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PSYC 236 Midterm 1 > Chapter 8: Mood Disorders and Suicide > Flashcards

Chapter 8: Mood Disorders and Suicide Flashcards

1
Q

Imagined Loss

A

Individuals unconsciously interprets other types of events such as severe loss events

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2
Q

Major Depressive Disorder

A

Symptoms must be present for most of the day, more days than not, for at least two weeks

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3
Q

Mood Disorders fall into two categories

A

1) Depressive Disorders
2) Bipolar and related disorders

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4
Q

Depressive Disorders

A

Chang in mood in the direction of depression

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5
Q

Bipolar and Related Disorders

A

Involve periods of depression cycling with period of mania

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6
Q

Major Depressive Disorders- MDD

A

A depressive disorder characterized by persistent feelings of sadness, loss of interest or ability to feel pleasure, unexplained weight loss, difficulty sleeping, fatigue, difficulty concentrating, feelings of worthlessness or guilt, suicidal thoughts, and either agitation or slowing down. The person must not be suffering from other disorders that may present as depression, such as schizoaffective disorder or a delusional disorder.

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7
Q

Persistent Depressive Disorder

A

defined as depressed mood for most of the day, more days than not, lasting for at least two years, along with at least three out of a list of six additional symptoms.
-appetite disturbance, sleep disturbance, low energy, low self-esteem, poor concentration or difficulty making decisions, and hopelessness

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8
Q

Bipolar Mood Disorders

A

Involves Mania and Hypomania

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9
Q

Mania

A

defined as a distinct period of elevated, expansive, or irritable mood that lasts at least one week and is accompanied by at least three associated symptoms
-increased energy, decreased need for sleep, racing thoughts, pressured speech, and problems with attention and concentration. Judgment is also impaired, and these individuals may go on spending sprees, engage in substance abuse or risky sexual behaviour, or may even become aggressive. Individuals in a manic episode may feel that they are special in some way, or that they have been “chosen” to fulfill a special mission

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10
Q

Hypermania

A

is a less severe form of mania that involves a similar number of symptoms, but those symptoms need to be present for only four days

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11
Q

Those with mania experience

A

-enjoyable
-Energy and can get a lot done
-Minds are clear and sharply focused (solve difficult problems and make insights)
-Results in they denying their negative impact their symptoms may have on their life

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12
Q

Bipolar I Disorder

A

an individual has a history of one or more manic episodes with or without one or more major depressive episodes. A depressive episode is not required for the diagnosis of bipolar I disorder, but most individuals have both manic and depressive episodes

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13
Q

Bipolar II Disorder

A

is defined as a history of one or more hypomanic episodes with one or more major depressive episodes

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14
Q

Hypomanic episodes in Bipolar II disorder

A

may be experienced as a period of successful high productivity, and, indeed, many people with bipolar II are reluctant to take mood-stabilizing medication because they experience their hypomania as enjoyable

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15
Q

Length of time for hypomanic.manic episodes

A

typically last between two weeks and four months, while the depressive episodes last between six and nine months

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16
Q

Cyclothymia

A

chronic, but less severe, form of bipolar disorder. It involves a history of at least two years of alternating hypomanic episodes and episodes of depression that do not meet the full criteria for major depression

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17
Q

Rapid Cycling bipolar Disorder

A

as the presence of four or more manic and/or major depressive episodes in a 12-month period. The episodes must be separated from each other by at least two months of full or partial remission, or by a switch to the opposite mood state

-higher rates of disability and lower rates of response to treatment

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18
Q

What can Rapid Cycling have a presentation of higher…?

A

Rates of disability and lower rates of response to treatment

-Made worse by antidepressant medications

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19
Q

Specifiers

A

Further descriptors of a patient’s condition that capture the natural variation in the expression of affective disturbances and therefore increase the specificity of diagnoses by conveying important information about salient features that might be otherwise overlooked. For example, one specifier used in conjunction with a diagnosis of major depressive disorder is “with melancholic features.”

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20
Q

Seasonal Affective Disorder (SAD)

A

can occur in both unipolar MDD and bipolar disorder and is characterized by recurrent depressive episodes that are tied to the changing seasons

-Generally in the winter months

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21
Q

Reasons for SAD

A

-focused on melatonin, a hormone that is secreted at night by the pineal gland
-Sun provides increased light in the morning, melatonin release is normally lowered. This causes body temperature to rise, triggering the body processes to move to their awake state

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22
Q

SAD need more light

A

To Trigger decreased melotonin secretion
-Nights grow longer in the winter months, melotonin levels remain high, and nothing to prompt the switch from the sleep state to the wake state

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23
Q

Phase-delayed circadian Rhythm

A

dysregulation of the natural biological pattern of sleep and wakefulness

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24
Q

Drugs and SAD

A

-Medications that suppress melatonin are not effective in relieving symptoms of SAD

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25
Q

SAD= phase delayed circadian rhythms

A

therapies that “reset” the circadian clock, such as exposure to morning light (“phototherapy”), may work for some individuals by inducing a “phase advancement” of temperature, melatonin, and other neurochemicals, such as the stress hormone cortisol

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26
Q

SAD and the sun

A

-Lower levels of vitamin D in winter months= and this is associated with serotonin activity

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27
Q

2 weeks after childbirth

A

Many experience mood swings and feelings of depression up to two weeks after childbirth

-sometimes these mood swings are chronic and severe enough to meet the critieria for a major depressive or manic episode

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28
Q

Postpartum Mood episodes rare symptom

A

Psychotic symptoms such as command hallucinations to kill their infant

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29
Q

Other disorders in Peripartum period

A

Mood disorders

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30
Q

Strongest psychological and environmental risk factors for postpartum depression include

A

a history of previous depressive episodes; severely stressful life events concurrent with, or immediately following, childbirth (e.g., divorce, eviction); a poor marital relationship or low support from their partner

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31
Q

Biological models of postpartum disorder

A

some women appear to be very sensitive to the rapid changes in reproductive hormones (e.g., progesterone and estradiol) that occur at delivery

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32
Q

Hormonal role

A

-hormones play a major role in regulating the brain systems associated with arousal, cognition, emotion, and motivation. Hormone fluctuations also affect multiple other biological systems, including the immune system and the hypothalamic-pituitary-adrenal (HPA) axis

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33
Q

Children can be affected too

A

-stunted growth
-Slower language development

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34
Q

Premenstrual Dysphoria Disorder (PMDD)

A

is characterized by marked affective lability, irritability/anger, depressed mood, and/or anxiety, plus the presence of additional symptoms of loss of interest in activities, concentration difficulties, low energy, changes in appetite and/or sleep, feelings of loss of control, and/or physical symptoms. Five symptoms must be present to meet DSM-5 criteria for PMDD, and these symptoms must significantly interfere with daily functioning. Further, these symptoms must be present for most menstrual cycles in the past year.

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35
Q

Hormones and PMDD

A

-cyclical changes in ovarian steroids in individuals with PMDD have been shown to cause decreases in the neurotransmitter serotonin, which is strongly implicated in mood disorders

-

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36
Q

Medications for PMDD

A

medications such as selective serotonin reuptake inhibitors (SSRIs) have shown better efficacy in treating PMDD than other types of antidepressants or cognitive-behavioural therapy

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37
Q

Biological Factors of Mood disorders

A

-the mood disorders are highly heritable, but a family history of a mood disorder does not guarantee the presence of disorder. A genetic vulnerability likely needs to be expressed as a vulnerable personality or cognitive trait and triggered by stress in the environment.
-Family history
-Stressful events

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38
Q

Five Factor Model of Personality

A

A model that characterizes human personality according to five traits: Openness to Experience, Conscientiousness, Extraversion, Agreeableness, and Neuroticism. (OCEAN/CANOE Model)

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39
Q

Neuroticism

A

Tendency to depression, anxiety, and high stress reactivity

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40
Q

Extraversion

A

Gregariousness, assertiveness, and activity, and excitement-seeking

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41
Q

Low Conscientiousness

A

Self disciplime, dutifulness, achievement striving and orderliness

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42
Q

Depression

A

Neuroticism, Extraversion, Low consciousness

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43
Q

Bipolar disorder

A

High extraversion and high openness to experience

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44
Q

Behavioural Inhibition system/behavioural activation system (BIS/BAS)

A

Two general motivational systems that underlie human behaviour. The BIS motivates behaviour away from unpleasant stimuli. The BAS motivates behaviour toward rewarding stimuli.

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45
Q

BIS

A

punishment system and regulates avoidance behaviours
-More fearful of novelty and uncertainty, and more sensitive to punishment
-Depression, anxiety, and frusteration

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46
Q

BAS

A

-Reward system
-Regulates Approach behaviour
-More impulsive and have more difficulty regulating their emotions and inhibiting their behaviour when faced with rewarding stimuli
-Fun seeking: impulsivity= I crave excitement, new activities

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47
Q

BAS and what disorder

A

Bipolar disorder

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48
Q

BIS

A

Depression

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49
Q

Beck’s Cognitive Theory

A

Beck’s great insight was in proposing that a person’s emotional response to a situation is determined by the manner in which that situation is appraised or evaluated

Ex: People with depression and people prone to depression are more likely to appraise situations negatively than those not prone to depression

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50
Q

Cognitive Distortions

A

Thoughts about the self, world, or future that are distortions of the true state of affairs.

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51
Q

Examples about Cognitive Distortions

A

1) All or nothing thinking= bacl and white, don’t do well on a test, failure

2) Overgeneralization= You are late to a doctors appointment and say= I’m always screwing up

3) Magnification (catastrophizing)= You exaggerate the importance of your errors or problems= You forgot someone’s name and say this is terrible

4) Jumping to conclusions
-You interpret things negatively when there are not definite facts to support your conclusion
Your partner does not return your call, so you tell yourself, “They probably don’t care about me anymore.”

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52
Q

Schemas

A

Mental structures used to organize information about the world.
-Develop from our early experiences with the world and represent stored memories, images, and thoughts from these experiences

-Depression: Negative Schemas

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53
Q

Cognitive triad

A

Negative views of the self, world, and future, as part of Beck’s cognitive model of depression.

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54
Q

Diathesis stress model

A

The view that a predisposition to develop a disorder (the “diathesis”), interacting with the experience of stress, causes mental disorders. According to this perspective, the interaction underlies the onset of all disorders, although either the predisposition or the stress may be more important in a particular disorder, or in a particular person.

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55
Q

Mothers who have depression

A

presence of a negative attentional bias predicted these girls’ development of depression later in adolescence

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56
Q

Those with bipolar disorder display what?

A

display preferential attention to positive stimuli, and particularly cues of reward or incentive, in the environment when they are in the manic or euthymic phases of the illness

-higher levels of manic symptoms are associated with more positive interpretations of ambiguous scenarios

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57
Q

Constance Hammen’s Stress Generation Hypothesis

A

A theory of depression recurrence stating that individuals with a history of depression have higher rates of stressful life events that are at least in part dependent on their own behaviour or characteristics than non-depressed individuals.

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58
Q

James Interpersonal Model of Depression

A

A model that individuals who are depressed (or at risk for depression) behave in ways that bother or alienate others. As a result, depressed individuals are more likely to experience interpersonal rejection and relationship stress, thereby reducing social support and perpetuating their depression.

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59
Q

Excessive reassurance seeking

A

Part of Coyne’s model of depression where a depressed person seeks reassurance about themself from non-depressed people.

-defined as the tendency to repeatedly seek assurance about one’s worth and lovability from others, regardless of whether such assurances have already been provided

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60
Q

Negative Feedback Setting

A

The tendency to actively seek out criticism and other negative interpersonal feedback from others.

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61
Q

William Swann’s Self Verification Theory

A

negative feedback seeking is defined as the tendency to actively seek out criticism and other negative interpersonal feedback from others that is consistent with one’s self-schemas.

-individuals experiencing depression do indeed seek more negative feedback from others and are consequently more rejected by others than individuals who are not depressed

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62
Q

Stressful Events Are linked to those who have

A

Depression

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63
Q

Childhood Stressful Life Events

A

-More likely to develop depression or a bipolar disorder

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64
Q

Child abuse and the brain

A

child abuse is associated with the death of cells in the hippocampus and amygdala, two areas of the brain that are critically involved in the regulation of mood and emotional memory

-hild abuse is associated with dysregulation of the body’s biological stress response system—the hypothalamic-pituitary-adrenal (HPA) axis

65
Q

MDD and bipolar disorders

A

-Run in the family

66
Q

Genome-wide association study

A

A research design that involves scanning the entire genome to find particular genetic loci that differentiate individuals with a specific disorder and those without.

67
Q

Neurotransmitters

A

chemical substances manufactured at the neuron and released at the synapse, or the gap between one neuron and another

68
Q

Synapse

A

central point of neural communication; when a neurotransmitter is released, it binds to receptors on the post-synaptic neuron.

69
Q

Excitatory effects on postsynaptic neurons

A

increasing their chances of firing new action potentials, or they can have inhibitory effects, thereby reducing the chances of their firing

70
Q

Dysfunction in two neurostransmitters in depression

A

catecholamine norepinephrine (NE) and the indoleamine serotonin (also known as 5-hydroxytryptamine, or 5-HT)

71
Q

first antidepressant medications (tricyclic antidepressants and monoamine oxidase inhibitors)

A

worked by increasing levels of these two monoamines.

72
Q

Depression is a deficit of

A

5-HT, NE, or DA activity

73
Q

Mania

A

too much NE or Da acivity in the context of too little 5-HT activity

74
Q

Facts about Neurotransmitter system

A

-most patients with unipolar depression do not show reductions in NE activity.

75
Q

Low NE activity

A

key feature of both bipolar disorder and severe unipolar depression.

76
Q

Depression have fewer

A

-5-HT receptors
-5-HT released at a synapse has fewer places to bind on the post-synaptic cells= leads to fewer subseuqent action potentials and lower 5-HT neurotransmitters

77
Q

Connection of DA neurotransmission and level of 5-HT

A

if there are low levels of 5-HT, DA levels will also decrease. DA is strongly implicated in the regulation of reward processing and motor behaviour and, thus, low levels of this neurotransmitter are thought to be responsible for a reduction in the capacity of individuals experiencing depression to experience pleasure and their symptoms of psychomotor retardation

78
Q

Neurotransmitters in manic episodes of bipolar disorder

A

NE, DA, and 5-HT

-abnormal DA levels may trigger the hyperactivity and psychosis seen in severe mania, whereas abnormal NE levels may trigger euphoria and grandiosity.

-5-HT, normal levels of this neurotransmitter act to inhibit the activity of some neurons, leading to inhibition of certain behaviours. Conversely, low levels of 5-HT can lead to activation (or disinhibition) of a variety of behaviours

79
Q

Role of DA in the etiology of MDD and bipolar disorder

A

Depression has long been associated with a lack of responsiveness to reward (anhedonia).

80
Q

Hypodepaminergia

A

deficits have been tied directly to reduced activity in mesocorticolimbic dopamine pathways

81
Q

Hyperdopaminergia

A

mania may result from too much dopamine signalling in these same pathways

82
Q

Bipoalr disorder in the manic phase

A

show abnormally elevated activity in areas of the brain with high DA receptor density during tasks that involve anticipating and consuming a reward such as money

83
Q

Stress and the Hypothalamic Pituitary Adrenal Axis

A

The biological stress response system responsible for the fight-or-flight response. It is overactive in major depression

84
Q

corticotropin-releasing hormone (CRH)

A

Encounters stress, this is activated

-Leads to the release of adrenocorticotropic hormone (ACTH) from the pituitary gland and, subsequently, release of the hormone cortisol from the adrenal gland.

85
Q

HPA axis

A

Helps us deal with the acute dangers we faced in prehistoric times

-today’s stresses are often more chronic, repeated, or uncontrollable (e.g., ongoing relationship problems, poverty, discrimination, or physical, psychological, or sexual abuse or harrassment).

86
Q

Activation of the HPA axis

A

results in the release of pro-inflammatory cytokines, which are part of the immune response. The evolutionary purpose of these cytokines is to prepare the body to repair wounds resulting from the stress of, say, being attacked by a predator.

87
Q

Depression and bipolar disorder

A

have higher levels of certain pro-inflammatory cytokines than individuals without depression, and that high levels of these same cytokines prospectively predict the onset of depression and manic episodes

88
Q

Bipolar and unipolar depression associated with a decrease in

A

blood flow and reduced glucose metabolism in the frontal regions of the cerebral cortex, particularly on the left side

89
Q

Side of the brain for mania

A

-greater right hemisphere reductions seen in mania

90
Q

Increased glucose metabolism has also been observed in several subcortical regions

A

In depression

91
Q

Structures in depression

A

differences in the functional connections between limbic structures involved in the processing of emotions and emotional memory (e.g., the amygdala and hippocampus) and cortical structures involved in higher-order decision making, impulse control, judgment, and motivation (e.g., the anterior cingulate cortex and dorsolateral prefrontal cortex

92
Q

Depression: Elevated activity in the

A

amygdala when they rated the negative words during the emotion-processing task.
-decreased relationship between amygdala activity and activity in the dorsolateral prefrontal cortex.

93
Q

Dorsolateral prefrontal cortex

A

Motivation and executive functioning

94
Q

Anterior Cingulate Cortex

A

Rewards anticipation, decision making, empathy, emotion, and impulse control

95
Q

Amygdala

A

Processing of emotions

96
Q

Hippocampus

A

Learning and memory

97
Q

Psychotherapy for Unipolar Disorder

A

-Cognitive behavioural therapy (CBT)
-Interpersonal Psychotherapy (IPT)
-Antidepressant Medication called Imipramine

98
Q

Cognitive Behavioural Therapy (CBT)-unipolar disorder

A

teach people to become aware of the meanings of and attributions to events in their lives, and to examine how these cognitions contribute to the emotional reactions that follow.
-These latter results suggest that CBT has more enduring effects than antidepressant medication.

99
Q

CBT-Thought Records- unipolar disorder

A

the client is encouraged to focus on a situation that occurred recently and that evoked a strong negative emotion.
-encouraged to write down all the thoughts that were running through their mind during this situation. Often, these thoughts will include cognitive distortions (e.g., all-or-nothing thinking)
-client is then encouraged to come up with alternative thoughts that represent a balance of the evidence

100
Q

CBT-Behavioural Experiments- Unipolar disorder

A

-encourage people to view these thoughts as scientific hypotheses that can be tested in an experiment.
-If I try to talk to new people, I will certainly be rejected” is easy to test empirically. The therapist and client collaboratively design the nature of the experiment and set out clear contingencies.

101
Q

CBT- Activity Scheduling- Unipolar disorder

A

encourage clients to start scheduling these activities back into their lives. The theory is that if people experiencing depression start engaging in these pleasurable activities again, they will correspondingly start to feel pleasure in their lives.
-Clients start by making a list of all the activities they used to engage in and rating these activities on a score of 0 to 10 in terms of how much pleasure or accomplishment these activities elicited.

102
Q

CBT- Behavioural Activation Therapy-Unipolar Disorder

A

An evidence-based treatment for depression that focuses on activating behaviour to improve mood

103
Q

Mindfulness Based Cognitive Therapy (MBCT)-Unipolar Disorder

A

purpose of mindfulness is to promote a non-evaluative awareness of the here and now in an effort to help individuals experiencing depression detach from ruminative thinking and cultivate a decentred, detached perspective to depression-related thoughts and feelings.

-“I feel sad; I must be getting depressed again. I’ll never be healthy,” the patient is taught to think, “This is just a transitory emotion; I’m observing it and letting it pass.” There is experimental evidence showing that mindfulness meditation does, indeed, decrease ruminative thinking

104
Q

Interpersonal Psychotherapy (IPT)- Unipolar Disorder

A

A therapy that uses a medical model to understand interpersonal conflicts and transitions as they relate to depression.
Toward the beginning of treatment, the client and therapist work collaboratively to identify the client’s source of interpersonal dysfunction with relevance to four areas: (1) interpersonal disputes, (2) role transitions, (3) grief, and (4) interpersonal deficits.

Interpersonal disputes are defined as conflicts in marital, family, or other social relationships. The IPT therapist intervenes by identifying sources of misunderstanding and using communication and problem-solving training to empower the client to change the situation.

-The IPT therapist tries to identify personality issues in the client (e.g., hostility, excessive dependency) that may be interfering with the formation of close relationships, and uses the therapeutic relationship as a model for improving social competence

105
Q

Family focused Therapy (FFT)- Bipolar Disorder

A

Adjunctive psychotherapy for bipolar and related disorders that focuses on educating the patient’s family about the disorder and improving family communication.

106
Q

Interpersonal and Social Rhythm Therapy (IPSRT)

A

Adjunctive psychotherapy for bipolar disorder that focuses on regularizing patients’ daily rhythms and routines.

107
Q

Cognitive Therapy (Bipolar Disorder)

A

Patients are taught strategies that address the unique issues faced in bipolar disorder, including (1) how to regularize their sleep and daily routines, (2) how to regularly monitor their mood to help identify early triggers for manic episode relapses, and (3) the importance of medication compliance.

108
Q

Medications for Depression

A

-Tricylic Antidepressants (TCAs)
-Monoamine oxidase inhibitors (MAoIs)
-Selective serotonin reuptake inhibitor (SSRI)- fluoxetine (prozac)

109
Q

Tricyclics Antidepressants (TCAs)

A

One of the three known major classes of antidepressants. Tricyclics enable more neurotransmitters to be released into the synaptic cleft. They include amoxapine (Asendin), amitriptyline (Elavil), imipramine (Tofranil), and doxepin (Sinequan).

110
Q

TCA role

A

blocking the reuptake from the synapse of NE and/or, less commonly, 5-HT. This means that more of these neurotransmitters are available in the synapse to bind to post-synaptic receptors and trigger new action potentials.

111
Q

Side effects of TCAs

A

including dry mouth, blurry vision, constipation, urinary hesitation, dizziness upon standing up, sedation, and weight gain. These drugs can also cause or exacerbate cardiac arrhythmias and thus cannot be used in patients with an existing cardiac condition. Finally, the tricyclics are highly lethal in overdose.

112
Q

Monoamine Oxidase Inhbitors (MAOIs)

A

A class of medications used to treat major depression by inhibiting the enzyme monoamine oxidase, which breaks down monoamines such as dopamine and norepinephrine, thus allowing more of these neurotransmitters to accumulate in the presynaptic cell.

113
Q

MAOIs role

A

work by inhibiting an enzyme (monoamine oxidase) that breaks down monoaminergic neurotransmitters (e.g., dopamine, norepinephrine, serotonin) in the presynaptic cell. This means that more monoamines are available to be released into the synapse, to bind with post-synaptic receptors, and to trigger new action potentials.

114
Q

Common MAOIs

A

Marplan (isocarboxazid), Nardil (phenelzine), and Parnate (tranylcypromine).

115
Q

Flaws of MAOIs

A

-side effects
-nhibit the breakdown of amines, patients taking these medications must limit their intake of foods containing amines, especially tyramine (e.g., aged cheese, chocolate, red wine). Too much tyramine can raise blood pressure to dangerous levels. Patients taking MAOIs also must avoid over-the-counter cold medicines that contain pseudoephedrine (e.g., Sudafed), as well as any drug that works on serotonin, such as another antidepressant.

116
Q

Selective Serotonin Reuptake Inhibitors

A

One of the three known major classes of antidepressants. SSRIs, as their name suggests, delay the process of reuptake of neurotransmitters so that they remain available longer to maintain optimal neuronal firing rates. They include fluoxetine (Prozac), sertraline (Zoloft), and paraxetine (Paxil).

117
Q

Side effects of SSRIs

A

nausea, insomnia, sedation, and sexual dysfunction

118
Q

Other classes of antidepressants

A

(1) serotonin-norepinephrine reuptake inhibitors (SNRIs) such as Wellbutrin (buproprion), Effexor (venlafaxine), Desyrel (trazodone), and Remeron (mirtazapine); (2) medications that work on increasing dopamine transmission, such as Mirapex (pramipexole) and Provigil (mondafinil); and (3) drugs that have other miscellaneous actions on other neurotransmitters such as GABA (e.g., Neurontin [gabapentin]).

119
Q

Patients with mildly to moderate severe unipolar depression, antidepressant medication was no more effective

A

than a placebo

120
Q

Medications for bipolar disorder

A

-Lithium, Antoconvulsants, Antipsychotics Antidepressents

121
Q

Lithium

A

Lithium salt, used to treat mania and depression. Has the effect of flattening out the peaks and valleys of the illness, allowing sufferers to achieve some stability in their lives with less disruption for family members. Apparently lithium has preventive effects for both unipolar mood disorders and bipolar mood disorders, and lithium is considered the treatment of choice for bipolar disorder.

122
Q

Lithium and the brain

A

-reduces the transmission of excitatory neurotransmitters, particularly dopamine and glutamate, and increases the transmission of inhibitory neurotransmitters, particularly GABA.
- lithium increases levels of proteins, such as brain-derived neurotrophic factor and B-cell lymphoma 2, that inhibit cell death
-lithium appears to preserve, or even increase, brain volumes in critical areas needed for emotion regulation and memory, such as the hippocampus, amygdala, and prefrontal cortex

123
Q

Lithium side effects

A

lithium interferes with the regulation of sodium and water levels, patients also require regular tests to monitor thyroid and kidney function. Common side effects of lithium include dehydration, weight gain, acne with scarring, thinning of hair, and hand tremor.

-Many do not respond to this

124
Q

Anticonvulsants

A

nclude Tegretol (carbamazepine), Depakote (valproate), Lamictal (lamotrigine), Neurontin (gabapentin), Topamax (topiramate), Trileptal (oxcarbazepine), Zonegran (zonisamide), Gabitril (tiagabine), Felbatol (felbamate), Keppra (levatiracetam), Dilantin (phenytoin), and Lyrica (pregabalin).

125
Q

How anticonvulsant drug works

A

increasing the synthesis and release of the neurotransmitter gamma-aminobutyric acid (GABA), which plays a general inhibitory role in the brain. Others work by decreasing the synthesis and release of the neurotransmitter glutamate, which has a general excitatory effect in the brain.

126
Q

Side effects of anticonvulsant

A

liver or kidney damage or decrease the amount of platelets in the blood. Finally, pregnant women should not take anticonvulsants because they increase the risk of birth defects.

127
Q

Antipsychotics

A

These medications may be used to control psychotic symptoms such as hallucinations or delusions and also may be used as sedatives to help with the insomnia and agitation that often accompany manic episodes. Finally, in some people antipsychotic medications have been found to have a mood-stabilizing effect on their own and, thus, can be used for those patients who do not respond to lithium or anticonvulsants.

128
Q

Antipsychotics for bipolar disorder

A

Abilify (aripiprazole), Clozaril (clozapine), Geodon (ziprasidone), Risperdal (risperidone), Seroquel (quetiapine), and Zyprexa (olanzapine).

129
Q

How antipsychotics work

A

are antagonists of multiple neurotransmitter receptors, including serotonin and dopamine.

130
Q

Side effects of antipsychotics

A

blurred vision, dry mouth, drowsiness, muscle spasms or tremor, facial tics, and weight gain.

-increase the risk of diabetes because they cause rapid weight gain and high cholesterol.

-ardive dyskinesia, an irreversible syndrome involving involuntary, dyskinetic movements. The risk of developing tardive dyskinesia increases with the duration and cumulative dose of medication, and it has no treatment.

131
Q

Antidepressants

A

Buproprion appears to be less likely to trigger manic episodes than some of the other antidepressants. In addition, there is some evidence that venlafaxine works more quickly than do other antidepressants. All antidepressants are associated with a risk for triggering mania in patients with bipolar disorder, however, so these medications are typically used in conjunction with one of the mood-stabilizing medications discussed above.

132
Q

Relapse ideas

A

(1) increased the dose of Tegretol, and (2) augmented Tegretol with another medication—the antidepressant buspirone (Buspar).

132
Q

Phototherapy for Seasonal Affective Disorder

A

Treatment for seasonal affective disorder that involves exposure to high-intensity full-spectrum lighting.

133
Q

What phototherapy does

A

it may mimic the natural effects of sunlight on a cascade of neurobiological processes, including gene expression in the adrenal gland, serotonin production in the hypothalamus, and inhibition of melatonin secretion from the pineal gland.

134
Q

Due to phototherapy’s potentiality to induce manic episodes, those with bipolar SAD

A

Should be maintained on an effective mood stabilizer

135
Q

CBT for SAD

A

it focuses specifically on challenging dysfunctional seasonal cognitions (e.g., the effect of low light and poor weather) and on scheduling pleasurable winter activities.

136
Q

Treatment-Resistant Depression

A

is defined as a failure to achieve remission following at least two trials of antidepressant medication at an appropriate dose and duration

-Treatment-resistant depression is associated with severe impairments in social, educational, occupational, and health functioning, and these individuals have a significantly lower quality of life than patients with non–treatment-resistant depression

137
Q

Electroconvulsive Therapy (ECT)

A

The use of electricity to induce a seizure in mental patients by placing electrodes on the skull and administering a convulsive rather than a lethal shock intensity.

138
Q

Present Day ECT

A

Patients are administered a general anaesthetic and muscle relaxant so that they do not convulse during the seizure. A blood pressure cuff is placed around the patient’s ankle, preventing the muscle relaxant from reaching the foot.

An electrical current is then applied to the patient’s brain through electrode pads placed on their temples. This induces a seizure that typically lasts for about 25 seconds. After the anaesthetic wears off, patients typically experience a period of confusion that can last up to a few hours

139
Q

Flaws of ECT

A

Most patients report persistent memory loss following ECT, involving both retrograde amnesia (forgetting events prior to the seizure) and anterograde amnesia (forgetting events after the seizure). These memory problems usually improve within a couple of months. However, a small percentage of patients complain of continuing memory impairment following ECT.

140
Q

ECT administered

A

administered two to three times per week, with a total of between six and 12 treatments. The best meta-analysis of ECT examined 73 randomized controlled research trials investigating the efficacy of ECT in treatment-resistant unipolar and bipolar depression.

141
Q

Transcranial Magnetic Stimulation (TMS)

A

Treatment for severe depression that uses a magnet to excite neurons in the brain.

-During the procedure, a large electromagnetic coil is held against the patient’s scalp. An electric current creates a magnetic pulse that travels through the skull and causes small electrical currents in the brain. These currents stimulate nerve cells in the region of the cortex under the coil. The procedure is non-invasive and painless, although patients sometimes report a tapping or knocking sensation in their head, as well as muscle contractions in their jaw or scalp.

142
Q

Other strategies for unipolar disorder

A

-Exercise
-Yoga

143
Q

Suicide

A

Intentional taking of one’s own life

144
Q

Suicidal Ideation

A

Refers to thoughts of death and plans for suicide
They make express this, yet never carry it out

145
Q

Suicidal gestures

A

are behaviours that look like a suicide attempt, but are clearly not life-threatening (e.g., taking pills, but not enough to overdose). People who engage in suicidal gestures often do not have an intent to die, but may want to alert others to their suffering.

146
Q

Suicide Attempt

A

is the carrying out of a suicide plan, which is unsuccessful but for which there was a clear intent to die.

147
Q

Completed suicide

A

is when someone dies by suicide

148
Q

Self harm

A

Cutting or burning, way of coping with emotional distress

149
Q

Gender that most common to die from it

A

Men

150
Q

Causes for suicide

A

-untreated mental disorder
-The feeling that one is rootless and lacking a sense of belonging
-Do not feel integrated in society
-Loss of identity (cultural and social)
-Biological factors (genes and low levels of serotonin
-Interpersonal model of suic
-Motivational volitenal model of suicide

151
Q

Interpersonal Model of suicide

A

A model that explains suicidal ideation and intent as resulting from beliefs that one is a burden on others and feelings of hopelessness and alienation from others. These can progress to capability for suicide through repeated self-harm and suicidal gestures.

152
Q

Motivational Volitional Model

A

A model of suicide that states that cognitions of defeat, humiliation, and entrapment (i.e., an inability to escape) in response to stressful life events will result in a motivation for suicidal ideation when motivational moderators, such as feelings of thwarted belongingness and perceived burdensomeness, are high.

153
Q

Prevention for Suicide

A

(1) provide guidelines to improve public awareness and knowledge of suicide; (2) disseminate information about suicide and its prevention; (3) make existing statistics about suicide and related risk factors publicly available; (4) promote collaboration and knowledge exchange across domains, sectors, regions, and jurisdictions; (5) define best practices for suicide prevention; and (6) promote the use of research and evidence-based practices for suicide prevention.

154
Q

Patients who have a clear suicide plan, access to lethal means, a clear intent to die, and who cannot guarantee their own safety

A

should be considered a medical emergency and be hospitalized immediately.

155
Q

Brown and Beck form of CBT

A

The central feature of this form of CBT is to identify and modify the thoughts, images, and core beliefs that were activated prior to previous suicide attempts. Therapists also address specific vulnerability factors for suicide, including hopelessness, poor problem solving, poor impulse control, and social isolation.

STANDARD CBT AND MEDICTION= DOES NOT WORK

156
Q

Pharmacological agent: Ketamine

A

A pharmacological agent, a glutamate N-methyl-d-aspartate (NMDA) receptor antagonist, that has been explored as an agent that can rapidly reduce suicidal ideation, and thus may be useful in emergency situations of acute suicidality.

157
Q

Zindel Segal

A

Distinguished Professor of Psychology in Mood Disorders, and the Director of Clinical Training in the Graduate Department of Psychological Clinical Sciences at the University of Toronto and is providing some of the most important research on cognitive models and treatments for depression.

he is trying to solve the very important problem of depression relapse.

PSYC 236 Midterm 1 (8 decks)

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