Antipsychotic agents:
- Dopamine hypothesis
- Excessive limbic dopamine is hypothesised to cause psychosis
- Many antipsychotics inhibit dopamine 2 receptors in mesolimbic and striatal frontal system in CNS
- Drugs that increase dopamine eg amphetamines, levodopa, bromocriptine –> aggravate schizophrenia psychosis.
- Diminished dopamine activity in cortex and hippocampus
- Cognitive impairment and negative symtoms of Schizophrenia eg emothional blunting, social withdrawal, lack of motivation.
- Dopamine hypothesis doesn’t explain all aspects of psychosis.
- Basis of action
- Typical antipsychotics – dopamine blockade
- Atypical antipsychotics eg clozapine, quetiapine are 5HT 2a receptor blockers (inverse agonists)
- Most are readily but incompletely absorbed
- Significant first pass metabolism
- Bioavail 25-35%(chlorpromazine), 65% (haloperidol)
- Highly lipid soluble and protein bound 92-99% –> large volume of distribution
- Long duration of action
- 6mo for average relapse post ceasing meds, clozapine is the exception – relapse is rapid and severe.
- Neuroleptic malignant syndrome – life threatening disorder due to excessive rapid blockade of Dopamine receptors. Sx – muscle rigidity, fever, altered BP and HR. Needs supportive treatment with cooling, muscle relaxants and anti-parkinsons drugs. Switch to atypical after recovery.
- OD – rarely fatal, Sx – hypotension, hypothermia, drowsiness, coma, convulsions, miosis.
Phenothiazines (Learn Chlorpromazine)
- D2 block >>> 5HT2a – low clinical potency
- Alpha adrenoceptor blockade – hypotension, impotence
- Anti muscarinic – urinary retention, constipation, vasodilation, dilated pupils
- H1 receptor blockade
- SE – sedation, wt gain, decreased seizure threshold, QT prolongation, EPS (akathisia, dystonia, parkinsons sx, tardive dyskinesia, hyperprolactinemia – due to nigrostriatal dopamine pathways), hypotension. Deposits in cornea and lens.
- Long half lives
- Metabolism dependent elimination. Almost completely metabolised by p450 system in liver
Butyrophenones (Learn Haloperidol)
- Typical antipsychotic
- Commonly used
- D2>5HT
- Highly potent with less autonomic SE but more EPS than phenothiazines
- Sedation and hypotension is low
Thioxanthenes
- (Don’t learn much in detail, just know the name of one Typical antipsychotic i.e. Thiothixene)
- Typical antipsychotic
Atypical antipsychotics
- Olanzapine, Risperidone, clozapine, quetiapine, aripiprazole
- Risperidone is rapidly converted into its active metabolite paliperidone except in 10% who are poor metabolisers
- Primary action is 5HT blockade, some minor dopamine blockade.
- Clozapine should never be abruptly stopped unless myocarditis or agranulocytosis. (rapid relapse rate)
- Olanzapine – effective against negative as well as positive sx
Lithium
- Uses – manic bipolar disorder, prev of recurrent manic or depressive bi polar disease
- PD
- Not clearly understood
- Supresses inositol signaling and inhibits GSK -3
- PK
- Virtually complete absorption in 6-8hrs, peak plasma levels in 0.5-2hrs
- Distribution – total body water, no protein binding, vD 0.7-0.9L/kg
- No metabolism
- Excreted in urine
- T 1/2 20 hrs
- Renal clearance reduced by 25% by diuretics/NSAIDS
- SE
- Tremor, ataxia, dysarthria, confusion, decreased thyroid function(reversible), nephrogenic diabetes insipidus, oedema, wt gain, bradycardia(Sinus node depression), acni
- OD
- Can be dialysed
Antidepressants:
- Basis of action (biogenic amine hypothesis).
- Depression is thought to be due to dysfunction or deficiency of monoamines in the CNS as well as deficiencies in neurotrophic and endocrine factors.
- The aim of antidepressants are to increase monoamines such as seretonin, NA and dopamine in CNS.
- TCAs:
- Act at seretonin, histamine, acetylcholine, and alpha adrenoceptors
- Amitriptyline, imipramine
- SE – anticholinergic (dry mouth, urinary retention, constipation, mydriasis, impotence), sedation(5HT/histamine), orthostatic hypotension ( adrenoceptor blockade), wt gain
- Well absorbed, long half life, extensive hepatic metabolism. 5% excreted unchanged in urine. Can induce or inhibit CytP450
- Amitriptyline – 45% bio avail, 90% protein bound, t 1/2 31-46hr, active metabolite, Vd 5-10L,
- Overdose – can be lethal – arrhythmias and seizures–> need cardiac monitoring, airway support and gastric lavage.
- Heterocyclics: Superficial knowledge.
- Mirtazepine – tetracyclic, has SE similar to TCA- sedation, wt gain, inhibit Cyt P450
- SSRIs:
- Inihibit seretonin transporter (SERT)
- Commonest antidepressant in use
- Use- generalised anxiety, PTSD, OCD, panic disorder, bulimia
- Fluoxetine, sertraline, paroxetine, citalopram, escitalopram
- Fluoxetine
- PK – 70% bioavail, 95% protein bound, highly lipiphilic, Vd 12-97L, metabolised into active norfluoxetine(t1/2 180hr). Long half life(48-72). Inhibits Cytochrome p450.
- Safe in OD
- SE – sexual dysfunction, nausea, GI upset, diarrhoea, seretonin syndrome
- MAO inhibitors:
- Moclobemide – reversible MOA-A inhibitor.
- Inhibit Monoamine breakdown
- SE – toxicity, potentially lethal food(tyramine breakdown prevented in gut –> high serum NA –> hypertension) and drug interactions, orthostatic hypotension, insomnia, sexual dysfunction
- PK – extensive 1st pass metabolism,
- OD – autonomic instability, psychotic sx, confusion, delerium, fever, seizures.
- Need to avoid cheese, tap beer, soy, dried sausages.
Serotonin syndrome.
- Over stimulation of 5HT receptors in medulla and central grey nuclei
- Cognitive
- Delerium, coma
- Autonomic
- Hypertension, tachycardia, diaphoresis
- Somatic
- Myoclonus, hyper-reflexia, tremor\
Viva questions:
- How do antipsychotics work ?
- Tell me about Chlorpromazine.
- Tell me about Haloperidol.
- Tell me about Lithium and Lithium overdose.
- Tell me about TCAs and TCA overdose.
- Tell me about Fluoxetine / Fluoxetine overdose.
- Tell me about Serotonin syndrome.
- Tell me about MAOs.
- Tell me about Benztropine
- Benzatropine is an anticholinergic drug used in patients to reduce the side effects of antipsychotic treatment, such as parkinsonism and dystonia.
- Muscarinic antagonist