Psychiatric drugs Flashcards
What are the broad categories of pharmacological treatments available for depression
- SSRIs
- SNRIs
- TCAs
- MAOIs (RIMA)
- NA reuptake inhibitors
- Noradrenergic and specific serotonergic antidepressanrs
Consider SSRIs
- examples
- indications
- what is their onset of action?
- how do they work?
- Indications: depression, anxiety disorders, PD, OCD, PTSD
- Sertraline, fluoxetine, paroxetine, citalopram
- Delayed onset of action (0-14 days)
- blocks uptake of serotonin into presynaptic neuron
Compare the half life of paroxetine to fluoxetine
What does this mean for patients?
Paroxetine has a half-life of 20 hours (shortest), fluoxetine has the longest (2-4 days)
Short half-life makes the effects of missed pill more pronounced as the active agent remains in body for less time. (DISCONTINUATION SYNDROME, if stopped abruptly)
A patient has been prescribed paroxetine for depression. They visit their GP as they havent felt themselves in recent days. The patient complains of nausea and diarrhoea. He appears agitated.
After asking about the patients compliance to medication you learn that he has missed his medication over the past week.
1) What is the likely diagnosis?
2) What other symptoms should you ask about/expect?
3) How would you treat?
1) Discontinuation syndrome
2) agitation, anxiety, dizziness, balance problems, nausea, diarrhoea, flu-like symptoms
3) Reassurance and monitoring; reintroduction of drug with tapered withdrawal; consider alternative antidepressant or anxiolytic
Give an example of a TCA
How does it work?
Describe the side effect profile
e.g. Amitriptyline
MOA: Binds to NA and serotonin reuptake transporters –> increased availability of monamines in synaptic cleft
Has anticholinergic effects: dry mouth, constipation, urinary retention, cognitive effects
psychotrophic effects (agitation, nightmares), sexual dysfunction, akathisia, muscle twitches, cardiac arrhythmias
You are the psychiatric trainee on-call in A&E. You are asked to see a patient known who has presented confused with tachycardia and hypotension. O/E his pupils are dilated
James Smith, 27, has been taking amitriptyline for his depression. No other relevant PMH
1) What is the most likely cause for this presentation?
2) What is the patient at risk of?
1) TCA overdose
2) Seizures, coma, cardiorespiratory arrest
Consider venlafaxine
1) What kind of drug is this?
2) How does is work?
3) Indications
4) Side effects
5) Give an example of another drug in this class
1) SNRI
2) Blocks uptake of serotonin and NA into presynaptic neuron
3) Depression, mixed anxiety
4) HEADACHE, nausea, hypertension, risk of discontinuation syndrome
5) Duloxetine
When would you consider using a RIMA drug?
How do they work?
Reserved for treatment resistant depression or atypical depression
Prevent action of monamine oxidase from breaking down serotonin, dopamine and noradrenaline (in presynaptic knob)
1) Give two examples of RIMAs
2) Before prescribing these drugs what must you discuss with the patient
3) What drugs should be avoided with these?
1) Moclobemide, selegiline
2) Tyramine-food interactions: cheese, red whine, broad bean pods and tyramine
- -> hypertensive effect –> hypertensive crisis (less with moclobemide)
3) Do not combine with SSRIs –> serotonin syndrome ;
interacts with adrenaline, NA, Levodopa
Reboxetine is an example of which class of drug?
NA reuptake inhibitor
- highly selective
How do NaSSa drugs work?
Give an example
Noradrenergic and specific serotonergic antidepressant
MOA: Increases release of serotonin and NA via alpha-2 receptors on presynaptic neuron
Mirtazapine
What are antipsychotics used to treat?
- psychotic illnesses (e.g. schizophrenia, schizoaffective disorder)
- bipolar
- adjunct therapy for depressive episodes
(Off license use: behavioural disturbance in dementia and LD, conduct disorder, PD, PTSD, anxiety)
How do the following drugs cause psychotic symptoms?
a) Cocaine, MDMA, ecstasy
b) LSD
b) PCP
a) Dopaminergic drugs can produce schizo-like symptoms. They block the action of dopamine via D2 receptor blockade
b) Hallucinergic drugs are structurally similar to serotonin, act at their receptors
c) PCP is a glutamate agonist and can produce schizo-affective symptoms
Give three examples of typical antipsychotics
Butyrophenones:
- Haloperidol
Phenothiazines:
- Chlorpromazine
- Trifluoperazine
- Fluphenazine
Thioxanthines:
- Flupenthixol
Describe the side effect profile of the typical antipsychotics. Why is this?
Selective dopamine receptor blockade –>
(Via nigrostriatal pathway)
EPS, parkinsonism, dystonias, tardive dyskinesia
(Via infundibular pathway)
Hyperprolantinaemia
Why do newer antipsychotics have a lower propensity to cause EPS?
Give 3 examples of atypical antipsychotics
- Less specificity for D2 receptors
- Also act on serotonin system
Risperidone, olanzepine, quetiapine, aripiprazole
Describe the side effect profile of the atypical antipsychotics. Why is this?
Anti-HAM side effects
Anti-Histaminic: sedation
Anti-alpha adrenergic: sexual dysfunction, orthostatic hypotension, palpitations, vertigo
Anti-muscarinic: dry mouth, tachycardia, urinary retention, constipation, blurry vision, dizziness, somnolence, impaired memory and cognition
Weight gain and metabolic syndrome
What kind of drug is clozapine?
When is it used?
Describe its side effect profile
- Atypical antipsychotic
- reserved for treatment resistant cases (although most effect antipsychotic)
- Most severe: granulocytosis (which necessitates blood test monitoring);
low propensity to cause EPS;
hypersalivation and hypotension;
extreme sedation;
metabolic syndrome
When is rapid tranquillisation needed?
What agents would you use?
Acute agitation/aggression where there is risk to self or others.
- always try to talk down first and offer oral medication
IM administration of
(1) antipsychotic: olanzepine/ haloperidol which have immediate sedative effect
or;
(2) benzodiazepines: lorazepam/midazolam
Also treat the underlying cause (e.g. sepsis)
What is the number one mood stabiliser indicated for long term maintenance therapy?
We dont completely understand its MOA but what do we know?
Lithium
- Causes inhibition of inositol via 2nd messenger model
- causes regulation of gene expression- protein kinase C
Lithium has a narrow therapeutic range which increases its risk of toxicity.
How might a person with lithium toxicity present?
What may precipitate this kind of reaction?
- nausea
- vomiting
- ataxia
- cerebellar signs
- confusion
Precipitants:
- salt depletion; dehydration i.e. in diarrhoea or vomiting; drug interactions with thiazides, NSAIDs; deteriorating renal function
Discuss the side effect profile of lithium as:
a) short term
b) long term
a) polydipsia, polyuria, nausea, fine tremor, loose stool
b) hypothyroidism, renal impairment, weight gain, acne
Why is it important to maintain adherance to lithium therapy?
- there is loss of efficacy if you keep stopping and starting
This question is about carbemazepine
- Indication
- Why should it be prescribed with caution in a person with multiple comorbidites?
- Antimanic mood stabiliser with lower efficacy than lithium
- Major drug interactions; induces liver enzymes so reducing levels of other agents and these agents in turn alter carbemazepine metabolism
