Pharmocology Essay

2181 words - 9 pages

Depression is one of the leading causes of morbidity worldwide and is thought to result in a decreased work productivity and the higher utilisation of health services (World Health Organisation, 2001) costing the United States over $83.1billion in research and treatment in 2001 (Gartlehner et al, 2008). The prevalence of depression varies from country to country, from 3% in Japan and 16.9% in the US (Andrade et al, 2006); prevalence also varies between genders, with at least 12% of American women diagnosed compared with only 8% of the male population (Medscape, 2014). Depression is also one of the most common mental illnesses in the UK and is estimated to affect one in five adults (Mental ...view middle of the document...

The combination of symptoms, their severity and the circumstances surrounding their occurrence all help the doctor diagnose the type of depression and the most appropriate treatment for it (National Health Service, 2014).
The precise pathophysiological cause of depression is still unclear, in the early 1950’s monoamine oxide inhibitors and various other drugs were discovered to hold mood elevating properties, this lead to the formation of The Monoamine Theory of Depression, first proposed by Schildkaurt in 1965 which states that depression is a result of the functional decrease of the monoamine transmitters noradrenaline and 5-Hydroxytryptamine (5-HT), also known as serotonin (Rang and Dale, 2012). The discovery prompted investigation into antidepressant drug therapy (Ferguson, 2001). Evidence from studies supports that the cause to depression is monoamine neurotransmitter deficiency (Sussman, 2003). Since the first Biogenetic Amine hypothesis was published by Schildkraut, Bunney and Davis in 1965 they have prevailed in the management and treatment of depression (Kramer et al, 2003).
The progression in research has led to a significant advance in the treatment of depression, specifically in the design of target drugs which act on specific neurobiological molecules linked to depression (Harvey, 1997). The availability of antidepressant drugs has increased since the 1950’s when the first tricyclic antidepressant, Imipramine was introduced (Briatta, 2002).
TCA’s are non-selective inhibitors of serotonin, dopamine and noradrenalin reuptake and are a completion of five or more different drugs taken as one, including a noradrenaline reuptake inhibitor, a serotonin reuptake inhibitor, an anticolinergic-antimuscarinic, an alfa-1-adneergic antagonist and an antilustanine (Yildiz et al, 2002) TCA’s are taken orally and are metabolised by the liver and absorbed into the blood plasma either through the N-demethylation route, which the removal of methyl groups from the molecule or the ring hydroxylation route which is the addition of a hydroxyl group to the molecule (Rang and Dale, 2012). TCA’s work by competitive binding to the neurotransmitter transporters and blocking the serotonin from being reabsorbed, dopamine (DAT) and noradrenalin transporters (NAT) (Tatsumi et al, 1997), however TCA’s do not only affect the 5-HT DAT and NAT transporters but also act as calcium channel blockers and sodium channel blockers (Pancrazio et al, 1998) along with acting as antagonist at the 5-HT sub transporters such as 5-HT2 and 5-HT1 (Cusack et al, 1994). It has been suggested that the improvement of emotional symptoms is due to the inhibitions of serotonin reuptake and the reliefs of biological symptoms is due to the inhibition of noradrenaline reuptake (Rang and Dale, 2012). Although TCA’s have shown efficacy in treating depression they also present harmful side effects such as incoordination, confusion and sedation in the first few weeks of treatment (Rang and...

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