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Psychiatry (Y4) > 5- Psychiatric emergencies > Flashcards

5- Psychiatric emergencies Flashcards

1
Q

name the key psychiatric emergencies

A
  • Neuroleptic malignant syndrome
  • Delirium tremens
  • Wernicke’s
  • Acute dystonia
  • Lithium toxicity
  • Clozapine induced agranulocytosis
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2
Q

antipsychotics are broadly divided into 2 categories

A

first generation
second generation

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3
Q

first generation antipsychotics

A

‘Typicals’
- Dopamine (D2) receptor antagonists.
- Developed in the 1950s.
- Examples include haloperidol, chlorprothixene
- Also exert antagonism on noradrenergic, cholinergic, and histaminergic neurones

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4
Q

second generation

A

‘atypicals’
- serotonin-dopamine receptor antagonists.
- Examples include aripiprazole, risperidone, olanzapine.

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5
Q

why are first gen antipsychotics associated with more side effects

A

Also exert antagonism on noradrenergic, cholinergic, and histaminergic neurons

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6
Q

First-generation antipsychotics are associated with more side-effects that include:

A
  • Extrapyramidal: movement disorders like parkinsonism and dystonia
  • Anti-cholinergic: dry mouth, dry eyes, constipation, urinary retention
  • Anti-histamine: sedating
  • Cardiovascular: prolonged QT interval, arrhythmias
  • Neuroleptic malignant syndrome
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7
Q

second-gen antipsychotics side effects

A
  • have a lower side-effect profile

However, there is still a risk of

  • extrapyramidal side-effects,
  • cardiovascular side-effects (e.g. prolonged QT interval, arrhythmias), and
  • neuroleptic malignant syndrome.
  • Weight gain and metabolic syndrome long-term
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8
Q

neuroleptic malignant syndrome (NMS)

A

is a rare, life-threatening disorder that is associated with the use of antipsychotic drugs (previously known as neuroleptic
medications).
- High mortality

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9
Q

prevalence of NMS

A
  • Up to 3% of those taking antipsychotics
  • Can occur at any age- predominant in young males
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10
Q

aetiology of NMS

A

The exact cause is unknown.
- Seen most commonly with potent first generation antipsychotic (typical antipsychotics)
o Haloperidol
o Fluphenazine
- Can also be precipitated by a sudden dose reduction or withdrawal of antiparkinsonian agents in patients with Parkinson’s disease

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11
Q

pathophysiology of NMS

A
  • Central blockade of dopamine in they hypothalamus leads to hyperthermic and dysautonomia. Blockage of other central pathways give rise to movement disorders
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12
Q

RF for NMS

A
  • High antipsychotic dose/ high potency antipsychotics
  • Concomitant drug use e.g. lithium
  • Depot
  • Medical illness
  • Previous NMS
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13
Q

presentation of NMS

A

Occurs within 2 weeks of starting

  • Altered mental state (confusion)
  • Fever >38 degrees
  • Muscular rigidity
  • Dysautonomia (autonomic instability)
    o Tachycardia,
    o Labile blood pressure
    o Profuse sweating
    o Arrhythmias
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14
Q

Investigations for NMS

A

Requires a low index of suspicion whilst taking antipsychotics

  • Clinical diagnosis
  • Raised creatine kinase (CK) due to muscle rigidity (may be normal if rigidity is not profound
    o Can lead to rhabdomyolysis
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15
Q

complications of NMS

A

cardiac arrest and arrhythmias, AKI, rhabdomyolysis, DIC, VTE

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16
Q

DD for NMS

A
  • Serotonin syndrome: similar presentation to NMS in association with selective serotonin reuptake inhibitor (SSRI) drug use. Characterised by nausea, vomiting, diarrhoea, shivering, hyperreflexia, myoclonus, and ataxia.
  • Malignant hyperthermia: a rare genetic disorder characterised by hyperthermia, muscle rigidity, and dysautonomia in the setting of exposure to certain anaesthetic agents (e.g. succinylcholine) or vigorous exercise.
  • Recreational drug use: both use of MDMA (i.e. ecstasy) and cocaine have been associated with an NMS-like syndrome.
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17
Q

management of NMS

A

Largely supportive. Most episodes resolve within two weeks of removing offending drug
1) Stop causative agent
2) Determine if mild or severe case

Mild cases- supportive care
1) Cardiac monitoring
2) CK and U&Es monitoring
3) IV fluids
4) Antipyretics
5) Cooling blankets for hyperthermia
6) Antihypertensive agents
7) Benzos for agitation

Severe cases- medical therapy
1) Supportive care
2) Dantrolene: ryanodine receptor antagonist (causes skeletal muscle relaxation). Helps treat hyperthermia and rigidity.
3) Bromocriptine: dopamine agonist. Prescribed to restore ‘dopaminergic tone’.

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18
Q

delirium tremens

A
  • Withdrawal delirium due to alcohol withdrawal
  • Only occurs in people with a high alcohol intake for more than a month
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19
Q

aetiology of delirium tremens

A
  • Due to long periods of drinking being stopped abruptly
  • When alcohol use ceases, the unregulated mechanisms result in hyperexcitability of neurons as natural GABAergic systems are down-regulated and excitatory glutamatergic systems are unregulated. This combined with increased noradrenergic activity results in the symptoms of delirium tremens

BASICALLY NOT ENOUGH GABA WHICH IS INHIBITORY

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20
Q

RF for delirium tremens

A
  • Physical illness
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21
Q

presentation of delirium tremens

A
  • cognitive impairment
  • vivid perceptual abnormalities
  • formication – tactile hallucinations e.g. bugs crawling on skin
  • paranoid delusions
  • marked tremor
  • autonomic arousal (e.g. tachy, fever, pupillary dilatation, increased sweating)

Signs- dehydration and electorlytre disturbance

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22
Q

complication of delirium tremens

A

death

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23
Q

investigations ofr DT

A
  • U&Es (electrolyte abnormalities), LFT (liver function tests) and alcoholic hepatitis
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24
Q

management of DT

A
  • large dose of benzodiazepine e.g. lorazepam, chlordiazepoxide until sleeping
  • haloperidol for any psychotic features
  • intravenous pabrinex
    o Contains thiamine (B1), riboflavin (B2), pyridoxine (B6) and nicotinamide, and also benzyl alcohol as a local anaesthetic.
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25
Q

Management

A
26
Q

summarise the course of Wernicke-korsakoff syndrome

A
27
Q

Wernicke-Korsakoff syndrome

A

refers to two distinct neurological syndromes resulting from thiamine (Vitamin B1) deficiency
- Wernicke’s encephalopathy
- Korsakoff syndrome

28
Q

prevalence of WE

A

Lesions associated with WE are found in up to 2.5% of autopsy- majority of which had been alcohol dependent
- Vascular congestion, microglial proliferation and petechial haemorrhage

29
Q

aetiology of WE

A
  • In presence of chronic alcoholism
  • Can also be caused by anorexia nervosa and hyperemesis gravidarum and GI disease

Due to thiamine (B1) deficiency
- Thiamine def leads to neuronal injury

30
Q

causes of thiamine deficiency

A

o Dietary def
o Reduce GI absorption e.g. gastric bypass
o Reduced hepatic uptake
o Impaired utilisation

31
Q

presentation of WE

A

triad of
o Confusion
o Ataxia
o Oculomotor dysfunction (Nystagmus)

32
Q

presentation of korsakoff syndrome

A
  • Chronic amnesic syndrome: Defects in Anterograde and retrograde memory
  • Confabulation: stories made up to fill gaps in memory
  • Poor insight: unaware of heir illness
33
Q

investigations for WE

A
  • Clinical diagnosis normally
  • Cane criteria
    o Dietary def
    o Oculomotor dysfunction
    o Altered mentals status or mild memory impairment
  • Neuroimaging e.g. CT to exclude alternative cause of confusion
34
Q

management of Wernickes

A

Intravenous thiamine e.g. Pabrinex
- Should be give 2-3 pairs up to three times a day for 3-5 days
- Should be administered before or alongside any glucose infusion
- After initial treatment, patients should be given orqal thiamine replacement and continued until patient not at risk
At risk patients
- Pabrinex prophylactically

35
Q

Management of Korsakoff syndrome

A
  • Patients rarely recover
  • no specific treatment
  • May need help with ADL e.g. carers
36
Q

acute dystonia background

A
  • Extrapyramidal side effect
  • An acute medication-induced dystonia- movement disorders characterised by involuntary contractions of muscles, and typically develop within minutes or hours following a trigger such as a medication.
37
Q

aetiology of acute dystonia

A

Adverse effect of antidopaminergic agents - EXTRAPYRAMIDAL
o Antiemetics e.g. metoclopramide
o Antipsychotics e.g. haloperidol and chlorpromazine

38
Q

presentation of acute dystonia

A

Extrapyramidal side effect within a few days of taking medication
o Onset of atypical posture or position of muscles within minutes or hours of taking medications
o Ocular muscles, jaw, tongue, face, neck and trunk of the body

39
Q

investigayions for acute dystonia

A
  • Medication history
  • Neuromuscular testing to examine
    o Range of motion
    o Breathing ability
    o Swallowing
    o Speech
  • Vaccine history
    o Tetanus
  • Bloods
    o ABG (rule out hyperventilation)
    o U&Es
     Hypomagnesemia
     Calcium
     Ceruloplasmin
     Wilsons disease
40
Q

management of acute dystonia

A
  • Procyclidine hydrochloride can be given parenterally and is effective emergency treatment for acute drug-induced dystonic reactions.
  • If treatment with an antimuscarinic is ineffective, intravenous diazepam can be given for life-threatening acute drug-induced dystonic reactions.
41
Q

lithium toxicity background

A

Lithium is the standard long-term therapy in bipolar affective disorder. It minimizes the risk of relapse and improves quality of life.

however can cause toxicity if used improperly

42
Q

how is lithium toxicity prevented

A
  • Contraindicated in:
    o Arrythmia
    o Renal impairment
    o Hypothyroidism (untreated)
    o Low sodium
    o Diabetes insipidus
    o Addison’s
  • Regular testing of lithium levels
43
Q

aetiology of lithium toxicity

A
  • Due to excessive intake (suicidal or accidental) or decreased excretion (dehydration- vomiting and diarrhoea, low sodium diet or kidney problems
44
Q

adverse reactions to lithium

A
  • initial: nausea, diarrhoea, vertigo, muscle weakness and dazed feeling
  • polydipsia/ polyuria
  • oedema
  • teratogenicity
  • hypothyroidisms
  • hyperthyroidism
  • hyperparathyroidism
    o high calcium
  • nephrotoxicity
45
Q

how is lithium prescribed to prevent toxicity

A
  • Before lithium is started: UEs, TFTs, pregnancy status, ECG
  • Due to its side effect profile and risk of toxicity lithium is strictly regulated:
46
Q

describe the measuring of lithium levles

A

o Lithium levels – 12 hours following first dose, then weekly until therapeutic level (0.5–1.0 mmol/L) has been stable for 4 weeks. Once stable check every 3 months.
o U&Es – every 6 months; TFTs – every 12 months.

47
Q

investigations/presentation of sign of toxicity

A

1.5–2.0 mmol/L: N+V, coarse tremor, ataxia, muscle weakness, apathy.

48
Q

investigations/presentation of severe toxicity

A

> 2.0 mmol/L : nystagmus, dysarthria, hyperreflexia, oliguria, hypotension, convulsions and coma

49
Q

management of lithium toxicity

A

Supportive treatment should be initiated, which includes correction of fluid and electrolyte balance.**

50
Q

Clozapine induced agranulocytosis

A
  • Antipsychotic used to treatment resistant Schizophrenia.
  • Decreases neutrophil count and susceptibility to infection.
  • Very effective antipsychotic but huge potential for side effects.
  • Doesn’t cause extrapyramidal side effects
51
Q

prevalence of clozapine induced agranulocytosis

A
  • 0.8% of patients on clozapine
52
Q

prevention and investgiations for agranuloytosis

A
53
Q

presentation of agranulocytosis

A

Occurs most frequently in the first 18 weeks of treatment
- Fever
- Sore mouth
- Sore throat
- infection

54
Q

management of Clozapine induced agranulocytosis

A

BEWARE if a patient stops smoking then amount of clozapine will need decreasing

55
Q

manageging neutropenia

A

give granulocyte colony-stimulating factor (G-CSF)

56
Q

which drug causes neuroleptic malignnat sydnrome

A

antipsychotivc drugs

57
Q

which drug causes delirium tremens

A

alcohol withdrawal

58
Q

what causes Wernicke-Korsakoff syndrome

A

B1 deficiency- thiamine def

  • give pabrinex- mix of B vitamins including B1
59
Q

which drugs cause acute dystonia

A

antidopaminergic agents e.g. metoclopramide and haloperidol

60
Q

whicch drug can induce agranulocytosis

A

clozapine

61
Q

which drug is associated with toxicity

A

lithium

62
Q

which drugs can cause seratonin sydnrome

A

SSRIs

Psychiatry (Y4) (15 decks)

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