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PSYCHIATRY > PPT - PSYCHOSIS, DEMENTIA, INSOMNIA, ALCOHOL, DRUGS, ADHD, ACUTE BEHAVIOURAL DISTUBANCES > Flashcards

PPT - PSYCHOSIS, DEMENTIA, INSOMNIA, ALCOHOL, DRUGS, ADHD, ACUTE BEHAVIOURAL DISTUBANCES Flashcards

1
Q

What are indications of antipsychotics?

A

Schizophrenia
Schizoaffective disorder
Delusional disorder
Depression or mania with psychotic features
Psychotic episodes secondary to a medical condition or psychoactive substance use
Delirium
Behavioural disturbance in dementia
Severe agitation, anxiety and violent or impulsive behaviour
Motor tics
Nausea and vomiting
Intractable hiccups

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2
Q

Why were atypical antipsychotics developed?

A

Because of the problematic EPS associated with first generation of typical antipsychotics

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3
Q

What are examples of typical antipsychotics?

A

Chlorpromazine
Flupentixol
Haloperidol
Levopromazine
Pericyazine
Perphenazine
Prochlorperazine

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4
Q

What are examples of atypical antipsychotics?

A

Aripiprazole
Clozapine
Risperidone
Quetiapine
Olanzapine
Ziprasidone

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5
Q

Whats the moa of typical antipsychotics?

A

D2 receptor antagonists blocking dopaminergic transmission in the mesolimbic pathway

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6
Q

Why do typical antipsychotics cause so many side effects?

A

They block dopamine receptors in entire brain
They can also block muscarinic, histaminergic and alpha adrenergic receptors

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7
Q

Whats the clinical effect of dopamine D2 receptor antagonism in the mesolimbic pathway?

A

Treatment of positive psychotic symptoms

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8
Q

Whats the clinical effect of dopamine D2 receptor antagonism in the mesocortical pathway?

A

Worsening of negative and cognitive symptoms of schizophrenia

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9
Q

Whats the clinical effect of dopamine D2 receptor antagonism in the nigrostriatal pathway?

A

Extrapyramidal side effects e.g. parkinsonian symptoms, acute dystonia, akathisia, tardive dyskinesia, NMS

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10
Q

Whats the clinical effect of dopamine D2 receptor antagonism in the tuberoinfundibular pathway?

A

Hyperprolactinaemia
- galactorrhoea
- amenorrhoea and infertility
- sexual dysfunction

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11
Q

Whats the clinical effect of dopamine D2 receptor antagonism in the CTZ?

A

Anti-emetic effect

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12
Q

What are anticholinergic side effects of typical antipsychotics?

A

Dry mouth
Constipation
Urinary retention
Blurred vision

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13
Q

What are alpha-adrenergic receptor blockade side effects of typical antipsychotics?

A

Postural hypotension

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14
Q

What are histaminergic receptor blockade side effects of typical antipsychotics?

A

Sedation
Weight gain

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15
Q

What are cardiac side effects of typical antipsychotics?

A

QTc prolongation, arrhythmias, myocarditis and sudden death

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16
Q

What are dermatological side effects of typical antipsychotics?

A

Photosensitivity
Skin rashes

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17
Q

What causes extrapyramidal side effects in antipsychotics?

A

A relative deficiency of dopamine and an excess of ACh induced by dopamine antagonism in the nigrostriatal pathway

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18
Q

What are the extrapyramidal side effects?

A

Parkinsonian symptms
Acute dystonia
Akathisia
Tardive dyskinesia
Neuroleptic malignant syndrome

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19
Q

Why is clozapine only used in treatment-resistant cases of schizophrenia?

A

Due to the life-threatening risk of bone marrow suppression with agranulocytosis
And it lowers the seizure threshold

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20
Q

Whats the concern with antipsychotic use in elderly patients?

A

Increased risk of stroke
Increased risk of venous thromboembolism
Particularly susceptible to postural hypotension

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21
Q

What important adverse effects can atypical antipsychotic causes?

A

Weight gain
Glucose intolerance
Hyperlipidaemia

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22
Q

Whats the moa of atypical antipsychotics?

A

D1, D2, D4 and 5-HT2 receptor antagonists
D2 antagonist potency is low

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23
Q

What are the benefits of atypical antipsychotics?

A

Reduce positive and negative symptoms (typical antipsychotics may not affect or may worsen negative symptoms)
Lowered risk of EPS and hyperprolactinaemia due to weaker D2 blockade

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24
Q

Why does clozapine have to be monitored differently if you are a smoker?

A

Cigarette smoke causes the body to metabolise clozapine faster than usual due to inducing CYP activity so you will need a higher dose to achieve the same benefit as a non-smoker

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25
Q

What are the recommendations when prescribing antipsychotics to the elderly?

A

Antipsychotic drugs should not be used in elderly patients with dementia, unless they are at risk of harming themselves or others, or experiencing agitation, hallucinations or delusions that are causing them severe distress.
The lowest effective dose should be used for the shortest period of time.
Treatment should be reviewed regularly; at least every 6 weeks

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26
Q

How can you manage hyperprolactinaemia from antipsychotics?

A

Give low dose treatment with aripiprazole (reduces prolactin concentration because its a dopamine-receptor partial agonist)

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27
Q

What are the clinical symptoms of hyperprolactinaemia?

A

sexual dysfunction, reduced bone mineral density, menstrual disturbances, breast enlargement, galactorrhoea, and a possible increased risk of breast cancer.

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28
Q

Why does sexual dysfunction occur with all antipsychotic medications?

A

Reduced dopamine transmission and hyperprolactinaemia decrease libido; antimuscarinic effects can cause disorders of arousal; and alpha1-adrenoceptor antagonists are associated with erection and ejaculation problems in men.

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29
Q

Which antipsychotic has a particular risk of QTc prolongation?

A

Pimozide

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30
Q

Which antipsychotics are most likely to cause postural hypotension?

A

Clozapine and quetiapine

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31
Q

Which antipsychotics most commonly cause weight gain?

A

Clozapine and olanzapine

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32
Q

Whats the monitoring required for antipsychotics?

A

Weight should be measured at the start of therapy with antipsychotic drugs, then weekly for the first 6 weeks, then at 12 weeks, at 1 year, and then yearly.

Fasting blood glucose, HbA1c, and blood lipid concentrations should be measured at baseline, at 12 weeks, at 1 year, and then yearly. Prolactin concentrations should also be measured at baseline.

Before initiating antipsychotic drugs, an ECG may be required, particularly if physical examination identifies cardiovascular risk factors (e.g. high blood pressure), if there is a personal history of cardiovascular disease, or if the patient is being admitted as an inpatient.

Blood pressure monitoring is advised before starting therapy, at 12 weeks, at 1 year and then yearly during treatment and dose titration of antipsychotic drugs.

Expert sources advise to monitor full blood count, urea and electrolytes, and liver function tests at the start of therapy with antipsychotic drugs, and then yearly thereafter.

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33
Q

Outline the timeline for EPS?

A

3 hrs - Acute Dystonia
3 days – weeks - Bradykinesia
3 months - Akathisia
3 years - Tardive dyskinesia

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34
Q

What pharmacological treatment can be offered to manage dementia?

A

Acetylcholinesterase inhibitors
Memantine

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35
Q

What are examples of acetylcholinesterase inhibitors?

A

Donepezil
Galantamine
Rivastigmine

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36
Q

Whats the moa of acetylcholinesterase inhibitors?

A

inhibit the cholinesterase enzyme from breaking down ACh, increasing both the level and duration of the neurotransmitter action.
It’s known that in pt with dementia, there are lower levels of acetylcholine

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37
Q

What are the indications for acetylcholinesterase inhibitors?

A

Mild tho moderate dementia in Alzheimer’s disease

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38
Q

Whats the moa of memantine?

A

An uncompetitive NMDA receptor antagonist that prevents glutamates action on the receptor
Continuous activation of NMDA receptors in CNS by glutamate is thought to cause some alzheimers symptoms

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39
Q

Who is memantine indicated in?

A

Second line teatment for Alzheimer’s:
- moderate Alzheimer’s who are intolerant of, or have a contraindication to, acetylcholinesterase inhibitors
- as an add-on drug to acetylcholinesterase inhibitors for patients with moderate or severe Alzheimer’s
- monotherapy in severe Alzheimer’s

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40
Q

What are AChE inhibitors and memantine often used for unlicensed?

A

Mild to moderate or severe dementia with Lewy bodies - donepezil or rivastigmine
Vascular dementia if comorbid Alzheimer’s disease, Parkinson’s disease dementia or dementia with Lewy bodies

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41
Q

Which types of dementia should not be offered AChE inhibitors or memantine?

A

Frontotemporal dementia

42
Q

What are non cognitive symptoms associated with dementia?

A

Psychosis
Mood disturbances
Personality changes
Agitation
Aggression
Altered sexual behaviours
Changed sleep patterns
Appetite disturbance

43
Q

How are non cognitive symptoms of dementia treated?

A

Antipsychotics risperidone and haloperidol

(Only initiated under specialist supervision)

44
Q

How do we manage pt with aggressive or challenging behaviour whos a threat to themselves or others’ safety?

A
  1. Use restrictive interventions
  2. Manual restraint, rapid tranquilisation, seclusion or mechanical restraint in high-secure settings for extreme behaviour
45
Q

Whats the NICE reccomendation for rapid tranquilisation?

A

First line - IM lorazepam
IM haloperidol + promethazine

46
Q

When should IM lorazepam be chosen for rapid tranquilisation?

A

If there is insufficient information to guide the choice of medication for rapid tranquillisation, or the service user has not taken antipsychotic medication before
f there is evidence of cardiovascular disease, including a prolonged QTc, or no ECG has been carried out

47
Q

What are the risks of rapid tranquilisation with benzos?

A

Loss of conciousness
Respiratory depression or arrest
Cardiovascular collapse
Disinhibition

48
Q

What are the risks of rapid tranquilisation with antipsychotics?

A

Loss of conciousness
Cardiovascular or resp complications and collapse
Seizures
Akathisia
Dystonia
Dyskinesia
NMS
Excessive sedation

49
Q

How do you monitor someone undergoing rapid tranquilisation?

A

Monitor temp, pulse, bp, hydration, level of conciousness, resp rate every 15 mins for at least 1 hour
Pt must remain under within eyesight observation until they are fully ambulatory again
ECG and haematological monitoring are strongly recommended for when antipsychotics are given

50
Q

What drugs should be offered to a person in acute alcohol withdrawal?

A

Chlordiazepoxide short term treatment for detoxification
thiamine if risk of wernickes encephalopathy

51
Q

Why is chlordiazepoxide the benzo of choice for managing alcohol withdrawal?

A

Because it has a long half life (6-3o hours)

52
Q

Whats the moa of Chlordiazepoxide used for alcohol dependance?

A

Benzodiazepines are cross-tolerant with alcohol and modulate anxiolysis by stimulating GABA-A receptors [24]. During withdrawal from one agent, the other may serve as a substitute. They are proven to reduce withdrawal severity and incidence of both seizures and delirium tremens

53
Q

How do we mange delirium terms?

A

Oral lorazepam first line

54
Q

How do we manage alcohol withdrawal seizures?

A

Quick acting benzos e.g. lorazepam

55
Q

How do we manage wernickes encephalopathy?

A

Prophylactic oral thiamine to harmful or dependant drinkers
Parenteral thiamine if suspected wernickes for a minimum of 5 days. Followed by oral thiamine treatment

56
Q

What drugs can be used to abstain from alcohol?

A

Disulfiram
Acamprosate
Naltrexone

57
Q

When is Disulfiram used?

A

Once the patient is abstinent from alcohol

58
Q

Whats the moa of Disulfiram?

A

It inhibits aldehyde dehydrogenase which leads to an accumulation of acetylaldehyde which causes unpleasant effects within 20 mins of drinking alcohol- nausea, vomiting, headaches flushing, palpitations, hypotension
Consumption of large amounts of alcohol can lead to collapse and death. Fear of this is an important aspect of its efficacy

59
Q

What should be patients be warned about when on Disulfiram

A

Patients should be aware that even small amounts of alcohol (e.g. In perfumes, foods, mouthwashes) can produce severe symptoms.

60
Q

What are contraindications of Disulfiram?

A

Cardiac failure; coronary artery disease; history of cerebrovascular accident; hypertension; psychosis; severe personality disorder; suicide risk

61
Q

Whats the purpose of acamprosate?

A

Improves rates of abistince as it reduces cravings and the urge to drink

62
Q

Whats the moa of acamprosate?

A

Its mechanism of action is uncertain, but the drug is thought to interact weakly with NMDA receptors and so enhances GABA transmission

63
Q

What are the indications of naltrexone?

A

Adjunct to prevent relapse in formerly alcohol-dependent patients

Adjunct to prevent relapse in formerly opioid-dependent patients

64
Q

What are contraindications for naltrexone?

A

Those currently on opioids

65
Q

What drugs can be given as opioid substitution therapy?

A

Methadone or Buprenorphine

66
Q

Whats the moa of methadone?

A

a synthetic opioid analgesic with full agonist activity at the µ-opioid receptor.

67
Q

Whats the moa of Buprenorphine?

A

a partial agonist at the mu-opioid receptor and an antagonist at the kappa-opioid receptor
It demonstrates a high affinity for the mu-opioid receptor but has lower intrinsic activity compared to other full mu-opioid agonists. This means that buprenorphine preferentially binds the opioid receptor and displaces lower affinity opioids without activating the receptor to a comparable degree

68
Q

What are the actions of opioid substitution therapy?

A

Suppresses cravings and withdrawal symptoms
Blocks the acute effects of other opioids

This prevents antisocial behaviours and allows the person to return to a productive lifestyle and address problems.

69
Q

What are the benefits of Buprenorphine?

A

Ceiling effects - once a certain dose is reached buprenorphine’s effects plateau.
dose-related side effects such as respiratory depression, sedation, and intoxication also plateau, resulting in a lower risk of overdose compared to full agonist opioids.
It also means that opioid-dependent patients do not experience sedation or euphoria at the same rate that they might experience with more potent opioids, reducing the reinforcing effects of opioids which can lead to drug-seeking behaviours

70
Q

Whats the moa of naltrexone?

A

Competes for opiate receptors and displaces opioid drugs from these receptors, thus reversing their effects

71
Q

What drugs can be used for nicotine dependancE?

A

Nicotine-replacement therapy
Bupropion
Varenicline

72
Q

Whats the moa of bupropion?

A

thought to confer its anti-craving and anti-withdrawal effects by inhibiting dopamine reuptake, which is thought to be involved in the reward pathways associated with nicotine, and through the antagonism of the nicotinic acetylcholinergic receptor (AChR), thereby blunting the effects of nicotine

73
Q

Whats the moa of varenicline?

A

an alpha-4 beta-2 neuronal nicotinic acetylcholine receptor partial agonist. The drug exerts mild agonistic activity at this site, though at a level much lower than nicotine; it is presumed that this activation eases withdrawal symptoms.

74
Q

What drug is used as an antidote for opioids?

A

Naloxone

75
Q

Whats the moa of naloxone?

A

competitive inhibitor of the µ-opioid receptor. Naloxone antagonizes the action of opioids, reversing their effects

76
Q

What happens if you use naloxone on someone who has not taken opioids?

A

No significant effect

77
Q

Whats the antidote for TCA poisoning ?

A

Sodium bicarbonate

78
Q

Whats the antidote for benzo poisoning?

A

Flumazenil

79
Q

Whats the antidote for methanol or ethylene glycol poisoning?

A

Fomepizol

80
Q

If you dont know whether a pt is suffering a benzo or opioid overdose what should you use as an antidote?

A

Naloxone - if it has no effect its likely benzos
Dont try flumezanil as it can be dangerous if the pt has taken other drugs i.e. mixed drug overdose

81
Q

Whats the moa of flumezanil?

A

It competitively inhibits the activity of benzodiazepine and non-benzodiazepine substances that interact with benzodiazepine receptors site on the GABA/benzodiazepine receptor complex. It can also reverse the binding of benzodiazepines to benzodiazepine receptors.

82
Q

Whats the moa of fomepizol?

A

a competitive inhibitor of alcohol dehydrogenase, the enzyme that catalyzes the initial steps in the metabolism of ethylene glycol and methanol to their toxic metabolites

83
Q

What drugs can be offered to manage ADHD in children??

A

Methylphenidate first line
Lisdexamfetamine, dexamfetamine and atomoxetine second line

84
Q

What medications can be offered to adults with ADHD?

A

Lisdexamfetamine or methylphenidate are usually offered first line

85
Q

What are the main risks with methylphenidate and lisdexamfetamine?

A

Cardiotoxicity
Perform a baseline ECG before starting treatment

86
Q

When are hypnotic drugs offered for insomnia?

A

When daytime impairment is severe

87
Q

What are the adverse effects of hypnotic drugs for short term insomnia use?

A

Daytime sedation
Poor motor coordination
Cognitive impairment
Concerns about accidents and injuries
Tolerance!!

88
Q

Whats the guidance on using hypnotics?

A

The hypnotics recommended for treating insomnia are 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. You should make the patient aware that repeat prescriptions are not usually given.
It is important to review after 2 weeks and consider referral for cognitive behavioural therapy (CBT).

89
Q

How is narcolepsy managed pharmacologically?

A

Daytime stimulants e.g. modafinil
Nighttime sodium oxybate (known as GHB)

90
Q

Whats the moa of sodium oxybate for managing narcolepsy?

A

It’s a metabolite of GABA = GABA_B receptor agonist activity

91
Q

Whats the moa of modafinil?

A

inhibit the reuptake of dopamine by binding to the dopamine reuptake pump, and lead to an increase in extracellular dopamine. Modafinil activates glutamatergic circuits while inhibiting GABA.

92
Q

How is long term insomnia managed?

A

Pharmacological therapy should be avoided but if severe symptoms or an acute exacerbation, a short course of a hypnotic drug <1 week may be considered as a temp adjunct to behavioural and cognitive treatment

If over 55 with persistent insomnia, modified0release melatonin may be offered

93
Q

How can sleep paralysis be managed pharmacologically?

A

If troublesome clonazepam may be used

94
Q

Whats the management for obstructive sleep apnoea?

A

◦ lifestyle changes - lose weight, stop smoking, reduce alcohol, avoid sedatives, goos sleeping habits
◦ Continuous positive airway pressure (CPAP)
◦ Mandibular advancement device
◦ Surgery

95
Q

Whats used in the management of patients following intoxication with benzos?

A

Flumazenil

96
Q

What is used to manage intoxication with amphetamines or cocaine?

A

Benzos

97
Q

Whats used in the management of cocaine intox?

A

Alpha blockers

98
Q

Whats used in a paracetamol overdose?

A

Activated charcoal if ingested <1 hour ago
N-acetylcysteine (helps replenish levels of glutathione and therefore helps metabolise paracetemol)
Liver transplant

99
Q

How do we manage TCA overdose?

A

IV bicarbonate may reduce risk of seizures and arrhythmias in severe toxicity
Bolus IV fluids to treat the hypotension

100
Q

How do we manage lithium toxicity:?

A

Volume rescuscitstin with normal saline or haemodialysis in severe cases

101
Q

How do we manage warfarin overdose?

A

Vitamin K
Prothrombin complex

102
Q

How do we manage heparin overdose?

A

Protamine sulphate

PSYCHIATRY (20 decks)

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