a person has trouble falling asleep or staying asleep at least three nights per week for 3 months or longer.

118
Q

Associations of insomnia

A 
Female gender
Increased age
Lower educational attainment
Unemployment
Economic inactivity
Widowed, divorced, or separated status
119
Q

Less common diagnostic factors for insomnia

A

Daytime napping
Enlarged tonsils or tongue
Micrognathia (small jaw) and retrognathia
Lateral narrowing of oropharynx

120
Q

Investigations for insomnia

A

Diagnosis is clinical
Sleep diaries and actigraphy may aid diagnosis.
Polysomnography is not routinely indicated.

121
Q

Actigraphy

A

Actigraphy is a non-invasive method for monitoring motor activity. A type of wearable sleep test that tracks your movements to analyze when you are asleep and when you are awake

122
Q

When is Polysomnography indicated for investigating insomnia?

A

Considered in patients with suspected obstructive sleep apnoea or periodic limb movement disorder, or when insomnia is poorly responsive to conventional treatments

123
Q

The use of hypnotics in insomnia

A

Short-acting benzodiazepines or non-benzodiazepines (zopiclone, zolpidem and zaleplon).

Diazepam is not recommended but can be useful if the insomnia is linked to daytime anxiety.

Use the lowest effective dose for the shortest period possible.

If there has been no response to the first hypnotic, do not prescribe another.

It is important to review after 2 weeks and consider referral for cognitive behavioural therapy (CBT).

124
Q

Korsakoff’s syndrome

A

Disorder that primarily affects the memory system in the brain. It usually results from a deficiency of thiamine (vitamin B1), which may be caused by alcohol abuse, dietary deficiencies, prolonged vomiting, eating disorders, or the effects of chemotherapy.

125
Q

Features of Korsakoff’s syndrome

A

anterograde amnesia
retrograde amnesia
confabulation

126
Q

Lithium

A

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

127
Q

Lithium mechanism of action

A

Mechanism of action - not fully understood, two theories:
> interferes with inositol triphosphate formation
> interferes with cAMP formation

128
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

129
Q

Monitoring Lithium levels

A

> when checking lithium levels, the sample should be taken 12 hours post-dose

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

> once established, lithium blood level should ‘normally’ be checked every 3 months

> after a change in dose, lithium levels should be taken a week later and weekly until the levels are stable.
thyroid and renal function should be checked every 6 months

130
Q

Circumstantiality

A

The inability to answer a question without giving excessive, unnecessary detail. H

131
Q

Tangentiality

A

Refers to wandering from a topic without returning to it.

132
Q

Clang associations

A

Are when ideas are related to each other only by the fact they sound similar or rhyme.

133
Q

Word salad

A

Is completely incoherent speech where real words are strung together into nonsense sentences.

134
Q

Knight’s move thinking

A

A severe type of loosening of associations, where there are unexpected and illogical leaps from one idea to another. It is a feature of schizophrenia.

135
Q

Perseveration

A

The repetition of ideas or words despite an attempt to change the topic.

136
Q

Echolalia

A

Is the repetition of someone else’s speech, including the question that was asked.

137
Q

Mirtazapine

A

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

138
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

139
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.

140
Q

Features of Post-concussion syndrome

A 
Seen after even minor head trauma
headache
fatigue
anxiety/depression
dizziness
141
Q

Seasonal affective disorder (SAD)

A

Describes depression which occurs predominately around the winter months. SAD should be treated the same way as depression.

142
Q

Section 136 of mental health Act

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

143
Q

Adverse effects of SSRIs

A

Gastrointestinal symptoms

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

144
Q

SSRI 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

Triptans: avoid SSRIs

145
Q

Side effects of TCAs

A 
drowsiness
dry mouth
blurred vision
constipation
urinary retention
lengthening of QT interval

Psychiatry (3 decks)

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