Chapter 7 – Mood Disorders And Suicide Flashcards
Explain the criteria for major depressive episodes
To receive this diagnosis the person must be markedly depressed or show a marked loss of interest in pleasurable activities for most of every day and for most days for at least two weeks. In addition to these obvious emotional symptoms, he or she must show at least three or four other symptoms that range from cognitive symptoms such as feelings of worthlessness or guilt and thoughts of suicide, to behavioural symptoms such as fatigue or physical agitation, to physical symptoms such as changes in appetite and sleep patterns
Explain the criteria for manic episodes
The person shows a markedly elevated, euphoric, or expensive mood, often interrupted by locational outbursts of intense irritability or even violence. These extreme mood must persist for at least a week for this diagnosis to be made. In addition, three or more additional symptoms must occur in the same time., Ranging from behavioural symptoms such as notable increase in goal-directed activity or often involving loosening of personal and cultural innovations as in multiple sexual, political, or religious activities, to mental symptoms were self-esteem becomes grossly inflated and mental activity may speed up such as flights of ideas or racing thoughts, to physical symptoms such as decreased need for sleep or psychomotor agitation
Explain the prevalence of mood disorders
The ochre with alarming frequency at least 15 to 20 times more frequently than schizophrenia, for example, and at almost the same rate as all the anxiety disorders taken together. Unipolar major depressive disorder is the most common at nearly 17% lifetime prevalence rates. Rates for unipolar depression are always much higher for women then for men.
Bipolar disorder is much less common and there is no discernable difference in the prevalence rates between the sexes. The lifetime risk for developing this disorder is about 1%.
Differentiate depressions that are not mood disorders from those that are
Normal depressions are nearly always the result of recent stress.
Includes loss and the grieving process which usually includes four phases of normal response: numbing and disbelief; yearning and searching for the dead person; disorganization and despair that sets in when the person accepts the loss as permanent; and some reorganization as the person gradually begins to rebuild his or her life. The normal nature of exhibiting a certain number of grief symptoms has led DSM to suggest that major depressive disorder usually not be diagnosed for the first two months following the loss, even if all the symptom criteria are met.
Also includes postpartum “blues”. Postpartum depression sometimes occurs in new mothers following the birth of a child but only postpartum blues are very common. His symptoms typically include changeable mood, crying easily, sadness, and irritability, often liberally intermixed with happy feelings. Such symptoms occur in as many as 50 to 70% of women within 10 days of the birth of their child and usually subsides on their own.
What is a mild to moderate form of depressive disorder?
Dysthymic disorder is generally considered to be mean of mild to moderate intensity, but it’s primary Hallmark is its chronicity. To qualify for a diagnosis, a person must have a persistently depressed mood most of the day, four more days than not, for at least two years. In addition, individuals must have at least two of six additional symptoms when depressed. Periods of normal mood may ochre briefly, but they usually last for only a few days to a few weeks and these normal mood are one of the most important characteristics distinguishing this disorder from major depressive disorder.
Describe criteria for diagnosing major depressive disorder and the subtypes
The diagnostic criteria for major depressive disorder or require that the person exhibit more symptoms that are required for dysthymia and that the symptoms be more persistent (not interwoven with periods of normal mood). To receive this diagnosis, a person must be in a major depressive episode (Single if initial, or recurrent) and never have had a manic, hypo manic, or mixed episode. And affected person must experience either markedly depressed moods or marked loss of interest in pleasurable activities most of every day, nearly every day, for at least two consecutive weeks. In addition to showing One or both of the symptoms, the person must experience at least three or four additional symptoms during the same period. In addition to the obvious emotional symptoms, these symptoms also include cognitive symptoms such as feelings of worthlessness or guilt and thoughts of suicide, behavioural symptoms such as fatigue or physical agitation, and physical symptoms such as changes in appetite and sleep patterns.
Subtypes include chronic major depressive disorder or, major depressive episode with melancholic features, severe major depressive episode with psychotic features, major depressive episode with atypical features, major depressive episode with catatonic features, recurrent major depressive episode with a seasonal pattern.
Discuss biological and psychological causal factors in unipolar mood disorders
Biological causal factors:
Genetic influences – family studies have shown that the prevalence of mood disorders is approximately 2 to 3 times higher among blood relatives of persons with clinically diagnosed unipolar depression than in the population at large. Twin studies also suggest a moderate genetic contribution. About 31 to 42% of the variance in liability to major depression is due to genetic influences. However, even more variance in the liability to most forms of major depression is due to non-shared environmental influences then to genetic factors.
Neurochemical factors – early attention in the 1960s and 70s focussed primarily on to neurotransmitter substances of the monoamine class – norepinephrine and serotonin – because researchers observed that antidepressant medication seem to have the effect of increasing these neurotransmitters availability synaptic junctions. This observation lead to the ones influential monoamine theory of depression, that depression was at least sometimes due to an absolute or relative depletion of one or more of these neurotransmitters at important receptor sites in the brain. However, by the 1980s it was clear that no such straightforward mechanisms could possibly be responsible for causing depression. More recent research also suggests that dopamine disfunction especially reduced activity plays a significant role in at least some forms of depression.
Abnormalities of hormonal regulatory and immune systems – the majority of attention has been focussed on the hypothalamus-pituitary-adrenaline or HPA axis. In particular on the hormone cortisol, which is excreted by the outermost portion of the adrenal glands and is regulated through a complex feedback loop. Blood plasma levels of cortisol are known to be elevated in some 20 to 40% of outpatients with depression and in about 60 to 80% of hospitalized patients with severe depression. Sustained elevations in cortisol can result from increased CRH activation, increased secretion of ACTH, or the failure of feedback mechanisms. One line of evidence that indicates the failure of feedback mechanisms in some patients with depression comes from robust findings that in about 45% of patients with serious depression, a potent suppressor of plasma cortisol in normal individuals, dexamethasone, either fails entirely to suppress cortisol or fails to sustain its suppression.
The other endocrine axis that has relevance to depression is the hypothalamus-pituitary-thyroid axis because disturbances to this axes are also linked to mood disorders.
In recent years, studies have shown that depression is also accompanied by dysregulation of the immune system.
Neurophysiological and neuroanatomical influences- exciting neurophysiological research in recent years has followed up on earlier neurological findings that damage to the left, but not the right, anterior prefrontal cortex often leads to depression. This led to the idea that depression in people without brain damage may nonetheless be linked to lower levels of brain activity in the same region. A number of studies have supported this idea. The relatively lower activity on the left side of the prefrontal cortex in depression is thought to be related to symptoms of reduced positive affect and approach behaviours to rewarding stimuli, and increased right side activity is thought to underlie increased anxiety symptoms and increased negative affect associated with increased vigilance for threatening information.
Abnormalities have also been detected in several other brain areas in patients with depression. For example, several regions of the prefrontal cortex including the orbital prefrontal cortex, which is involved in responsivity to reward, show decreased volume in individuals with recurrent depression relative to normal controls. Lower levels of activity in the dorsolateral prefrontal cortex , Which are associated with decreased cognitive control, have also been observed in individuals with depression compared to controls. Another area involved is the hippocampus. Another area is the anterior cingulate cortex, which both shows decreased volume and abnormally low levels of activation in patients with depression. This area is involved in selective attention.
Finally, the amygdala, which is involved in the perception of thread and in directing attention, tends to show increased activation in individuals with depression, which may be related to their biased attention to negative emotional information.
Sleep and other biological rhythms – patients who are depressed often show one or more of a variety of sleep problems, ranging from early-morning awakening, periodic awakening during the night, and for some, difficulty falling asleep. Such changes occur in about 80% of hospitalized patients with depression and in about 50% of outpatients. Also, research using EEG recordings has found that many patients with depression and through the first. Of REM sleep after only 60 minutes or less of sleep which is 15 to 20 minutes sooner then patients who are not depressed, and also show greater amounts of REM sleep during the early cycles that are seen in person without depression. The person with depression also get a lower than normal amount of deep sleep.
Research has found some abnormalities in all of the normal human rhythms such as circadian cycles, body temperature, propensity to REM sleep, and secretion of cortisol, thyroid stimulating hormone, and growth hormone.
Sunlight and seasons – another kind of rhythm abnormality or disturbance is seen in people with seasonal affective disorder, in which most of those affected seem to be responsive to the total quantity of available light in the environment.
Biological explanations were sex differences – it has been suggested that hormonal factors such as normal fluctuations in ovarian hormones account for sex differences. However, studies examining this hypothesis have yielded inconsistent results and overall are not very supportive.
Psychological causal factors:
Stressful life events – psychological stressors are known to be involved in the onset of a variety of disorders such as unipolar major depression. Most involve loss of a loved one, serious threats to important close relationships or to ones occupation, or severe economic or serious health problems. An important distinction has been made between stressful life events that are independent of the person’s behaviour and personality such as losing a job because ones company is shutting down we’re having one’s house hit by hurricane, and events that may have been at least partly generated by the depressed person’s behaviour or personality. These are called dependent life events and an example is being unable to resolve conflicts with a spouse. Evidence suggests that dependent life events play an even stronger role in the onset of major depression then do independent life events.
People with depression often also have a distinctly negative view of themselves and the world around them so their own perceptions of stress may resolve at least to some extent from the cognitive symptoms of their disorder rather than cause their disorder.
A number of good studies have demonstrated that chronic stress is associated with increased risk for the onset, maintenance, and recurrence of major depression.
Vulnerability and invulnerability factors in responses to stressors – there are important individual differences in how people respond to the experience of episodic or chronic life stress such as genetics.
Different types of vulnerabilities for unipolar depression – includes personality traits, negative styles of thinking about the world and one’s experiences, early childhood adversity, and lack of social support.
Personality and cognitive diathesis- neuroticism is the primary personality variable that serves as a vulnerability factor for depression. Refers to a stable and heritable personality trait that involves a temperamental sensitivity to negative stimuli. There is some evidence that high levels of introversion may also serve as vulnerability factors. The cognitive diathesis that have been studied for depression generally focus on particular negative patterns of thinking that make people who are prone to depression more likely to become depressed when faced with one or more stressful life events.
Early adversity as a diathesis – A range of adversities in the early environment such as family turmoil, parental psychopathology, physical or sexual abuse, and other forms of intrusive, harsh, and coercive parenting, can create both a short-term and a long-term vulnerability to depression. Such factors operate by increasing an individual sensitivity to stressful life events in adulthood.
Psychodynamic theories – Depression is anger turned inward. Freud hypothesize that depression can also occur in response to imagine or symbolic losses. The most important contribution of the psychodynamic approach is to depression has been their noting the importance of loss, both real and symbolic or imagined, to the onset of depression and noting the striking similarities between the symptoms of mourning and the symptoms of depression.
Behavioural theories – people become depressed either when their response is no longer produce positive reinforcement or when the rate of negative reinforcements increases. Because these ideas do not show that depression is caused by these factors, behavioural theories are no longer very influential when it comes to depression.
Becks cognitive theory –. Neck hypothesized that the cognitive symptoms of depression often proceed and cause the affect of or mood symptoms rather than vice versa. It is a diathesis-stress theory in which negative cognitions are central. First, there are the underlying dysfunctional beliefs known as depressogenic schemas which are rigid, extreme, and counterproductive. These dysfunctional beliefs need to be activated by the occurrence of some form of stress and are thought to develop during childhood and adolescence as a function of one’s negative experiences with one’s parents and significant others. Although these dysfunctional beliefs may lie dormant for years in the absence of significant stressors, when they are activated by current stressors or depressed food, they tend to feel the current thinking pattern, creating a pattern of negative automatic thoughts Dash thoughts that often occur just below the surface of awareness and involve unpleasant, pessimistic predictions. These pessimistic predictions tend to centre on the three themes of what Beck calls the negative cognitive triad: negative thoughts about the self; negative thoughts about one’s experiences and this rounding world; negative thoughts about one’s future. This tree ad is maintained by a variety of negative comment devices or errors such as dichotomous or all or none reasoning, selective abstraction, arbitrary inference.
Recent research has shown that stressors are not necessary to activate the latent depressive schemas. Simply inducing a depressed mood, for example through listening to sad music or recalling sad memories, in an individual who was previously depressed is generally sufficient to activate these schemas.
The helplessness and hopelessness theories of depression – Martin Seligman first proposed that the laboratory phenomenon known as learned helplessness might provide a useful animal model of depression. He noted that laboratory dogs who were first exposed to uncontrollable shocks later acted in a passive and helpless matter when they were in a situation where they could control the shocks. In contrast, animals first exposed to equal amounts of controllable shops had no trouble learning to control the shocks. When animals or humans find that they have no control over aversive events, they may learn that they are helpless, which makes them unmotivated to try to respond in the future. Instead they exhibit passivity and even depressive symptoms. They are also slow to learn that any response they do make is effective, which may parallel the negative cognitive set in human depression.
The reformulated helplessness theory proposes that when people are exposed to uncontrollable negative events, they ask themselves why, and the kinds of attributions they make are, in turn, central to whether they become depressed. Three critical by mentions on which attributions are made our internal/external, global/specific, and stable/unstable. People who have a relatively stable and consistent pessimistic attributional style have a vulnerability or diathesis for depression when faced with uncontrollable negative life events. This style seems to develop at least in part through social learning.
The hopelessness theory proposes that having a pessimistic attributional style in conjunction with one or more negative life events was not sufficient to reduce depression in less one first experienced a state of hopelessness. A hopelessness expectancy was defined by the perception that one had no control over what was going to happen and by the absolute certainty that an important bad outcome was going to occur or that a highly desired good outcome was not going to occur. They propose that depression-prone individuals not only tend to make global and stable attributions for negative events but also tend to make negative inferences about other likely negative consequences of the event and negative inference is about the implications of the event for the self-concept.
The ruminative response styles theory of depression – focusses on different kinds of responses that people have when they experience feelings and symptoms of sadness and distress, and how their differing response styles affect the course of their depressed feelings. When some people have such feelings, they tend to focus intently on how they feel and why they feel that way, a process called rumination, which involves a pattern of repetitive and relatively passive mental activity. Women are more likely than men to ruminate, and men are more likely to engage in a distracting activity.
These disorders are distinguished from unipolar disorders by the presence of manic or hypomanic episodes, which are nearly always preceded or followed by periods of depression.
Bipolar disorders
Describe the causal factors in bipolar disorders
Biological causal factors:
Genetic influences – there is a greater genetic contribution to bipolar I disorder then to unipolar disorder. Genes account for about 80 to 90% of the variance in the liability to develop bipolar I disorder.
Neurochemical factors – The early monoamine hypothesis for unipolar disorder was extended to bipolar disorder. There is good evidence for increased norepinephrine activity during manic episodes and less consistent evidence for lowered norepinephrine activity during depressive episodes. Serotonin Activity appears to be low in both depressive and manic phases.
Abnormalities of hormonal regulatory systems – cortisol levels are elevated, but they are usually not elevated during manic episodes. Show evidence of abnormalities on the dexamethasone suppression test, The hypothalamus-pituitary-thyroid axis
Neurophysiological and neuroanatomical influences – whereas blood flow to the left prefrontal cortex is produced during depression, during mania it is increased in certain other parts of the prefrontal cortex. There are shifting patterns of brain activity during mania and during depressed and normal moods.
Sleep and other biological rhythms – there are disturbances in biological rhythms such as circadian rhythm’s, even when symptoms have mostly remitted. During manic episodes, patients tend to sleep very little seemingly by choice, and this is the most common symptom to occur prior to the onset of a manic episode. During depressive episodes, they tend toward hypersomnia or too much sleep.
Psychological causal factors:
Stressful life events – the stressful life events are thought to influence the timing of an episode, perhaps by activating the underlying vulnerability.
Other psychological factors – Low social support, personality and Kaban to variables that interact with stressful life events such as the personality variable neuroticism.
Explain how various socio-cultural factors affect unipolar and bipolar disorders
Cross-cultural differences in depressive symptoms: for example, in some non-western cultures such as China and Japan where Rachel depression are relatively low, many of the psychological symptoms of depression are often not present and instead people tend to exhibit so-called somatic and vegetative manifestation such a sleep disturbance, loss of appetite, weight loss, and loss of sexual interest. Affected individuals May also think that physical symptoms have more legitimacy and that it is more appropriate to reveal and discuss these rather than psychological symptoms. Several possible reasons for the symptom differences stem from Asian beliefs in the unity of the mind and body, a lack of expressiveness about emotions more generally, and the stigma attached to mental illness in these cultures.
Assess treatments and outcomes of mood disorders
Pharmacotherapy: antidepressant, mood stabilizing, and antipsychotic drugs are all used in the treatment of unipolar and bipolar disorders.
In the 1950s, monoamine oxidase inhibitor’s were used because they inhibit the action of monoamine oxidase, the enzyme responsible for the breakdown of norepinephrine and serotonin once released but the adverse effects can be dangerous and sometimes fatal if foods rich in the amino acid tyramine are consumed. They are not used very often today.
The drug treatment of choice since the early 1960s until about 1990 was one of the standard antidepressants called tricyclic antidepressants because of their chemical structure such as imipramine, which are known to increase neurotransmission of the monoamine’s, primarily norepinephrine and to a lesser extent Serotonin. They are effective, however only about 50% show what is considered clinically significant improvement, and many still have significant residual depressive symptoms. Also have unpleasant side effects for some including dry mouth, constipation, sexual dysfunction, and weight gain. Highly toxic when taken in large doses.
Increasingly popular are antidepressants from the selective serotonin reuptake inhibitory or SSRI category because they have less side effects and toxicity then tricyclics. Side effects are problems with orgasm and lowered interest in sexual activity, although insomnia, increased physical agitation, and gastrointestinal distress also occur.
Recently, several new atypical antidepressants have also become increasingly popular such as bupropion (Wellbutrin) which does not have as many side effects especially sexual ones as the SSRIs, and is good for depressions with significant weight gain, loss of energy, and oversleeping.
Venlafaxine (Effexor) seems superior to the SSRIs in the treatment of severe or chronic depression, although the profile of side effects is similar to that of the SSRIs.
Ease drugs usually require at least 3 to 5 weeks to take effect and discontinuing them when symptoms have remitted may result in relapse.
Lithium has become widely used as a mood stabilizer in the treatment of both depressive and Maddock episodes of bipolar disorder her. Mood stabilizer means they have both antimanic and antidepressant effects, they exert mood stabilizing effects in either direction. Lithium has been more widely studied as a treatment of manic episodes that then of depressive episodes, and estimates are that about three quarters of manic patients show at least partial improvement. Treatment with antidepressants is associated with significant risk of precipitating manic episodes or rapid cycling although this risk is low or if the person also takes lithium. Unpleasant side effects include lethargy, cognitive slowing, weight gain, decreased motor coordination, and gastrointestinal difficulties and long-term use is occasionally associated with kidney malfunction and sometimes permanent kidney damage.
Anticonvulsants have also recently been used in the treatment of bipolar disorder her and are often effective in patients who do not respond well to lithium or who develop unacceptable side effects from it. However, the risk for attempted and completed suicide was nearly 2 to 3 times higher for patients on anticonvulsant medications then for those on lithium.
Both bipolar and unipolar patients who show signs of psychosis may also receive treatment with antipsychotic medications in conjunction with their antidepressant or mood stabilizing drugs.
Alternative biological treatments:
Electroconvulsive therapy – often used with severely depressed patients who may present an immediate and serious suicidal risk. Also used in patients who cannot take antidepressant medications or who are resistant to them. A complete remission of symptoms occur as for many patients after about 6 to 12 treatments, which induce seizures and are delivered under general anaesthesia and with muscle relaxants. Immediate side effects include confusion, although there is some evidence for lasting adverse affects on cognitions, such as amnesia and slow response time. Also very useful in the treatment of manic episodes
Trans cranial magnetic stimulation or TMS – a noninvasive technique allowing focal stimulation of the brain in patients who are awake. Brief but intense pulsating magnetic fields that induce electrical activity in certain parts of the cortex are delivered. It is painless , Effective, and has less side effects than ECT
Deep brain stimulation – explored for individuals with refractory depression who have not responded to other treatment approaches. Involves implanting an electrode in the brain and then stimulating that area with electric current
Bright light therapy – originally used in the treatment of seasonal affective disorder
Psychotherapy:
Cognitive-behavioral therapy – one of the two best-known psychotherapies for unipolar depression with documented effectiveness is cognitive-behavioral therapy or CBT which is a relatively brief form of treatment that focusses on here-and-now problems rather than on the more remote causal issues that psychodynamic psychotherapy often addresses. Cognitive therapy relies heavily on Adam Paracle approach in that patients are taught to treat their beliefs as hypotheses that can be tested through the use of behavioural experiments.
Mindfulness-based cognitive therapy can be used with people with highly recurrent depression who have been treated with medication in order to help prevent further occurrences. The logic of this treatment is based on findings that people with recurrent depression are likely to have negative thinking patterns activated when they are simply in a depressed mood. Rather than trying to alter the content of their negative thinking as in traditional cognitive therapy, it might be more useful to change the way in which these people relate to their thoughts, feelings, and bodily sensations. Involves training in mindfulness meditation techniques aimed at developing patients awareness of their unwanted thoughts, feelings, and sensations so that they are no longer automatically try to avoid them but learn to accept them for what they are.
Behavioural activation treatment – focus is intensively on getting patients to become more active and engaged with their environment and with their interpersonal relationships. Includes scheduling daily activities and reading pleasure and mastery while engaging in them, exploring alternative behaviours to reach goals, and role-playing to address specific deficits.
Interpersonal therapy – focusses on current relationship issues, trying to help the person understand and change maladaptive interaction patterns
Family and marital therapy – deals with unusual stressors in a patient’s life and behaviour by a spouse.
Explain the prevalence rates of suicide among people with mood disorders
50 to 90% of those who complete a suicide attempt do so during a depressive episode or in the recovery phase. The act often occurs at a point when the person appears to be emerging from the deepest phase of the depressive attack. The risk of suicide is about 1% during the year in which a depressive episode occurs, but the lifetime risk is about 15%.
Describe who is likely to attempt suicide and who is likely to complete suicide
Until recently, suicide attempts for most common in people between 25 and 44 years old, but it is now people between 18 and 24 years old who have the highest rates. Women are about three times as likely to attempt suicide as men. Rates of suicide are also about three or four times higher in people who are separated or divorced then in those with any other marital status. Completed suicides are more common in men than women, however when people have bipolar disorder, as many or even more women as men actually complete suicide. The highest rate of completed suicide is in the elderly.
For women, the method most commonly used is drug ingestion; men tend to use methods more likely to be lethal, particularly gunshot, which may be a good part of the reason why completed suicide are higher among men
Other high-risk groups include people with fairly severe and recurrent mood disorders, people with schizophrenia, those hospitalized for alcohol dependence, people living alone or with low levels of perceive social support, people from socially disorganized areas, certain highly creative or successful individuals.
Describe the various motives for why someone takes their own life
Personality traits such as impulsivity, aggression, pessimism, and negative affect you buddy. Often associated with negative events such as severe financial reversals, imprisonment, and interpersonal crises of various sorts. Hopelessness about the future. Severe psychic anxiety, panic attacks, severe anhedonia or inability to experience pleasure, Global insomnia, delusions, and alcohol abuse.
Suicide sometimes runs in families and genetic factors may play a role. Genetic vulnerability may be linked to the neurochemical correlates of suicide such as alterations in serotonin functioning, with reduced serotonin activity.
Socio-cultural factors. Whites have significantly higher rates of suicide that African-Americans, except among young males, where rates are similar. Young native American men show a suicide rate similar to that of white males. Japan is one of the few societies in which suicide has been socially approved under certain circumstances.
Evaluate the ethical issues involved in the right to die
Fears that the right to suicide might be abused. For example, people who are terminally ill and severely incapacitated might feel pressured to end their own lives rather than bird and their families.
Suicidal people who are not terminally ill and you have dependent children, parents, a spouse, or other loved ones may want the right to die as well.
Suicide is generally considered tragic but also wrong because of the respect in our society of the preservation of human life as a worthwhile value.
People who are chronically ill and in chronic and debilitating pain wants to shorten their agony.
