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CPD 20: DEPRESSION Biography - Ciaran Mullins graduated in 2006 from Aberdeen’s Robert Gordon University and worked in retail for three years in the UK and in Ireland. He then worked in hospital pharmacy in the UK on orthopaedic and medical wards, before spending a year and a half working in oncology at the South East Scotland Cancer Network at the Western General, Edinburgh. Mullins returned to University College Cork to study medicine in September 2010 and is set to enter his third year. He is currently a part-time pharmacist with Unicare/Doc Morris. 1. REFLECT - Before reading this module, consider the following: Will this clinical area be relevant to my practice. 2. IDENTIFY - If the answer is no, I may still be interested in the area but the article may not contribute towards my continuing professional development (CPD). If the answer is yes, I should identify any knowledge gaps in the clinical area. 3. PLAN - If I have identified a knowledge gap

- will this article satisfy those needs - or will more reading be required? 4. EVALUATE - Did this article meet my learning needs - and how has my practise changed as a result? Have I identified further learning needs? 5. WHAT NEXT - At this time you may like to record your learning for future use or assessment. Follow the 4 previous steps, log and record your findings.

DEPRESSION INTRODUCTION Depression is a common illness. It is almost twice as common in females as males and may cause substantial disability. 1 It has an estimated lifetime prevalence ranging from 2-15% and is reported as the fourth leading cause of disease burden, in terms of cost and impact on workplace productivity.2 Therefore, depression is an important global public health issue. Whilst recognised by the public primarily as a disorder of affect, the healthcare practitioner must appreciate that depression may manifest initially with entirely somatic symptoms. Many patients seek treatment for a constellation of symptoms that, when not considered in the context of mental illness, may seem entirely innocuous. Such symptoms could range from non-specific aches, fatigue or headache to vague descriptions of abdominal discomfort or sleeping problems. This inherent complexity, compounded by the still widespread ignorance and misperceptions of the disease by public as a personal failing or lack of self control, mean that many will avoid a diagnosis of depression for fear of stigmatisation. Clinically, depression is described as a condition of disturbed mood, speech, energy and ideas.3 This is often accompanied by pessimistic thinking and, in extreme cases, suicidal ideation. Commonly, patients describe their symptoms in physical terms as lacking an enthusiasm for living life. They may feel unable to derive pleasure from, or have an interest in, activities that formerly provided joy. Biological features, such as sleep disturbance, weight loss and loss of appetite are not uncommon.4 Episodes

of anxiety and panic attacks often occur concurrently, while secondary obsessional and phobic symptoms may also emerge. In more severe cases, psychotic symptoms, such as hallucinations or delusion may be present. Normal sex drive may be reduced and some may lose interest in sex altogether. Rarely, a paradoxical reversal of symptoms occurs, with excessive eating and sleeping the most common features.3,4 The term depression can be misleading and it is equally important not to overcall patients’ symptoms. We all, at some time or another, feel ‘down in the dumps’ or ‘hacked off’ about something. Lowered mood as a response to life’s ups and downs is normal and simply termed sadness or unhappiness. It is when these symptoms take on a more pervasive nature and interfere with normal functioning that a depressive illness has occurred.3 DIAGNOSIS Depression is a clinical diagnosis, but symptom severity and clinical presentation varies between patients. There are two main diagnostic criteria used to identify and classify depression (Table 1.). The International Classification of Diseases (ICD-10) is a WHO-sponsored classification of mental and behavioural disorders.5 An alternative, the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) is favoured by many physicians and produced by the American Psychiatric Association.6 The extent to which these symptoms are present is of crucial importance in determining the severity of the underlying depressive illness and serves as a guide for determining the ultimate treatment plan for individual patients.

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60 Second Summary Depression is a major cause of global disease burden, with an estimated lifetime prevalence of 2-15%. Patients do not always present with overt psychological symptoms. Diagnosis is clinical and often aided by internationally recognised diagnostic criteria. The pathogenesis of depression is still not fully understood and depressive syndromes are heterogeneous and diverse in their aetiologies. Antidepressants are effective for the treatment of moderate-to-severe depression and, once instituted, should be continued for at least sixto-nine months, with close monitoring. Several antidepressant drugs are available in Ireland, with choice guided largely by clinical experience, patient preference and recognition of likely adverse effects. Antidepressant drugs constitute a great variety of chemical types with wide variations in half lives, pharmacokinetic properties and side effects. Great care must be undertaken when initiating treatment (especially in incidences of polypharmacy), changing treatment and withdrawing treatment. The selective serotonin reuptake inhibitor (SSRIs) are considered amongst the safest agents despite, at best, comparable efficacy with the previously favoured tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs). The serotonin/norepinephrine reuptake inhibitors (SNRIs), with their short half-lives, are emerging as beneficial agents in those at risk of the adverse events associated with overdoses of TCAs and SSRIs. Some atypical antidepressants like trazodone, mianserin, mirtazapine and agomelatine may be beneficial in selected patient groups or in those suffering from treatment failure on more established antidepressants. Recognising the possibility of drug-drug interactions with the many antidepressants available is clinically important.

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CPD 20: DEPRESSION TABLE 1 ICD-10 classification Individual usually suffers from: * Depressed mood, loss of interest and enjoyment; * Reduced energy -> to increased fatigability and reduced activity; * Marked tiredness with only slight effort. Other common symptoms: * Reduced concentration and attention; * Reduced self-esteem and self-confidence; * Ideas of guilt and unworthiness; * Bleak and pessimistic views of the future; * Ideas acts of self-harm or suicide; * Reduced appetite; * Disturbed sleep. DSM-IV Criteria Two-to-four of the following symptoms must be present; at least one symptom must be (a) or (b) (a) Depressed mood; (b) Markedly diminished interest or pleasure in all or almost all activities; (c) Significant weight loss (when not dieting) or weight gain with increased or reduced appetite; (d) Insomnia or hypersomnia; (e) Psychomotor agitation/retardation; (f) Fatigue or loss of energy; (g) Feelings of worthlessness or excessive and inappropriate guilt; (h) Reduced ability to think or concentrate; (i) Recurrent thoughts of death; suicidal ideation or suicide attempt or specific suicide plan. It is very important that any diagnosis takes into account not just the symptoms outlined in Table 1, but the degree of functional impairment or disability.7 For example, in order for a diagnosis of mild depression, the presence of two or more of ICD-10 symptoms for every day for at least two consecutive weeks must be established. Similarly, moderate depression requires greater than four ICD-10 symptoms or greater than five DSM-IV symptoms with some functional impairment, while severe depression involves most of the symptoms with marked interference of function. The DSM also advises for sub-threshold or minor depression, typically consisting of twoto-four DSM-IV symptoms and dysthymia (mild-to-moderate depressive illness lasting intermittently for two years or more, relapsing and remitting with longer periods of feeling unwell), and seasonal affective disorder

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(SAD).6,8 It remains important to identify such patients because of the risk of future major depression and the associated morbidity.8,9 Depression classifications include major depressive disorder, depression with melancholic or catatonic features, atypical depression, single or recurrent episode depression and dysthymia. PATHOPHYSIOLOGY The pathological events underlying depressive illness have not yet been clearly elucidated.10-12 The latest thinking posits a complex interaction between neurotransmitter availability and both receptor regulation and sensitivity as being key to the emergence of affective symptoms. Clearly, CNS serotonin (5-HT) activity is important, but other key players include norepinephrine, dopamine, glutamate and, in more recent work, brain-derived neurotropic factor (BDNF). Interestingly, drugs producing exclusively acute rises in neurotransmitter availability at CNS synapses, such as cocaine and amphetamines, do not demonstrate the efficacy over protracted periods that antidepressants do, implying that it is not merely synaptic availability of neurotransmitter that is responsible for the antidepressant action of therapeutic agents.10 The importance of 5-HT in the pathophysiology of depression has been clearly demonstrated by the long-term efficacy of selective serotonin reuptake inhibitors. Additionally, experimentally induced depletion of tryptophan (the amino acid precursor of 5-HT) in research subjects in remission produced a transient relapse of depressive symptoms. Whilst the effects of these drugs on synaptic 5-HT is immediate, the antidepressant effect requires exposure to therapeutic levels of the drug for several weeks.3 This strongly suggests a role for neurolemmal receptor regulation, intracellular signalling events and altered gene expression over time, in concert with the enhanced neurotransmitter availability. AETIOLOGY In common with many psychiatric illnesses, the precise causes of affective disorders are largely unknown. However, they do appear to be multifactorial, involving genetic, biochemical, endocrine and environmental factors. The original monoamine hypothesis suggested that depression was related to either a quantitative or qualitative deficiency of limbic and cortical serotonin, norepinephrine (noradrenaline) and dopamine.13 This theory is now known to be overly simplified, since it takes many weeks at therapeutic doses for antidepressants affecting these transmitter systems to produce a clinically recognisable effect. Recent work combining behavioural, molecular and electrophysiological techniques reveal that certain aspects of depression result from maladaptive stressinduced neuroplastic changes in specific

neural circuits.14 Indeed, depression is known to be associated with a number of hormonal abnormalities, including hypothalamicpituitary-adrenal (HPA) axis dysregulation, thyroid dysfunction, and oestrogen deficiency. Substantial recent evidence also points to the importance of neural plasticity in recovery from depression. Antidepressant drugs increase the expression of several molecules associated with neuronal plasticity, in particular the neurotrophin BDNF and its receptor TrkB. Indeed, drug treatment has been found to increase neurogenesis and synaptic numbers in several brain areas.14,15 Conversely, depression, in its most severe forms is associated with reduced volumes of the hippocampus and prefrontal cortex. Genetic and environmental factors are known to influence the onset of depressive illness.8,13 The heritability of depression is estimated to range between 30-40%. No single gene has been identified and it is likely that multiple loci are responsible for this contribution. Moreover, epigenetic factors, influenced by environmental exposure in-utero are garnering much recent research interest.14 Co-morbidities and on-going life stresses may increase the duration or severity of depressive episodes but a causal link has been more difficult to establish. Certain drugs and substance misuse have also been implicated in the onset of depressive episodes; such drugs include steroids, propranolol, metoclopramide, progestin releasing implants and H-2 receptor antagonists.16,17 MANAGEMENT A wide range of effective treatments are available for depression. While medication alone can relieve symptoms, successful management of the depressed patient often involves additional physical, psychological and social interventions.4,10,11 Psychotherapy alone, or in combination with drug treatment, has been shown to be effective for acute treatment of mild-to-moderate depression and for reduction in the number of recurring episodes. However, the combination of medication and psychotherapy provides the fastest and most sustained response in all patient populations. Further, combination therapy improves treatment compliance and is associated with higher rates of improvement in depressive symptoms. Antidepressants, when given at therapeutic doses, are considered effective in up to 80% of patients with moderate to severe depression (assuming compliance).3 Generally, four to six weeks in adequate doses is required for the full effects to be seen. However, this may extend to up to twelve weeks in a small subset of patients. The choice of medication should be guided by expected safety and tolerability, familiarity with the drug, compliance issues, such as dosage schedule and history of previous treatments. The latest

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CPD 20: DEPRESSION guidance from the American College of Physicians places emphasis on patient preference when choosing the best course of pharmacotherapy, especially if he/she has had a previous depressive episode.18 The American Psychiatric Association in its Practice Guideline for the Treatment of Patients with Major Depressive Disorder advises customised treatment plans for individual patients, based on assessment of symptoms, recognition of potential therapeutic benefits and likely side effects. Any treatment should aim to improve patient function within a realistic time frame through the establishment of attainable goals. The choice of treatment should be chosen on the basis of the following18: * clinical assessment; * presence of other disorders; * stressors; * patient preference; * reactions to any previous treatment. PHARMACOTHERAPY Despite the myriad antidepressant drugs currently available, therapeutic effectiveness has improved little over the past number of decades. There is no convincing evidence that one class of antidepressants provides better relief of symptoms than another, nor is there concrete data showing increased efficacy of individual drugs versus each other.3,10 There is some data demonstrating better responses in severely depressed patients to drugs affecting more than one neurotransmitter system. The greatest differences between the available agents lie in their side effect profiles, toxicity in overdose, cost and propensity to interact with other therapeutic agents. Drugs currently used in the treatment of depression include the following: * Selective serotonin reuptake inhibitors (SSRIs); * Tricyclic antidepressants (TCAs);

hypotension or sedation, are safer in overdose and less cardiotoxic than the TCA drugs.10,11 The SSRIs available make up a remarkable variety of chemical types but they all have a specific effect of inhibiting synaptic serotonin re-uptake. They have similar side effect profiles but there are differences in the intensity of these side effects. Generally the SSRIs are well absorbed following oral administration, undergo hepatic metabolism and are cleared via the kidneys. There are some important differences between individual agents and, as such these impact their clinical use. Fluoxetine, paroxetine and fluvoxamine have the greatest potential for drug-drug interations while citalopram and its S-isomer,S-citalopram have minimal potential and sertraline has a dose related potential (see table). Additionally fluoextine has a very long half life (4-6 days), a factor which must be taken into account when switching from one antidepressant to another.19-23 The commonest adverse events associated with SSRIs are GI complaints (nausea, vomiting and diarrhoea) and sleep disturbances. These complaints are usually only a problem in the first weeks of treatment and a degree of tolerance develops. Problematic sexual dysfunction has also been reported in up to 70% of users. SSRIs are associated with an increased bleeding Drug Class and MOA

Drug name

SSRIs (Inhibition of synaptic SERT*)

Citalopram S-citalopram Fluoxetine

* Atypical antidepressants. TABLE 2. PHARMACOLOGY OF MOST COMMONLY PRESCRIBED ANTIDEPRESSANT DRUGS19-30 1. SSRIs: These drugs were developed in order to reduce some of the problems associated with the earlier tricylic compounds. While no more (or less) effective than the TCAs, their favourable toxicity profile and lower incidence of troublesome side effects make them first line for many physicians. They are the most widely used antidepressants in Ireland.19 As a class they are associated with less anticholinergic side effects, are less likely to cause postural

Metabolised by 3A4 and 2D6 Moderate inhibitor of 2D6 (also metabolised by 1A2



Dosulepin/Dothiepin Trimeprimine

Metabolised by 2D6, 2C19 Metabolised by 2D6 Metabolised by 2D6

14-45hrs 7-23hrs


Minimal effect



Minimal effect


SNRIs (Inhibition of 5HT and norepinephrine reuptake)


TCAs (Inhibition of 5HT and norepinephrine reuptake)


Increased norepinephrine activity but not by reuptake

Other effects thought to be relevant include increased alpha1 and beta1 receptor sensitivity. These drugs are well absorbed, are metabolised by the CYP450 system, and have variable half lives. Importantly, pharmacokinetic interactions with other drugs, as a result of heterogeneity of Half-life

Paroxetine Sertraline

Others (Increased 5HT and norepinephrine activity with antagonists effects at Histamine H1 receptors)

2. TCAs: These were the drugs of first choice before the advent of the SSRIs and SNRIs.3,10 In addition to inhibiting the reuptake of 5HT and norepinephrine, they also have effects on other neurotransmitter systems, resulting in troublesome toxicities. With chronic administration, biochemical adaptations result in altered pre and post synaptic receptor sensitivity, a reduction in alpha2 receptor sensitivity pre-synaptically in particular being associated with increased norepinephrine availability.

Effect on CYP450 system Minimal effects Minimal effects Inhibitor of 3A4 and minimally of 2D6 Inhibits 2D6 Dose related inhibition of 2D6


* Serotonin/norepinephrine reuptake inhibitors (SNRIs); * Monoamine oxidase inhibitors (MAOIs);

tendency, particulary GI bleeding and this risk is increased with concomitant therapy with NSAIDs. Hyponatraemia may be a problem with increasing age, female gender and low body weight all predisposing factors. The toxicity profile varies as much as the chemical nature of each of the compounds; paroxetine is associated with greater risks of sweating, dry mouth, sedation and weight gain (anticholinergic effect, sertraline with increased risk of diarrhoea and fluvoxamine with increased nausea, headache and nervousness.4,10, 19-23

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36hrs 30hrs 4-6days 24hrs 22-36hrs


CPD 20: DEPRESSION metabolism within the CYP system are common and metabolites often have longer half lives than the parent compound.3, 10, 26-28 The commonest adverse events with these agents include dry mouth, blurred vision, constipation, urinary retention, sweating and weight gain (anticholinergic effects), sedation (antihistamine effects) and orthostatic hypotension (alpha-adrenergic antagonistic effects). TCAs should be avoided in those with an underlying cardiac disorder, or those at high risk of overdose.29-31 3. SNRIs: These drugs were developed in an attempt to improve efficacy over standard agents.3 They inhibit the reuptake of both 5HT and norepinephrine but without the antimuscarinic, cardiac or other toxic effects of the older drugs.10 Similar to the SSRIs, they are well absorbed, undergo hepatic metabolism and with excretion predominantly by the kidneys. Their low risk for drug interactions and short half lives make them popular for use in those at risk for self harm.24, 25 Adverse reactions with these drugs are very similar to the profile for SSRIs with many appearing in the early stages of treatment and subsiding with continuing therapy. Venlafaxine has been associated with a dose dependent increase in blood pressure and heart rate and it should be prescribed with caution in patients at risk of arrythmias.24 4. MAOIs: Two types are available: the traditional, non-selective and irreversible agents and moclobemide, which is a selective and reversible inhibitor of MAO-A. Inhibition of MAO, a mitochondrial enzyme, reduces the breakdown of 5HT and norepinephrine, increasing the levels of these neurotransmtters available for synaptic transmission. Strict dietary restrictions are required with the original drugs of this class, e.g. tranylcypromine and phenelzine because patients were unable to metabolise the tyramine in common foodstuffs, predisposing to them to hypertensive crisis (as a result of sympathomimmetic effects). 3, 10, 32 Moclobemide does not require dietary modifications.33 Currently, they are rarely prescribed in primary care and advice is that they should be initiated under specialist supervision.8 Extreme care must be taken switching between and MAOI and other antidepressants because of a risk of serotonin syndrome. 5. Atypical agents: Mirtazepine, trazodone and mianserin are chemically distinct drugs and exert their antidepressant effects via differing effects on neurotransmission. Mirtazepine has few pharmacokinetic interactions and produces fewer GI side effects and sexual dysfunction compared with SSRIs but it can cause weight gain and sedation. Trazodone also causes sedation through action at central histamine receptors and may also cause postural hypotension (alpha adreneric

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antagonist effects). Mianserin increases norepinephrine transmission (pre-synaptic alpha adrenoceptor blockade), has little anticholinergic effects but causes marked sedation.29-31 Agomelatine, a recently available melatonergic agonist (at MT1 and MT2 receptors) with 5HT-2c antagonist properties has been shown to improve sleeping patterns in those with depression associated with disturbed circadian rhythms. Whilst having no direct effect on the reuptake of monoamines, it has been shown to increase norepinephrine and dopamine release in the frontal cortex.34 CLINICAL CONSIDERATIONS Switching\stopping antidepressant agents Much caution must be exercised when changing antidepressant therapy.35 The risks involved include withdrawal symptoms, serotonin syndrome and pharmacokinetic and pharmacodynamic interactions. Abrupt withdrawal is ill-advised, except in the case of fluoxetine, wherein the long half life of the parent drug and its metabolite desmethylfluoxetine allow for cessation without a tapering period (provided a 20mg dose schedule has been followed). Should the prescriber wish to change to a MAOI, however a five week wait to clear fluoxetine and its metabolites must be adhered to.3 Cross tapering, where one drug is initiated slowly as the other is withdrawn is the usual standard in clinical practice.36 The rate of such tapering should be tailored to the individual patient, typically taking up to four weeks. Switching from one SSRI to another cross tapering is not required and may actually prove beneficial (by reducing the incidence of withdrawal symptoms) except with fluoxetine. TCAs should not be initiated until at least two weeks after MAOI treatment has stopped and vice versa. SSRIs and SNRIs should not be started until two weeks after an MAOI, except in the case of fluoxetine. Serotonin syndrome is a potentially life threatening adverse reaction that may result from therapeutic use of a serotonin enhancing antidepressant after an interaction with two or more serotonin enhancing medications, e.g. SSRI with a MAOI, tramadol or a triptan) or following an overdose of a serotonin enhancing medicine. Co-administration of MAOIs with SSRIs is absolutely contraindicated for this reason. Signs and symptoms are diverse and range from mild diarrhoea and tremor to restlessness, myoclonus, confusion, convulsions and death. A particular problem is the rapidity of both symptom onset and progression.10, 37 Since all antidepressants have the potential to cause withdrawal symptoms, it is recommended that when taken continuously for greater than six weeks an antidepressant should not be stopped

suddenly, unless in the case of a serious adverse event. Slow tapering over four weeks is the recommended regimen to reduce the incidence of adverse events.36,38 Drug interactions The myriad antidepressant drugs available for prescription, coupled with the prevalence of depression mean that the potential for interaction with other drugs, either prescription or otherwise is high. Given this risk, pharmacists must be vigilant of prescriptions for medications known to interact with antidepressant drugs from the different classes. This can only be achieved from a thorough understanding of the relevant pharmacology. Some important drug-drug interactions include39: * Increased bleeding risk when SSRIs used with NSAIDs; * lowering of seizure threshold when SSRIs used with antiepileptics and fluoxetine increases plasma levels of phenytoin; * fluoxetine reduces the antiplatelet effect of clopidogrel; * fluoxetine and paroxetine possibly inhibit metabolism of tamoxifen to active metabolite (venlafaxine is a safer alternative); * increased risk of CNS toxicity when TCAs and tramadol used concomitantly; * increased risk of ventricular arrhythmias when TCAs used with amiodarone; ìncreased risk of ventricular arrhythmias when TCAs given moxifloxacin. REFERENCES 1.    Bleakley S, How best to recognise and manage depression. Pharmacy in Practice April 2008: 84-7 2.    Moussavi S et al, Depression, chronic diseases and decrements in health: results from the World Health surverys. Lancet 2007; 370: 851-8 3.    Walker R, Edwards C, Clinical Pharmacy and Therapeutics. Churchill Livingstone, 3rd Edition,2004. Chapter on affective disorders. Pp 439-454 4.    Kumar P and Clark M, Clinical Medicine. Pubs: Saunders Elsevier, 7th Edition, 2009. Chapter on psychological medicine, depressive disorders pp11981205 5.    ICD-10 Classification of Mental and Behavioural Disorders, WHO publications, Geneva, 1992. 6.    APA Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, American Psychiatric Association, Washington DC, 1994. 7.    Depression, Treatment and management of depression in adults, including adults

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CPD 20: DEPRESSION with a chronic physical health problem: Quick reference guide (incorporating CG 90 and 91. NICE, UK October 2009. Available at Accessed 15th July 2012. 8.    Depression : The treatment and management of depression in adults (CG90). NICE, UK 2009. Available at Accessed 15th July 2012.

depression? A review of the evidence. J Psychiatr Neurosci 1993; 18: 92-101 18. APA. Practice Guideline for the Treatment of Patients with Major Depressive Disorder (3rd edition). Accessed 15th July 2012. American Psychiatric Association. 19. SPC Prozac®. Available on www., accessed 15th July 2012

9.    Hermens M, Prognosis of minor depression in the general population : a systematic review. Gen Hosp Psychiatr 2004l 26:453-62

20. SPC Cipramil®. Available on www., accessed 16th July 2012

10. DeBattista C, Antidepressant Agents (Chapter 30 ) in Basic and Clinical Pharmacology, 11th Edition. Editors: Katzung B, Masters S, Trevor A. Pubs: McGraw Hill, US, 2009.

22. SPC Seroxat®. Available on www., accessed 17th July 2012

11. Drugs used in affective disorders (Chapter 35) in Pharmacology (4th Edition).Eds: HP Rang, MM Dale, JM Ritter. Publishers Churchill Livingstone, UK, 2002 12.  Dunlop BW, Nemeroff CB. The role of dopamine in the pathophysiology of depression. Arch Gen Psychiatry. Mar 2007;64(3):327-37. 13. Ebmeier K et al, Recent developments and current controversies in depression. Lancet 2006; 367: 153-67

21. SPC Lexapro®. Available on www., accessed 17th July 2012

23. SPC Lustral®. Available on www., accessed 17th July 2012 24. SPC Efexor XL®. Available on www., 18th July 2012 25. SPC Cymbalta®. Available on www., 18th July 2012 26. SPC amitriptyline. Available online at, 18th July 2012 27. SPC Prothiaden®. Available online at, 18th July 2012 28. SPC Surmontil®. Available online at, 18th July 2012

14. Vaishnav K and Nestler Eric J, The Molecular Neurobiology of Depression. Nature 455, 894-902 (16 October 2008) | doi:10.1038/nature07455; Published online 15 October 2008

29. SPC Zispin®. Available online at www., 18th July 2012

15. Maletic V et al, Neurobiology of depression: An integrated view of key finings. Int J Clin Pract. 2007 December; 61(12): 2030–2040.

31. SPC Mianserin. Available online at www., 19th July 2012

16. Psychotropic Drug Directory 2010. Ed: Stephen Bazire. Publishers:HEALTHCOMM UK Ltd

33. SPC Manerix®. Available online at www., 19th July 2012

17. Patten S, Love E, Can drugs cause

30. SPC Molipaxin®. Available online at, 19th July 2012

32. SPC Parnate®. Available online at www., 19th July 2012

35. Bleakley S, Treatment pathways for managing depression. Pharmacy in Practice May 2008: 118-121 36. The Maudsley Prescribing Guidelines 10th Edition. Eds: D Taylor, C Paton, S Kapur. Publishers Informa Healthcare UK 2009. [pages 155-229] 37. Bleakley S, Treatment pathways for managing depression. Pharmacy in Practice May 2008: 118-121 38. Mann JJ, The medical management of depression. NEJM 2005; 353: 1819-34 39. British National Formulary No. 63, March 2012, BNF online, available at www.BNF. org accessed 20th July 2012. Pfizer Healthcare Ireland are committed to supporting the continuous professional development of pharmacists in Ireland. We are delighted to be partnering with Irish Pharmacy News in order to succeed with this. Throughout the year, Irish Pharmacy News will deliver 12 separate modules of continuous professional development, across a wide range of therapy areas. These topics are chosen to support the more common interactions with pharmacy patients, and to optimise the patient experience with retail pharmacy. We began the 2011 programme with a section on the Gastrointestinal System. Other topics include Diabetes (Types I and II), the Cardiovascular System, Smoking Cessation, Infections, Parkinson’s Disease, Alzheimer’s Disease, Depression and others. We hope you will find value in all topics. Pfizer’s support of this programme is the latest element in a range of activities designed to benefit retail pharmacy. Other initiatives include the Multilingual Pharmacy Tool, a tailored Medical Communications Programme, Educational Meetings and Grants, our Patient Information Pack, new pharmacy Consultation Room brochures and other patient-assist programmes including the Quit with Help programme and If you would like additional information on any of these pharmacy programmes, please contact Pfizer Healthcare Ireland on 01-4676500 and ask for the Established Products Business Unit.

34. SPC Valdoxan®. Available online at www., 19th July 2012

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60 Second Summary : Depression is a major cause of global disease burden, with an estimated lifetime prevalence of 2-15%. Patients do not al...


60 Second Summary : Depression is a major cause of global disease burden, with an estimated lifetime prevalence of 2-15%. Patients do not al...