Ch.6, Panic etc Disorders Flashcards

1
Q

Diff between anxiety and fear

A

Anxiety involves a general feeling of apprehension about possible future danger
whereas fear is an alarm reaction that occurs in response to immediate danger: fight flight, ANS, adaptive

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2
Q

Most common categories of disorders for women and earliest age onset

A

anxiety disorders, 2nd most common for men
anxiety disorders have earliest age onset of all mntal disorders

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3
Q

Panic attack/ 3 components of fear/panic

A

when a sudden fear response occurs with no fearful stimuli,
cognitive/subjective components (e.g., “I’m going to die”)

physiological components (e.g., increased heart rate and heavy breathing)

behavioral components (e.g., a strong urge to escape or flee).

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4
Q

3 components of anxiety and how they differ from fear

A

still has the cognitive/subjective, physiological, and behavioural
1- cognitive/subjective: worried about what might happen
2-physiological: tension/chronic overarousal
3-general avoidance
- anxiety is descriptively and functionally distinct from fear or panic, proven by statistical analyses of subjective reports of panic and anxiety and from a great deal of neurobiological evidence

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5
Q

Adaptive value of anxiety/conditioning in anxiety

A

may help us plan and prepare for possible threat
in mild/moderate degrees, anxiety enhances learning and performance
much of our anxiety may be conditioned into us

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6
Q

list of anxiety disorders

A

specific phobia

social anxiety disorder (social phobia)

panic disorder

agoraphobia

generalized anxiety disorder.

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7
Q

Personality trait most related to anxiety

A

neuroticism a proneness or disposition to experience negative mood states that is a common risk factor for both anxiety and mood disorders

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8
Q

common psychological causal factors of anxiety disorders

A

-classical conditioning of fear, panic, or anxiety to a range of stimuli plays an important role in many of these disorders
-people who have perceptions of a lack of control over either their environments or their own emotions (or both) seem more vulnerable to developing anxiety disorders
-faulty or distorted patterns of cognition also may play an important role.

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9
Q

most effective treatment for anxiety disorders (3)

A

-graduated exposure to feared cues, objects, and situations—until fear or anxiety begins to habituate— constitutes the single most powerful therapeutic ingredient.
-cognitive restructuring techniques can provide added benefit by helping the individual understand his or her distorted patterns of thinking about anxiety-related situations and how these patterns can be changed.
-Medications also can be useful in treating all disorders except specific phobias, and nearly all tend to fall into two primary categories: antianxiety medications (anxiolytics) and antidepressant medications.

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10
Q

Specific phobias

A

said to be present if a person shows strong and persistent fear that is triggered by the presence of a specific object or situation and leads to significant distress and/or impairment in a person’s ability to function
-people with specific phobias encounter a phobic stimulus, they often show an immediate fear response that often resembles a panic attack except for the existence of a clear external trigger

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11
Q

5 subtypes of specific phobias, DSM 5

A

animal, natural environement, blood injection injury (seeing blood or injury), situational, other (choking)

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12
Q

Why is blood-injury phobia potentially adaptive? why does it onset?

A

-From an evolutionary and functional standpoint, this unique physiological response pattern may have evolved for a specific purpose: By fainting, the person being attacked might inhibit further attack, and if an attack did occur, the drop in blood pressure would minimize blood loss
&***This type of phobia appears to be highly heritable

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13
Q

Phobias from psycoanalytic vs phobias as learned behavior

A

-According to the psychoanalytic view, phobias represent a defense against anxiety that stems from repressed impulses from the id. Because it is too dangerous to “know” the repressed id impulse, the anxiety is displaced onto some external object or situation that has some symbolic relationship to the real object of the anxiety (too speculative)
-vicarious conditioning: Simply watching a phobic person behaving fearfully with his or her phobic object can be distressing to the observer and can result in fear being transmitted from one person to another through vicarious or observational classical conditioning.

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14
Q

Given all the traumas that people undergo and watch others experience, why don’t more people develop phobias

A

-individual differences in life experiences strongly affect whether conditioned fears or phobias actually develop: some life experiences may serve as risk factors and make certain people more vulnerable to phobias than others, whereas other experiences may serve as protective factors for the development of phobias

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15
Q

What impacts the level of fear acquired during conditioning?

A

-experiencing an inescapable and uncontrollable event is expected to condition fear much more powerfully than experiencing the same intensity of trauma that is escapable or to some extent controllable
-cognitions:” can help maintain our phobias once they have been acquired = people with phobias are constantly on the alert for their phobic objects or situations and for other stimuli relevant to their phobia

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16
Q

Phobias and prepared learning

A

evolutionary history has affected which stimuli we are most likely to come to fear. Primates and humans seem to be evolutionarily prepared to rapidly associate certain objects—such as snakes, spiders, water, and enclosed spaces—with frightening or unpleasant events
occurs bc: primates and humans who rapidly acquired fears of certain objects or situations that posed real threats to our early ancestors had a selective advantage (they survived more often than those who had no fear of such things)

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17
Q

Preparedness and conditioning fears experimentally

A

fear is conditioned more effectively to fear-relevant stimuli (slides of snakes and spiders) than to fear-irrelevant stimuli (slides of flowers and mushrooms

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18
Q

why can people with phobias not control their fear due to brain pathology?

A

amygdala reacts to even subliminal presentation of the stimuli

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19
Q

biological causal factors of specific phobias

A

-Genetic and temperamental variables also affect the speed and strength of conditioning of fear
-individuals who are carriers of one of the two variants of the serotonin-transporter gene (the s allele, which has been linked to heightened neuroticism) show superior fear conditioning than those without the s allele
-behaviorally inhibited toddlers (who are excessively timid, shy, easily distressed, etc.) at 21 months of age were at higher risk of developing multiple specific phobias by 7 to 8 years of age than were uninhibited children

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20
Q

Treatments for specific phobias

A

is exposure therapy—a form of behavior therapy that involves controlled exposure to the stimuli or situations that elicit phobic fear
-participant modeling: more effective than reg exposure therapy; the therapist calmly models ways of interacting with the phobic stimulus or situation

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20
Q

Why do antianxiety meds and cognitive techniques not eliminate specific phobias?

A

COGNITIVE RESTRUCTURING TECHNIQUES ARE NOT AS USEFUL** AND ANTIANXIETY MEDS MIGHT INTERFERE WITH THE BENEFITS OF EXPOSURE THERAPY

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21
Q

Drug known to facilitate the extinction of conditioned fear in animals

A

D-cycloserine: can also help the effectiveness of exposure therapy in a virtual reality environment, but by itself has no effect

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22
Q

social anxiety disorder and most common type of social anxiety; gender differences in social anxiety

A

characterized by disabling fears of one or more specific social situations
-Intense fear of public speaking is the single most common type of social anxiety
-women experience it far more

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23
Q

Learned behavior and social anxiety

A

-social anxiety often seems to originate from simple instances of direct or vicarious classical conditioning such as experiencing or witnessing a perceived social defeat or humiliation, or being or witnessing the target of anger or criticism

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24
Q

social fears an evolution

A

proposed that social fears and phobia evolved as a by-product of dominance hierarchies that are a common social arrangement among primates

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25
Q

social anxiety and amygdala activation when compared to controls

A

people who have social anxiety show greater activation of the amygdala (and other brain areas involved in emotion processing) in response to negative facial expressions (such as angry faces) than do normal controls = explains the seemingly irrational quality of social anxiety, in that the angry faces are processed very quickly and an emotional reaction can be activated without a person’s awareness of any threat = The hyperactivity to negative facial expressions is paralleled by heightened neural responses to criticism

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26
Q

Social anxiety and sense of control

A

people with social anxiety have a diminished sense of personal control over events in their lives

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27
Q

cognitive biases in the maintence of social anxiety

A

(1) people with social anxiety tend to expect that other people will reject or negatively evaluate them. They argued that this leads to a sense of vulnerability when they are around people who might pose a threat.
(2) cognitive bias seen in social anxiety is a tendency to interpret ambiguous social information in a negative rather than a benign manner
MAINTAIN AND CONTRIBUTE TO THE DEVELOPMENT OF SOCIAL ANXIETY

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28
Q

Treatment for social anxiety

A

cognitive and behaviural therapies
cognitive restructuring: e therapist attempts to help clients with social anxiety identify their underlying negative, automatic thoughts
External focus on cognitive restructuring: clients may be assigned exercises in which they manipulate their focus of attention (internally versus externally) to demonstrate to themselves the adverse effects of internal self-focus

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29
Q

social anxiety and pharmaceutical treatments

A
  • several categories of antidepressants (including the monoamine oxidase inhibitors and the selective serotonin reuptake inhibitors
    -however external focus cognitive restructuring therapy produced much more improvement than these drugs
    -produce shorter-term benefits than behavioral therapy
    -D-cycloserine added to exposure therapy may also work
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30
Q

Panic disorder/gender differences

A

occurrence of panic attacks that often seem to come “out of the blue.”/ person must have experienced recurrent, unexpected attacks and must have been persistently concerned about having another attack or worried about the consequences of having an attack for at least a month
more common in women

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31
Q

Anticipatory anxiety/nocturnal panic

A

fearing another panic attack
nocturnal panic: panic attack that occurs during sleep

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32
Q

Agoraphobia/ gender differences

A

most commonly feared and avoided situations include streets and crowded places such as shopping malls, movie theaters, and stores./ more common in women

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33
Q

How might agoraphobia and panic disorder might be different?

A

Could include panic attack like symptoms, but many people do not experience panic = led to it being a distinct DSM 5 diagnosis

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34
Q

recurrence

A

new onset of te disorder

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35
Q

why is there a large gender difference in agoraphobia?

A

it is more acceptable for women who experience panic to avoid the situations they fear and to need a trusted companion to accompany them when they enter feared situations. Men who experience panic are more prone to “tough it out” because of societal expectations and their more assertive, instrumental approach to life

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36
Q

Panic disorder and comorbidities

A

The vast majority of people with panic disorder (83 percent) have at least one comorbid disorder, most often generalized anxiety disorder, social anxiety, specific phobia, PTSD, depression, and substance-use disorders
DEPRESSION MOST COMMON

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37
Q

PANIC disorder and suicidal behavior

A

panic disorder is indeed associated with increased risk for suicidal ideation and attempts independent of its relationship with comorbid disorders EVEN OUTSIDE OF DEPRESSION

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38
Q

Biological causal factors of panic disorder

A

genetics, brain activity, and biochemical abnormalities.
-s, panic disorder has a moderate heritable component

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39
Q

locus coeruleus and panic attacks, early theory

A

One relatively early prominent theory about the neurobiology of panic attacks implicated the locus coeruleus in the brain stem and a particular neurotransmitter—norepinephrine—that is centrally involved in brain activity in this area
NOT TRUE: increased activity in the amygdala that plays a more central role in panic attacks than does activity in the locus coeruleus.

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40
Q

fear networks/sensitivity/panic disorder

A

panic disorder is likely to develop in people who have abnormally sensitive fear networks that get activated too readily to be adaptive. This theory about abnormally sensitive fear networks is also consistent with findings that individuals with panic disorder showed heightened startle responses to loud noise stimuli as well as slower habituation of such responding

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41
Q

Region of the brain that generates conditioned anxiety

A

HPC, involved in emotional memory

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42
Q

Panic Provocation procedures

A

lab experiments showing that people with panic disorder are much more likely to experience panic attacks when they are exposed to various biological challenge procedures than are normal people or people with other psychiatric disorders (caffeine etc)

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43
Q

2 primary NT systems most implicated in panic attacks

A

Noradrenergic activity in certain brain areas can stimulate cardiovascular symptoms associated with panic
Increased serotonergic activity also decreases noradrenergic activity.

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44
Q

How do SSRIs work to treat panic disorder?

A

This fits with results showing that the medications most widely used to treat panic disorder today—the selective serotonin reuptake inhibitors (SSRIs)—seem to increase serotonergic activity in the brain but also to decrease noradrenergic activity.
=By decreasing noradrenergic activity, these medications decrease many of the cardiovascular symptoms associated with panic that are ordinarily stimulated by noradrenergic activity

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45
Q

Anticipatory anxiety and GABA

A

The inhibitory neurotransmitter GABA has also been implicated in the anticipatory anxiety that many people with panic disorder have about experiencing another attack. GABA is known to inhibit anxiety and has been shown to be abnormally low in certain parts of the cortex in people with panic disorder

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46
Q

Cognitive Theory of Panic

A

-The cognitive theory of panic disorder proposes that people with panic disorder are hypersensitive to their bodily sensations and are very prone to giving them the most dire interpretation possible
- tendency to catastrophize about the meaning of their bodily sensations.

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47
Q

automatic thoughts, during panic attacks

A

-the triggers of panic.
-catastrophizing the meaning of bodily sensations/ The person is not necessarily aware of making these catastrophic interpretations; rather, the thoughts are often just barely out of the realm of awareness

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48
Q

Describe the panic circle of panic disorder

A

1) Any kind of perceived threat may lead to apprehension or worry, which is accompanied by various bodily sensations. (the intial physical sensations do not have to arise from the perceived threa, but might come from other sources like excercise, anger, etc)
2) person then catastrophizes about the meaning of his or her bodily sensations, this will raise the level of perceived threat, thus creating more apprehension and worry as well as more physical symptoms
=fuel further catastrophic thoughts.
= culminate in a panic attack

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49
Q

Comprehensive Learning Theory of Panic Disorder

A

suggests that initial panic attacks become associated with initially neutral internal (interoceptive) and external (exteroceptive) cues through an interoceptive conditioning (or exteroceptive conditioning) process = leads anxiety to become conditioned to these CSs (conditioned stimuli) = the more intense the panic attack = the more robust the conditioning that will occur.

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50
Q

3 components of panic disorder

A

1, anticipatory anxiety, 2 agoraphobic fears, 3 panic attacks themselves

51
Q

Conditioning of anxiety and developing two panic disorder components

A

anticipatory anxiety and, sometimes, agoraphobic fears.

52
Q

Generalization and panic disorder cues

A

nce an individual has developed panic disorder, that person shows greater generalization of conditioned responding to other similar cues than do controls without panic disorder

53
Q

Extinction and panic disorder cases

A

Because extinction involves inhibitory learning, which seems to be impaired in panic disorder, it is not surprising that individuals with panic disorder also show impaired discriminative conditioning because of their deficits in learning that a CS is a safety cue

54
Q

Internal CS that trigger panic attack

A

panic attacks themselves (the third component of panic disorder) are also likely to be conditioned to certain internal cues: even excitement that raises the heart rate can trigger a panic attack bc it is an internal CS IF a person is hyperattentitve to their heart rate

55
Q

anxiety sensitivity and perceived control

A

anxiety sensitivity—a trait-like belief that certain bodily symptoms may have harmful consequences—are more prone to developing panic attacks and perhaps panic disorder

56
Q

Rem sleep vs non rem sleep and when nocturnal panic attacks occur

A

one stage called REM sleep (rapid eye movement sleep) during which vivid dreaming occurs, and four stages of non-REM sleep (Stages 1–4) when vivid dreams do not occur; f nocturnal panic attacks occurred in response to dreams, we would expect them to occur during REM sleep (when nightmares usually occur), but in fact they occur during Stage 2 and early Stage 3 sleep, usually a few hours after falling asleep.

57
Q

How are nocturnal panic attackls different from “sleep terrors/night terrors” and sleep paralysis?

A

night terrors: usually experienced by children; don’t wake up durtinjg them
sleep paralysis: can occur during the transition from sleep to waking: involves awareness of one’s surrounding accompanied by a stark sense of terror and inability to move = occcurs bc the individuals are waking from REM when muscle activity below the neck is surpressed

58
Q

Perceived control and anxiety

A

Moreover, anxiety sensitivity has a greater effect on panic symptoms in people with low perceived control/ individuals with panic disorder may also be protected against the development of agoraphobic avoidance if they have relatively high levels of perceived control over their emotions and threatening situations

59
Q

Why do people who have developed panic disorder continue to have panic attacks in spite of the fact that their predictions of heart attacks, death, and insanity rarely, if ever, come true?

A

evidence suggests that such disconfirmation does not occur because people with panic disorder frequently engage in safety behaviors (such as breathing slowly or carrying a bottle with anxiolytic medication) before or during an attack. They then mistakenly tend to attribute the lack of catastrophe to their having engaged in this safety behavior rather than to the idea that panic attacks actually do not lead to heart attacks

60
Q

Safety behaviours/dropping safety behaviors in panic disorder

A

asking people to drop their safety behaviors during cognitive-behavioral treatment can increase the effectiveness of the treatment

61
Q

cognitive biases and the maintence of panic

A

studies have shown that people with panic disorder are biased in the way they process threatening information. Such people not only interpret ambiguous bodily sensations as threatening but they also interpret other ambiguous situations as more threatening than controls.

62
Q

1970s original behavioral treatment for agoraphobioa

A

involved prolonged exposure to feared situations, often with the help of a therapist or family member. Similar to what is done with specific phobia and social anxiety disorder, the idea was to make people gradually face the situations they feared and learn that there was nothing to fear.

63
Q

difference between clinical and statistical significance

A

Not all statistically significant changes are of sufficient magnitude to be clinically significant = Clinical significance reflects how large the effects of a particular treatment or intervention are with respect to how much meaningful change they provide in a person’s level of functioning or well-being.
statistical significance is more just the math

64
Q

Criticisms of 1970s treatments for agoraphobia

A

they did not specifically target panic attacks.

65
Q

Interoceptive exposure

A

deliberate exposure to feared internal sensations; The idea was that fear of these internal sensations should be treated in the same way that fear of external agoraphobic situations is treated—namely, through prolonged exposure to those internal sensations so that the fear may extinguish

66
Q

panic control treatment (PCT)

A

targets both agoraphobic avoidance and panic attacks
1) clients are educated about the nature of anxiety and panic and how the capacity to experience both is adaptive.
2) teaching people with panic disorder to control their breathing.
3) clients are taught about the logical errors that people who have panic disorders are prone to making and learn to subject their own automatic thoughts to a logical reanalysis.
4)exposed to feared situations and feared bodily sensations to build up a tolerance to the discomfort.
= produces better results than the original exposure-based techniques that focused exclusively on exposure to external situations

67
Q

Anxiolytics

A

(antianxiety medications) from the benzodiazepine category

68
Q

Two anxiolytics, benefits and side effects

A

alprazolam (Xanax) or clonazepam (Klonopin).
act very quickly (30–60 minutes) and so can be useful in acute situations of intense panic or anxiety.
cons: have side effects such as drowsiness and sedation, which can lead to impaired cognitive and motor performance/ with prolonged use, most people using moderate to high doses develop physiological dependence on the drug, which results in withdrawal symptoms when the drug is discontinued
NOT CONSIDERED A FIRST CHOICE TREATMENRT

69
Q

SSRIs, tricyclics, and the serotonin-norepinephrine reuptake inhibitors benefits and cons for panic disorder treatment

A

-major advantage is that they do not create physiological dependence in the way benzodiazepines can, and they also can alleviate any comorbid depressive symptoms or disorders
-takes about 4 weeks before they have any beneficial effects, so they are not useful in an acute situation where a person is having a panic attack.
cons: dry mouth, constipation, blurred vision with the tricyclics, and interference with sexual arousal with the SSRIs)

70
Q

Why are SSRIs more widely prescribed than tricyclics?

A

bc SSRI’S are generally better tolerated by most patients

71
Q

Antianxiety medication used with CBT

A

in the short term, such combined treatment sometimes produces a slightly superior result compared to either type of treatment alone
- long term, after medication has been tapered (especially benzodiazepine medications), clients who have been on medication with or without cognitive or behavioral treatment seem to show a greater likelihood of relapse

72
Q

drug that enhances responsiveness of panic disorder to CBT

A

d-cycloserine

73
Q

GAD frequency criteria

A

DSM-5 criteria specify that the worry must occur on more days than not for at least 6 months and that it must be experienced as difficult to control

74
Q

GAD and future apprehension “basic anxiety disorder”

A

People suffering from GAD live in a relatively constant, future-oriented mood state of anxious apprehension, chronic tension, worry, and diffuse uneasiness that they cannot control. They also show marked vigilance for possible signs of threat in the environment and frequently engage in subtle avoidance activities such as procrastination, checking, or calling a loved one frequently to see if he or she is safe
basic anxiety disorder: apprehension is the essence of GAD

75
Q

GAD duration/ gender difference/ age distribution

A

tends to be chronic/ twice as common in women
GAD is the most common in older adults

76
Q

psycoanalytic viewpoint of GAD

A

-generalized or free-floating anxiety results from an unconscious conflict between ego and id impulses that is not adequately dealt with because the person’s defense mechanisms have either broken down or have never developed
- primarily sexual and aggressive impulses that had been either blocked from expression or punished upon expression that led to free-floating anxiety
-. Defense mechanisms may become overwhelmed when a person experiences frequent and extreme levels of anxiety, as might happen if id impulses are recurrently blocked from expression
- primary difference between specific phobias and free- floating anxiety is that in phobias, the defense mechanisms of repression and displacement of an external object or situation actually work, whereas in free-floating anxiety these defense mechanisms do not work, leaving the person anxious nearly all the time.
NOT TESABLE INVALID

77
Q

Predicting future/ GAD/ parenting

A

the unpredictability of the future is a huge source of anxiety
-parents of anxious children often have an intrusive, overcontrolling parenting style, which may serve only to promote their children’s anxious behaviors by making them think of the world as an unsafe place in which they require protection and have little control themselves

78
Q

If worrying is so anxiety-provoking and distressing, why do GAD people keep doing it?

A

superstitious avoidance of catastrophe (“Worrying makes it less likely that the feared event will occur”)

Avoidance of deeper emotional topics (“Worrying about most of the things I worry about is a way to distract myself from worrying about even more emotional things, things that I don’t want to think about”)

Coping and preparation (“Worrying about a predicted negative event helps me to prepare for its occurrence”

79
Q

GAD worry patterns and response suppression

A

. When people with GAD worry, their emotional and physiological responses to aversive imagery are actually suppressed. This suppression of aversive emotional physiological responding may serve to reinforce the process of worry (that is, to increase its probability
-worry suppresses physiological responding, it also insulates the person from fully experiencing or processing the topic that she or he is worrying about, and it is known that such full processing is necessary if extinction of that anxiety is to occur

80
Q

cognitive biases and GAD

A

-process threatening information in a biased way, perhaps because they have prominent danger schemas. Anxious people tend to preferentially allocate their attention toward threatening cues when both threat and nonthreat cues are present in the environment.

81
Q

negative consequences of worry

A

worry also has some negative consequences, including the fact that worry begets further worry and creates a sense of perceived uncontrollability over the worry process, which further enhances anxiety

82
Q

genetic factors GAD and environmental influence

A

Risk for GAD does seem to run in families and has a heritability estimate of approximately 30%: part of this common genetic predisposition for GAD and major depression is best conceptualized as neuroticism
-what determines whether individuals with a genetic risk for GAD and/or major depression develop one or the other disorder seems to depend entirely on the specific environmental experiences they have

83
Q

GABA and GAD/norepinephrine, serotonin

A

-f GABA, a neurotransmitter now strongly implicated in generalized anxiety
- highly anxious people have a kind of functional deficiency in GABA, which ordinarily plays an important role in the way our brain inhibits anxiety in stressful situations
-The benzodiazepine drugs appear to reduce anxiety by increasing GABA activity in certain parts of the brain implicated in anxiety, such as the limbic system, and by suppressing the stress hormone cortisol. Whether the functional deficiency in GABA in anxious people causes their anxiety or occurs as a consequence of it is not yet known, but it does appear that this functional deficiency promotes the maintenance of anxiety.
-GABA, serotonin, and perhaps norepinephrine

84
Q

(CRH) and GAD

A

-When activated by stress or perceived threat, CRH stimulates the release of ACTH (adrenocorticotropic hormone) from the pituitary gland, which in turn causes release of the stress hormone cortisol from the adrenal gland
-CRH may play an important role in generalized anxiety through its effects on the bed nucleus of the stria terminalis (an extension of the amygdala: important brain area mediating generalized anxiety

85
Q

Neurobiological Differences Between Anxiety and Panic

A

Fear and panic involve activation of the fight-or-flight response, and the brain areas and neurotransmitters that seem most strongly implicated in these emotional responses are the amygdala (and locus coeruleus) and the neurotransmitters norepinephrine and serotonin. -Generalized anxiety (or anxious apprehension) is a more diffuse emotional state than acute fear or phobia that involves arousal and a preparation for possible impending threat; and the brain area, neurotransmitters, and hormones that seem most strongly implicated are the limbic system (especially the bed nucleus of the stria terminalis, an extension of the amygdala), GABA, and CRH

86
Q

CBT for gad

A

-involves a combination of behavioral techniques, such as training in applied muscle relaxation, and cognitive restructuring techniques aimed at reducing distorted cognitions and information-processing biases associated with GAD as well as reducing catastrophizing about minor events
-GAD initially appeared to be among the most difficult of the anxiety disorders to treat

87
Q

Problems with benzodiazepines at the emotional/fear level

A

. Their effects on worry and other psychological symptoms are not as great. Moreover, they can create physiological and psychological dependence and withdrawal and are therefore difficult to taper.

88
Q

Buspirone

A

effective, and it is neither sedating nor does it lead to physiological dependence. It also has greater effects on psychic anxiety than do the benzodiazepines. However, it may take 2 to 4 weeks to show results

89
Q

OCD definition/ difference between obsessions and compulsions

A

is defined by the occurrence of both obsessive thoughts and compulsive ­behaviors performed in an attempt to neutralize such thoughts
Obsessions = persistent and recurrent intrusive thoughts, images, or impulses that are experienced as disturbing, inappropriate, and uncontrollable. People who have such obsessions actively try to resist or suppress them or to neutralize them with some other thought or action.
Compulsions involve overt repetitive behaviors that are performed as lengthy rituals (such as hand washing, checking, putting things in order over and over again). Compulsions may also involve more covert mental rituals = performance of the compulsive act or the ritualized series of acts usually brings a feeling of reduced tension and satisfaction, as well as a sense of control, although this anxiety relief is typically fleeting

90
Q

Why Is OCD No Longer Considered to Be an Anxiety Disorder?

A

-In DSM-5, obsessive-compulsive disorder was removed from the anxiety disorders category and placed into a new category called “obsessive-compulsive and related disorders.”
-One reason for moving OCD into the new category was that anxiety is not generally used as an indicator of OCD severity.
-neurobiological underpinnings of OCD appear to be rather different from those of other anxiety disorders, focusing on frontal-striatal neural circuitry including the orbitofrontal cortex, anterior cingulate cortex, and striatum (especially the caudate nucleus

91
Q

trichotillomania

A

chronic hair pulling)

92
Q

OCD gender differenes

A

Childhood or early adolescent onset is more common in boys than in girls and is often associated with greater severity
-In most cases the disorder has a gradual onset, and once it becomes a serious condition, it tends to be chronic, although the severity of symptoms sometimes waxes and wanes over time

93
Q

OCD as learned behavior/ Mowrer’s two process theory of avoidance learning

A

-neutral stimuli become associated with frightening thoughts or experiences through classical conditioning and come to elicit anxiety
-Once learned, such avoidance responses are extremely resistant to extinction
-model predicts that exposure to feared objects or situations should be useful in treating OCD if the exposure is followed by prevention of the ritual, enabling the person to see that the anxiety will subside naturally in time without the ritual = TRUE

94
Q

OCD and evolutionary Preparedness

A

-r=the fact that many people with OCD have obsessions and compulsions focused on dirt, contamination, and other potentially dangerous situations has led many researchers to conclude that these features of the disorder likely have deep evolutionary roots

95
Q

The Effects of Attempting to Suppress Obsessive Thoughts

A

one factor contributing to the frequency of obsessive thoughts, and the negative moods with which they are often associated, may be these attempts to suppress them (similar to what was discussed earlier about the effects of attempts to control worry in people with GAD)
- thought suppression leads to a more general increase in obsessive-compulsive symptoms beyond just the frequency of obsessions

96
Q

Appraisals of Responsibility for Intrusive Thoughts in OCD: THOUGHT-ACT FUSION

A

people with OCD often seem to have an inflated sense of responsibility. In turn, in some vulnerable people, this inflated sense of responsibility can be associated with beliefs that simply having a thought about doing something (e.g., a mother’s thought about harming her infant) is morally equivalent to actually having done it, or that thinking about the behavior increases the chances of actually doing so

97
Q

Memory confidence and OCD

A

those with OCD have low confidence in their memory ability (especially for situations they feel responsible for), which may contribute to their repeating their ritualistic behaviors over and over again
-. An additional factor contributing to their repetitive behavior is that people with OCD have deficits in their ability to inhibit both motor responses

98
Q

heritability rates of OCD

A

, most family studies have found 3 to 12 times higher rates of OCD in first-degree relatives of OCD clients than would be expected from current estimates of the prevalence of OCD
- early-onset OCD has a higher genetic loading than later-onset OCD

99
Q

OCD and Tourette’s genetic relationship

A

tic-related OCD is linked to Tourette’s syndrome, a disorder characterized by severe chronic motor and vocal tics that is known to have a substantial genetic basis

100
Q

OCD and basal ganglia/other brain region pathologies

A

-The basal ganglia are in turn linked at the amygdala to the limbic system, which controls emotional behaviors.
- people with OCD have abnormally high levels of activity in two parts of the frontal cortex (the orbital frontal cortex and the cingulate cortex/gyrus), which are also linked to the limbic area.
-People with OCD also have abnormally high levels of activity in the subcortical caudate nucleus, which is part of the basal ganglia

101
Q

OFC

A

The orbital frontal cortex seems to be where primitive urges regarding sex, aggression, hygiene, and danger come from

102
Q

caudate nucleus or corpus striatum function

A

part of the set of structures called the basal ganglia, which are involved in the execution of voluntary, goal-directed movements)

103
Q

cortico–basal–ganglionic–thalamic circuit

A

involved in the preparation of complex sets of interrelated behavioral responses used in specific situations such as those involved in territorial or social concerns= dysfunctions in this circuit in turn prevent people with OCD from showing the normal inhibition of sensations, thoughts, and behaviors that would occur if the circuit were functioning properly. In this case, impulses toward aggression, sex, hygiene, and danger that most people keep under control with relative ease “leak through” as obsessions and distract people with OCD from ordinary goal-directed behavior.

104
Q

clomipramine (Anafranil) and fluoxetine (PROZAC)/ short term vs long term serotonin regulation

A
  • tricyclic drug
    -often effective in the treatment of OCD even though other tricyclic antidepressants are generally not very effective
  • because clomipramine has greater effects on the neurotransmitter serotonin, which is now strongly implicated in OCD
    =long-term administration of clomipramine (or fluoxetine) causes a downregulation of certain serotonin receptors, further causing a functional decrease in the availability of serotonin = the immediate short-term effects of clomipramine or fluoxetine may be to increase serotonin levels (and exacerbate OCD symptoms too), the long-term effects are quite different: 6-12 WEEKS TO SEE IMPROVEMENT
105
Q

serotonergic system and OCD

A

increased serotonin activity and increased sensitivity of some brain structures to serotonin are involved in OCD symptoms.
-drugs that stimulate serotonergic systems lead to a worsening of symptoms.

106
Q

OCD, exposure and response prevention therapy

A

. The exposure component involves having individuals with OCD repeatedly expose themselves (either in guided fantasy or directly) to stimuli that provoke their obsessions
-response prevention component requires that they then refrain from engaging in the rituals that they ordinarily would perform to reduce their anxiety or distress. Preventing the rituals is essential so that they can see that if they allow enough time to pass, the anxiety created by the obsession will dissipate naturally down to at least 40 to 50 on a 100-point scale, even if this takes several hours

107
Q

D-cycloserine and extinction in OCD/ potential antidepressant interactions

A

at D-cycloserine (the drug known to facilitate extinction of fear) enhances the effectiveness of behavioral treatments like this one; however, this enhancement is blocked if the person is taking an antidepressant as well

108
Q

Major disadvantage of medication treatment for OCD

A

when the medication is discontinued relapse rates are generally very high
-people who do not seek alternative forms of behavior therapy that have more long-lasting benefits may have to stay on these medications indefinitely

109
Q

Neurosurgery for OCD

A

-for the treatment of severe, intractable OCD
- person must have had severe OCD for at least 5 years and must not have responded to any of the known treatments discussed so far (medication or behavior therapy)

110
Q

BREAK; BODY DYSMORPHIA
Why was body dysmphoric disorder BDD classified as a somatoform disorder in the DSM IV and how do we classify it now in DSM-5?

A

because it involves preoccupation with certain aspects of the body.
DSM-5: because of its very strong similarities with OCD, it was moved out of the somatoform category and into the OCD and related disorders category in DSM-5.

111
Q

BDD/perceived/imagined flaws

A

-People with BDD are obsessed with some perceived or imagined flaw or flaws in their appearance to the point they firmly believe they are disfigured or ugly

112
Q

What is the most common bodily regions for BDD fixations? differences in gender in these obsessions?

A

-skin (73 percent), hair (56 percent), nose (37 percent), eyes (20 percent), breasts/chest/nipples (21 percent), stomach (22 percent), and face size/shape (12 percent)
-Men are more likely to obsess about their genitals, body build, and balding, whereas women tend to obsess more about their skin, stomach, breasts, buttocks, hips, and legs

113
Q

BDD and most common comorbid disorder

A

very commonly also have a depressive diagnosis (with most estimates being over 50 percent; Allen & Hollander, 2004), and it can even lead to suicide attempts or death

114
Q

plastic surgery outcomes of BDD

A

patient does get what he or she requests—and unfortunately is almost never satisfied with the outcome. Even if they are satisfied with the outcome, such patients still tend to retain their diagnosis of BDD

115
Q

Treatments and NTs implicated OCD and BDD commonalities and symptom simalrities

A

People with BDD, like those with OCD, have prominent obsessions, and they engage in a variety of ritualistic behaviors such as reassurance seeking, mirror checking, comparing themselves to others, and camouflage. Moreover, they are even more convinced that their obsessive beliefs are accurate than are people with OCD
the same neurotransmitter (serotonin) and the same sets of brain structures are implicated in the two disorders , and the same kinds of treatments that work for OCD are also the treatments of choice for BDD

116
Q

Difference between BDD and anorexia

A

people with BDD look normal and yet are terribly obsessed and distressed about some aspect of their appearance. By contrast, people with anorexia are emaciated and generally satisfied with this aspect of their appearance

117
Q

Why did BDD only become an important subject in the literature recently?

A

-? One possible reason is that its prevalence may actually have increased in recent years as contemporary Western culture has become increasingly focused on “looks as everything,” with billions of dollars spent each year on enhancing appearance through makeup, clothes, plastic surgery, and other means
-A second reason BDD has been understudied is that most people with this condition never seek psychological or psychiatric treatment. Rather, they suffer silently or go to dermatologists or plastic surgeons

118
Q

Biopsycosocial approach to BDD

A
  • overconcern with a perceived or slight defect in physical appearance is a moderately heritable trait
    -BDD seems to be occurring, at least today, in a sociocultural context that places great value on attractiveness and beauty, and people who develop BDD often hold attractiveness as their primary value
    -people with BDD were reinforced as children for their overall appearance more than for their behavior
  • people with BDD show biased attention and interpretation of information relating to attractiveness
    -fMRI studies have found that patients with BDD showed fundamental differences in visually processing other people’s faces relative to controls. Specifically, they showed a bias for extracting local, detailed features rather than the more global or holistic processing of faces seen in controls
119
Q

Treatments of BDD

A

-higher doses of antidepressants needed for BDD than OCD
-, a form of cognitive-behavioral treatment emphasizing exposure and response prevention has been shown to produce marked improvement
-These treatment approaches focus on getting the patient to identify and change distorted perceptions of his or her body during exposure to anxiety-provoking situations

120
Q

**BREAK, Hoarding Disorder

A

People with hoarding disorder both acquire and fail to discard many possessions that seem useless or of very limited value, in part because of the emotional attachment they develop to their possessions.

121
Q

Compulsive hoarding and OCD differences neurobiologically

A

people with compulsive hoarding may be neurologically distinct from people with OCD
-This conclusion would also be consistent with some findings of a relative lack of responsiveness to the same medications that are often successful in reducing the severity of other forms of OCD and with recent findings that different genes seem to be implicated in OCD without hoarding versus OCD with hoarding

122
Q

treatment for hoarding disorder

A

new intensive and prolonged behavioral treatments that include home visits, which seem to be more effective
- Traditional behavioral therapy using exposure and response prevention is also less effective than for traditional OCD

123
Q

Earlier addition definitions of Trichotillomania vs dsm 5/ onset

A

In earlier editions of the DSM, trichotillomania was categorized as an impulse-control disorder. However, reflecting its relationship to OCD, in DSM-5 it is now placed in the obsessive-compulsive and related disorders category.
onset: The onset can be in childhood or later, with onset post-puberty being associated with a more severe course

124
Q

Yoruba culture of nigeria anxiety, 3 symptom clusters

A

: worry, dreams, and bodily complaints. However, the sources of worry are very different than those in Western society; they focus on creating and maintaining a large family and on fertility. Dreams are a major source of anxiety because they are thought to indicate that one may be bewitched. The common somatic complaints are also unusual from a Western standpoint: “I have the feeling of something like water in my brain,”

125
Q

difference between western social anxiety taijin kyofusho

A

Westerners with social anxiety are afraid of social situations where they may be the object of scrutiny or criticism. By contrast, most people with taijin kyofusho are concerned about doing something that will embarrass or offend others
-BDD IS ALSO COMMON IN TAIJIN KYOFUSO

126
Q

koro,

A

hich for men involves intense, acute fear that the penis is retracting into the body and that when this process is complete the sufferer will die. Koro occurs less frequently in women, for whom the fear is that their nipples are retracting and their breasts shrinking. Koro tends to occur in epidemics (sometimes referred to as a form of mass hysterIA: is often attributed to either malicious spirits or contaminated food.