Kk&s Ch.15 Mood Ds

Front 1

Lifetime prevalence of MDD? Which disorder has higher lifetime prevalence?

Back 1

17% (Actual Range =5-17, avg =12)
None

Front 2

Yearly incidence rate of major depression/major depressive episode?
Men/Women incidence rate?

Back 2

1.59%
Men: 1.1
women: 1.89

Front 3

Annual incidence rate of bipolar disorder?

Back 3

less than 1%

Front 4

Give Range and Average for Lifetime prevalence of
1. MDEpisode
2. Dysthymic Ds
3. Minor Depressive Ds
4. Recurrent brief depressive ds
5. Full unipolar spectrum

Back 4

1. 5-17, Avg 12
2. 3-6, Avg 5
3. 10, -
4. 16, -
5. 20-25

Front 5

Lifetime prev of
1. BP I
2. BP II
3. Cyclothymia
4. Hypomania
5. Full bipolar spectrum

Back 5

1. 0 to 2.4
2. 0.3-4.8
3. 0.5-6.3
4. 2.6-7.8
5. 2.6-7.8

Front 6

MDD prevalence of females versus males

Back 6

independent of culture or country, twofold or greater prevalence

Front 7

why greater women than men with depression?

Back 7

1. hormonal differences,
2. childbirth
3. different stressors
4. learned helplessness

Front 8

bipolar 1 disorder, prevalent more in women or men?

Back 8

=

Front 9

1 bipolar manic episodes, more common in women or men?
2 bipolar depressive episodes

Back 9

1. men
2 women

Front 10

mixed mania/depression seen more in which gender?

Back 10

women

Front 11

rapid cycler greater in which gender?

Back 11

women

Front 12

Bipolar Disorder I onset range, and mean?

Back 12

mean=30
onset 5 or 6 to 50

Front 13

MDD mean age of onset?

Back 13

40

Front 14

What percent of patients onset MDD between 20 and 50?

Back 14

50%

Front 15

Is incidence of MDD among people younger than 20 increasing or decreasing? Why?

Back 15

increasing
increased alcohol and drug abuse

Front 16

MDD and relationship to marital status?

Back 16

MDD most often in people without close interpersonal relationships or in those divorced/seperated

Front 17

Bipolar I marital status association?

Back 17

more common in divorced/seperated than married

Front 18

MDD and correlation with SES?

Back 18

none

Front 19

Bipolar I and correlation with SES?

Back 19

BP1 assoc with higher SES (incidence)

Front 20

BP1 and college?

Back 20

BP1 more common in non-college grads

Front 21

Depression: greater in rural, urban or no trend?

Back 21

greater in rural

Front 22

Mood disorder prevalence and race?

Back 22

no difference but examiners overpredict Sz in different to their own cultures and see less Mood

Front 23

Comorbidity with Mood Ds?

Back 23

alcohol abuse/dependence
PD
OCD
Social Anxiety

Front 24

People with Mood Ds, which gender has more substance issues?

Back 24

men

Front 25

Which ds will give higher rate of lifetime or co-morbid mood ds?

Back 25

substance use
anxiety

Front 26

what is difference lifetime hx of substance use, panic ds, and ocd in ECA study between people with Bipolar 1 and MDD?

Back 26

In the Epidemiological Catchment Area (ECA) study, the lifetime history of substance use disorders, panic disorder, and OCD was approximately twice as high among patients with bipolar I disorder (61 percent, 21 percent, and 21 percent, respectively) than in patients with unipolar major depression (27 percent, 10 percent, and 12 percent, respectively).

Front 27

What problem does comorbid anxiety and substance use cause for mood ds?

Back 27

Comorbid substance use disorders and anxiety disorders worsen the prognosis of the illness and markedly increase the risk of suicide among patients who are unipolar major depressive and bipolar

Front 28

which nt's most implicated in mood disorders?

Back 28

Of the biogenic amines, norepinephrine and serotonin are the two neurotransmitters most implicated in the pathophysiology of mood disorders.

Front 29

how is NE related to depression?
what are key receptors?

Back 29

The correlation suggested by basic science studies between the downregulation or decreased sensitivity of β-adrenergic receptors and clinical antidepressant responses is probably the single most compelling piece of data indicating a direct role for the noradrenergic system in depression.

presynaptic β2-receptors in depression, because activation of these receptors results in a decrease of the amount of norepinephrine released. Presynaptic β2-receptors are also located on serotonergic neurons and regulate the amount of serotonin released.
Venlafaxine also points to role of NE in role of depression.

Front 30

what data points to serotonin in MDD

Back 30

Besides that SSRIs and other serotonergic antidepressants are effective in the treatment of depression, other data indicate that serotonin is involved in the pathophysiology of depression. Depletion of serotonin may precipitate depression, and some patients with suicidal impulses have low cerebrospinal fluid (CSF) concentrations of serotonin metabolites and low concentrations of serotonin uptake sites on platelets.

Front 31

what is role of Dopamine in depression? mania?

Back 31

The data suggest that dopamine activity may be reduced in depression and increased in mania. T

Front 32

What is relationship of drugs that decrease DA and mood ds?

Back 32

Drugs that reduce dopamine concentrations—for example, reserpine (Serpasil)—and diseases that reduce dopamine concentrations (e.g., Parkinson's disease) are associated with depressive symptoms

Front 33

What is relationship of drugs that increase DA and mood ds?

Back 33

In contrast, drugs that increase dopamine concentrations, such as tyrosine, amphetamine, and bupropion (Wellbutrin), reduce the symptoms of depression.

Front 34

what are other theories of depression and DA relationship?

Back 34

maybe mesolimbic dopamine pathways messsed up?
Dopamine D1 receptor may be HYPOactive in depression

Front 35

Is dopamine increased or decreased in mania? depression?

Back 35

Suspected to be decreased

Front 36

Why do people think reduced dopamine associated with depression?

Back 36

Drugs that decrease DA such as reserpine (Serpasil) and diseases that reduce domapine (like Parkinson's) associated with depression.
Also, drugs that increase Dopamine, reduce sx of depression

Front 37

What drugs increase dopamine concentrations?

Back 37

tyrosine, amphetamine, and bupropion (Wellbutrin)

Front 38

Which pathway may be dysfxn in depression related to dopamine?

Back 38

Mesolimbic

Front 39

Is the dopamine D1 receptor hyper or hypoactive in depression?

Back 39

hypo

Front 40

What effect do cholinergic drugs have on mood?

Back 40

Cholinergic Agonists can produce lethargy, anergia, and psychomotor retardation in healthy subjects, can exacerbate symptoms in depression, and can reduce symptoms in mania.
These effects generally are not sufficiently robust to have clinical applications, and adverse effects are problematic.

Front 41

What is relationship of cholinergic agonists to learned helplessness in mice?

Back 41

Cholinergic agonist and antagonist drugs have differential clinical effects on depression and mania. Agonists can produce lethargy, anergia, and psychomotor retardation in healthy subjects, can exacerbate symptoms in depression, and can reduce symptoms in mania. These effects generally are not sufficiently robust to have clinical applications, and adverse effects are problematic.

Front 42

What is relationship of depression and cholinergic agonists?

Back 42

Cholinergic agonists can induce changes in hypothalamic-pituitary adrenal (HPA) activity and sleep that mimic those associated with severe depression.

Some patients with mood disorders in remission, as well as their never-ill first-degree relatives, have a trait-like increase in sensitivity to cholinergic agonists.

Front 43

Is there relationship with GABA and depression? What is it?

Back 43

Reductions of GABA have been observed in plasma, CSF, and brain GABA levels in depression.

Animal studies have also found that chronic stress can reduce and eventually can deplete GABA levels.

By contrast, GABA receptors are upregulated by antidepressants, and some GABAergic medications have weak antidepressant effects.

Front 44

Is there relationship between Glutamate and Depression? What is it?

Back 44

Glutamate, thus, may work in conjunction with hypercortisolemia to mediate the deleterious neurocognitive effects of severe recurrent depression. Emerging evidence suggests that drugs that antagonize NMDA receptors have antidepressant effects.

Front 45

What is bio relationship of stress and depression?

Back 45

Glutamate, thus, may work in conjunction with hypercortisolemia to mediate the deleterious neurocognitive effects of severe recurrent depression. Emerging evidence suggests that drugs that antagonize NMDA receptors have antidepressant effects.

Front 46

Stress is associated how to HPA axis?

Back 46

Elevated HPA activity is a hallmark of mammalian stress responses and one of the clearest links between depression and the biology of chronic stress.

Front 47

In depression, what levels of cortisol is seen and what does it suggest?

Back 47

Hypercortisolema in depression suggests one or more of the following central disturbances:

decreased inhibitory serotonin tone;
increased drive from norepinephrine (NE), ACh, or corticotropin releasing hormone (CRH);
or decreased feedback inhibition from the hippocampus.

Front 48

hypercortisolema in depression is associated how with
1. inhibitory serotonin tone,
2. drive from NE, ACh, CRH
3. feedback inhibition from hippocampus?

Back 48

1. decreased
2. increased
3. decreased

Front 49

HPA activity is increased in what % of depressed outpatients? inpatients?

Back 49

Evidence of increased HPA activity is apparent in 20 to 40 percent of depressed outpatients and 40 to 60 percent of depressed inpatients

Front 50

How is Dexamathosone used?
i.e. what is normal, abnormal response

Back 50

normally suppresses HPA axis activity for 24 hours

Nonsuppression of cortisol secretion at 8:00 AM the following morning or subsequent escape from suppression at 4:00 PM or 11:00 PM is indicative of impaired feedback inhibition.

Hypersecretion of cortisol and dexamethasone nonsuppression are imperfectly correlated (approximately 60 percent concordance). A more recent development to improve the sensitivity of the test involves infusion of a test dose of CRH after dexamethasone suppression.

Front 51

Why are the tests of adrenocortical hyperactivity not used?

Back 51

These tests of feedback inhibition are not used as a diagnostic test because adrenocortical hyperactivity (albeit usually less prevalent) is observed in mania, schizophrenia, dementia, and other psychiatric disorders

Front 52

What Percent of depressed patients have thyroid dysfxn? How does it show?

Back 52

Approximately 5 to 10 percent of people evaluated for depression have previously undetected thyroid dysfunction

Increased TSH

Front 53

What is TRH challenge?

Back 53

increased TSH response to a 500-mg infusion of the hypothalamic neuropeptide thyroid-releasing hormone (TRH).

Front 54

What % of depressed patient show abnormal response to TRH challenge?

Back 54

depressed patients (e.g., 20 to 30 percent) shows a blunted TSH response to TRH challenge.

Front 55

What is clinical meaning does a blunted TSH response mean?

Back 55

the major therapeutic implication of a blunted TSH response is evidence of an increased risk of relapse despite preventive antidepressant therapy

Front 56

Does the dexamethasone suppression test normalize with tx?

Back 56

No

Front 57

Does the blunted TSH response to TRH normalize to treatment?

Back 57

No

Front 58

Somostatin levels and relation to mood ds?

Back 58

Growth hormone (GH) is secreted from the anterior pituitary after stimulation by NE and Dopamine (DA). Secretion is inhibited by somatostatin, a hypothalamic neuropeptide, and CRH. Decreased CSF somatostatin levels have been reported in depression, and increased levels have been observed in mania

Front 59

What causes release of prolactin from pituitary? what inhibits?

Back 59

serotonin
dopamine

Front 60

Any relation of prolactin to depression?

Back 60

Most studies have not found significant abnormalities of basal or circadian prolactin secretion in depression, although a blunted prolactin response to various serotonin agonists has been described. This response is uncommon among premenopausal women, suggesting that estrogen has a moderating effect.

Front 61

Depression & Sleep: relation to
1. deep/slow wave sleep
2. nocturnal arousal
2a. nocturnal awakenings
2b. total sleep time
2c. REM
2d. Core Body temp

Back 61

1. deep/slow wave sleep increased
2. nocturnal arousal increased
2a. nocturnal awakenings increased
2b. total sleep time: decreased
2c. REM: increased
2d. Core Body temp: increased

Front 62

Depression and REM latency?

Back 62

reduced

Front 63

Define REM latency

Back 63

The combination of increased REM drive and decreased slow wave sleep results in a significant reduction in the first period of non-REM (NREM) sleep, a phenomenon referred to as reduced REM latency

Front 64

Relationship of REM latency and slow wave sleep after recovery of depressive episode?

Back 64

Reduced REM latency and deficits of slow wave sleep typically persist after recovery of a depressive episode.

Front 65

(Increased or decreased) secretion of GH after sleep onset is associated with decreased slow wave sleep and shows similar state-independent or trait-like behavior.

Back 65

Decreased

Front 66

increased or decreased in depression?
1. REM LATENCY
2. REM Density
3. Sleep maintainence

Back 66

1. REM LATENCY: reduced
2. REM Density: increased
3. Sleep maintainence: decreased

Front 67

The combination of reduced REM latency, increased REM density, and decreased sleep maintenance identifies approximately XX percent of depressed outpatients and YY percent of depressed inpatients

Back 67

XX = 40 %
YY = 80%

Front 68

What is relationship of slow wave sleep to younger patients and depression?

Back 68

may see increased slow wave sleep

Front 69

what % of healthy individuals have abnormal sleep profiles?

Back 69

10%

Front 70

Do people with abn sleep profiles respond better to psychotherapy or pharmacotherapy?

Back 70

pharm

Front 71

Any relation of depressive disorders to immune system?

Back 71

decreased lymphocyte proliferation in response to mitogens
Interleukin 1 may induce glucocorticoid synthesis via gene activity

Front 72

What does brain imaging show in depression?

Back 72

abnormal hyperintensities in subcortical regions, such as periventricular regions, the basal ganglia, and the thalamus

Front 73

What structures have altered volumes in depression?

Back 73

Some depressed patients also may have reduced hippocampal or caudate nucleus volumes

Front 74

What does PET show in depression?

Back 74

The most widely replicated positron emission tomography (PET) finding in depression is decreased anterior brain metabolism, which is generally more pronounced on the left side

Front 75

In depression which side of brain is less active? more?

Back 75

generally left side less active, meaning non-dominant ride side more active

Front 76

In hypomania, how does brain activity (seen via PET) differ than depression?

Back 76

greater right hemisphere reduction of activity (ie increased left hemisphere)

Front 77

cerebral blood flow/metabolism is changed how in what tracts?

Back 77

reductions of reduced cerebral blood flow or metabolism, or both, in the dopaminergically innervated tracts of the mesocortical and mesolimbic systems in depression

Front 78

anterior cerebral metabolism and depression relationship?

Back 78

global reduction of activity

Front 79

relationship of activity to limbic regions in depression?

Back 79

increased activity (increased glucose metabolism), especially in patients with severe recurrent depression and a family history of depression

Front 80

Which patients to you especially see increased limbic activity increased?

Back 80

severe recurrent depression, family history of mood disorder

Front 81

what is increased glucose metabolism areaas in depression associated with?

Back 81

intrusive ruminations

Front 82

Which brain areas are considered heavily involved in depression?

Back 82

prefrontal cortex
anterior cingulate
hippocampus
amygdala

Front 83

prefrontal cortex function?

Back 83

The PFC is viewed as the structure that holds representations of goals and appropriate responses to obtain these goals
Subregions in the PFC appear to localize representations of behaviors related to reward and punishmen

Front 84

prefrontal cortext function in left-hemi versus right hemi?

Back 84

left-sided activation of regions of the PFC is more involved in goal-directed or appetitive behaviors, whereas regions of the right PFC are implicated in avoidance behaviors and inhibition of appetitive pursuits

Front 85

Anterior Cingulate Cortex function?

Back 85

The anterior cingulate cortex (ACC) is thought to serve as the point of integration of attentional and emotional inputs

Front 86

What are the subdivisions of the Anterior Cingulate Cortex and their function?

Back 86

Two subdivisions have been identified: an affective subdivision in the rostral and ventral regions of the ACC and a cognitive subdivision involving the dorsal ACC.

Front 87

What does activation of the Anterior Cingulate Cortex help people with?

Back 87

control of emotional arousal, particularly when goal attainment has been thwarted or when novel problems have been encountered.

Front 88

Hippocampus function?

Back 88

The hippocampus is most clearly involved in various forms of learning and memory, including fear conditioning, as well as inhibitory regulation of the HPA axis activity. Emotional or contextual learning appears to involve a direct connection between the hippocampus and the amygdala

Front 89

Amygdala function

Back 89

The amygdala appears to be a crucial way station for processing novel stimuli of emotional significance and coordinating or organizing cortical responses

Although most research has focused on the role of the amygdala in responding to fearful or painful stimuli, it may be ambiguity or novelty, rather than the aversive nature of the stimulus per se, that brings the amygdala on line

Front 90

What do family studies show about mood disorders?

Back 90

Family data indicate that if one parent has a mood disorder, a child will have a risk of between 10 and 25 percent for mood disorder. If both parents are affected, this risk roughly doubles.

Front 91

Does severity of illness in family relative change risk?

Back 91

Yes, greater risk if relation has more severe form of illness.

Front 92

Genes are considered to explain what percent of the cause of the mood disorder?

Back 92

50 to 70%

Front 93

When considering unipolar and bipolar disorders together, what is the twin (monozygotic) concordance of disorders? how about same sex dizygotic?

Back 93

1. 70 to 90
2. 16 to 35%

Front 94

Which is the most convincing evidence (family, adoption, twin studies) for the role of genetics?

Back 94

twin studies

Front 95

Which chromosomes most linked to bipolar disorder via linkage study?

Back 95

18 and 22q

Front 96

Unipolar depression linked to what chromosome?

Back 96

2

Front 97

What is the theory explaining why stressful life events often precede the first episode of a mood disorder but not so much 2nd, 3rd episodes?

Back 97

The stress that comes from the first episode results in long-lasting changes in the brains biology; i.e., changes brain to be more vulnerable so that can depressed without an external stressor

Front 98

Which life event is most associated with development of depression?

Back 98

Losing a parent before age 11

Front 99

Which environmental stressor is most associated with onset of an episode of depression?

Back 99

loss of a spouse

Front 100

What is the difference between being employed and unemployed in terms of depression risk?

Back 100

persons out of work are three times more likely to report symptoms of an episode of major depression than those who are employe

Front 101

What is relationship between personality disorders and depression.

Back 101

Persons with certain personality disorders—OCD, histrionic, and borderline—may be at greater risk for depression than persons with antisocial or paranoid personality disorder.
Why ...
The latter can use projection and other externalizing defense mechanisms to protect themselves from their inner rage

Front 102

What is the most powerful predictor of the onset of a depressive episode?

Back 102

recent stressful events

Front 103

Which stressors are more likely to produce depression?

Back 103

onces that reflect negatively on self-esteem ...

Front 104

What is the psychodynamic explanation of depression

Back 104

Freud/Karl Abraham
1. infant-mother relationship 0 to 18 months ... disturbed (oral phase) ... this creates vulnerability to depression
2. depressed linked to real or imagined object loss
3. lost/departed object is introject as a defense (to minimize distress associated with loss)
4. lost object seen with mix of love and hate, feelings of anger are directed inward to self.

Overall, depression = aggresssion toward oneself

Front 105

Silvano Arieti view on depression

Back 105

Silvano Arieti observed that many depressed people have lived their lives for someone else rather than for themselves. He referred to the person for whom depressed patients live as the dominant other, which may be a principle, an ideal, or an institution, as well as an individual

Depression sets in when patients realize that the person or ideal for which they have been living is never going to respond in a manner that will meet their expectations.

Front 106

Edward Bibring view on depression

Back 106

Edward Bibring regarded depression as a phenomenon that sets in when a person becomes aware of the discrepancy between extraordinarily high ideals and the inability to meet those goals

Front 107

Edith Jacobson view on depression

Back 107

Edith Jacobson saw the state of depression as similar to a powerless, helpless child victimized by a tormenting parent.

Front 108

Heinz Kohut view of depression

Back 108

Heinz Kohut's conceptualization of depression, derived from his self-psychological theory, rests on the assumption that the developing self has specific needs that must be met by parents to give the child a positive sense of self-esteem and self-cohesion. When others do not meet these needs, there is a massive loss of self-esteem that presents as depression.

Front 109

John Bowlby view of depression

Back 109

John Bowlby believed that damaged early attachments and traumatic separation in childhood predispose to depression. Adult losses are said to revive the traumatic childhood loss and so precipitate adult depressive episodes.

Front 110

What is psychodynamic view of mania?

Back 110

defense against depression

Front 111

Abraham view of mania?

Back 111

Abraham, for example, believed that the manic episodes may reflect an inability to tolerate a developmental tragedy, such as the loss of a parent. The manic state may also result from a tyrannical superego, which produces intolerable self-criticism that is then replaced by euphoric self-satisfaction.

Front 112

Bertram Lewin view of mania

Back 112

Bertram Lewin regarded the manic patient's ego as overwhelmed by pleasurable impulses, such as sex, or by feared impulses, such as aggression.

Front 113

Klein view of mania?

Back 113

Klein also viewed mania as a defensive reaction to depression, using manic defenses such as omnipotence, in which the person develops delusions of grandeur.

Front 114

What is Aaron Beck triad view of depression?

Back 114

Aaron Beck postulated a cognitive triad of depression that consists of (1) views about the self—a negative self-precept; (2) about the environment—a tendency to experience the world as hostile and demanding, and (3) about the future—the expectation of suffering and failure

Front 115

What is learned helplessness view of depression?

Back 115

In the reformulated view of learned helplessness as applied to human depression, internal causal explanations are thought to produce a loss of self-esteem after adverse external events. Behaviorists who subscribe to the theory stress that improvement of depression is contingent on the patient's learning a sense of control and mastery of the environment.

Front 116

How stable is the diagnosis of depression?

Back 116

One type of study assessed the stability of a diagnosis of major depression in a patient over time. The study found that 25 to 50 percent of the patients were later reclassified as having a different psychiatric condition or a nonpsychiatric medical condition with psychiatric symptoms

Front 117

Which dx is more stable unipolar or bipolar depression?

Back 117

bipolar

Front 118

How much minimum time is needed between mood episodes to consider then seperate?

Back 118

At least two months without significant symptoms

Front 119

What is a major difference between psychotic and non-psychotic depression?

Back 119

One difference is that bipolar I disorder is more common in the families of probands with psychotic depression than in the families of probands with nonpsychotic depression

Front 120

What is the difference between mood congruent and mood incongruent psychosis?

Back 120

Mood congruent usually means more likely mood ds while incongruent means Szaffective/Sz

Front 121

What has been associated with poor prognosis in mood disorders (along with psychosis)

Back 121

long duration of episodes, temporal dissociation between the mood disorder and the psychotic symptoms, and a poor premorbid history of social adjustment. The presence of psychotic features also has significant treatment implications.

Front 122

Melancholia features?

Back 122

by severe anhedonia,
early morning awakening,
weight loss, and
profound feelings of guilt (often over trivial events)

Front 123

Melancholia associated with biology?

Back 123

yes, changes in autonomic and endocrine function

Front 124

Does melancholia occur more with life stressors or not?

Back 124

more endogenous, without external life stresors

Front 125

What are atypical features of depression?

Back 125

reversed veg s:
increased eating and sleeping

Front 126

How to patients with MDD atypical features compare with MDD typical features?

Back 126

When patients with major depressive disorder with atypical features are compared with patients with typical depression features, the patients with atypical features are found to have a younger age of onset, more severe psychomotor slowing, and more frequent coexisting diagnoses of panic disorder, substance abuse or dependence, and somatization disorder.
Patients with atypical features may also have a long-term course, a diagnosis of bipolar I disorder, or a seasonal pattern to their disorder.

Front 127

How are these patients often misdiagnosed?

Back 127

The high incidence and severity of anxiety symptoms in patients with atypical features have sometimes been correlated with the likelihood of their being misclassified as having an anxiety disorder rather than a mood disorder.

Front 128

What are the key features of catatonia and when do you see them?

Back 128

The hallmark symptoms of catatonia—stuporousness, blunted affect, extreme withdrawal, negativism, and marked psychomotor retardation—can be seen in both catatonic and noncatatonic schizophrenia, major depressive disorder (often with psychotic features), and medical and neurological disorders

Front 129

How much time are you allowed to add specififier post-partum onset

Back 129

1 month/4 weeks post-partum

Front 130

Rapid cycling more common in?

Back 130

Patients with rapid cycling bipolar I disorder are likely to be female and to have had depressive and hypomanic episodes

Front 131

Is Rapid cycling inherited or is an external factor like stress or drug tx more likely involved?

Back 131

Not inherited
more likely external factor

Front 132

What is evidence showing SAD is different perhaps than nonseasonal depression?

Back 132

1. Patients respond to light tx (although no studies with controls)
2. decreased metabolic activity in orbital frontal cortex and left inferior parietal lobe

Front 133

Endogenous features of depression (although controversial)

Back 133

diurnal variation,
delusions,
psychomotor retardation,
early morning awakening, and
feelings of guilt

Front 134

reactive (to stress) features of depression

Back 134

initial insomnia,
anxiety,
emotional lability, and
multiple somatic complaints

Front 135

What is difference between primary and secondary depression?

Back 135

primary = mood ds
secondary = GMC, substance induced

Front 136

How differentiate Bipolar I depression with Unipolar depression?

Back 136

In a clinical situation, only the patient's history,
family history, and
future course can help differentiate the two conditions.

Front 137

What percent of depresed patients contemplate suicide?

Back 137

2/3's
66%

Front 138

When percent of depressed patients commit suicide?

Back 138

10 to 15%

Front 139

Which people with MDD have higher lifetime risk of successful suicide

Back 139

HOSPITALIZED
Those recently hospitalized with a suicide attempt or suicidal ideation have a higher lifetime risk of successful suicide than those never hospitalized for suicidal ideation.

Front 140

What % of depressed patients complain of reduced energy?

Back 140

97%

Front 141

What % complain of trouble sleeping?

Back 141

80%

Front 142

Anxiety affect as many as XX% of depressed patients?

Back 142

90%

Front 143

What % of patients have a diurnal variation in sx, increased severity in AM and better by eve?

Back 143

50%

Front 144

What % have poor concentration?
trouble thinking?

Back 144

84%
67%

Front 145

What may be symptoms of depression in children?

Back 145

School phobia and excessive clinging to parents may be symptoms of depression in children.

Front 146

What may be sx of depression in teens?

Back 146

Poor academic performance,
substance abuse,
antisocial behavior,
sexual promiscuity,
truancy, and
running away may be symptoms of depression in adolescents.

Front 147

Is depression more common in the general population or the older person?

Back 147

the older person

Front 148

what is prevalence rate in older persons for MDD?

Back 148

25 to 50%

Front 149

What is depression in older persons correlated with?

Back 149

Several studies indicate that depression in older persons may be correlated with
low socioeconomic status,
the loss of a spouse, a
concurrent physical illness, and social isolation

Front 150

What do we often underdx depression in elderly?

Back 150

because greater somatic complaints
ageism: ie.., we think depressive sx are normal in old age

Front 151

How is mania misdiagnosed in teens?

Back 151

seen as antisocial personality ds
schizophrenia

Front 152

What are teen sx of mania?

Back 152

Symptoms of mania in adolescents may include psychosis, alcohol or other substance abuse, suicide attempts, academic problems, philosophical brooding, OCD symptoms, multiple somatic complaints, marked irritability resulting in fights, and other antisocial behaviors. Although many of these symptoms are seen in normal adolescents, severe or persistent symptoms should cause clinicians to consider bipolar I disorder in the differential diagnosis

Front 153

Biplar 1 versus 2: which has more marital disruption?

Back 153

2 more marital disruption

Front 154

Biplar 1 versus 2: which has early onset?

Back 154

2 earlier onset

Front 155

Biplar 1 versus 2: attempting suicide

Back 155

2

Front 156

Bipolar 1 versus 2: completing suicide

Back 156

2

Front 157

The available data indicate that alcohol dependence is more strongly associated with a coexisting diagnosis of depression in (gender) than in (gender)

Back 157

> in women than in men

Front 158

What does the genetic and family data suggest about men with both mood ds and alcohol dependence?

Back 158

two genetically SEPERATE disease processes

Front 159

What is the most common symptom of depression?

Back 159

generalized psychomotor slowing
although can also see agitation, especially in elderly (hand-wringing and hair-pulling)

Front 160

Signs of psychomotor retardation?

Back 160

stooped posture, no spontaneous movements, downcast averted gaze

Front 161

What percent of depressed patients deny depressive feelings and do not appear to be very depressed?

Back 161

50%

Front 162

How do they non-depressed appearing people get tx?

Back 162

brought in by family members or employers because of social withdrawal and generally decreased activity

Front 163

Give examples of mood-congruent delusions in depression

Back 163

Mood-congruent delusions in a depressed person include those of guilt,
sinfulness,
worthlessness,
poverty,
failure,
persecution, and
terminal somatic illnesses (such as cancer and “rotting” brain)

Front 164

What is Veraguth's fold?

Back 164

The Swiss neuropsychiatrist Otto Veraguth described a peculiar triangle-shaped fold in the nasal corner of the upper eyelid. The fold is often associated with depression and referred to as Veraguth's fold.

Front 165

About XX percent of all depressed patients have marked symptoms of a thought disorder, usually thought blocking and profound poverty of content.

Back 165

10%

Front 166

About XX to XX percent of all depressed patients have a cognitive impairment, sometimes referred to as depressive pseudodementia. Such patients commonly complain of impaired concentration and forgetfulness

Back 166

50 to 75

Front 167

About XX to XX percent of all depressed patients commit suicide, and about XX have suicidal ideation

Back 167

10 to 15
66%

Front 168

When are depressed patients at increased risk of suicide?

Back 168

Patients with depressive disorders are at increased risk of suicide as they begin to improve and regain the energy needed to plan and carry out a suicide (paradoxical suicide)

Front 169

What is advice around tx of depressed patient with SI and rx?

Back 169

avoid TCA's
consider giving benzo while giving activiating rx like fluoxetine

Front 170

Describe Zung Scale

Back 170

self-rating scale
20 items
normal score = 34
depressed is 50 or more
global index of intensity of sx

Front 171

Describe Raskin

Back 171

clinician sale
5 point scale of three dimensions: verbal report, displayed behavior, and secondary sx
Range: 3 o 13
Normal: 3 and depressed is 7 or more

Front 172

Describe Hamilton scale

Back 172

The Hamilton Rating Scale for Depression (HAM-D) is a widely used depression scale with up to 24 items, each of which is rated 0 to 4 or 0 to 2, with a total score of 0 to 76. The clinician evaluates the patient's answers to questions about feelings of guilt, thoughts of suicide, sleep habits, and other symptoms of depression, and the ratings are derived from the clinical interview.

Front 173

Gives stages of manic speech

Back 173

1. louder, rapid, difficult to interpret
2. puns, jokes, rhymes, plays on words, irrelevancies
3. loosed associations, concentration fades, flight of ideas, claning, and neologisms
4. incoherent, indistinguishable from say sz

Front 174

Delusions occur in XX percent of all manic patients

Back 174

75%

Front 175

Describe manic thought content

Back 175

The manic patient's thought content includes themes of self-confidence and self-aggrandizement. Manic patients are often easily distracted, and their cognitive functioning in the manic state is characterized by an unrestrained and accelerated flow of ideas.

Front 176

What are cognitive deficits in BP1?

Back 176

These deficits can be interpreted as reflecting diffuse cortical dysfunction; subsequent work may localize the abnormal areas. Grossly, orientation and memory are intact, although some manic patients may be so euphoric that they answer questions testing orientation incorrectly

Front 177

About XX percent of all manic patients are assaultive or threatening

Back 177

75%

Front 178

What % of manic patients attempt suicide?

Back 178

unknwn

Front 179

What % of manic patients attempt homicide?

Back 179

unknown

Front 180

If seen teen with depression, what GMC to consider?

Back 180

mono

Front 181

If depressed and overweight, what to test?

Back 181

adrenal and thyroid fxn

Front 182

What endocrine tests should be done for MDD?

Back 182

Thyroid and
Adrenal Fxn

Front 183

Which drugs are associated with depression?

Back 183

Cardiac drugs,
antihypertensives,
sedatives,
hypnotics,
antipsychotics,
antiepileptics,
antiparkinsonian drugs,
analgesics,
antibacterials, and
antineoplastics are all commonly associated with depressive symptoms

Front 184

Which neuro problems most commonly associated with depression?

Back 184

Parkinson's disease, dementing illnesses (including dementia of the Alzheimer's type), epilepsy, cerebrovascular diseases, and tumors

Front 185

About XX to XX percent of all patients with Parkinson's disease have marked symptoms of depressive disorder

Back 185

50 to 75

Front 186

What does the MDD in Parkinson's correlate with?

Back 186

not correlate with the patient's physical disability, age, or duration of illness but do correlate with the presence of abnormalities found on neuropsychological tests.

Front 187

How does epilepsy correlate with depression?

Back 187

The interictal changes associated with temporal lobe epilepsy can mimic a depressive disorder,

Front 188

What side epileptic focus is associated with depressive disorder?

Back 188

especially if the epileptic focus is on the right side.

Front 189

Depression is a common complicating feature of cerebrovascular diseases, particularly in the (time) after the episode.

Back 189

2 years

Front 190

Depression is (more or less common) in anterior brain lesions than in posterior brain lesions and, in both cases, (does not, often) responds to antidepressant medications.

Back 190

more common in anterior brain lesions
both respond to Rx

Front 191

What types of tumours are associated with depressive ds?

Back 191

Tumors of the diencephalic and temporal regions are particularly likely to be associated with depressive disorder symptoms.

Front 192

How do you distinguish pseudodementia of depression with dementia?

Back 192

MDD cog Sx have: sudden onset
also, have self-reproach
have diurnal variation in cog sx
patients often answer I don't know (versus confabulate)
in interview, depressed patients can be coached to remembering but demented can't

Front 193

What do you distinguish between Anxiety disorder with depression
and Depressive Ds with marked anxiety?

Back 193

An abnormal result on the dexamethasone-suppression test,

the presence of shortened REM latency on a sleep electroencephalogram (EEG),

and a negative lactate infusion test result support a diagnosis of

major depressive disorder in particularly ambiguous cases

Front 194

about XX of all bereaved spouses for a time meet the diagnostic criteria for major depressive disorder

Back 194

1/3

Front 195

What are MDD sx of unresolved bereavement?

Back 195

morbid preoccupation with worthlessness,
suicidal ideation,
feelings that the person has committed an act (not just an omission) that caused the spouse's death,
mummification (keeping the deceased's belongings exactly as they were),
and a particularly severe anniversary reaction, which sometimes includes a suicide attempt

Front 196

What happens for some people with severe spousal bereavement depression?

Back 196

end up with serious medical condition - immune function depressed, cardiovascular status precarious
... death within a few months of spouse, especially among elderly men

Front 197

How distinguish schizophrenia from mania?

Back 197

Merriment, elation, and infectiousness of mood are much more common in manic episodes than in schizophrenia.

The combination of a manic mood, rapid or pressured speech, and hyperactivity weighs heavily toward a diagnosis of a manic episode.

onset in mania often rapid, and seen as marked change

Front 198

What % of patients with bipolar 1 ds have a family history of mood disorder?

Back 198

Half of all patients with bipolar I disorder have a family history of mood disorde

Front 199

Which PD are associated with manic sx?

Back 199

borderline, narcissistic, histrionic, and antisocial personality disorders

Front 200

What is DDX of BP2?

Back 200

Mood Ds
Psychotic Ds
and Borderline PD

Front 201

How are BP2 and BPD similar

Back 201

both often have severely disrupted life
multiple episodes of mood ds sx

Front 202

List as many clinical features predictive of bipolar disorder

Back 202

Early age at onset
Psychotic depression before 25 years of age
Postpartum depression, especially one with psychotic features
Rapid onset and offset of depressive episodes of short duration (<3 months)
Recurrent depression (more than five episodes)
Depression with marked psychomotor retardation
Atypical features (reverse vegetative signs)
Seasonality
Bipolar family history
High-density, three-generation pedigrees
Trait mood lability (cyclothymia)
Hyperthymic temperament
Hypomania associated with antidepressants
Repeated (at least three times) loss of efficacy of antidepressants after initial response
Depressive mixed state (with psychomotor excitement, irritable hostility, racing thoughts, and sexual arousal during major depression)

Front 203

What conditions might suggest Bipolar Ds more than MDD?

Back 203

agitated depression,
cyclical depression,
episodic sleep dysregulation, or a combination of these;

refractory depression (failed antidepressants from three different classes);
depression in someone with an extroverted profession,
periodic impulsivity,
such as gambling,
sexual misconduct, and wanderlust, or periodic irritability, suicidal crises, or both;
and depression with erratic personality disorders.

Front 204

About XX percent of patients having their first episode of major depressive disorder exhibited significant depressive symptoms before the first identified episode

Back 204

50%

Front 205

The first depressive episode occurs before age XX in about XX percent of patients

Back 205

before age 40
50%

Front 206

late onset depression is associated with?

Back 206

absence of a family history of mood disorders,
antisocial personality disorder,
and alcohol abuse

Front 207

How long does untx depressive episode last?

Back 207

6 to 13 months

Front 208

How long does treated episode last?

Back 208

3months

Front 209

The withdrawal of antidepressants before X months has elapsed almost always results in the return of the symptoms

Back 209

3

Front 210

Over a 20-year period, the mean number of episodes is XX

Back 210

5 or 6 episodes over 20 years

Front 211

About XX percent of patients with an initial diagnosis of major depressive disorder have a manic episode XX years after the first depressive episode

Back 211

5 to 10 percent

6 to 10 years

Front 212

What is the average age of a switch to manic episode in MDD?

Back 212

32

Front 213

Switching occurs after how many depressive episodes?

Back 213

often after two to four episodes

Front 214

Although the data are inconsistent and controversial, some clinicians report that the depression of patients who are later classified as having bipolar I disorder is often characterized by?

Back 214

hypersomnia
psychomotor retardation
psychotic sx
hx of postpartum episodes
family hx of BP1
hx of antidepressant induced hypomania

Front 215

Patients who have been HOSPITALIZED for a FIRST episode of major depressive disorder have about a XX percent chance of recovering in the FIRST year.

Back 215

50%

Front 216

About AA percent of patients experience a recurrence of major depressive disorder in the first BB months after release from a hospital, about CC percent in the following DD years, and about EE percent in FF years

Back 216

A: 25% B, first 6 months
C: 30 to 50% in following D: 2 years
E: 50 to 75% in F: 5 years

Front 217

What lowers relapse?

Back 217

Rx
Patients who have had only 1 or 2 episodes

Front 218

What happens as pt experiences more depressive episodes?

Back 218

time between decrease
severity increases

Front 219

What are good prognositic indicators of MDD?

Back 219

Mild episodes,
the absence of psychotic symptoms, and a short hospital stay are good prognostic indicators

good prognostic signs are the absence of a comorbid psychiatric disorder and of a personality disorder,
no more than one previous hospitalization for major depressive disorder, and
an advanced age of onset.

Front 220

What are good prognositic indicators of MDD, psychosocial indicators:

Back 220

a history of solid friendships during adolescence,
stable family functioning, and
generally sound social functioning for the 5 years preceding the illness.

Front 221

Poor prognostic factors for MDD

Back 221

increased by coexisting dysthymic disorder,
abuse of alcohol and other substances,
anxiety disorder symptoms, and a history of more than one previous depressive episode.

Front 222

Gender1 are more likely than Gender2 to experience a chronically impaired course.

Back 222

Men > women in terms of chronically impaired course

Front 223

Which personality traits are associated with BP1?

Back 223

None

Front 224

What % of time does BP1 start with depression?

Back 224

Bipolar I disorder most often starts with depression (75 percent of the time in women, 67 percent in men) and is a recurring disorder.

Front 225

(Few, Some, Most) patients experience both depressive and manic episodes, although (XX) percent experience only manic episodes.

Back 225

Most
10 to 20 %

Front 226

BP1 manic episode onset ?

Back 226

rapid onset: hours or days ... sometimes evolve over a few weeks

Front 227

Untreated manic episode lasts about XX months

Back 227

3 months

Front 228

Of persons who have a single manic episode, XX percent are likely to have another.

Back 228

90%

Front 229

As the disorder progresses, the time between episodes often (increases or decreases)?

Back 229

decreases

Front 230

What happens over time in terms of interepisode interval?

Back 230

after about 5 episodes,
interepisode interval stablizes at 6 to 9 months

Front 231

What % of BP have rapid cycling (4 or more episodes per year?)

Back 231

5 to 15%

Front 232

The incidence of bipolar I disorder in children and adolescents is about XX percent, and the onset can be as early as age X.

Back 232

1%
as early as age 8

Front 233

BP in kids/teens often misdiagnosed as?

Back 233

Sz or ODD

Front 234

Is early onset associated with poor, ok, or good prognosis?

Back 234

Poor

Front 235

Onset of BP1 in older persons is?
common, or uncommon?

Back 235

uncommon

Front 236

Do patients with MDD or BP1 have worse prognosis?

Back 236

BP1

Front 237

About XX percent of patients with bipolar I disorder may have a second manic episode within X years of the first episode

Back 237

40 to 50%
2 years

Front 238

XX percent of patients achieve significant control of their symptoms with lithium

Back 238

50 to 60

Front 239

What are predictors of poor prognosis in BP1?

Back 239

premorbid poor occupational status, alcohol dependence,
psychotic features,
depressive features,
interepisode depressive features, and
male gender were all factors that contributed a poor prognosis.

Front 240

Predictors of good prognosis in BP1?

Back 240

Short duration of manic episodes,
advanced age of onset,
few suicidal thoughts, and
few coexisting psychiatric or medical problems predict a better outcome.

Front 241

About XX percent of patients with bipolar I disorder do not have a recurrence of symptoms; YY percent have more than one episode, and ZZ percent have a chronic disorde

Back 241

X 7 percent
Y 45% have more than one episode
Z 40% have a chronic disorder

Front 242

What is mean number of manic episodes?

Back 242

9

Front 243

What % have more than ten episodes of mania in BP1?

Back 243

40%

Front 244

On long-term follow-up, XX percent of all patients with bipolar I disorder are well, XX percent are well but have multiple relapses, XX percent are in partial remission, and XX percent are chronically ill.

Back 244

15% are well
45% well with relapses
30% partial remission
10% chronically ill

Front 245

XX percent of all patients with bipolar I disorder have chronic symptoms and evidence of significant social decline

Back 245

One third of all patients with bipolar I disorder have chronic symptoms and evidence of significant social decline

Front 246

Do stressful life events increase relapse rates in BP1?

Back 246

yes

Front 247

List indicators for hospitalization in MDD:

Back 247

Clear indications for hospitalization are the risk of suicide or homicide,
a patient's grossly reduced ability to get food and shelter, and the
need for diagnostic procedures.

A history of rapidly progressing symptoms and the
rupture of a patient's usual support systems are also indications for hospitalization.

Front 248

Explain three psychotherapeutic approaches to depression:
1. Major Theorists
2. Concepts of pathology and cause

Back 248

A. Psychodynamic
1. Freud, Abraham, Jacobson, Kohut
2. Ego regression: damaged self-esteem, unresolved conflict due to childhood object loss and disappointment
B: Cognitive approach
1. Plato, Adler, Beck, Rush
2. Distorted thinking: dysphoria due to learned negative view of self, others, and world
Interpersonal Approach: impaired relations, absent or unsatisfactor significant social bonds

Front 249

Explain Psychodynamic approaches to depression:
1. major goals
2. mechanism of change
3. primary techniques
4. therapist role
5. Marital role

Back 249

1. promote personality change through understanding of past conflicts, to achieve insight into defenses, ego disortions, and superego defects; to provide a role model; to permit cathartic release of aggression
2. Techniques
Expressive empathy, transference and resistance analysis, confront defenses, clarifying ego and super-ego disortions
3. Interpreter-reflector: establishment and exploration of transference; therapeutic alliance for benign dependence and empathic understanding
4. Marital role: exclusion, confidentiality unless life-threatening

Front 250

Explain CBT approaches to depression:
1. major goals
2. mechanism of change
3. primary techniques
4. therapist role
5. Marital role

Back 250

CBT
1. Major Goals
sx relief through change thoughts; identify self-destructive cognitions, to modify specific eorroneous assumptoms; to promote self-control over thinking problems
2. Primary Techniques:
record and monitor thoughts, correcting distored themes with logic and experimental testing
providing alternative thought content
homework
3. Therapist Role: Educator, shaper; positive relationship instead of transference, collaborative empiricism as basis for joint scientific logical task
4. Spouse as objective reporter; couple therapy for disturbed cognitions sustained in marital relationship

Front 251

Explain IPT approaches to depression:
1. major goals
2. mechanism of change
3. primary techniques
4. therapist role
5. Marital role

Back 251

1/2/ Major Goals:
- relief through soloving interpersonal problems
- reduce stress involving family or work
- improve interpersonal communication skills
3. primary techniques:
communication, environmental, clarifying managing maladaptive relationships and learning new ones through communicatoin and social skills training; providing information on illness
4. Tx role:
- explorer prescriber: positive relationship transference without interpretation; active therapist role for influence and advocacy
5. Marital role:
intergral role of spouse in tx; examine role of spouses' role in patients predisposition to depression and effects on illness on marriage

Front 252

What is Weltan-schauung?

Back 252

world-view

Front 253

What is best tx for mild depression: Rx, Psychotherapy, or both?

Back 253

either alone is effective, probably more likely psychotherapy for mild

Front 254

In a randomized, controlled trial comparing psychodynamic therapy with cognitive behavior therapy, the outcome of the depressed patients was ?

Back 254

same outcome

Front 255

National Institute of Mental Health (NIMH) Treatment of Depression Collaborative Research Program found the following predictors of response to various treatments:
1. IPT?
2. CBT?
3. Rx?
4. Combined (Rx + IPT)

Back 255

1. low social dysfunction good for IPT
2. low cognitive dysfunction good for CBT AND Rx
3. High work dysfunction and Rx
4. high depression severity - combined

Front 256

Match variable to mode of therapy
Nonselective
Psychodynamic (Pd)
CBT
IPT
1. Feeling of hopelessness/helplessness

Back 256

Non-selective

Front 257

What patient variables would make you choose Pd Tx?

Back 257

long term feelings
Unresolved conflict
Insightful
Accessible (to dreams/fantasy)
Little need for guidance/direction
Stable environment

Front 258

What patient variables would make you choose CT?

Back 258

Distorted thoughts
Logical thinking problems
Moderate to high need for direction
responsive to behavioural training and self-help

Front 259

What patient variables would make you select IPT?

Back 259

Recent social conflict
Recent life change
abnormal grief
moderate need for direction
Responsiveness to environmental manipulation (available support network)

Front 260

Goals of CT?

Back 260

The goal of cognitive therapy is to alleviate depressive episodes and prevent their recurrence by helping patients identify and test negative cognitions; develop alternative, flexible, and positive ways of thinking; and rehearse new cognitive and behavioral responses

Front 261

How does CT compare to phamacotherapy?

Back 261

Most studies found that :
cognitive therapy is equal in efficacy to pharmacotherapy and
is associated with fewer adverse effects and better follow-up than pharmacotherapy.

Front 262

NIMH Treatment of Depression Collaborative Research Program, found that pharmacotherapy, either alone or with psychotherapy, may be the treatment of choice for patients with (mild, moderate or severe) major depressive episodes

Back 262

Severe

Front 263

What is Interpersonal Therapy have in terms of basic assumptions?

Back 263

1. Current interpersonal problems likely have roots in early dysfxn relationship
2. Current problems likely involved in precipitating or perpetuating current depressive symptoms

Front 264

Can IPT work in severe MDD?

Back 264

yes, some studies indicate is best method in severe depression

Front 265

How many sessions is IPT?

Back 265

12 to 16 sessions

Front 266

Are intra-psychic phenomena like defense mechanisms or internal conflicts addressed in IPT?

Back 266

No

Front 267

How about discrete bheaviours such as lack of assertiveness, impaired social skills, disorted thinking addressed in IPT?

Back 267

Only in context of effect on interpersonal relationships

Front 268

What is behaviour therapy based on?

Back 268

Maladaptive behavioural patterns based on lack of + feedback and outright rejection from society

Front 269

Does behavior tx work in MDD?

Back 269

yes

Front 270

What are aims of Psychoanalytic therapy

Back 270

Improvements in interpersonal trust, capacity for intimacy, coping mechanisms, the capacity to grieve, and the ability to experience a wide range of emotions are some of the aims of psychoanalytic therapy.

Front 271

Compare Pd, CT, and IPT in terms of advantages and disadvantages in domains of:
1. Theory
2. Goals,
3. Structure
4. Therapist Role
5. Techniques
6. Research Status
7. Relation to other modalities
8. Patient Population

Back 271

See Table 15.1- 33

Front 272

When is family tx indicated for mood ds?

Back 272

Family therapy is indicated if the disorder jeopardizes a patient's marriage or family functioning or if the mood disorder is promoted or maintained by the family situation.

Front 273

Patients with mood disorders have a high rate of divorce, and about XX percent of all spouses report that they would not have married or had children if they had known that the patient was going to develop a mood disorder.

Back 273

50%

Front 274

How was vagal nerve stimulation discovered?

Back 274

Vagal Nerve Stimulation in tx for epilepsy helped mood also

Front 275

Which side is used in vagal nerve stim?

Back 275

left side

Front 276

How does vagal nerve stim work?

Back 276

vagus nerve connected to enteric system and may be involved in release of enteric peptides that act as neurotransmitters

Front 277

Which tx: Rx or Ptx?
1. Vegative Sx

Back 277

Rx

Front 278

Which tx: Rx or Ptx?
mild to moderate situation or characterological depressed mood

Back 278

Ptx

Front 279

Which tx: Rx or Ptx?
Anhedonia, loss of libido, impaired sexual fxn

Back 279

Rx

Front 280

Which tx: Rx or Ptx?
apathy, decreased enjoyment
diminished sexual desire or gratification

Back 280

Ptx

Front 281

Which tx: Rx or Ptx?
1. Major weight loss
2. Minor weight gain

Back 281

1. Rx
2. Ptx

Front 282

Which tx: Rx or Ptx?
1. Early morning awakening
2. Oversleeping, morbid dreams or nightmares

Back 282

1. Rx
2. Ptx

Front 283

Which tx: Rx or Ptx?
1. Restlessness or feelings of being slowed down
2. Hyperactivity or motor retardation

Back 283

1. Ptx
2. Rx

Front 284

Which tx: Rx or Ptx?
1. Lack of motivation or will
2. Depressive Stupor

Back 284

1. Ptx
2. Rx

Front 285

Which tx: Rx or Ptx?
1. Nihilistic or self-deprecatory delusions, self-berating auditory hallucinations
2. Low self-esteem, inappropriate guilt feelings, self-reporach

Back 285

1. Rx
2. Ptx

Front 286

Which tx: Rx or Ptx?
1. Loss of control, over thinking, obsessive rumination, inability to focus or act
2. Distractibility, sluggish thinking or decision making; negative cognitions

Back 286

1. Rx
2. Ptx

Front 287

Which tx: Rx or Ptx?
1. Acute, episodic, and uncontrolled suicidal acts or plans
2. Chronic feelings of hopelessness or helplessness

Back 287

1. Rx
2. Rx or Ptx

Front 288

Which tx: Rx or Ptx?
1. Social withdrawal or fears of rejection or failure; psychosomatic complaints or hypochondriasis
2. Panic attacks or phobias; persecutory delusions, pseudodementia; physicial sx or somatic delusions

Back 288

1. Ptx
2. Rx

Front 289

Which tx: Rx or Ptx?
1. Genetic loading
2. No genetic loading

Back 289

1. Rx
2. Ptx

Front 290

Which tx: Rx or Ptx?
1. Psychosocial stressors, e.g., loss of significant other, change in status or role
2. Other mental disorders, e.g. Sz, alcohol dependence, AN

Back 290

1. Ptx
2. Rx

Front 291

Which tx: Rx or Ptx?
1. Borderline PD
2. Histrionic PD
3. OCPD
4. Dependent PD
5. Inadequate
6. Masochistic

Back 291

1, 2, 3 Rx
4, 5, 6 Ptx

Front 292

Approximately XX percent of depressive disorder patients exhibit significant but transient benefit from total sleep deprivation.

Back 292

60

Front 293

The positive results are typically reversed (time period)

Back 293

by the next night of sleep.

Front 294

What methods have been used to sustain benefits of sleep deprivation help in MDD?

Back 294

1. Serial TOTAL sleep deprivation, with a day or two of normal sleep in between
... not so effective
2. Phase DELAY ... time patient goes to sleep each night, o stay away from 2am to 10pm daily ... wears off in time
3. serial PARTIAL sleep deprivation
helps to treat insomnia ...
4. Sleep depression combined with Rx:

Front 295

How are combo sleep dep and rx studies in MDD done?

Back 295

total and partial sleep deprivation folllowed by immediate tx with antidepressant or lithium
or
sleep deprivation accelerates response of antidepressans like prozac and nortriptyline

Front 296

along with MDD, what does sleep deprivation help?

Back 296

Premenstrual dysphoria

Front 297

GENDER represent at least XX percent of all patients with seasonal depression, and the mean age of presentation is XX. Patients (commonly, rarely) present over the age of XX with seasonal affective disorder.

Back 297

Women
75%
40
rarely
50%

Front 298

Phototherapy parameters?

Back 298

hototherapy typically involves exposing the afflicted patient to bright light in the range of 1,500 to 10,000 lux or more, typically with a light box that sits on a table or desk. Patients sit in front of the box for approximately 1 to 2 hours before dawn each day, although some patients may also benefit from exposure after dusk

Front 299

Along with SAD, what else is phototx used for?

Back 299

Sleep disorders
helps decrase irratability and decreased fxn associated with shift work.
Geriatric sleep ds improved with bright light.
Jet lag.
OCD with a seasonal variation.

Front 300

The use of specific pharmacotherapy approximately XX the chances that a depressed patient will recover in X month

Back 300

doubles the chance in 1 month

Front 301

Name 3 factors in choosing an antidepressant for MDD

Back 301

Choice of antidepressants is determined by the side effect profile least objectionable to a given patient's physical status, temperament, and lifestyle.

Front 302

Common reason for poor Rx response?

Back 302

1. Too low
2. Too short

Front 303

When would you consider drug trial unsuccessful?

Back 303

Max tolerated dose at 4 to 5 weeks

Front 304

What would you do if patient improving on low dosage of drug?

Back 304

Don't increase (at least wait until max benefit achieved); i.e., if improving, watchi.

Front 305

If no response at all after 2 to 3 weeks what can be done?

Back 305

Drug level ... may tell adherence or unusual pharmacokinetics

Front 306

What is recommendation re: Antidepressant duration of Tx for MDD?

Back 306

at least 6 months or
length of previous epsidode, (which ever is more)

Front 307

What would you do if episodes are less than 2.5 years apart?

Back 307

Tx prophylactically for 5 years

Front 308

How do available antidepressants differ in overall efficacy, speed of response, or long-term effectiveness.

Back 308

They don't

Front 309

What do antidepressants differ in?

Back 309

Side effect profile
interactions
side effects
chance of discontinuation syndrome
ease of dose adjustment

Front 310

How do you select intial Rx?

Back 310

Selection of the initial treatment depends on the chronicity of the condition,
course of illness (a recurrent or chronic course is associated with increased likelihood of subsequent depressive symptoms without treatment),
family history of illness and treatment response,
symptom severity,
concurrent general medical or other psychiatric conditions,
prior treatment responses to other acute phase treatments,
potential drug–drug interactions,
and patient preference.

Front 311

What % of uncomplicated MDD respond to Rx?

Back 311

In general, approximately 45 to 60 percent of all outpatients with uncomplicated (i.e., minimal psychiatric and general medical comorbidity), nonchronic, nonpsychotic major depressive disorder who begin treatment with medication respond (i.e., achieve at least a 50 percent reduction in baseline symptoms);

Front 312

How is response defined?

Back 312

50% reduction in baseline sx

Front 313

What percent achieve Remission, absensce of depressive symptoms?

Back 313

up to 50% (35-50%)

Front 314

Patients with major depressive disorder with atypical features (sometimes called hysteriod dysphoria) may preferentially respond to treatment with

Back 314

MAOIs or SSRIs.

Front 315

How about melancholic depression, which drug to use?

Back 315

Antidepressants with dual action on both serotonergic and noradrenergic receptors demonstrate greater efficacy in melancholic depressions

Front 316

Tx of MDD with psychotic features

Back 316

add antipsychotic
use ECT

Front 317

Which rx for atypical features of depression?

Back 317

For those with atypical symptom features, strong evidence exists for the effectiveness of MAOIs
SSRI's and bupropion also usable in atypical depression

Front 318

Tx of MDD with comorbid Panic Ds, which Rx?

Back 318

SSRI
tricyclics

Front 319

In comorbid MDD, what decides choice of treatment, MDD or the comorbidity

Back 319

the comorbidity

Front 320

Which GMC diseases does MDD worsen morb and mort?

Back 320

The presence of a major depressive episode is associated with increased morbidity or mortality of many general medical conditions (e.g., cardiovascular disease, diabetes, cerebrovascular disease, and cancer

Front 321

Is it useful to use antidepressants side effects to treat depression sx?

Back 321

No.
Choosing more sedating antidepressants (e.g., amitriptyline [Elavil, Endep]) for more anxious, depressed patients or more activating agents (e.g., desipramine) for more psychomotor-retarded patients is not generally helpful. For example, any short-term benefits with paroxetine, mirtazapine, or amitriptyline (more sedating drugs) on symptoms of anxiety or insomnia may become liabilities over time.

Front 322

So how should you manage sx relief?

Back 322

use adjunctive medications (e.g., sleeping pills or anxiolytics) combined with antidepressants to provide more immediate symptom relief or to cover those side effects to which most patients ultimately adapt

Front 323

What factors might help you in choosing rx?

Back 323

failure to previous class well documented
First degree relative responding well to classs

Front 324

List reasons why patient may not acutely respond to rx?

Back 324

1. intolerance of side fx
2. idiosyncratic adverse event
3. poor clinical reponse
4. wrong diagnosis

Front 325

By week 4, if dose is adequate, what % of people who will fully respond show at least a partial response?

Back 325

20 to 25%

Front 326

What happens if don't even get partial response by week 4 to 6 in MDD?

Back 326

switch

Front 327

How long, if getting response, would you wait before saying ultimate response achieved?

Back 327

8 to 12 weeks.

Front 328

What % of patients require 2nd medication treatment trial b/c 1st trial is poorly tolerated or ineffective

Back 328

50%

Front 329

Options when 1st trial unsuccessful?

Back 329

Switch (preferred over augmenting)
Augment

Front 330

Best augmenters?

Back 330

Li,
T3
also Wellbutrin (bupropion)

Front 331

Which drug is not approved for acute Mania by FDA?

Back 331

Lamotrigine

Front 332

Which drugs ARE approved for Bipolar Maintenance

Back 332

Lamotrigine,
Lithium,
Olanzapine

Front 333

What could happen if physician thinks rx will not work in mood ds?

Back 333

may result in poor response,
nonadherence,
inadequate dosage

Front 334

How is acute mania often tx?

Back 334

in hospital

Front 335

What is tx range of lithium level?

Back 335

0.6 to 1.2

Front 336

What is used more for acute mania - lithium or valproate?

Back 336

valproate, b/c easier earlier on

Front 337

Valproate dosing range? blood level target?

Back 337

750mg to 2.5 grams
50 to 120 ug/ml

Front 338

Valproate loading dose?

Back 338

15 to 20 mg/kg

Front 339

Carbamazepine use?
Doses?

Back 339

acute mania
600 to 1800 mg/day

Front 340

carbamazapine drug level target?

Back 340

4 to 12 ug/m

Front 341

do you need higher or lower doses of OXcarbazepine?

Back 341

higher, 1500mg of ox = 1000 of carb

Front 342

What Rx might you use in bipolar depression?

Back 342

olanzapine/fluoxetine combo (Symbyax)
Lamotrigine,
Ziprasidone (low dose ... 20 to 80 mg a day)

Front 343

How can verapamil be used? what is it?

Back 343

calcium channel antagonist ....
antimanic

Front 344

WHat type of ECT works best in mania?

Back 344

Bilateral treatment (versus unilateral non-domniant)

Front 345

When might you use ECT for mania?

Back 345

patients with rare refractory mania,
patients with medical complications,
extreme exhaustion (malignant hyperthermia or lethal catatonia)

Front 346

What % of bipolar patients relapse in first 5 months off lithium?

Back 346

50 percent relapse in first 5 months off lithiu

Front 347

Which Rx best in long term for bipolar ds?

Back 347

Lithium, carbamazepine, and valproic acid, alone or in combination, are the most widely used agents in the long-term treatment of patients who are bipolar.

Front 348

Does lamotrigine protect against mania in BP1?

Back 348

switch into mania same rate as placebo so answer is no

Front 349

What is incidence of severe rash in Lamotrigine?

Back 349

2/10, 000
4 in 10, 000 kids

Front 350

What happens in long term on lithium?

Back 350

over needs thyroid supplementation, i.e., T3 25 to 50 ug per day because of SHORT-half life
T4 used in long-term maintenance

Front 351

Role of T4 in BP1?

Back 351

hypermetabolic doses of T4 seems to help in BP1 (both manic and depressive phases)

Front 352

describe onset of dysthymic ds

Back 352

most cases are of early onset, beginning in childhood or adolescence and certainly occurring by the time patients reach their 20s

Front 353

Key Features of Dysthymia

Back 353

(1) low-grade chronicity for at least 2 years;
(2) insidious onset, with origin often in childhood or adolescence; and
(3) persistent or intermittent course.

Front 354

Dysthymia link to Mood Disorders?

Back 354

The family history of patients with dysthymia is typically replete with both depressive and bipolar disorders, which is one of the more robust findings supporting its link to primary mood disorder

Front 355

Dysthymic disorder is common among the general population and affects XX to XX percent of all persons.

Back 355

5 to 6

Front 356

Dysthymia is seen among patients in general psychiatric clinics, where it affects between XX of all patients

Back 356

50% and 33%

Front 357

Dysthymia gender differences in rates?

Back 357

no difference in incidence rates

Front 358

Dysthymia common in?

Back 358

women younger than 64 (than men)
unmarried vs married
young people
low incomes

Front 359

Dysthymia relation to MDD

Back 359

Dysthymic disorder frequently coexists with other mental disorders, particularly major depressive disorder, and in persons with major depressive disorder there is less likelihood of full remission between episodes.

Front 360

Dsthymia coexists often with?

Back 360

The patients may also have coexisting anxiety disorders (especially panic disorder),
substance abuse, and
borderline personality disorder

Front 361

genetic risk?

Back 361

> if have 1st degree rel with MDD

Front 362

Do you see similar sleep pattern in Dysthymia like MDD?

Back 362

yes, less REM latency, increased REM density

Front 363

Dys compared to MDD in terms of DexSupTest?

Back 363

Less likely to be abnormal

Front 364

What are DSM things to remember about dysthym

Back 364

1 year for teens or less,
early onset = before age 21 or late =21 or older

Front 365

Differnce between MDD and Dysthymia?

Back 365

The profile of dysthymic disorder overlaps with that of major depressive disorder, but differs from it in that symptoms tend to outnumber signs (more subjective than objective depression). This means that disturbances in appetite and libido are uncharacteristic, and psychomotor agitation or retardation is not observed.

Front 366

Research Criteria is different how from DSMIV Dysth

Back 366

Research Criteria is different how:

- REgular criteria emphasize vegetate dysfxn while research criteria more cognitive
Has three (versus two)

Presence, while depressed, of three (or more) of the following:

1. low self-esteem or self-confidence, or feelings of inadequacy
2. feelings of pessimism, despair, or hopelessness
3. generalized loss of interest or pleasure
4. social withdrawal
5. chronic fatigue or tiredness
6. feelings of guilt, brooding about the past
7. subjective feelings of irritability or excessive anger
8. decreased activity, effectiveness, or productivity
9. difficulty in thinking, reflected by poor concentration, poor memory, or indecisiveness

Front 367

What are some attributes of depressive and hyperthymic temperaments:

Back 367

Depressive (vs Hyperthymic):
1. Gloomy vs Cheerful
2. Humorless vs Articulate
3. Pessimisitic, overoptimistic and carefree
4. Guilt prone, low self-esteem and pre-occupied with failure versus overconfident, self-assured, boastful, and grandiose
5. Introverted vs extroverted
6. Sluggish vs High Energy
7. Few but constant interests and versatile with broad interests
8. Passive vs overinvolved and meddlesome
9. Reliable, dependpendable, and devoted vs Unihibited and stimulus seeking

Front 368

What conditions does dysth aggravate?

Back 368

stroke

Front 369

What % of dsythmic kids go onto hypomanic, manic or mixed episodes after puberty?

Back 369

up to 20%

Front 370

What is relation of adult onset dysthymic ds and hypomania and mania?

Back 370

rarely get spontaneous hypomania or mania

Front 371

DDX of Dysthymia?

Back 371

pretty much same as MDD;
think substance and GMC
especially think:
MINOR depressive disorder (episodic versus no euthymia) and
Recurrent Brief (less than 2 weeks) Depressive Ds

Front 372

What % of people with MDD meet also criteria for Dysthymia?

Back 372

40%

Front 373

About XX percent of patients with dysthymic disorder experience an insidious onset of symptoms before age XX.

Back 373

50%,
Age 25

Front 374

Dysthmia Duration untreated usually?

Back 374

10 years

Front 375

Studies of patients with the diagnosis of dysthymic disorder indicate that about XX percent progressed to major depressive disorder, YY percent to bipolar II disorder, and less than ZZ percent to bipolar I disorder

Back 375

XX 20
YY 15
Z 5

Front 376

The available data about DYSTHMIA previously available treatments indicate that only XX percent of patients are in remission 1 year after the initial diagnosis

Back 376

10 to 15%

Front 377

Best tx for Dysthymia?

Back 377

The combination of pharmacotherapy and some form of psychotherapy may be the most effective treatment for the disorder.

Individual insight-oriented psychotherapy is the most common treatment method for dysthymic disorder, and many clinicians consider it the treatment of choice.

Front 378

Rx in Dysthymia?

Back 378

The data generally indicate that selective serotonin reuptake inhibitors (SSRIs) venlafaxine and bupropion are an effective treatment for patients with dysthymic disorder. Monoamine oxidase inhibitors (MAOIs) are effective in a subgroup of patients with dysthymic disorder, a group who may also respond to the judicious use of amphetamines.

Front 379

Patients with cyclothymic disorder may constitute from XX percent of all psychiatric outpatients, perhaps particularly those with significant complaints about marital and interpersonal difficulties

Back 379

3 to 5

Front 380

In the general population, the lifetime prevalence of cyclothymic disorder is estimated to be about X percent

Back 380

1

Front 381

Cyclothymic disorder, as with dysthymic disorder, frequently coexists with ?

Back 381

Borderline PD

Front 382

An estimated XX percent of outpatients and YY percent of inpatients with borderline personality disorder have a coexisting diagnosis of cyclothymic disorder

Back 382

XX: 10%
YY: 20%

Front 383

The female-to-male ratio in cyclothymic disorder is about ?

Back 383

3 to 2

Front 384

Cyclothymia onset?

Back 384

15 to 25 for
50 to 75%

Front 385

About XX percent of all patients with cyclothymic disorder have positive family histories for bipolar I disorder.

Back 385

30%

Front 386

How does the + family hx rate in cyclothymia compare to BP1?

Back 386

same, 30%

Front 387

How does having BP1 and having a relative then with cyclothymia compare with having some other ds and having cyclothymia?

Back 387

much higher if BP1

Front 388

What evidence suggests cyclothymia may be milder form of BP2 ds?

Back 388

The observations that about
one third of patients with cyclothymic disorder subsequently have major mood disorders,
that they are particularly sensitive to antidepressant-induced hypomania, and that about
60 percent respond to lithium

Front 389

What is psychodynamic theory of cyclothymia?

Back 389

Most psychodynamic theories postulate that the development of cyclothymic disorder lies in traumas and fixations during the oral stage of infant development. Freud hypothesized that the cyclothymic state is the ego's attempt to overcome a harsh and punitive superego. Hypomania is explained psychodynamically as the lack of self-criticism and an absence of inhibitions occurring when a depressed person throws off the burden of an overly harsh superego. The major defense mechanism in hypomania is denial, by which the patient avoids external problems and internal feelings of depression.

Hypomania is frequently triggered by a profound interpersonal loss. The false euphoria generated in such instances is a patient's way to deny dependence on love objects and simultaneously disavowing any aggression or destructiveness that may have contributed to the loss of the loved person

Front 390

About % of all patients with cyclothymic disorder have depression as their major symptom

Back 390

50%

Front 391

% patients with cyclothymic disorder have periods of mixed symptoms with marked irritability.

Back 391

Almost all

Front 392

About XX percent of all patients with cyclothymic disorder have substance dependence.

Back 392

5 to 10

Front 393

Which PD to consider in DDX of Cyclothymic ds?

Back 393

Borderline,
Antisocial,
Histrionic,
Narcissitic

Front 394

How stimulants (i.e. for suspected ADHD) impact on cyclothymia?

Back 394

worsen it

Front 395

About XX % of all patients with cyclothymic disorder develop a major mood disorder, most often ?

Back 395

33%
BIpolar 2

Front 396

About XX percent of all patients with cyclothymic disorder who are treated with antidepressants experience antidepressant induced hypomanic or manic episodes

Back 396

40 to 50%

Front 397

Which disorders meet criteria for Dep Ds NOS

Back 397

1. Minor depressive Ds
2. Recurrent Brief Depressive Ds
3. Premenstrual Dsyphoric Ds

Front 398

Minor depressive disorder prevelance?

Back 398

Minor depressive disorder may be as common as major depressive disorder—that is, about 5 percent prevalence in the general population.

Front 399

Difference between minor and major depressive ds?

Back 399

same duration, different number of sx
only need two sx; i.e., 1 low mood or anhedonia + other

Front 400

Define Recurrent Brief Depressive Disorder:

Back 400

meet criteria for MDD EXcept for duration of two weeks (at least 2 days)

Front 401

Recurrent Brief Depressive Ds
The 10-year prevalence rate for the disorder is estimated to be XX percent for people in their 20s; the 1-year prevalence rate for the general population is estimated to be X %

Back 401

The 10-year prevalence rate for the disorder is estimated to be 10 percent for people in their 20s; the 1-year prevalence rate for the general population is estimated to be 5 percent

Front 402

In terms of bio abnormalities with recurrent brief depressive disorder, how do they compare to patients with major depressive disorder

Back 402

same; i.e.,
1/ NON suppression on DST
2. Blunt reponse to TRH
3. Shortening of REM sleep latency

Front 403

What symptoms don't you get in Premenstrual Dysphoric Disorder?

Back 403

GPS
Guilt
Psychomotor Slowing
SI

Front 404

What are categories of sx of Premenstrual Dysphoric Disorder

Back 404

The syndrome involves mood symptoms (e.g., lability), behavior symptoms (e.g., changes in eating patterns), and physical symptoms (e.g., breast tenderness, edema, and headaches).

Front 405

Which patients with Sz likely to get postpsychotic depressive episode?

Back 405

Patients with postpsychotic depressive disorder of schizophrenia are likely to have had
poor premorbid adjustment,
marked schizoid personality disorder traits, and an
insidious onset of their psychotic symptoms. They are also likely to have first-degree relatives with mood disorders. Although the findings have not been consistent, postpsychotic depressive disorder of schizophrenia has been associated with a less-favorable prognosis, a higher likelihood of relapse, and a higher incidence of suicide than is seen in patients with schizophrenia without postpsychotic depressive disorder.

Front 406

Define mixed anxiety-depressive disorder?

Back 406

Mixed anxiety-depressive disorder is characterized by a persistent or recurrent depressed mood lasting at least 1 MONTH (KEY) and by symptoms of anxiety, such as sleep disturbance, fatigue or low energy, irritability, and worry

Front 407

Which type of patients especially prone to mixed anxiety-depressive disorder?

Back 407

patients in general medical setting

Front 408

People with Mixed anxiety-depressive disorder often have what prominent
complaint?
Diagnosed with what in ICD-10?

Back 408

chronic fatigue
diagnosed with neurasthenia

Front 409

Atypical depression key features?

Back 409

Atypical depression refers to fatigue superimposed on a history of somatic anxiety and phobias, together with reverse vegetative signs (mood worse in the evening, insomnia, tendency to oversleep and overeat), so that weight gain occurs rather than weight loss

Front 410

Hysertoid Dysphoria criteria?

Back 410

he category of non-DSM hysteroid dysphoria combines reverse vegetative signs with the following characteristics:
(1) giddy responses to romantic opportunities and an avalanche of dysphoria (angry-depressive, even suicidal responses) on romantic disappointment;
(2) impaired anticipatory pleasure, yet the capability to respond with pleasure when such is provided by others (i.e., preservation of consummatory reward);
(3) craving for chocolate and sweets, which contain phenylethylamine compounds and sugars believed to facilitate cellular and neuronal intake of the amino acid L-tryptophan, hypothetically leading to synthesis of endogenous antidepressants in the brain

Front 411

List 11 drug categories than can cause Depression:

Back 411

1. Cardiac and antihypertensive drugs
2. Sedatives and hypnotics
3. Steroids and hormones
4. Stimulants and appetite suppressants
5. Psychotropic drugs
6. Neurological agents
7. Analgesics and anti-inflammatory drugs
8. Antibacterial and antifungal drugs
9. Antineoplastic drugs
10. Nonsteroidal anti-inflammatory drugs (NSAIDs)
11. Anticholinesterases

Front 412

Which is worse: motility psychosis or catatonia?

Back 412

catatonia,
the difference being that motility psychosis has better, more favorable course

Front 413

List as many Rx as you can that cause mania:

Back 413

Amphetamines
Baclofen
Bromide
Bromocriptine
Captopril
Cimetidine
Cocaine
Corticosteroids (including adrenocorticoid hormone [ACTH])
Cyclosporine
Disulfiram
Hallucinogens (intoxication and flashbacks)
Hydralazine
Isoniazid
Levodopa
Methylphenidate
Metrizamide (following myelography)
Opiates and opioids
Phencyclidine (PCP)
Procarbazine
Procyclidine
Yohimbine

Front 414

Describe Anxiety-Blissfulness Psychosis

Back 414

Anxiety-blissfulness psychosis may resemble agitated depression but can also be characterized by so much inhibition that a patient can hardly move. Periodic states of overwhelming anxiety and paranoid ideas of reference are characteristic of the condition, but self-accusation, hypochondriacal preoccupation, other depressive symptoms, and hallucinations may also accompany it. The blissful phase manifests most frequently in expansive behavior and grandiose ideas, which are concerned less with self-aggrandizement than with the mission of making others happy and saving the world.