TCAs modulate neurotransmission by blocking 5-HT and NE transporters. This leads to elevated synaptic concentrations of the neurotransmitters, respectively. It is important to consider that TCAs do not have much affinity for dopamine (3,4-dihydroxyphenethylamine, DA) transporters, and thus have limited effect on this particular neurotransmitter.
TCAs are highly lipid-soluble and therefore, rapidly absorbed.
These drugs lead to CNS stimulation and cause a wide range of presenting symptoms, such as confusion, mania, agitation, tremor, seizures, and sedation.
Side effects tied to the antimuscarinic properties of these medications include impaired gastric motility, dry mouth, blurry vision, increased temperature, and urinary impairment.
Tricyclic antidepressants exhibit antihistamine effects, with the most severe manifestations being seizures and arrhythmias, though uncommon. There are also minor anti-histamine symptoms, which mostly mimic anticholinergic effects.
A major collection of side effects attributed to TCAs can be described as the three C's. These are convulsions, coma and cardiotoxicity. Cardiac effects are predominantly due to sodium channel blockade, and these cardiotoxic effects can take the form of QRS widening, QT prolongation and torsades de pointes. Additional side effects of these drugs include hyperpyrexia and respiratory depression.
Tricyclic antidepressants display alpha-1 blockade effects and can lead to postural hypotension.
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