Psych basics Flashcards

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1
Q

What is mnemonic for MSE?

A

ASEPTIC

  • Appearance & behaviour
  • Speech
  • Emotion (mood)
  • Perception (all 5 senses)
  • Thought
  • Insight
  • Cognition
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2
Q

What should be reported in Appearance and behaviour in the MSE?

A
  • General appearance
    • Age, gender, build, ethnicity
    • Hair, make-up, clothing, piercings, tattoos
    • Physical problems
    • Self-care (well-kempt or self-neglecting)
  • Body language
    • Facial expression, e.g. smiling, scowling, fearful
    • Eye contact, e.g. responsive and appropriate, avoidant, too intense
    • Posture, e.g. hunched shoulders in depression
    • Activity level
    • Describe what they are doing, e.g. pacing around the room, responding to hallucinations
  • Other movements
    • Extrapyramidal SEs
    • Repeated movements
  • Rapport:
    • Withdrawn and cold, polite and friendly, guarded (suspicious/deliberately withholding info), disinhibited (e.g. removing clothing)
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3
Q

Give some examples of repeated movements that may be seen, and their defintions

A
  • Mannerism: appear goal-directed (e.g. sweeping hair from face)
  • Stereotypes: not goal-directed (e.g. flicking fingers at hair)
  • Tics: purposeless, involuntary movements involving a group of muscles (e.g. blinking)
  • Compulsions: rituals the patient feels compelled to undertake (e.g. hand-washing)
  • Echopraxia: patients senselessly imitate actions of those around them; associated with echolalia
  • Catatonic symptoms: extreme negativism, lack of response to stimuli
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4
Q

What should be commented on in the speech section of the MSE?

A
  • Rate: fast, slow, normal
  • Volume: loud, soft, normal
  • Tone: emotional quality of speech, e.g. sarcastic, angry, calm
  • Flow: speech may be spontaneous, only when prompted, hesitant, with long pauses before answers, uninterruptible etc.
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5
Q

Name some disorders of speech and give their defintions

A
  • Dysarthria: impaired articulation
  • Dysphasia: impaired ability to comprehend or generate speech
  • Clang association: rhyming connections (e.g. gang, bang)
  • Punning: playing on words with the same sounds but different meanings (e.g. tyre, tire)
  • Neologisms: made-up words
  • Pressure of speech: reflects underlying pressure of thought  will be hard to interrupt the patient
  • Poverty of speech: reflects underlying poverty of thought  typically seen in depression
  • Thought block: complete emptying of the mind of thoughts  shown as a sudden halt in speech; may be seen in schizophrenia
  • Circumstantial speech: reflecting underlying over-inclusive thinking which adds excessive details and subclauses to every sentences, but eventually reaches the original destination
  • Tangential speech: patient diverts from the initial train of thought and never returns to the original destination
  • Flight of ideas: patient’s ideas jump from one to another, but may eventually come back to the point; may be linked normally (i.e. via rhymes, puns, distractions in the room)
  • Derailment/loosening of associations/knights move thinking: thoughts start at one place but end up in a completely unrelated place to the original route
    • Word salad is its worst form → mixture of incoherent words and phrases
  • Perseveration: thoughts remain in one place, e.g. “what is your name?” “John”, “how are you?” “John”
  • Echolalia: senselessly repeating words or phrases spoken by others, like a parrot
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6
Q

What should be commented on in the mood and affect section of the MSE?

A
  • Mood:
    • subjective
    • objective
  • Affect (how they express their emotional state):
    • Appropriateness or congruity
    • Range of emotional expressivity
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7
Q

What should be commented on regarding thought in an MSE?

A
  • Form (can be ordered or disordered)
    • e.g. circumstantial and tangential thinking, loosening of association, neologisms, flight of ideas, thought blocking
  • Content
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8
Q

Give some examples of disorders of thought content

A
  • Delusions
  • Overvalued ideas
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9
Q

Give some examples of disorders of thought content

A
  • Delusions
  • Overvalued ideas
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10
Q

Define delusion

A

a fixed belief, held despite rational argument or evidence to the contrary, which cannot be fully explained by a patient’s cultural, religious or educational background

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11
Q

What are the different classifications of delusions?

A
  • Primary, secondary and systematised:
    • Primary: arise completely out of the blue in someone without prior mental health problems
    • Secondary: follow another abnormal experience, such as an abnormal mood or hallucination (e.g. perception of hearing a voice, so patient believes they are being stalked)
    • Systematised: when delusions grow and build on each other, connecting into a delusional system
  • Mood congruent or incongruent:
    • Mood congruent are commonly seen in depression or mania
  • Bizarre or non-bizarre:
    • Bizarre are completely impossible (characteristic of schizophrenia
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12
Q

Name some themes of delusions

A
  • Grandiose
  • Persecutory
  • Nihilistic
  • Delusions of reference
    • beliefs that ordinary objects, events or other people’s actions have a special meaning or significance for the patient (e.g. news reports related to them)
  • Delusions of control
  • Delusions of thought interference
  • Passivity
  • Delusions of infidelity/morbid jealousy/Othello syndrome
  • Erotomanic
  • Delusions of guilt
  • Hypochondriacal/somatic delusions
  • Religious delusions
  • Delusions of misidentification
  • Delusions of infestation
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13
Q

Name 2 types of delusions of misindentification

A
  • Capgras syndrome
    • belief that a familiar person has been replaced by an imposter;
  • Fregoli syndrome
    • belief that a complete stranger is actually a familiar person already known to the patient
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14
Q

What is Ekbom’s syndrome?

A

i. e. Delusions of infestation
* delusion that body is infested with small but visible organisms. May occur secondary to tactile hallucinations

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15
Q

What is an overvalued idea?

A
  • Plausible belief that a patient becomes preoccupied with to an unreasonable extent, leading to distress to patient/those around them
  • Distinguished from delusions due to lack of gross abnormality of reasoning → can give fairly logical reasons for their beliefs
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16
Q

What is an illusion

A
  • Illusions: misperception of a stimulus
    • Can occur if patient is drowsy, very emotional, seen in delirium
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17
Q

Define hallucination

A
  • Hallucinations: perception in the absence of a stimulus
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18
Q

Name the types of auditory hallucinations

A
  • 1st person (audible thoughts): patients hear own thoughts spoken aloud as they think them
    • Thought echo: thoughts are echoed after being thought
  • 2nd person: voice(s) addressing patient directly
    • May be persecutory, critical, complementary, command
    • Often mood congruent
  • 3rd person: voices speak about the patient, e.g. running commentary, conversation
  • Elementary hallucinations: simple sounds, e.g. whistling, single words (voices are complex)
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19
Q

What do visual hallucinations suggest? give an example of one

A
  • Suggest organic illness or psychoactive substance use
  • E.g. Lilliputian hallucinations: miniature people or animals
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20
Q

When may visual hallucinations occur in the absence of pathology?

A
  • occur briefly when waking (hypnopompic hallucinations) or
  • falling asleep (hypnagogic hallucinations) or
  • following a bereavement (still seeing loved one)
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21
Q

What are:

  • extracampine hallucinations
  • functional hallucinations
  • reflex hallucinations
A
  • Extracampine hallucinations: outside the limits of a person’s normal sensory field, e.g. hearing voices 100 miles away
  • Functional hallucinations: normal sensory stimulus is needed to precipitate the hallucination in the same modality (e.g. hear voices when doorbell rings)
  • Reflex hallucinations: normal sensory stimulus precipitates hallucination in another modality (e.g. hear voices when light is switched on)
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22
Q

What is the difference between depersonalisation and derealisation?

A
  • Depersonalisation: person feels unreal, detached, numb, distant
    • “Do you ever feel as if you aren’t quite real?”
  • Derealisation: the world feels unreal, e.g., like a film set
    • “Do you ever feel as if the world around you is not quite real?”
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23
Q

What does cognition mean in the MSE?

A
  • Umbrella term covering thinking and remembering
  • Includes:
    • orientation,
    • attention,
    • concentration
    • memory,
    • all of which are affected by a patient’s level of consciousness
  • Any concern → formal testing (e.g. MMSE)
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24
Q

What is the Abbreviated Mental Test Score (AMTS)?

A

A quick way to assess confusion with 10 questions – screening tool

Score ≤6 is significant for dementia/delirium

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25
Q

What are the qs in the Abbreviated Mental Test Score (AMTS)??

A

Questions:

  1. How old are you?
  2. What is your DOB?
  3. What time is it? (to nearest hour)
  4. What year is it?
  5. Where are we?
  6. Remember the address 42 West Street (recall later)
  7. Do you know who I am? Do you know who that is (point to nurse/family member)
  8. Do you know who the prime minister/queen is?
  9. Dates of WW2? (or other memorable date)
  10. Count down from 20-1

Address recall

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26
Q

What is the Mini Mental State Exam (MMSE)?

A
  • Test to assess cognitive impairment,
  • usually as a screening tool for dementia (also used to assess progression of cognitive impairment)
  • Marked out of 30
    • 20-24 suggests mild dementia;
    • 13-20 suggests moderate dementia;
    • <12 suggests severe dementia
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27
Q

What are the qs in the Mini Mental State Exam (MMSE)?

A
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28
Q

Name some members of the psych MDT

A
  • Psychiatrists
  • Psychiatric nurse
  • Community psychiatric nurse
  • Social worker
  • OT
  • Clinical psychologist
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29
Q

Name the levels in the Hierarchy of Diagnosis

What is its use and why is it used?

A
  • Consider higher levels first (e.g. first rule out/treat organic brain disorder)
  • This is because higher levels can lead to conditions below it, e.g. organic brain disorder can cause psychosis; depression (affective disorder) can cause anxiety (neurotic disorder)
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30
Q

What are the different types of psychotropic medication?

A

antidepressants,

antipsychotics,

mood stabilisers

sedatives/hypnotics

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31
Q

What is the common mechanism of action of antidepressants?

A

common action is to elevate levels of monoamines (NA, DA, 5-HT)

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32
Q

Give some e.g. of SSRIs. What is their mechanism of action?

A
  • E.g. fluoxetine, citalopram, paroxetine, sertraline
  • Mechanism: selective presynaptic blockade of serotonin reuptake pumps
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33
Q

What are the side effets of SSRIs?

A
  • GI: N+V, diarrhoea, anorexia/weight loss
    • Usually resolve in time
  • Sexual: low libido, delayed orgasm
  • Neuro: headache, anxiety, sleep disturbance, restlessness
  • Fewer anticholinergic SEs than TCAs; not sedating
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34
Q

What are the contraindications of SSRIs?

A
  • Mania  use with caution in bipolar
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35
Q

How long do SSRIs take to work? What can abrupt stopping of SSRIs cause?

A
  • May take 2wks for any effect & 6wks for full effect
  • May cause suicidal ideation/anxiety/restlessness on initiation
    • Esp citalopram in young adults
    • Warn patients of this and follow-up
  • Abrupt withdrawal of any antidepressant can cause discontinuation syndrome
    • Most common in SSRIs with short half-lives (paroxetine, sertraline)
    • Therefore, need to taper the dose down (except fluoxetine which has long half-life)
    • Do not cause dependence (don’t become addicted or crave them)
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36
Q

What are the symptoms of discontinuation syndrome?

A
  • GI: GI disturbance
  • Neuro: agitation, dizziness, headache, tremor,
  • insomnia
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37
Q

Give some e.g. of TCAs. What is their mechanism of action?

A
  • E.g. amitriptyline, iofe-, clomi-, imi- pramine,
  • Mechanism:
    • presynaptic blockade of both NA and 5-HT reuptake pumps (and to a lesser extent DA);
    • also blockade of muscarinic, histaminergic and alpha-adrenergic receptors
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38
Q

What are the indications of TCAs?

A
  • Depression
  • OCD (clomipramine)
  • Neuropathic pain (amitriptyline)
  • Nocturnal enuresis in children (imipramine)
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39
Q

What are the SEs of TCAs?

A
  • Antimuscarinic: dry mouth, blurred vision, constipation, urinary retention, confusion
  • Alpha-adrenergic blockade: postural hypotension, dizziness, syncope
  • Histaminergic blockade: weight gain, sedation/drowsiness
  • Cardiotoxic effects: arrhythmias, heart block, QT interval prolongation, ST elevation
  • Toxic in overdose: cardiotoxic, respiratory failure, seizures, convulsions, coma
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40
Q

What are the contraindications of TCAs?

A
  • Recent MI
  • Arrhythmias
  • Severe liver disease
  • Mania → use with caution in bipolar
  • High suicide risk (as lethal in overdose)
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41
Q

How long do TCAs take to work? What is a major caution that patients should be warned about regarding TCAs?

A
  • May take 2wks for any effects and 6wks for full effect
  • May cause drowsiness → advise patients to avoid driving
    • Sedation can be useful in patients with insomnia
      • Prominent sedative effects → amitriptyline, clomipramine
      • Less sedative effects → iofepramine, imipramine
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42
Q

Give some e.g. of MOAIs. What is their mechanism of action?

A
  • E.g. phenelzine, moclobemide, tranylcypromide, isocarboxazid
  • Mechanism: non-selective and irreversible inhibition of monoamine oxidase A and B → decreased degradation of monoamines
    • Moclobemide is a RIMA (reversible inhibitor of monoamine oxidase) → less risk of hypertensive crisis
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43
Q

What are the indications of MAOIs?

A
  • Refractory/atypical depression (2nd line due to SEs)
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44
Q

What are the SEs of MAOIs?

A
  • Postural hypotension
  • Antimuscarinic: dry mouth, blurred vision, constipation, urinary retention, confusion
  • Increased appetite, weight gain
  • Hepatotoxicity
  • Hypertensive crisis
  • Serotonin syndrome
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45
Q

Why can a hypertensive crisis occur in MAOI use?

A
  • Due to interaction between MAOIs and tyramine-containing foods
  • Inhibition of MAO A causes accumulation of monoamine NTs and impairs metabolism of tyramine → accumulation of amines (esp NA) → tachycardia, HTN, vasoconstriction
  • May lead to intracerebral or subarachnoid haemorrhage
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46
Q

What is serotonin syndrome? What is the Tx for it?

A
  • Occurs because MAOIs increase 5-HT
  • Giving other antidepressants with a strong serotonergic effect (SSRIs, clomipramine, imipramine) at the same time increases the risk of serotonin syndrome; so does giving opiates
  • Triad of neuromuscular abnormalities, altered consciousness, autonomic instability
  • Tx: Cyproheptadine
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47
Q

What are the contraindications for MAOIs?

A
  • Mania → use with caution in bipolar
  • Hepatic impairment
  • Cerebrovascular disease
  • Phaeochromocytoma
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48
Q

What are some things that patients should be advised about when starting a MAOI?

A
  • Patients must carry a card indicating that they are taking a MAOI; must be education and given written info about diet
  • Foods to avoid: cheese, degraded protein (smoked fish, chicken liver), yeast and protein extract (Marmite/Oxo), broad beans, unfresh/overripe foods, decongestants, alcohol (esp beer)
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49
Q

What is the advised timing of starting another antidepressant alongside an MAOI?

A
  • Should be prescribed at least 1wk after cessation of other antidepressants;
  • other antidepressants should not be prescribed until 2wks after discontinuing MAOIs
  • → to decrease risk of serotonin syndrome
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50
Q

Give some e.g. of SNRIs. What is their mechanism of action?

A
  • E.g. venlafaxine
  • Mechanism: presynaptic blockade of both NA and 5-HT reuptake pumps (also DA in high doses); negligible effects of muscarinic, histaminergic or alpha-adrenergic receptors
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51
Q

What are the indications of SNRIs?

A
  • Generalised anxiety disorder
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52
Q

What are the SEs of SNRIs?

A
  • Similar SEs to SSRIs (but tend to be more severe)
  • GI: Constipation, nausea
  • Neuro: Dizziness, Sleep disturbances
  • Cardio: HTN
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53
Q

What are the contraindications of SNRIs?

A
  • High risk of cardiac arrhythmia
  • Uncontrolled HTN
  • Pregnancy
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54
Q

Which medical professional needs to supervise SNRI use? What monitoring is required?

A
  • Should be used as 2nd-line treatment under specialist supervision
  • Requires BP monitoring
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55
Q

Give some e.g. of Noradrenergic and specific serotonergic antidepressants (NaSSA).

What is their mechanism of action?

A
  • E.g. mirtazapine
  • Mechanism: presynaptic alpha-2 receptor blockade  results in increased release of NA and 5-HT from presynaptic neurons
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56
Q

What are the indications of NaSSA?

A
  • Depression (esp when sedation or increased oral intake is wanted)
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57
Q

What are the SEs of NaSSA?

A
  • Increased appetite, weight gain
  • Oedema
  • Sedation
  • Few antimuscarinic SEs → useful in elderly
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58
Q

What are the contraindications of NaSSA?

A
  • Hypersensitivity
  • Mania → use with caution in bipolar
  • Patients taking MAOIs
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59
Q

Name some other antidepressant classes and give some e.g.

A
  • Selective NA reuptake inhibitor (NARI):
    • E.g. reboxetine
    • Selective presynaptic blockade of NA reuptake pumps
  • Serotonin 2A antagonist/serotonin reuptake inhibitor (SARI):
    • E.g. trazodone
    • Trazodone is molecularly similar to TCAs but clinically different  weak antidepressant but good sedative. Safe in overdose and negligible anticholinergic SEs. Often used as adjunct antidepressant in people taking non-sedative antidepressant, e.g. SSRI
  • Tetracyclic antidepressants:
    • E.g. mianserin
  • Dopaminergic and noradrenergic antidepressants
    • E.g. bupropion, pramipexole
60
Q

Which patients should be prescribed antidepressants with caution? Why?

A

All antidepressants should be used with caution in epilepsy (as they lower seizure threshold)

61
Q

What is the general mechanism of action of antipsychotics?

A
  • Primary mechanism of all antipsychotics (possibly except clozapine) is antagonism of dopamine D2 receptors in the mesolimbic pathway
  • Atypical antipsychotics have more effects on other receptors, e.g. 5-HT2, histamine, muscarinic, a-adrenergic
  • Clozapine is a comparatively weak D2-antagonist but has high affinity for 5-HT2 and D4 receptors (among many others)
  • Blockade of D2 receptors occurs throughout the brain → side effects
    • SEs are also caused by blocking muscarinic, histaminergic and a-adrenergic receptors
62
Q

Name some typical antipsychotics

A
  • E.g. phenothiazines (chlorpromazine, fluphenazine), butyrophenones (haloperidol), thioxanthines (flupentixol)
63
Q

What are the indications for typical antipsychotics?

A
  • Schizophrenia
  • Other psychotic illnesses (schizoaffective disorder, delusional disorder)
  • Depression/mania with psychotic features
  • Psychotic episodes secondary to an organic condition or psychoactive substance misuse
  • Delirium (caution in alcohol withdrawal as they lower seizure threshold)
  • Behavioural disturbance in dementia
  • Severe agitation, anxiety, violent or impulsive behaviour
64
Q

What are the SEs of typical antipsychotics?

A
  • Extrapyramidal SEs (EPSEs) at normal doses
    • They are due to relative deficiency of DA and excess of ACh produced by dopamine antagonism in the nigrostriatal pathway
  • Neuroleptic malignant syndrome:
    • A rare but potentially fatal complication of antipsychotic treatments
  • Hyperprolactinaemia: Sexual dysfunction, reduced bone mineral density, menstrual disturbances, gynaecomastia, galactorrhoea
65
Q

Name the ESPEs of atypical antipsychotics

A
  • Parkinsonism: tremor, rigidity, bradykinesia
    • Usually occurs within 1 months of starting antipsychotic
  • Acute dystonia: involuntary sustained muscular contractions or spasms, e.g. neck (spasmodic torticollis), clenched jaw, protruding tongue, eyes roll upwards, grimacing
    • May lead to jaw dislocation, torticollis, limb rigidity, altered behaviour
    • More common in young men
    • Usually occurs within 72hrs of treatment
  • Akathisia: severe restlessness and muscular discomfort
    • Occurs within 6-60 days
  • Tardive dyskinesia: rhythmic involuntary movements of the head/limbs/trunk, esp chewing, grimacing, protruding tongue
    • Develops in 20% patients who receive long-term typical antipsychotics
66
Q

What is the Tx of parkinsonism?

A
  • Anticholinergics – oral if able to swallow; otherwise IV/IM
    • Often procyclidine IM 5mg bolus, then continue 8hrly if necessary
      • Consider reducing dose of antipsychotic or switching to atypical
67
Q

What is the Tx of acute dystonia?

A
  • Anticholinergics – oral if able to swallow; otherwise IV/IM
    • Often procyclidine IM 5mg bolus, then continue 8hrly if necessary
      • Consider reducing dose of antipsychotic or switching to atypical
68
Q

What is the Tx of akisthesia?

A
  • Propranolol or short-term benzodiazepines
  • Consider reducing dose of antipsychotic or switching to atypical
69
Q

What is the Tx of Tardive dyskinesia?

A
  • No effective treatment
  • Withdraw antipsychotic if possible
  • Clozapine might be helpful
  • Consider benzodiazepines
  • Do not give anticholinergics (may worsen)
70
Q

What is neuroleptic malignant syndrome?

A
  • Presents with:
    • hyperthermia,
    • fluctuating levels of consciousness,
    • muscle rigidity,
    • autonomic dysfunction: pallor, tachycardia, labile BP, sweating, urinary incontinence
  • Bloods: Increased WBC + creatinine
71
Q

What is the Tx of Neuroleptic malignant syndrome?

A
  • ABCDE approach
    • CVS and respiratory support in ICU
  • Stop antipsychotics
  • Give bromocriptine and dantrolene (post-synaptic muscle relaxant)
  • Usually lasts 5-7d after discontinuation of antipsychotics
72
Q

Name some atypical antipsychotics

A
  • -PINES:
    • olanzapine,
    • quetiapine
    • clozapine (discussed separately)
  • Other:
    • risperidone,
    • aripiprazole,
    • amisulpride
73
Q

What are the indications of atypical antipsychotics

A
  • Schizophrenia
  • Other psychotic illnesses (schizoaffective disorder, delusional disorder)
  • Depression/mania with psychotic features
  • Psychotic episodes secondary to an organic condition or psychoactive substance misuse
  • Delirium (caution in alcohol withdrawal as they lower seizure threshold)
  • Behavioural disturbance in dementia
  • Severe agitation, anxiety, violent or impulsive behaviour
74
Q

What are some SEs of atypical antipsychotics

A
  • Metabolic syndrome
  • Postural hypotension
  • Drowsiness
  • EPSEs (less common)
75
Q

What is metabolic syndrome/

A
  • obesity,
  • diabetes,
  • HTN, dyslipidaemia
76
Q

What are the contraindications of atypical antipsychotics?

A
  • Use with caution in those with: cardiovascular disease, metabolic syndrome, epilepsy and elderly
77
Q

What must be monitored during atypical antipsychotic use?

A
  • Monitor:
    • weight,
    • BP,
    • ECG,
    • lipids,
    • glucose/HbA1c,
    • FBC,
    • U&Es,
    • LFTs
78
Q

What are the indications of clozapine?

A
  • Treatment-resistant schizophrenia (failure to respond to 2 antipsychotics, at least 1 of which is an atypical)
79
Q

What are the SEs of clozapine?

A
  • Immuno:
    • Agranulocytosis (rare (0.8%) but fatal)
  • Cardio:
    • Myocarditis,
    • cardiomyopathy,
    • Tachycardia (treat with beta-blockers)
  • Metabolic:
    • Metabolic syndrome → obesity, diabetes, HTN, dyslipidaemia
  • GI:
    • Constipation (use laxatives)
  • Neuro:
    • Sedation
    • Convulsions
80
Q

What are the contraindications of clozapine?

A
  • Severe cardiac disease
  • Acute liver disease
  • Severe renal impairment
  • History of bone marrow disorders
81
Q

What must be monitored during clozapine use?

A
  • Must be monitored with regular FBC (for agranulocytosis)
    • Before starting, weekly for 1st 18wks, then fortnightly, then monthly
    • If leukocyte count <3000/mm3 or absolute neutrophil count <1500mm3 → discontinue permanently and refer to haematologist
  • weight,
  • lipids,
  • ECG,
  • LFTs
82
Q

When can clozapine be initiated?

A

as inpatient

83
Q

Name some mood stabilisers

A
  • lithium,
  • sodium valproate
  • carbamazepine
84
Q

What is the mechanism of action of mood stablisers?

A
  • Uncertain
  • May act on sodium transport or GABA in nerve and muscle cells
  • May inhibit the recycling of neuronal membrane phosphoinositides involved in generation of second messengers
  • These inhibitory mechanisms are thought to decrease neuronal signalling → decreasing the hyperactive circuits involved in mania
85
Q

What are the indications for lithium?

A
  • Mania
  • Prophylaxis in BAD
  • Augments antidepressants in treatment of refractory depression
  • Adjunct to antipsychotics in schizoaffective disorder and schizophrenia
  • Aggressive or self-mutilating behaviours
86
Q

What are the SEs of lithium?

A
  • General:
    • weight gain, fine tremor, muscle weakness, oedema, worsening acne and psoriasis
  • GI:
    • diarrhoea, nausea, vomiting, metallic taste
  • Renal:
    • nephrogenic DI, impaired renal function
  • Endo:
    • hypothyroidism, hyperparathyroidism
  • Cardiac:
    • T-wave inversion
  • Haem:
    • leucocytosis
  • Teratogenic
  • Lithium toxicity:
87
Q

Describe lithium toxicity (levels, precipitants, presentation)

A
  • Toxic over levels of 1.5mmol/l
  • Can be precipitated by antidepressants, anticonvulsants, antipsychotics, diuretics, CCBs, dehydration
  • Presentation:
    • 1.5-2mmol/L: nausea and vomiting, apathy, coarse tremor, ataxia, muscle weakness
    • >2mmol/L: nystagmus, dysarthria, impaired consciousness, disorientation, seizures
88
Q

What is the Tx of lithium toxicity?

A
  • Stop lithium
  • Check levels
  • Fluids → ensure adequate hydration and electrolyte balance
  • Anticonvulsants if necessary
  • Haemodialysis if necessary for renal failure
89
Q

What are the contraindications of lithium?

A
  • Pregnancy and breastfeeding
  • Caution in renal disease, cardiac disease and thyroid disease
  • Caution in conditions causing Na imbalance, e.g. Addison’s disease
90
Q

Who can prescribe lithium? What pre-Tx monitoring is required? What monitoring is required during Tx?

A
  • Prescribed only on specialist advice
  • Needs pre-treatment Ix: medication review, blood tests (FBC, U&Es, TFTs), pregnancy test, ECG
  • Monitoring during treatment: lithium plasma levels weekly until level has been stable for 4wks, then every 3 months, regular monitoring of FBC, U&Es, Ca, TFTs
91
Q

Which drugs does lithium interact with?

A
  • Lithium is taken orally and excreted by kidneys  clearance is decreased with renal impairment (elderly, dehydration) and Na depletion
  • Some drugs (diuretics (esp thiazide), NSAIDs & ACE inhibitors can also increase lithium levels → prescribe with caution
  • Antipsychotics may synergistically increase lithium-induced neurotoxicity → important because often co-administered in acute mania
92
Q

Which patients is lithium not used in?

A

avoid in women of child-bearing age

93
Q

What are the SEs of sodium valproate?

A
  • Nausea and vomiting
  • Weight gain
  • Sedation and dizziness
  • Oedema
  • Hair loss
  • Hepatic failure (rare)
  • Pancreatitis
  • Pancytopenia
  • Teratogenic  neural tube defects
94
Q

What are the indications of sodium valproate?

A
  • Mania in BAD
  • Epilepsy
  • Prophylaxis in BAD (unlicensed)
  • Refractory depression
95
Q

What are the contraindications for sodium valproate?

A
  • Hepatic dysfunction
  • Porphyria
  • Pregnancy and breastfeeding
96
Q

Which patients is sodium valproate useful in?

Which bloods should be checked. and when?

What should female patients have prior to starting?

A
  • May be useful in patients with rapid cycling BAD
  • LFTs should be checked before and just after starting
  • Patients MUST have effective contraception (e.g. depot, implant)
97
Q

What are the indications of Carbamazepine?

A
  • Epilepsy
  • Prophylaxis in BAD (2nd line)
98
Q

What are the SEs of Carbamazepine?

A
  • Erythematous rash (common but rarely serious)
  • GI: diarrhoea, nausea, vomiting, anorexia, liver damage
  • Neuro: dizziness, headache, ataxia, diplopia, drowsiness
  • Haem: leucopenia, thrombocytopenia, agranulocytosis, aplastic anaemia
  • Biochem: hyponatraemia and fluid retention
  • Teratogenic
99
Q

What are the contraindications of Carbamazepine?

A
  • Atrioventricular conduction abnormalities (unless paced)
  • History of BM depression
  • Acute porphyria
  • Pregnancy and breastfeeding
100
Q

What monitoring is required prior to starting and during Tx with Carbamazepine?

A
  • Pre-treatment Ix: bloods (FBC, LFTs, U&Es), pregnancy test, ECG
  • Monitoring during treatment: FBC
101
Q

What are the indications of lamotrigine?

A
  • Epilepsy
  • Prophylaxis in BAD (most effective when depression is predominant feature)
102
Q

What are the SEs of lamotrigine?

A
  • Nausea and vomiting
  • Skin rashes  Stevens-Johnson syndrome can occur (esp in 1st 8wks)
  • Headache, blurred vision
  • Aggression, irritability
103
Q

What are the contraindications of lamotrigine?

A
  • Caution in myoclonic seizures and Parkinson’s (may be exaggerated)
  • Caution in hepatic and renal failure
104
Q

Which are the most important classes of drugs in the anxiolytic and hypnotic groups?

A
  • benzodiazepines (oxazepam, temazepam, lorazepam, diazepam)
  • Z drugs (zopiclone, zaleplon, zolpidem)
105
Q

Give some e.g. of benzodiazepines. What is the mechanism of action?

A
  • E.g. diazepam and nitrazepam (prolonged action); temazepam and lorazepam (shorter action)
  • Potentiate the action of GABA (the main inhibitory NT in the brain)
  • They bind to specific benzodiazepine receptors on the GABA receptor complex → results in increased affinity of the complex for GAA → increased flow of Cl- into cell → hyperpolarises the post-synaptic membrane and reduces neuronal excitability
106
Q

What are the indications for benzodiazepines?

A
  • Short-term relief of severe anxiety
  • Insomnia (hypnotic effect)
  • Alcohol withdrawal
  • Status epilepticus (diazepam)
  • Premedication before minor surgery
107
Q

What are the SEs of benzodiazepines?

A
  • Drowsiness
  • Paradoxical agitation and aggression
  • Confusion
  • Dependence and tolerance with prolonged use
  • Withdrawal syndrome after prolonged use
108
Q

What are the symptoms of benzodiazepine use? How is this managed?

A
  • Insomnia, anxiety, loss of appetite, weight loss, tremor, sweating, perceptual disturbances
  • Patient should be transferred to equivalent daily dose of diazepam, which is withdrawn gradually
109
Q

What are the contraindications of benzodiazepines?

A
  • Caution in patients with chronic respiratory disease – may cause respiratory depression
  • Severe hepatic impairment (metabolised in liver so accumulation of active metabolites
110
Q

When can benzodiazepine use be fatal? What is the Tx for their overdose?

A
  • Not usually fatal in overdose if taken alone but can be if taken in combination with other sedatives
    • Flumazenil is a benzodiazepine antagonist that can be given as an antidote in overdose
111
Q

What advice should be given to patients when starting benzodiazepines?

A
  • Care with alcohol and other minor tranquilisers (as they enhance sedative effect)
  • Caution with driving and operating machinery (due to drowsiness)
112
Q

Name some Z drugs. What is their mechanism of action?

A
  • E.g. zopiclone, zolpidem, zaleplon
  • Mechanism:
    • Believed to modulate benzodiazepine specific subunit sites (different site on the benzodiazepine receptor), as specific agonists of GABAA receptors
    • Similar to benzos, but slightly more specific
113
Q

What are the indications of Z drugs?

A
  • Short-term treatment of insomnia
114
Q

What are the SEs of Z drugs?

A
  • GI disturbances
  • Headache
  • Tolerance, dependence and withdrawal symptoms
  • Memory disturbances
115
Q

What are the contraindications of Z drugs?

A
  • Obstructive sleep apnoea
  • Caution in patients with chronic respiratory disease – may cause respiratory depression
  • Myasthenia gravis
  • Pregnancy and breastfeeding
  • Alcohol/drug abuse
  • Hepatic/renal impairment
116
Q

When should Z drugs be prescribed?

What is the length of prescription?

What advice should be given to patients?

A
  • Before prescribing hypnotics, alternative methods should be tried, e.g. advice about sleep hygiene
  • Only give short-term (up to 4wks)
  • Caution with driving and operating machinery (due to drowsiness
117
Q

Name some Acetylcholinesterase inhibitors. What are they used to treat? What is their mechanism of action?

A
  • Tx for dementia
  • E.g. donepezil, galantamine, rivastigmine
  • Mechanism: increase the amount of ACh in the brain (by preventing breakdown)
118
Q

What are the indications of Acetylcholinesterase inhibitors?

A
  • Mild-moderate dementia related to Alzheimer’s disease
  • Mild-moderate dementia related to Parkinson’s disease (rivastigmine)
  • May be beneficial in vascular dementia (but evidence is less strong)
119
Q

What are the SEs of Acetylcholinesterase inhibitors?

A
  • GI: nausea, vomiting, gastric and duodenal ulcers, GI haemorrhages
  • CVS: dizziness, syncope, bradycardia, AV heart blocks, MI
  • Psych: hallucinations, agitation
  • Others: rash, muscle cramps
120
Q

What are the contraindications of Acetylcholinesterase inhibitors?

A
  • Renal impairment (galantamine)
  • Caution in cardiac disease and those with susceptibility to peptic ulcers
121
Q

What should be monitored during Acetylcholinesterase inhibitors use? How should their Tx be started?

A
  • Start with the lowest dose and increase gradually, whilst monitoring for SEs
  • Monitor cognition and pulse regularly (at least every 6 months)
  • Review appropriateness in severe dementia (MMSE <10)
122
Q

Name some NMDA receptor antagonists. What is their mechanism of action?

A
  • E.g. memantine
  • Mechanism: reduces excitotoxic damage by blocking NMDA receptors, preventing calcium reflux
    • This is thought to work because excess glutamate (acting on NMDA receptors) leads to excitotoxicity and cell death
      • Appropriate amounts of glutamate facilitates learning and memory; excess glutamate causes excess calcium ion influx leading to excitotoxicity
123
Q

What are the indications of NMDA receptor antagonists?

A
  • Moderate-severe dementia related to Alzheimer’s disease
124
Q

What are the SEs of NMDA receptor antagonists

A
125
Q

What are the contraindications of NMDA receptor antagonists?

A
  • Caution in renal impairment + Hx of seizures
126
Q

Name some drugs to treat overdose and their corresponding overdose drug

A
  • Activated charcoal
    • Very large surface area and can bind drugs when taken orally to stop absorption in the GI tract
    • Must be taken shortly after the overdose
    • Not effective for lithium
  • Acetylcysteine (paracetamol)
  • Methionine (paracetamol)
  • Calcium resonium (may decrease lithium absorption)
  • Flumazenil (benzodiazepines)
  • Naloxone (opioid)
127
Q

What are the indications of ECT?

A
  • Most effective treatment for severe depression
    • Considered if life-threatening poor fluid intake, strong suicidal intent, psychotic features of stupor, when antidepressants are not effective/not tolerated
    • Especially effective in older patients
  • May precipitate manic episode in bipolar patients, but is an effective treatment for established mania
  • Some types of schizophrenia – catatonic states, positive psychotic symptoms and schizoaffective disorder
  • Puerperal psychosis with prominent mood symptoms or severe postnatal depression where rapid improvement is necessary to reunite mother with baby
128
Q

What should be done prior to ECT?

A
  • Patients must have full preoperative work-up, including any necessary Ix (e.g. ECG, U&Es, CXR, anaesthetic assessment)
  • Antiepileptic and benzodiazepines should be discontinued before treatment if possible (as they increase seizure threshold)
129
Q

What are some SEs and complications of ECT?

A
  • Short-term memory loss (esp for events surrounding the ECT)
    • Occasionally causes impaired autobiographical memory
  • Confusion
  • Headache
  • Anaesthetic complications
  • Status epilepticus
    • Prolonged seizures may occur in patients taking drugs that lower seizure threshold (antidepressants, antipsychotics)
130
Q

What are the contraindications of ECT?

A
  • No absolute
  • Relative: anaesthetic risk, raised ICP, risk of cerebral bleeding, heart disease
131
Q

Do advance decisions apply to the MHA?

A
  • Does not apply to treatment under the MHA
132
Q

What are the types of admission to hopsital?

A

MHA applies to any patient with a mental disorder who needs to be detained in hospital

Admission to hosp can be:

  • Informal/voluntary: patient consents and has capacity  this is ideal
  • Under the MCA: patient lacks capacity to consent
  • Under the MHA: either has or doesn’t have capacity to consent (i.e. capacity doesn’t matter)

The MHA sections people → it provides power to admit people to hospital by force

133
Q

Who is involved in a MHA assessment? What are the possible outcomes?

A
  • These are done when somebody might need to sectioned under section 2 or 3
  • 5 people are involved:
    • Patient
    • AMHP
    • Medical recommendation 1 and 2
    • Nearest relative
      • Should be consulted for S2; must be consulted for S3
      • NB this is not next of kin (which you choose yourself) – there is strict guidance on who the NR is
  • Possible outcomes:
    • Section 2
    • Section 3
    • No section (or removal of section if on 5(2)/4/135/136 etc.
134
Q

Who is involved in a MHA assessment? What are the possible outcomes?

A
  • These are done when somebody might need to sectioned under section 2 or 3
  • 5 people are involved:
    • Patient
    • AMHP
    • Medical recommendation 1 and 2
    • Nearest relative
      • Should be consulted for S2; must be consulted for S3
      • NB this is not next of kin (which you choose yourself) – there is strict guidance on who the NR is
  • Possible outcomes:
    • Section 2
    • Section 3
    • No section (or removal of section if on 5(2)/4/135/136 etc.
135
Q

Summarise section 2 of the MHA

A
  • For assessment of a mental disorder
    • Treatment can be given, but once this is the sole objective it must be converted to section 3
  • Used to:
    • Admit patient from community
    • Prevent voluntary patient leaving hospital
    • Following short-term section
    • Requires 2 medical recommendations and the recommendation of an AMHP (described above)
  • Maximum duration: 28d
  • Legal rights:
    • Patient can appeal to MH review tribunal
    • Right to independent MH advocate
136
Q

Summarise section 3 of the MHA

A
  • For treatment of a mental disorder
    • Patient must have a diagnosis, and being must be being treated for an improvement in condition or to prevent deterioration
  • Requires 2 medical recommendations and the recommendation of an AMHP (described above)
    • Also needs the consent of the nearest relative → if they object the section cannot proceed, unless NR is displaced by court hearing
  • Initial duration is 6 months; can be extended by a further 6 months, and then for periods of 1yr at a time
  • Legal rights:
    • Patient can appeal to MH review tribunal
    • Right to independent MH advocate
  • Discharge may be done if:
    • Tribunal decision, manager’s hearing, nearest relative’s decision, or safe for discharge
    • May be transferred to CTO
137
Q

Summarise community treatment orders

A
  • May be used for patients under section 3 (or 37)
  • They allow patients to live in the community, whilst still being subject to the powers of the MHA for the purpose of receiving medical treatment
  • Patients can be recalled to hospital if they do not comply with the terms
  • Lasts 6 months, renewed for 6 months, then 1yr
  • Cannot be used to treat patients with capacity (but terms of CTO may state that patient must comply with treatment  can recall to hospital if they do not comply)
138
Q

Summarise section 5(2) of the MHA

A
  • Doctor’s holding power
  • For patients already in hospital, to stop them leaving
    • Inpatients only (not in A&E or outpatients)
      • May be used on psych wards (if not possible to wait for S2/3) or general wards
    • Requires a recommendation by the responsible clinician or their nominated deputy, who may be a doctor or an approved clinician (often the on-call psychiatric trainee, can be F2 or above)

Maximum duration: 72hrs (during which a full MHA assessment should take place

139
Q

Summarise section 5(4) of the MHA

A
  • Nurses’ holding power (for urgent detention in the absence of a doctor)
  • Lasts for up to 6hrs
140
Q

Summarise section 135

A
  • Police section
  • Warrant to search and remove
  • AMHP applies to Magistrates Court for warrant to enter the property and move an ill patient to a ‘place of safety’ (usually a hospital)
  • Done by police, must be accompanied by AMHP and doctor
  • Maximum duration: 72hrs (during which a full MHA assessment should take place)
141
Q

Summarise section 136

A
  • Police power of arrest
  • Power for police to remove a mentally ill person from a public place to a place of safety
  • Maximum duration: 72hrs (during which a full MHA assessment should take place)
142
Q

Summarise section 4 of the MHA

A
  • Emergency section in the community, requiring only 1 medical recommendation and application by an AMHP
    • Used when waiting for a 2nd doctor would cause too much delay (i.e. waiting for 2nd doctor for S2 would take too long)
    • Up to 72hrs (during which a full MHA assessment should take place)
143
Q

Summarise section 17 of the MHA

A
  • Leave from the hospital for patients detained under the MHA
  • Must be approved by the responsible clinician
144
Q

Summarise Tx under the MHA

A
  • Section 3:
    • Can treat for 3 months without the patient’s consent
    • After 3 months you need a SOAD (second opinion appointed doctor) to agree
      • Also need SOAD for ECT at any time
  • Section 2:
    • Can treat, but is mainly for assessment
    • If treatment becomes the sole objective, section must be converted to S3
  • Other sections (including CTO) do not allow treatment
  • Patients can also be treated under the MCA (if they lack capacity)
145
Q

What is metabolic syndrome/

A
  • obesity,
  • diabetes,
  • HTN, dyslipidaemia