Depressive Disorders-oxford shoter

Depressed mood is a unique symptom of depressive disorders.

Depressive disorders always present with depressed mood as the most prominent symptom.

The clinical presentations of depressive states are uniform and consistent.

The concept of an 'episode' of clinical depression is universally agreed upon.

The ICD-10 classification provides a clear distinction between severe and less severe depressive disorders.

Reduced energy is not a central feature of depressive disorders.

Neurological disorders can cause depressed mood as a symptom of the disorder.

The mood of a patient with severe depressive episode is alleviated in circumstances where ordinary feelings of sadness would be alleviated, such as in pleasant company or after hearing good news.

Some patients with severe depressive episode maintain a smiling exterior despite deep feelings of depression.

The gestalt of a patient with severe depressive episode is characterized by erect posture and an upright head.

Patients with severe depressive episode often experience a diurnal variation of mood, with their mood improving as the day wears on.

Depressive cognitions in patients with severe depressive episode are limited to feelings of worthlessness and pessimism.

Feelings of guilt in patients with severe depressive episode are always attached to specific past events.

Lack of interest and enjoyment is a rare symptom in patients with severe depressive episode.

In depression, psychomotor changes include increased energy and speed of thought.

Anhedonia is not a key symptom of melancholic depression.

Biological symptoms include decreased appetite and weight gain.

Depressed patients always experience sleep disturbance in the form of excessive sleeping.

Anxiety is a rare symptom in severe depression.

Irritability is never a core presenting feature in adolescents with depression.

Depressed patients never experience depersonalization or dissociative symptoms.

Depressive pseudodementia is a condition that is more common in younger individuals than in the elderly.

In psychotic depression, there is no impairment of insight and patients are aware of their mistaken beliefs.

Delusions of severe depressive disorders are always mood-incongruent.

Patients with a delusion of guilt may believe that they have done something good and will be rewarded.

Cotard's syndrome is a mild depressive disorder characterized by a lack of energy.

Agitated depression is a condition that is seen more commonly among younger individuals than among middle-aged and elderly patients.

Retarded depression is a condition that is characterized by excessive motor activity.

Inattention to basic hygiene and nutrition is a common feature of mild depressive disorders.

Depressive disorders are always characterized by a complete loss of function in social and occupational spheres.

Depressive stupor is a common occurrence in patients with severe depressive disorder.

Patients in depressive stupor often exhibit aggressive behavior.

Patients in depressive stupor always recall events that took place during the period of stupor.

Atypical depression is a severe form of depressive disorder.

Kraepelin's description of depressive stupor mentioned that patients often defend themselves from pinprick.

Patients in depressive stupor often feed themselves without assistance.

Patients with atypical depression have a later onset of illness and a more acute course.

Depressive stupor is characterized by a high level of physical activity.

Mixed depression is characterized by a complete lack of anxiety and agitation.

Mild depressive disorders are characterized by delusions and hallucinations.

Patients with mild depressive disorders often experience early-morning waking.

The diagnosis of atypical depression predicts a poor response to modern antidepressant drug treatment.

Mixed depression is only seen in patients with bipolar disorder.

The ICD-10 classification provides a clear distinction between mild and severe depressive disorders.

In ICD-10, patients with minor anxiety– depressive disorder are diagnosed under the category of mood disorders.

The DSM-5 includes a category of 'Mixed Anxiety and Depressive Disorder'.

Patients with minor anxiety– depressive disorders rarely present to primary care doctors with somatic symptoms.

In DSM-5, Persistent Depressive Disorder (Dysthymia) requires symptoms to have persisted for at least 1 year.

Dysthymia is characterized by depressive symptoms that are severe enough to meet criteria for a depressive episode.

The diagnosis of minor anxiety– depressive disorder is clearly defined in both ICD-10 and DSM-5.

Patients with minor anxiety– depressive disorders typically present with a uniform set of symptoms.

In most cultures, sadness, joylessness, anxiety, and lack of energy are uncommon symptoms of depression.

Somatization of depression is more frequent and prominent in western cultures.

Particular cultures have no unique ways of dealing with painful emotions produced by loss.

The diagnosis of depression should not take cultural variations into account.

The term ‘minor’ accurately captures the serious consequences of affective disorders for an individual.

Depression is overdiagnosed in primary care, particularly in most countries.

Somatic presentations of depression are rare in non-western cultures.

Cultural stigmatization of mental illness has no impact on the presentation of depression.

The use of somatic metaphors for emotional suffering is uncommon in non-western cultures.

The classification of depressive disorders based on presumed aetiology is widely accepted.

The symptomatic picture of melancholic depression is uniform and consistent across patients.

The concept of reactive depression is no longer used in modern classification systems.

The distinction between severe and less severe depressive disorders is clearly defined in ICD-10.

Lewis (1934) suggested that every illness is solely the result of environmental factors.

Aetiological factors are not considered in classifying depressive disorders.

Classification by symptomatic picture is a widely accepted method of classifying depressive disorders.

DSM-5 and ICD-10 have a unified approach to classifying depressive disorders.

According to the classification by symptom profile, melancholic depression is a type of non-major depressive episode.

The presence of psychotic features in depression is always accompanied by melancholic symptoms.

Kraepelin's classification included a division into three groups: unipolar depression, bipolar disorder, and schizoaffective disorder.

Atypical depression is a type of melancholic depression.

Most patients with depressive disorders have melancholic symptoms of some kind.

Neurobiological abnormalities are more commonly found in patients with non-melancholic depression.

The diagnosis of melancholic depression is not a distinct subtype of depression, but rather a point on a continuum of severity of depression.

Tricyclic antidepressants are less effective in treating melancholic depression than selective serotonin reuptake inhibitors (SSRIs).

DSM-5 and ICD-10 are entirely satisfactory classification systems.

Comorbidity with anxiety disorders is a rare occurrence in depressive disorders.

In DSM-5, the term 'unipolar mania' is still used to describe a specific type of mania.

The 12-month prevalence of major depression in the community is around 10–20%

The full diagnostic criteria for major depression are always met in adjustment disorders.

Rates of major depression are about three times as high in women as in men, across different cultures.

Seasonal affective disorder is characterized by symptoms such as insomnia and decreased appetite.

Dementia and depressive disorders can be easily distinguished based on cognitive impairment.

Recurrent brief depression is a type of depression that is only seen in women and is linked to the menstrual cycle.

The epidemiology of depressive disorders is well-established and easily determinable.

The lifetime rates of major depression in different studies vary considerably, in the range 1–10%.

The mean age of onset of major depression is about 35 years.

In DSM-5, mood disorders secondary to a medical condition are classified as a separate category.

The distinction between depressive disorders and schizophrenia is always clear-cut.

Major depression has a low comorbidity with other disorders, particularly anxiety disorders and substance misuse.

The ICD-10 classification provides a clear distinction between depressive disorders and anxiety disorders.

ICD-10 and DSM-5 both classify depressive episodes based on the presence of psychotic features.

The lifetime risk for dysthymia is around 10%.

For most clinical purposes, it is better to classify disorders rather than describe them systematically.

Atypical depression is a separate category in ICD-10, but is classified as a specifier in DSM-5.

The ICD-10 classification provides a clear distinction between severe and less severe depressive disorders, but does not specify the exact criteria for the distinction.

The 1-week prevalence of mixed anxiety and depression in the community is around 5%.

Recurrent brief depression is classified under the same heading in both ICD-10 and DSM-5.

Rates of dysthymia are higher in men and in the unemployed.

The risk of depression in a first-degree relative of a proband is increased about twofold.

Investigators have employed only one main conceptual approach to elucidate the mechanisms of depression.

The aetiology section in the current chapter is not structured to illustrate various ways of approaching research into the causation of psychiatric disorder.

Family and twin studies have not found any correlation between depression and genetic factors.

The psychological and biological approaches to depression research represent the same level of enquiry.

The current chapter does not provide any information about the role of current life difficulties and stresses in provoking depression.

The text does not mention anything about the predisposing factors of depression in adulthood.

There is complete knowledge about the mechanisms involved in the translation of predisposing and provoking factors into clinical symptomatology.

The heritability of major depression is estimated to be higher than that of bipolar disorder or schizophrenia.

Twin studies have suggested that susceptibility to major depression and generalized anxiety disorder involves different genes and environmental risk factors.

The genetic liability to depression results from the combined action of a single gene of major effect.

The gene coding for the serotonin transporter has a single allelic variant that influences the expression of transporter sites.

GWAS studies in depression have reported several convincingly replicated loci.

A recent whole genome sequencing study identified multiple genetic markers associated with depression.

The mode of inheritance of depression fits a simple Mendelian pattern.

The heritability estimates for depression are consistently higher in men than in women.

The first approach to overcome the third problem of association is to separate events that are undoubtedly independent of illness from events that may have been secondary to the illness.

There is a sixfold excess of adverse life events in the months before the onset of depressive disorder, but only in established melancholic-type disorders.

Life events are important antecedents of all forms of depression, but are relatively more important in established melancholic-type disorders.

Neuroticism, as measured by the Eysenck Personality Questionnaire, is associated with decreased risk of depression after adverse life events.

Loss of a parent by death in childhood increases the risk of depressive disorder in adulthood.

Remission from depression is often associated with 'threat' life events.

Gross disruption of parent-child relationships, such as physical and sexual abuse, is a risk factor for anxiety disorders only.

The importance of life events in the onset of a depressive episode increases as the number of episodes increases.

Mothers with postnatal depression often manifest a rearing style that is characterized by overprotection and excessive care.

Vulnerability factors, such as poor social support, are not associated with an increased risk of depression.

The mechanism of the association between poor social support and depression is clear and well-established.

Stressful events are not a precipitating factor for depressive disorders.

Cognitive style characterized by sociotropy is associated with decreased risk of depression after adverse life events.

The events immediately preceding a depressive disorder are always the direct cause of the disorder.

Personality features have no influence on the way people respond to adverse circumstances and, thus, do not affect the likelihood of depressive disorders.

The genetic risk of depression is not influenced by inheritance of particular character traits and cognitive styles.

The effects of physical illness can only lead to mood disorders in predisposed individuals.

Endocrine disorders are a type of brain disease that can cause mood disorders.

Major depression occurs in all patients with Cushing’s disease.

Organic mood disorders can never provide clues to aetiology.

The puerperium is a medical illness that can cause mood disorders.

Cushing’s disease is the only medical condition that can cause mood disorders.

Depressive disorders in patients with Cushing’s disease always remit after cortisol levels are restored to normal.

The distinction between organic and non-organic mood disorders is always clear-cut.

Cognitive theories propose that depressive cognitions are a result of a primary disturbance of mood.

Patients with severe depressive episode often experience a diurnal variation of mood, with their mood worsening as the day wears on.

Cognitive distortions include arbitrary inference, selective abstraction, and rationalization.

Beck's theory proposes that depressive cognitions are limited to feelings of worthlessness and pessimism.

Cognitive theories suggest that depressive disorders are a result of illogical ways of thinking, but do not specify what these ways are.

Most psychiatrists regard depressive cognitions as a primary cause of depressive disorders.

Dysfunctional beliefs or schemas, such as 'No-one really likes me', are established in adulthood and affect the way a person responds to stress and adversity.

Abnormalities in information processing, such as negative biases in facial expression recognition, can only be demonstrated in depressed patients.

The monoamine hypothesis suggests that depressive disorder is due to an abnormality in the release of a single neurotransmitter, serotonin, in the brain.

Structural and functional imaging techniques have not been used to elicit changes in the neural circuitry that underpins the expression of clinical affective symptomatology.

Depressive disorders are not associated with distinct and persistent neuropathological changes in relevant brain regions.

The prognosis of mood disorders improves as the number of episodes increases.

Plasma tryptophan levels are increased in untreated depressed patients, particularly in those with melancholic depression.

There is consistent evidence that depressed patients who have died, usually by suicide, have lowered brain concentrations of 5-HT or 5-HIAA.

Cerebrospinal fluid (CSF) studies have found a consistent reduction in CSF concentrations of 5-hydroxyindoleacetic acid (5-HIAA) in drug-free patients with major depression.

Neurochemical brain imaging studies have found a widespread increase in 5-HT1A receptor binding throughout the cortical and subcortical regions in depressed individuals.

The synthesis of 5-HT in the brain is independent of the availability of its precursor amino acid, l-tryptophan.

Decreases in plasma tryptophan levels are likely to be an important causal factor in the impairments of brain 5-HT function in depressed patients.

Tryptophan depletion in healthy subjects with a family history of mood disorder produces significant clinical depressive symptomatology.

Noradrenaline receptors in the brain can be divided into only two subclasses.

Low brain 5-HT function is sufficient to cause depression.

Increasing brain noradrenaline function decreases plasma concentrations of adrenocorticotropic hormone (ACTH), cortisol, and growth hormone.

The synthesis of brain 5-HT is dependent on the availability of its amino acid precursor, tyrosine.

Unmedicated euthymic patients with a personal history of mood disorder do not undergo a rapid but temporary depressive relapse when exposed to tryptophan depletion.

GABA concentrations are higher in patients with panic disorder.

There is evidence for increased levels of glutamate in the anterior brain regions in depressed patients.

The NMDA-receptor antagonist ketamine has no effect on patients with treatment-refractory depression.

About 20% of patients with Cushing's syndrome suffer from major depression.

Endocrine abnormalities are not found in depressive disorder.

The hypothalamic-pituitary-adrenal axis is not affected in depressive disorders.

Plasma cortisol secretion is decreased in about 50% of patients with depressive disorder.

The adrenal gland is decreased in size in patients with depressive disorder.

Cortisol response to corticotropin (ACTH) challenge is decreased in patients with depressive disorder.

Glutamate levels are not being studied in mood disorders.

Desipramine and clonidine stimulate the release of growth hormone in patients with melancholic depression.

α-Methyl-para-tyrosine (AMPT) causes significant depressive symptoms in healthy subjects.

Dopamine function is well studied and clearly understood in depression.

Low levels of homovanillic acid (HVA) are found only in patients with psychomotor retardation.

Abnormalities in monoamine function are only found in unmedicated depressed patients.

Lowering 5-HT and dopamine function is sufficient to cause clinical depression in anyone, regardless of prior illness.

Decreased levels of free thyroxine are commonly found in depressed patients.

Administration of CRH to animals produces changes in neuroendocrine regulation, sleep, and appetite that are opposite to those found in depressed patients.

Childhood trauma does not affect HPA axis regulation.

CRH has a neurotransmitter role in cortical regions of the brain.

About 50% of depressed patients have a blunted TSH response to intravenous TRH.

Cytokines can induce expression of the tryptophan-metabolizing enzyme indoleamine 2, 3-dioxygenase, which increases tryptophan levels.

HPA axis changes in depressed patients are always state abnormalities that remit when the patient recovers.

About 80% of depressed inpatients do not show the normal suppression of cortisol secretion induced by administering 1 mg of the synthetic corticosteroid dexamethasone.

In experimental animal studies, early adverse experiences do not produce longstanding changes in HPA axis regulation.

Dexamethasone non-suppression is more common in depressed patients with anxiety.

Abnormalities in the dexamethasone suppression test are confined to mood disorders.

The glucocorticoid receptor hypothesis of depression suggests that dysfunction of the HPA axis and the resulting depressive syndrome are linked to genetic or acquired defects of serotonin receptors.

Animal experimental studies have found that antidepressant medication decreases expression of glucocorticoid receptors.

The dexamethasone suppression test is a diagnostic marker of melancholic depression.

The dexamethasone suppression test is a specific test for mood disorders.

The dexamethasone suppression test is a highly sensitive test for diagnosing depression.

Abnormalities in functional brain imaging in depression support a single structure model of mood disorders.

The default mode network becomes active during task-based activity.

Deficits in executive function are not prominent in patients with depression.

Cognitive impairments in patients with depression persist even after the mood disorder remits.

The neural circuitry that underpins emotional processing in depression is characterized by decreased limbic processing of aversive material.

Adverse early experiences such as parental conflict or abuse do not play a part in shaping features of personality that determine vulnerability to depression.

The predisposition to develop depressive disorders has no genetic contribution.

Neuropsychological changes in mood disorders are limited to attention and learning.

Recordings of the sleep EEG have shown a decrease in deep sleep in patients with major depression.

Selective REM sleep deprivation can produce a temporary worsening of mood in depressed patients.

Enlarged lateral ventricles are typically seen in younger subjects with early-onset depression.

The neurotrophic hypothesis of depression suggests that stress can lead to an increase in neurons and upregulation of adult neurogenesis, particularly in the hippocampus.

In major depression, decreased deep white matter hyperintensities are associated with late onset of depressive disorder.

Cerebral blood flow and metabolism are negatively correlated.

Decreased REM sleep latency is not a characteristic of sleep changes in depression.

Many effective antidepressant drugs increase REM sleep time and the latency to its onset.

The neural basis of emotional processing is not closely related to the pathophysiology of depressive disorders.

Monoamine neurotransmission is not capable of altering emotional processing at both a behavioural and neural level.

Adverse childhood experiences do not play a significant role in the risk of subsequent depression.

Genetic factors do not interact with environmental and interpersonal factors in a complex manner to contribute to the development of depressive disorders.

Recent stressful life events and difficulties are not significant risk factors for the development of depressive disorders.

Neurobiological and psychological mechanisms of depressive disorders are mutually exclusive.

The impact of genetic factors on the risk of depression is not partially mediated through an increased risk of early adverse experiences.

Major depression is not a disorder with important genetic, environmental, and interpersonal determinants.

About 75% of patients with recurrent depression achieve a period of 5 years of clinical stability with good social and occupational performance.

About 5% of patients who present with a depressive disorder will eventually have a manic illness.

Dysthymia is a chronic disorder that lasts for less than a year.

The development of mania is a common occurrence in patients with dysthymia.

The average length of a depressive episode is about 1 year.

Patients with minor depressive disorders have a higher recurrence rate than those with major depression.

Around 50% of patients with major depression will experience further episodes.

Mortality is decreased in patients with depression due to lower rates of suicide.

Patients with recurrent major depression experience on average about 2 further episodes over a 25-year follow-up.

Treatment of depression has no impact on mortality rates.

About 20% of depressed patients do not achieve complete symptom remission between episodes.

The risk of suicide is higher in bipolar disorder than in unipolar disorder.

The age of onset of major depression typically occurs after the age of 21.

The interval between episodes of major depression becomes progressively longer.

Duloxetine fatalities have been reported after consumption of as little as 500 mg.

MAOIs are recommended as first-line antidepressant drugs.

Moclobemide is more effective than conventional MAOIs for patients with resistant depression.

Reboxetine is a sedating antidepressant drug.

Lithium has established efficacy as a sole treatment for unipolar depression.

Lithium augmentation can produce a rapid amelioration of the depressed state within 48 hours.

The effects of lithium augmentation are restricted to patients taking tricyclic antidepressants.

Agomelatine may have a different mechanism of action, involving the activation of serotonin receptors.

Trazodone and mirtazapine are safer than tricyclic antidepressants in overdose.

Antidepressant drugs have similar clinical response rates in patients with dysthymia and major depression.

Tricyclic antidepressants are more effective than SSRIs in the treatment of moderate depression.

Antidepressants are effective in the treatment of minor depression.

Lofepramine is a tricyclic antidepressant that is particularly hazardous in overdose.

Venlafaxine is an SSRI that is more effective than tricyclic antidepressants in patients with more severe depressive states.

Duloxetine is an SNRI that is more effective than SSRIs in the treatment of depression.

Tricyclic antidepressants have a higher dropout rate due to side effects compared to SSRIs in short-term clinical trials.

Anticonvulsants such as carbamazepine, valproate, and lamotrigine are not useful in the management of bipolar disorder.

Lamotrigine has not been shown to have antidepressant effects in placebo-controlled trials in bipolar depressed patients.

Atypical antipsychotic agents, used at low doses, are not of benefit when combined with antidepressants in non-psychotically depressed patients who have failed to respond to antidepressant treatment alone.

The addition of atypical antipsychotic drugs to ineffective SSRI treatment does not result in clinical remission.

Electroconvulsive therapy is not described in Chapter 25.

Antipsychotic drugs are not combined with antidepressant drugs in the treatment of patients with depressive psychosis.

The addition of olanzapine to antidepressant treatment does not result in clinical remission.

Cognitive behaviour therapy is superior to a waiting list control in relieving depressive symptomatology, but it is not generally superior to other structured psychological treatments.

Supportive psychotherapy is a type of therapy that focuses on the identification and resolution of current life difficulties, and it is less effective than problem-solving therapy in moderately depressed patients in primary care.

Randomized trials suggest that problem-solving treatment is as effective as drug treatment in moderately depressed patients in primary care.

Cognitive behaviour therapy is not effective as a sole treatment for patients with severe depression, and this view is supported by trial evidence.

Behavioural activation is a type of therapy that uses the principles of operant conditioning to track the links between actions and emotional outcomes, and it is less effective than cognitive behaviour therapy in depression.

Interpersonal therapy is less effective than antidepressant medication in depressed patients.

The National Institute for Health and Clinical Excellence concluded that cognitive behaviour therapy is superior to drug treatment in moderately depressed outpatients.

In severely depressed inpatients, ECT is probably inferior to antidepressant drug treatment in the short term.

Delusions are not a feature that distinguishes patients who respond to full ECT from those who respond to placebo.

Relapse rates are low in depressed patients who have not responded to full trials of medication and are treated with ECT.

In major depression, psychotherapies have been extensively evaluated and are proven to be more effective than antidepressant medication.

The overall response rate is about 30% for ECT and 20% for simulated treatment.

Cognitive behaviour therapy is superior to other structured therapies such as interpersonal therapy in the management of mild to moderate depression.

ECT is considered to be a relatively ineffective treatment for depressive disorders with marked weight loss, early-morning waking, retardation, and delusions.

Couple therapy is not significantly more effective than a waiting list control.

Dynamic psychotherapy aims to resolve underlying developmental conflicts and attendant life difficulties that are believed to be causing or maintaining the depressive disorder.

More recent meta-analyses have shown that short-term psychodynamic therapy is less effective than cognitive behaviour therapy in depressed patients.

The antidepressant effect of sleep deprivation is permanent and does not disappear after the next night’s sleep.

Bright light treatment is usually given for a few minutes in the morning.

Patients with ‘atypical’ depressive features such as overeating and oversleeping respond poorly to bright light treatment.

The usual onset of the antidepressant effect of bright light is within 2–5 months.

Lieverse et al. (2011) showed that bright light treatment is not effective in non-seasonal depression.

The duration of exposure to bright light usually needs to be less than an hour.

In patients with recurrent depression, maintenance antidepressant treatment for 1–2 years has been shown to lower the relapse rate from 78% to 18%.

Cognitive therapy given during an acute phase of depression has been shown to lead to a less sustained improvement in depressive symptomatology compared to antidepressant drug treatment.

Lithium carbonate has been shown to be highly effective in the prevention of recurrent unipolar depression.

Maintenance treatment with cognitive therapy has been shown to be less effective in preventing relapse compared to maintenance medication.

Mindfulness-based cognitive therapy (MBCT) has been shown to be less effective in lowering the risk of relapse in patients with recurrent depression compared to maintenance antidepressant treatment.

Combining interpersonal therapy with medication in the treatment of the acute episode has been shown to increase relapse rates over the following 12 months.

In patients who achieve remission from depression with interpersonal therapy as a sole treatment, continuation therapy has been shown to be unhelpful in preventing recurrence.

Stopping antidepressants soon after a treatment response has been obtained is associated with a low risk of relapse.

Continuing antidepressant treatment for 6 months past the point of remission doubles the relapse rate.

Relapse refers to the worsening of symptoms after a period of complete recovery from a single episode of mood disorder.

Treatment to prevent relapse should be called prophylactic or maintenance treatment.

About two-thirds of patients who are withdrawn from medication will relapse during the next year.

Involvement of the family in the management of depressive disorders is unlikely to improve the outcome.

The majority of relapses occur in the last 6 months of the first year after medication withdrawal.

Antidepressant drug treatment is indicated for patients with mild depressive conditions.

Placebo-controlled studies have reached the conclusion that continuing antidepressant treatment for less than 6 months halves the relapse rate.

Patients with severe depressive disorders can be treated at home if they have a supportive family.

Work can provide a valuable distraction from depressive thoughts for patients with severe depression.

Inpatient treatment is necessary for patients who live alone or whose families cannot care for them during the day.

The risk of suicide is a key factor in determining the level of care and supervision required for a patient with a depressive disorder.

Dysthymia is not an indication for antidepressant medication.

Guidelines for a stepped-care approach to the management of depression have not been developed by the National Institute for Health and Clinical Excellence.

Patients with a depressive disorder of moderate or greater severity may not require any treatment if they have a supportive family.

A depressive disorder can be diagnosed simply based on the presence of prominent depressive symptoms.

A patient's social resources are not an important consideration in the diagnosis of depressive disorder.

The effects of the disorder on other people, such as family members, are not a significant consideration in the diagnosis of depressive disorder.

A patient's history of previous mood disturbance is not an important factor in assessing the current disorder.

The severity of a depressive disorder is solely determined by the presence of biological symptoms.

Aetiology is not an important consideration in the diagnosis of depressive disorder.

The risk of suicide is not a significant consideration in the diagnosis of depressive disorder.

SSRIs are never used as a first-choice treatment for depression.

Lofepramine is a sedating compound.

Tricyclic antidepressants are commonly used as first-choice agents for patients with severe depression.

Mirtazapine is used to treat patients who require concomitant sedation.

Concomitant treatment with nonsteroidal anti-inflammatory drugs increases the risk of bleeding with SSRIs.

The dosage and precautions for antidepressant drugs are described in Chapter 25.

Amitriptyline is a commonly used first-choice agent for treating depression.

The choice of antidepressant drug should be made without considering the patient's medical history and potential side effects.

In patients with moderate to severe depression, adding cognitive behaviour therapy to antidepressant medication is unhelpful.

If a depressive disorder does not respond within a reasonable time to a chosen combination of antidepressant drugs, graded activity, and psychological treatment, switching to a different antidepressant is the first step.

SSRIs have a clear dose–response relationship.

Switching from an SSRI to a different class of drug has been shown to be significantly better in terms of remission rate than switching to a second SSRI.

If a patient does not respond to one antidepressant, the next step is to increase the dose of the same medication.

Couple therapy is not a helpful addition in depressed patients where problems with a partner are playing a role in maintaining the disorder.

Therapy directed towards self-examination is particularly helpful in patients with severe depression.

In patients with recurrent depressive disorders, therapy directed towards self-examination may be offered during acute episodes.

ECT is usually considered as a first-line treatment of depression.

The therapeutic effect of antidepressant drugs is usually faster than that of ECT.

Patients who refuse to drink enough fluid to maintain an adequate output of urine are candidates for ECT.

Patients with depressive psychosis respond better to ECT than to a combination of an antidepressant drug and an antipsychotic drug.

The patient should be encouraged to engage in activities that they are likely to fail at due to slowness or poor concentration.

Psychotherapy can be used as the sole therapy for patients with severe depression with melancholic features.

The therapeutic response to psychotherapy is usually faster than that to antidepressant drugs.

The more structured therapies such as interpersonal therapy and cognitive behaviour therapy have a weaker evidence base with regard to the treatment of moderate to severe depression.

Aripiprazole is more likely to cause metabolic side effects than other atypical antipsychotics.

The combination of lithium with SSRIs is contraindicated due to the risk of 5-HT neurotoxicity.

The aim of lithium augmentation is to obtain a lithium concentration within the range of 1.0-1.5 mmol/l.

Risperidone is less likely to cause weight gain compared to olanzapine and quetiapine.

Lithium augmentation is usually not well tolerated in depressed patients.

About 20% of depressed patients will show a useful response to lithium augmentation over 1-3 weeks.

The discontinuation rate due to adverse effects is significantly lower with atypical antipsychotics than with placebo.

The combination of lithium with MAOIs or clomipramine is not effective in depressed patients who are otherwise refractory to treatment.

SSRIs are usually combined with serotonergic agents like bupropion in combination treatment.

When switching between agents with different pharmacological properties, cross-tapering can be employed.

Amitriptyline is slightly less effective than SSRIs in patients with severe depression.

The evidence for combination treatment with antidepressants is abundant and well-documented.

Combination of a tricyclic antidepressant with SSRIs is a recommended approach.

Antipsychotic drugs are not useful in non-psychotic resistant depression except at high doses.

Atypical antipsychotic drugs are used in high doses to augment SSRIs in nonpsychotic depression.

In patients with psychotic depression, it is usually best to prescribe a combination treatment of antidepressant and antipsychotic medication.

The addition of tri-iodothyronine (T3) to ineffective tricyclic antidepressant treatment has consistently shown to be highly effective in all studies.

Tri-iodothyronine (T3) is typically started at a dose of 20 μg daily and increased to 40 μg after 1 week if tolerance is good.

The use of ECT is contraindicated in patients with evidence of cardiovascular disease.

The response to ECT is not affected by medication resistance.

Tri-iodothyronine (T3) augmentation is only effective in treating depressive disorders with underlying thyroid activity.

The addition of tri-iodothyronine (T3) to antidepressant treatment is always associated with severe side effects.

ECT is only beneficial in patients who have not responded to antidepressant drugs and have no psychotic features.

The efficacy of tri-iodothyronine (T3) augmentation is established for all types of antidepressant drugs.

Among patients who have had three episodes of major depression, the likelihood of another episode is 80%.

Lithium is a first choice medication for long-term maintenance treatment of recurrent depression in most patients.

In patients with prolonged depression, it is particularly important to watch carefully for suicidal intentions.

Maintenance treatment should be considered if a patient has had one previous episode of depression within a 5-year period.

Cognitive behaviour therapy is only effective in lowering the risk of relapse in patients with no residual depressive symptomatology.

A study found that cognitive behaviour therapy was less effective than treatment as usual in bringing about a therapeutic response.

General practitioners do not play a key role in the long-term monitoring of patients with depressive disorders.

Annual monitoring of body weight, blood pressure, glucose, and lipids is not recommended for patients with depressive disorders.

The relapse rate in the year after ECT may be as low as 20%.

A randomized study found post-ECT prophylaxis with a combination of lithium and nortriptyline to be less effective than maintenance ECT in sustaining remission.

The choice of antidepressant medication is not influenced by the patient's response in the acute or continuation phase of treatment.

After recovery, the patient should be followed up for several weeks by the psychiatric team or general practitioner.

Lithium does not have a specific effect on lowering the risk of suicidal behaviour in patients with mood disorders.

If residual symptoms are still present, it is safer to withdraw medication.

Psychotherapy is not helpful in readjusting lifestyle to reduce the risk of further depressive episodes.

Community nurses and nurse therapists do not play a valuable role in delivering treatment for depressive disorders.

Newer antidepressant drugs are not better tolerated in the longer term than older antidepressant drugs.

A mild depressive episode requires at least three symptoms of A and two symptoms of B.

The severity of symptoms and degree of functional impairment are not considered in the classification of depressive episodes.

All three symptoms of A are required for a severe depressive episode, but only three symptoms of B are required.

Reduced concentration is a symptom of A in the ICD-10 classification.

The ICD-10 classification provides a clear distinction between moderate and mild depressive episodes.

According to the ICD-10, at least three of the symptoms listed are required to make a diagnosis of depression 'with somatic features'

In DSM-5, the diagnosis of depression 'with melancholic features' requires either 'loss of interest' or 'lack of emotional reactivity' to be present

Weight loss of 3% or more of body weight in the last month is a diagnostic criterion for depression 'with somatic features' in ICD-10

Early-morning waking (2 hours or more before usual time) is a diagnostic criterion for depression 'with melancholic features' in DSM-5

Marked loss of appetite is a diagnostic criterion for depression 'with melancholic features' in both ICD-10 and DSM-5

What is the classification term used for a depressive episode that is characterized by a lack of energy and depression?

What is the DSM-5 classification term used for a depressive disorder that is characterized by persistent depressive symptoms that have persisted for at least 1 year?

What is the ICD-10 classification term used for a depressive disorder that is characterized by recurrent episodes of depression?

What is the classification term used for a depressive disorder that is characterized by brief episodes of depression?

What is the ICD-10 classification term used for a depressive disorder that is characterized by mild depressive symptoms?

The DSM-5 includes a specifier 'with peripartum onset' for depressive disorders.

The ICD-10 classification provides a clear distinction between mild and moderate depressive disorders.

Depressive cognitions in patients with severe depressive episode are limited to feelings of worthlessness and pessimism.

Agitated depression is a condition that is seen more commonly among middle-aged and elderly patients than among younger individuals.

In DSM-5, Persistent Depressive Disorder (Dysthymia) requires symptoms to have persisted for at least 2 years.

The hypothalamic-pituitary-adrenal axis is studied in the context of genetic epidemiology.

Neurogenesis, neurotropins, and synaptic plasticity are related to neuropsychology and brain imaging.

Cognitive style is investigated in the context of early environment.

Monoamines are related to psychological investigations.

Personality is investigated in the context of genetic epidemiology.

What is the primary genetic contribution to mood disorders?

How do adverse early life experiences affect development?

What triggers depressive disorders in people who lack social support?

What is associated with changes in the activity of monoamine neurons and the HPA axis?

What may involve a loss of synaptic plasticity and dendrite formation?

What suggests persistent biological vulnerability in mood disorders?

Freud suggested that melancholia results from the loss of a loved one through death.

Depressed patients often appear to be critical of others, according to Freud's theory.

Freud's theory proposes that depression occurs when feelings of love and hostility are present at the same time, but not simultaneously.

Melanie Klein believed that weaning represents a significant symbolic gain for the infant.

According to Melanie Klein, 'depressive anxiety' leads to attempts at revenge and hatred towards others.

Freud's theory of depression is based on the idea that the patient's feelings of love are redirected against themselves as self-reproach.