Passmedicine Psychiatry Flashcards

1
Q

What is acute stress disorder?

A

Acute stress disorder is defined as an acute stress reaction that occurs in the first 4 weeks after a person has been exposed to a traumatic event (threatened death, serious injury e.g. road traffic accident, sexual assault etc).

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2
Q

Acute stress disorder features?

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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3
Q

Acute stress disorder management?

A

trauma-focused cognitive-behavioural therapy (CBT) is usually used first-line
benzodiazepines
sometimes used for acute symptoms e.g. agitation, sleep disturbance
should only be used with caution due to addictive potential and concerns that they may be detrimental to adaptation`

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4
Q

Mode of action: Chronic alcohol consumption & alcohol withdrawal

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)

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5
Q

Alcohol withdrawals features and timeline?

A

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

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6
Q

Alcohol withdrawal management?

A

patients with 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. Typically given as part of a reducing dose protocol
carbamazepine also effective in treatment of alcohol withdrawal
phenytoin is said not to be as effective in the treatment of alcohol withdrawal seizures

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7
Q

What must be given to patients undergoing alcohol withdrawal in the inpatient setting?

A

This patient will be undergoing assisted alcohol withdrawal in the inpatient setting, and as such will require prophylaxis of Wernicke’s encephalopathy also (IM B vitamin)

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8
Q

Disulfiram mechanism of action?

A

Disulfiram (also known as Antabuse) is an irreversible inhibitor of acetaldehyde dehydrogenase. This inhibition causes the buildup of acetaldehyde. The build-up of acetaldehyde within twenty to thirty minutes of alcohol consumption results in unpleasant symptoms, including facial flushing and nausea and vomiting. The reaction can be life-threatening, so disulfiram is not recommended for patients with underlying frailty, neurological, cardiac or hepatic conditions.

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9
Q

Acamprosate mechanism of action?

A

Acamprosate (or Campral) is taken three times a day and has shown to be effective in preventing alcohol relapse in combination with psychological support following detoxification in alcohol dependence syndrome. It is typically described as an ‘anti-craving’ medication and the underlying mechanism of action remains unclear

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10
Q

Buprenorphine mechanism of action

A

Buprenorphine is a mixed opioid agonist/antagonist. It is typically given as a sublingual tablet and provides an alternative opiate replacement therapy to methadone. Patient’s often describe buprenorphine as less sedating, which can be a benefit or drawback depending on the context and patient. Prescribers must also be aware that because of the opioid antagonist properties of methadone it can render regularly prescribed analgesia, such as co-codamol, ineffective

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11
Q

Assessment tool for alcohol withdrawal severity?

A

The revised Clinical Institute Withdrawal Assessment for Alcohol (CIWA) scale can be used to assess alcohol withdrawal severity

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12
Q

Diagnosis criteria anorexia nervosa

A

Diagnosis is now based on the DSM 5 criteria. Note that BMI and amenorrhoea are no longer specifically mentioned:
1. Restriction of energy intake relative to requirements leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health.
2. Intense fear of gaining weight or becoming fat, even though underweight.
3. Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or denial of the seriousness of the current low body weight.

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12
Q

Anorexia nervosa epidemiology

A

Epidemiology
90% of patients are female
predominately affects teenage and young-adult females
prevalence of between 1:100 and 1:200

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13
Q

Anorexia nervosa management

A

For adults with anorexia nervosa, NICE recommend we consider one of:
individual eating-disorder-focused cognitive behavioural therapy (CBT-ED)
Maudsley Anorexia Nervosa Treatment for Adults (MANTRA)
specialist supportive clinical management (SSCM).

In children and young people, NICE recommend ‘anorexia focused family therapy’ as the first-line treatment. The second-line treatment is cognitive behavioural therapy.

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14
Q

Anorexia nervosa prognosis

A

The prognosis of patients with anorexia nervosa remains poor. Up to 10% of patients will eventually die because of the disorder.

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15
Q

Anorexia nervosa biochemical features trend?

A

Anorexia features
most things low
G’s and C’s raised: growth hormone, glucose, salivary glands, cortisol, cholesterol, carotinaemia

15
Q

Anorexia nervosa features

A

reduced body mass index
bradycardia
hypotension
enlarged salivary glands

16
Q

Anorexia nervosa biochemical features

A

hypokalaemia
low FSH, LH, oestrogens and testosterone
raised cortisol and growth hormone
impaired glucose tolerance
hypercholesterolaemia
hypercarotinaemia
low T3

17
Q

What is a physical finding in anorexia nervosa patients?

A

Physical findings characteristic of lanugo hair (fine downy hair growth in response to the loss of body fat) may support the diagnosis of anorexia nervosa.

This should be considered with other features of anorexia nervosa e.g. failure of secondary sexual characteristics, bradycardia, cold-intolerance and yellow tinge on the skin (hypercarotenaemia)

18
Q

Typical antipsychotics mode of action?

A

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

19
Q

Typical antipsychotics side effects?

A

Extrapyramidal side-effects and hyperprolactinaemia common

20
Q

Examples of typical antipsychotics?

A

Haloperidol
Chlopromazine

21
Q

Atypical antipsychotics mode of action?

A

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

21
Q

Atypical antipsychotics S/E?

A

Extrapyramidal side-effects and hyperprolactinaemia less common
Metabolic effects

22
Q

Examples of atypical antipsychotics?

A

Clozapine
Risperidone
Olanzapine

22
Q

What are examples of EPSEs?

A

Extrapyramidal side-effects (EPSEs)
Parkinsonism

acute dystonia
sustained muscle contraction (e.g. torticollis, oculogyric crisis)
may be managed with procyclidine

akathisia (severe restlessness)

tardive dyskinesia (late onset of choreoathetoid movements, abnormal, involuntary, may occur in 40% of patients, may be irreversible, most common is chewing and pouting of jaw)

23
Q

Why are there specific warnings for antipsychotics in elderly?

A

increased risk of stroke
increased risk of venous thromboembolism

24
Q

Other side effects of antipsychotics?

A

antimuscarinic: dry mouth, blurred vision, urinary retention, constipation
sedation, weight gain
raised prolactin
may result in galactorrhoea
due to inhibition of the dopaminergic tuberoinfundibular pathway
impaired glucose tolerance
neuroleptic malignant syndrome: pyrexia, muscle stiffness
reduced seizure threshold (greater with atypicals)
prolonged QT interval (particularly haloperidol)

25
Q

What is used to treat tardive dyskinesia?

A

Tetrabenazine may be used to treat moderate/severe tardive dyskinesia

26
Q

What to do if clozapine is missed in 48 hours and why?

A

If doses are missed for more than 2 consecutive days (48 hours), you will need to restart their clozapine slowly (like when they first started on it). This restart of treatment needs to be under the direction of a Psychiatrist. This is because when you start Clozapine after a break of >48 hours, it can make side effects worse, such as blood pressure changes, drowsiness and dizziness. If there is a gap in treatment of 3 days (72 hours) then you may also require more frequent blood tests for a short period.

27
Q

Clozapine S/E?

A

Clozapine is an effective medication but carries a number of serious side effects which you must be aware of: agranulocytosis, neutropenia, reduced seizure threshold, and myocarditis.

28
Q

Clozapine monitoring: FBC

A

Monitor leucocyte and differential blood counts. Clozapine requires differential white blood cell monitoring weekly for 18 weeks, then fortnightly for up to one year, and then monthly as part of the clozapine patient monitoring service.

29
Q

Clozapine monitoring: Weight and lipids

A

Blood lipids and weight should be measured at baseline, at 3 months (weight should be measured at frequent intervals during the first 3 months), and then yearly with antipsychotics. Patients taking clozapine require more frequent monitoring of these parameters: every 3 months for the first year, then yearly.

30
Q

Clozapine monitoring: FBG

A

Fasting blood glucose should be measured at baseline, at 4–6 months, and then yearly. Patients taking clozapine should have fasting blood glucose tested at baseline, after one months’ treatment, then every 4–6 months.

31
Q
A