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BSMS308 > 1. Drugs for psych disorders > Flashcards

1. Drugs for psych disorders Flashcards

1
Q

Main classes of psych drugs

A 
Antidepressants
Anxiolytics
Mood stabilisers
Antipsychotics
Hypnotics
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2
Q

SSRI examples

A 
Fluoxetine
Paroxetine
Sertraline
Citalopram
Escitalopram
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3
Q

SSRI indications

A 
Depression
Anxiety disorders
Panic disorder
OCD
PTSD
other
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4
Q

SSRI similarities

A 
Indications
Mechanism of action
Delayed onset of action (10-14 days)
Efficacy
Relative safety in overdose
Advisability of prolonged course e.g. 6 months in major depression
Interactions
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5
Q

SSRI differences

A

Half-life:
shortest is paroxetine (20 hours)
longest in fluoxetine (2-4 days, w active metabolite half life of 14 days)

Propensity to cause discontinuation syndrome if stopped abruptly

Side effect profiles: fluoxetine causes agitation most commonly

Individual differences: people are different

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6
Q

SSRI mechanism of action

A

Blocks 5-HT (serotonin) re-uptake transporter and so keeps 5-HT in the synaptic cleft to prolong its action

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7
Q

SSRI discontinuation syndrome

A

SSRI discontinuation syndrome happens when SSRIs are stopped, especially if they are stopped abruptly

Commonest with paroxetine

Symptoms: agitation and anxiety, dizziness, balance problems, nausea and diarrhoea, flu-like symptoms

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8
Q

How to treat SSRI discontinuation syndrome

A

Reassurance and monitoring
Reintroducing drug with a tapered withdrawal
Consider an alternative antidepressant or anxiolytic

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9
Q

Tricyclic antidepressants examples

A

Amitriptyline
Imipraine
Lofepramine
Dothiepin

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10
Q

TCA indications

A

similar to SSRIs (depression, anxiety, OCD, panic disorder, PTSD) although not used as widely outside of depression. Efficacy in major depression similar to SSRIs

Rarely used first-line nowadays due to adverse effects and overdose risk

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11
Q

TCA mechanism of action

A

Bind to noradrenaline (NA) and 5HT reuptake inhibitors which increases monoamine levels in synaptic cleft, increasing their action
Also pronounced anticholinergic/antimuscarinic effects

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12
Q

What is notable about different TCAs?

A

They have widely varying specific affinities between different compounds so have different properties. This can be clinically relevant as you can prescribe them depending on the effect you want e.g. if you want sedative effects prescribe amitriptyline or dothiepin

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13
Q

TCA adverse effects

A

Two types - anticholinergic and other

Anticholinergic - dry mouth, constipation, urinary retention, cognitive effects

Other: psychotropic effects e.g. agitation, nightmares; sexual dysfunction e.g. ED; akathisia (restlessness), muscle twitches, cardiac arrhythmias

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14
Q

TCA overdose

A

neurological and cardiovascular effects:

neuro: mydriasis, confusion, seizures, coma,
cardio: tachycardia and other arrhythmias, hypotension, cardiorespiratory arrest

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15
Q

Are TCAs or SSRIs more dangerous in overdose?

A

TCAs! almost 17 times as much

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16
Q

Venlafaxine

A

Serotonin and noradrenaline reuptake inhibitor (SNRI) antidepressant
Appears to have a more pronounced dose-response effect than other antidepressants.

Might be mildly useful for anxiety and depression

Side effects: headache, nausea, hypertension, discontinuation syndrome

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17
Q

Duloxetine

A

SNRI, without concerns re hypertension

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18
Q

Moclobemide

A

monoamine oxidase inhibitor (RIMA)- usually reserved for treatment resistant depression or atypical depression

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19
Q

Reboxetine

A

highly selective NA reuptake inhibitor

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20
Q

MAOIs

A

Inhibits monoamine oxidase which breaks down 5-HT, DA and NA, so preserves them

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21
Q

MAOIs interactions - non-drug

A

A lot of foods - most cheeses, red wine, yeast production liver, broad bean pods, fermented sausages, salami etc
Tyramine

Hypertensive effect -> hypertensive crisis
Moclobamide is much lower risk of causing hypertensive crisis

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22
Q

MAOI drug interactions

A

DO NOT COMBINE WITH SSRI because will get serotonin syndrome

Adrenaline and noradrenaline

L-DOPA

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23
Q

Mirtazapine

A

NaSSA - noradrenergic and specific serotonergic antidepressant

Acts as an antagonist at alpha 2 receptors so cuts the brake cable on serotonin and noradrenaline release

24
Q

Mild depression

A

no pharmacology, psychological measures/reassurance

25
Moderate depression
Select antidepressant - SSRI and consider side effects If full response -> continuation therapy If incomplete response -> referral to specialist
26
Severe depression without psychotic features
1st line SSRI, 2nd line diff SSRI or mirtazepine, third line mertazapine, escitalopram, SNRI, TCA -> refractory depression -> augment: - SSRI and mirtazapine or venlafaxine and mirtazapine - others e.g. lithium, antipsychotic, CBT - venlafaxine at max doses
27
Severe depression with psychotic features
add antipsychotic
28
Continuation therapy
single episode - 6 months after resolution of symptoms | Recurrant depression - 2 years after resolution of symptoms
29
Antipsychotic indications
psychotic illnesses bipolar affective disorder adjunctive therapy for depressive episodes off-licensed uses: behavioural disturbance in dementia and learning disability, conduct disorder, personality disorder, PTSD, anxiety disorders, many more
30
Dopamine hypothesis
dopaminergic drugs especially amphetamine can produce symptoms very similar to schizophrenia symptoms AND drugs which block dopamine must have antipsychotic properties (D2 receptor blockade) too much dopamine-> psychosis? Major dopamine pathways in brain: Nigostriatal system: Substantia nigra to basal ganglia, striatum Tuberoinfundibular system Ventral tegmental area to frontal cortex
31
Serotonin hypothesis
some hallucinogenic drugs e.g. LSD structurally resemble serotonin Some newer antipsychotic drugs especially clozapine acts at serotonin receptors Too much serotonin -> psychosis?
32
Glutamate hypothesis
Phencyclidine (PCP/angel dust) is a glutamate agonist which produces schizophrennia-like symptoms There's also evidence of abnormal glutamate activity in schizophrenia too much glutamate -> schizophrenia?
33
Neuropleptics or typical antipsychotics
Introduced in 1950s Various different classes of drugs Have roughly similar efficacy SERIOUS NEUROLOGICAL SIDE EFFECTS: Extrapyramidal symptoms - parkinsonism, akathisia, dystonia Tardive dyskinesia - devellops in 5% of patients on long term antipsychotic meds per year
34
Example typical antipsychotics
Butyrophenones e.g. halperidol Phenothiazines e.g. chlorpromazine, trifluoperazine, fluphenazine Thioxanthines e.g. flupenthixol
35
How do different typical antipsychotics differ?
Side effect profiles Degree of sedation preparations available e.g. depot forms
36
Atypical antipsychotics
Newer drugs, less likely to cause EPS Different mechanisms of action, some not as specific for D2 receptors, and also act on 5HT system Not necessarily more effective than typical antipsychotics
37
Examples of atypical antipsychotics
risperidone olanzapaine quetiapine aripiprazole neurological side effects less common/severe than with typicals problems w weight gain and metabolic syndrome especially with olanzapine
38
What causes side effects?
receptor action happen because: the side effect of the direct action of a drug e.g. antipsychotics and dopamine also due to other receptors affected by the drug e.g. antipsychotics and histamine, muscarinic, alpha 1 & 2 receptors
39
Dopamine receptor blockade side effects
``` Extrapyramidal side effects Parkinsonism dystonias tardive dyskinesia hyperprolactinaemia ```
40
Muscarinic/cholinergic receptor side effects
``` Blurred vision - iris/ciliary bodies Dry eyes - lacrimal gland Dry mouth - salivary glands Tachycardia - heart Dyspepsia - stomach and oesophagus Constipation - colon Urinary retention - bladder Dizziness, somnolence, impaired memory and cognition - CNS ```
41
Alpha-adrenergic receptor side effects
Orthostatic hypotension Vertigo Palpitations Sexual dysfunction
42
Clozapine
reserved for treatment-resistant cases most effective antipsychotic Problems with haematological side effects necessitate blood test monitoring Acts on range of neurotransmitter systems including D4 receptors and serotonin system Low propensity to cause EPS hypersalivation and hypotension may occur
43
Rapid tranquillisation
for acute agitation/aggression where risk of harm to self or others Oral first then IM antipsychotics - haloperidol or olanzapine benzodiazepines - lorazepam or midazolam CHECK LOCAL PROTOCOLS treat underlying cause
44
Mood stabilisers
``` lithium valproarte carbamezapine lamotrigine other anticonvulsants e.g. gabapentin ```
45
Lithium
uncertain mode of action?? second messenger inhibition of inositol Regulation of gene expression - protein kinase C Side effects: toxicity, interactions, monitoring loss of efficacy?
46
Lithium side effects
short term: polydipsia and polyuria, nausea, fine tremor, loose stools long term: hypothyroidism, renal impairment, weight gain, acne
47
Lithium toxicity
narrow therapeutic index Coarse tremor, nausea and vomiting, ataxia and cerebellar signs, confusion Precipitants: salt depletion, dehydration e.g. in diarrhoea, drug interactions - thiazides, NSAIDs, deteriorating renal function
48
Carbamezapine
antimanic but less effective than lithium major problem with drug interactions induces liver enzymes so reducing levels of other agents other agents in turn alter CBZ metabolism
49
Valproate
effect on inhibition of Ca and Na channels Enhances inhibitory GABA Reduces excitatory glutamate Equal efficacy to Li in acute mania, ease of use, improved tolerablity, weight gain, teratogenic plus developmental disorders May have role in emotional liability following brain injury especially orbitofrontal cortex
50
benzodiazepines
commonly used: diazepam, lorazepam, clonazepam, temazepam, clobazam (benzo derivative) differ mainly in: potency, half-life, duration of action e.g. lorazepam is short acting, clonazepam is longer-acting
51
Benzodiazepines use in psychiatry
hypnotics, anxiolytics, minor tranquilisers - role in acute tranquilisation, management of alcohol withdrawal also anticonvulsant esp clobasam and muscle relaxant
52
Benzodiazepine mechanism of action
bind to BZP site on GABA-A receptor | GABA is main inhibitory neurotransmitter in CNS
53
Drugs acting on chloride channel
barbiturates - depressants benzodazepine (agonists - depressants), antagnoists, inverse agonists Steroid site - anaesthetic Picrotexin site - convulsants
54
Benzodiazepine dependency
tolerance Withdrawal: abrupt withdrawal can precipitate acute delirium, rarely psychosis, convulsion Other withdrawal symptoms: nausea, hyperacusis, dizziness and imbalance, tinnitus, depersonalisation Avoid lengthy prescriptions Tapered withdrawal using diazepam equivalents
55
Managing alcohol withdrawal
reducing regimen of benzodiazepines vitamin supplementation - oral/IM/IV additional aids to maintain abstinence: acamprosate- reduces cravings naltrexone - reduces cravings/enjoyment via opiod receptors Disulfiram (anatbuse) - induces severe reaction if alcohol consumed - risk of fulminating hepatitis so check LFTs frequently
56
Buspirone
partial agonist at 5HT-1a receptors generalised anxiety disorder may have applications in other neuro/psych disorders e.g. can decrease side effect of medication in Parkinson's disease, may have a role in behavioural desturbance in dementia
57
Pregabalin
binds to and modulates voltage-gated calcium channels in CNS originally developed for use in neuropathic pain but has a growing role in anxiety and panic disorder, also in partial seizures

BSMS308 (9 decks)

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