Q1 Mrs Ford appears to be suffering from depression. Depression is a common psychiatric condition which occurs when sadness or grief is abnormally prolonged and causes dysfunction. It is classified as an affective disorder, that is a disorder of mood rather than a disorder involving disturbances of cognition or thought.
Q2 Depression ranges from a mild condition, perhaps associated with a stressful or sad event, such as bereavement, to a severe state which may be accom-panied by delusions or hallucinations (psychotic depression). Depressed patients may experience a range of emotional and biological symptoms. They are unhappy, sad and cry for no apparent reason. They are generally negative about life and may be very self-critical, expressing feelings of worthlessness.
Patients’ energy level appears to be low: they feel constantly tired, lethargic and lack motivation. Patients’ sleep may also be disturbed, with charac-teristic patterns of early waking and inability to return to sleep. Appetite may be reduced or increased and the individual may exhibit psychomotor retardation, a pattern of slow physical movement and response. They may also develop constipation, reduction in libido, anxiety, irritability or tension.
Some depressed people show different behaviour patterns and may eat and sleep to excess.
Clinical Physiology and Pharmacology Farideh Javid and Janice McCurrie
2008 John Wiley & Sons, Ltd
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2-3 weeks
Following Antidepressant Drugs
Q3 Mrs Ford’s symptoms included: feeling constantly down, hopelessness, feeling that life is meaningless, suicidal thoughts, lack of energy and motivation, abandonment of socializing, social activities and other plans, disturbed sleep and eating patterns. These are consistent with the profile of depression.
Q4 The pathophysiology of depression is believed to involve the depletion of noradrenaline (norepinephrine) and serotonin (5-HT) at nerve endings in the brain. These monoamines are important in determining mood.
Q5 There are two main treatments for depression:
(1) drug therapy, for example using antidepressant tablets
(2) talk therapy, such as cognitive behaviour therapy or counselling.
Both of these treatments can be used as a course of therapy over a period of months. They can be used singly or together; the latter will increase the speed of recovery from a period of depression.
In addition, electroconvulsive therapy is available for patients with severe refractory depression. The mechanism by which this treatment alleviates depression is controversial: it may increase the ability of the nerves in the central nervous system (CNS) to respond to noradrenaline and serotonin (5-HT).
Q6
(1) Tricyclic antidepressants, which inhibit or reduce the reabsorption (reup-take) of the main neurotransmitters (noradrenaline and serotonin) into nerve endings.
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(2) Monoamine oxidase inhibitors (MAOIs), which were amongst the first antidepressant drugs to be used clinically. They affect one or both of the brain monoamine oxidase enzymes that play a role in the metabolism of serotonin, noradrenaline, dopamine and adrenaline. MAOIs inhibit breakdown of the neurotransmitters important in determining mood, which results in the antidepressant effect.
(3) Selective serotonin reuptake inhibitors (SSRIs), which work by increasing the actions of serotonin at nerve endings. These agents increase the life of serotonin in the synapse and facilitate neurotransmission. The choice of drug is based on the requirement of the individual patient. Any other illness, current drug therapy and previous responses to antidepressants are taken into consideration in choosing an appropriate agent.
Q7 Amitriptyline hydrochloride belongs to the tricyclic group of antidepressant drugs.
Q8 Dosage can be started at 75 mg per day and increased to 150–200 mg per day if necessary. When taken at night, the sedative effect of this agent has a beneficial effect on the patient’s sleep pattern.
Q9 Tricyclic antidepressants cause sedation and possess several other side effects.
The antimuscarinic (atropine-like) effects of these agents include dry mouth, blurred vision, raised intraocular pressure, postural hypotension, impo-tence, changes in cardiac rhythm and muscle tremors. They can also cause obstruction of the bladder neck, followed by difficulty in initiating micturition.
Q10 There is a delay of one to two weeks in the onset of response to all antidepressants. This might be due to the time taken to override the feedback mechanisms at the nerve endings. Therefore, Mrs Ford does not need a different medication at this stage, only reassurance that the drug will soon become effective.
Q11 The patient can be prescribed an SSRI as an alternative to amitriptyline.
Q12 An SSRI, such as fluoxetine, can be started at a dose of 20 mg per day. Although similar in their efficacy and time course to the tricyclic drugs, the advantage of the SSRIs is their lack of serious side effects, such as cardiotoxicity, sedation, blurred vision, dry mouth and so on, which are associated with tricyclic antidepressants.
Q13 Patients who take SSRIs might develop gastrointestinal disturbances such as dyspepsia, nausea and vomiting, weight gain, headaches because of the vasodilator effects of serotonin; in some patients insomnia may occur.
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Q14 MAOIs, such as phenelzine and isocarboxazid, affect the sympathetic nervous system by inhibiting one or both forms of brain monoamine oxidase. Their sympathomimetic effects can produce a feeling of well-being and increased energy, which is helpful for depressed patients. However, psychosis may occur in a susceptible individual or may follow over-administration of these agents. An increase in sympathomimetic action (such as occurs with use of amphetamines, which increase the release of noradrenaline) can result in a lethal hypertensive crisis. In addition, a hypertensive crisis can also be initiated if the patient consumes a diet rich in amines; foods with a high amine content include cheese, pickles, broad beans and wine.