Anxiety Disoders Flashcards

1
Q

Generalised Anxiety disorder

- WHAT/ FIGS (prev, gender, race)

A

Excessive anxiety under most circumstances and worry about practically anything. Able to maintain relationships + life but on edge/restless/tired

  • symptoms must last for 6+ months

FFs –>

a) Common in Western society (more than 6% will dev in their life)
b) 2:1 women

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2
Q
BRIEF aetiology of GAD --
Sociocultural perspective (2)
A
  • Dangerous situations are likely to give rise to it
    a) Katrina + earthquake in Hati – the residence who survived – anxiety disorders are twice as high (Derivois & Cenat, 2015)
    b) Poverty – high poverty places there is higher crime rates, fewer educational & job opportunities and have greater rate of GAD (McLaughlin et al. 2012)
    BUT
    ** not the whole picture as not everyone in poorer areas has it & people in wealthier areas can get it**
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3
Q

indepth aetiology

Cognitive perspective of GAD brief summary

A
  • GAD caused by a maladaptive way of thinking; excessive worry is a cognitive symptom.
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4
Q

Metacognitive theory of GAD

WHO+WHAT

A

Wells’ model

Two types of worry

a) Type 1 worry: worrying about a non-cognitive process. Provokes an anxiety response. They try & cope with this arousal + decrease the arousal by creating positive beliefs about worry. THIS MAY DECREASE AROUSAL
b) Type 2 worry: worrying that your worrying is becoming uncontrollable === leads to ineffective strategies aimed at avoiding worrying (i.e. thought suppression,distraction)

***often unsuccessful –> can’t control their worry –> reinforce the belief that worrying is uncontrollable and dangerous

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5
Q

Meta cognitive theory GAD evaluation

A

FOR
1) Individuals with GAD experience more negative beliefs about worry and Type 2 worry relative to individuals without a diagnosis of an anxiety disorder
AGAINST
2) Similar levels of negative beliefs about worry and Type 2 worry as do those with OCD and panic disorder
3) most studies use MCQ + AnTI - two measures focus on perceived lack of control over worry, which are defining DSM-IV criteria of GAD. Thus, employment of these measures assert that an established diagnostic criterion for GAD discriminates individuals with GAD from those without GAD. Constructs of Type 2 worry and negative beliefs about worry need to be refined in these studies, or that different methodological approaches be employed
4) It doesn’t explain why many studies have shown an sustained physiological arousal

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6
Q

Contrast avoidance model

WHO + WHAT GAD

A

(Newmann + Llera, 2011)

  • Rather than precluding negative emotional experiences, worry creates and prolongs a negative emotional state to prevent a sharp increase in negative emotions
  • Based on findings that – compared to relaxation and neutral mood – worry led to greater negative emotions and physiological arousal and was later associated with lower subjective reactivity to negative emotional stimuli
  • **Worry leads to sustained emotionality evidence – not reduces somatic activation **
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7
Q

Worry leads to sustained emotionality evidence – not reduces somatic activation
GAD

A
  • Worry during a stressful period predicted higher anxiety and depression after the stress had ended (Segerstromet al. 2000)
  • those with GAD report heightened emotional intensity and greater difficulty recovering from a negative mood state than non-anxious control participants (Mennin et al., 2005)
  • Worry episodes heightened both concurrent and succeeding cardiac activity for 2 h following each worry episode (Pieper, Brosschot, van der Leeden, & Thayer, 2010)
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8
Q

MC vs Contrast avoidance model AREAS OF DIVERGENCE GAD

A

1) beliefs about worry fuel the maintenance of GAD. MC focuses on the role of negative beliefs (i.e. worrying about worrying),
CAM focuses on the fact persons with GAD and non-anxious controls demonstrate significant differences in their beliefs toward the utility of worry to control their emotional responses to external events (Type I worry)

2) the concept that Type I worry (i.e. the positive beliefs about worry) reduces somatic activation. BUT, substantial data suggest that worry is associated with sustained tonic somatic activation (and as a result it mutes acute reactivity to brief images

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9
Q

Biological perspective - GAD

  • heredity
  • GABA activity for/against
A

1) heredity - Researchers have found that biological relatives are more likely to have GAD than non-relatives (Shienle et al. 2011)
2) GABA - involved in feedback loop of fear; when GABA is released –> physical symptoms decrease (i.e. fear) BUT in GAD this GABA release = prohibited or prevented. Malfunction in this feedback system can cause fear and anxiety to go unchecked

well supported but has critics BC unsure if cause or consequence ALSO may be a circuit NOT just 1 neuroT*

BUT these brain circuits contain GABAgernic neurones

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10
Q

specific PHOBIAS
WHAT/FIGS (prev, gender, race)

what may phobia be also diagnosed with?

A
  • Persistent + unreasonable fear of a particular object, activity or situation. People with a phobia become fearful if they even think about the object or situation they dread, but they usually remain comfortable as long as they avoid it or thoughts about it.
    CAN BE SPEC OR GENERAL (agrophobia)
  • Almost 14% of people will develop a specific phobia at some point in their lives
  • Women > men
  • Race also influences phobia prevalence; black and Hispanic americans > white americans
  • Not many in treatment
  • agoraphobia
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11
Q

GAD anxiety circuit

A

in limbic system; amygdala –> hypothalamus –> muscles/brainstem –> reflexes; hyperactive in anxiety (Those with anxiety have a greater startle reflex)

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12
Q

Behavioural explanations of phobias (2)

+ one “but”

A

1) Modelling – observation + imitation. Person may observe that others are afraid of certain objects or events & develop fears of the same things
2) 2 events in proximity might come to be a trigger - classical conditioning

***leads to avoidance of X **

BUT to keep in mind:
phobias are highly resistant to extinction, whereas laboratory fear conditioning, unlike avoidance conditioning, extinguishes rapidly

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13
Q

what may phobia disorder become if there is “stimulus generalisation” ?

A

learned phobias may BECOME GAD

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14
Q

Social anxiety disorder

WHAT + FIGS (prev, gender, race)

A
  • Severe, persistent and irrational anxiety about social or performance in which they may face scrutiny by others and possibly feel embarrassment
  • Can be narrow i.e. about only public speaking OR broad such as a general fear of functioning poorly in front of others
  • narrow: fear response + general: anxiety response
  • ** either way = judgement as performing worse than everyone else***

1) 13% develop this disorder in their lives
2) women > men
3) minority > white

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15
Q

SAD culturally bound?

A

‘taijin kyofusho’ – fear of making OTHERS uncomfortable in Japan and Korea – may actually be fear of being evaluated negatively by others(?)

  • Though there is evidence to suggest that different expressions of TKS overlap with SAD in other cultures, the rate of this disorder, and the meanings of the symptoms in those cultural contexts will greatly differ.
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16
Q

Cognitive explanation of SAD (leading exp)

A
  • People with this disorder hold a group of social beliefs and expectations that consistently work against them: EG
    a) They hold unrealistically high social standards thta they must achieve
    b) See themselves as unattractive
    c) Socially unskilled and inadequate

THUS avoid + fear social interaction; after a social situation –> will review + criticize how they “did”

  • Cognitive theorists do not necessarily agree on why some have these cognitions and others do not – trait tendencies, genetic predispositions, child relationships, parental upbringing, biological tendencies
17
Q

where do these thought patterns come from in SAD?

- temperament?

A
  • shyness seems to be an important variable (this is heritable too)
18
Q

where do these thought patterns come from in SAD?

- social experiences?

A

negative social experiences with peers may hasten the development of SAD or maintenance

19
Q

where do these thought patterns come from in SAD?

- genetics

A
  • family, twin, at risk studies
    a) risk of developing SAD in a family with SAD was three times higher when compared with families with no SAD
    b) twin studies: identical - 24% + frat 15%
20
Q

Panic disorder

what + figs (prev, gender, race)

A
  • Experiencing panic attacks unexpectedly and repeatedly
  • May experience dysfunctional changes in their thinking and behaviour as a result of these attacks (i.e. plan their lives around the possibility of another attack)
  • 5% will develop in their life
  • women > men
  • white > minority; experience of panic attack varies among cultures
21
Q

what is panic disorder commonly linked with + why?

A

* often accompanied by agrophobia; said to set the stage for agrophobia. May become fearful of having panic attacks in busy places*

22
Q

Biological explanation for panic disorder (2)

A

1) Norepinephrine activity is abnormal in people who suffer from panic attacks + antidepressants which help panic disorder affect norepinephrine activity
2) Norepinephrine is a part of a much bigger circuit - PANIC CIRCUIT (THIS IS DIFFERENT FROM ANXIETY CIRCUIT THUS THE TWO DIFFER)
a) anxiety used the lateral amygdala + prefrotnal cortex
b) panic pathway = central amygdala + periaqueductal grey

23
Q

cognitive explanation of panic disorder

1

A

RECOGNISE THAT BIO ONLY EXPLAINS A BIT OF THE DEALIO

    • Have a high degree of anxiety sensitivity – they focus on their bodily sensations much of the time + interpret them as threatening —-
  • Also an intolerance to uncertainty?

1) People prone to panic disorder - overly sensitive to certain bodily reactions; they misinterpret them as medical catastrophe
EXAMPLE
i.e. people with panic disorder tend to ‘over breathe’ in stressful situs, abnormal breathing makes them think they are in danger of suffocation so they panic

24
Q

Evidence surrounding cognitive theories of panic disorder

A
  • Findings support the incremental, predictive
    validity of panic-related interpretation biases
  • Said that interpretation bias is predictive of new onsets
    of panic disorder (even when controlling for bodily sensations) (panic spec schema)
  • those who interpret things as threatening –> likely to dev PD later on
  • those who have exp trauma = more likely to dev PD (congruent w this idea)
25
Q

OCD

Figures (Prev, gender, race, how many in treatment?)

A

Check things repeatedly, perform certain routines repeatedly (called “rituals”), or have certain thoughts repeatedly (called “obsessions”).
“Just right” obsessions are thoughts and/or feelings that something is not quite right or that something is
incomplete

  • Between 3% will develop during their lifetime
  • Equally common in men & women
  • Equally common among races
  • 40% of people with OCD seek treatment
26
Q

IS OCD categorised as an anxiety disorder in DSM?

A

• NOT classified as an anxiety disorder (IT IS ITS OWN CATEGORY IN DSM5)
BUT REMEMBER anxiety does play a major role in this pattern * obsessions cause great anxiety while compulsions are targeted at reducing anxiety.
Also, anxiety arises when the person tries to resist the compulsions + obsessions

27
Q

Behavioural Perspective of OCD (1)

A

Focus on compulsions rather than obsessions;
suggest the cause = CLASSICAL conditioning.
- The compulsion might occur after a fearful/negative situation + reduces anxiety (repeated no. of times)
- Eventually becomes a method of reducing anxiety
- Compulsions have been shown to reduce anxiety

28
Q

Evidence for the behavioural perspective of OCD

A
  • People with OCD have shown an impaired fear extinction response (with correlated neural areas) vs controls; i.e. there is no disappearance of the fear when it is not reinforced.
  • brain areas associated with fear response (extinction) are overactive in OCD (drives compulsive behaviour) (mofc)

NOT the best exp but helpful for therapies - extinction based therapies

29
Q

Cognitive Perspective of OCD

A
  • Cognitive theorists pointed out that everyone has intrusive + repetitive thoughts BUT we can dismiss them with ease
  • develop into obsessions when they are appraised as posing a threat for which the individual is personally responsible; THOUGHT ACTION FUSION (thinking = doing)
  • they typically blame themselves for such thoughts & expect somehow terrible things will happen - To avoid negative outcomes they try and think of ways to put matters right = called neutralising acts.
  • These acts can be reinforced + likely to be repeated

Belief that they need to be in control of these thoughts at all times is the key in OCD population

30
Q

Evidence for the cognitive perspective of OCD

A
  • Correlational evidence has provided support for
    association between inflated responsibility beliefs and OCD symptoms.

BUT
- inflated responsibility was originally hypothesised to underlie all OCD symptoms –> evidence that maladaptive responsibility appraisals
may be more closely linked to CHECKING compulsions than to other compulsions.
- such biases are not completely automatic or fixed, but may be modified by repeated practice in rehearsing more adaptive interpretations of ambiguity

31
Q

Biological perspective of OCD (2)

A

BIG area of research

1) Role of serotonin:
- findings that for many, antidepressant drugs (that only affect serotonin) reduce symptoms of OCD
- Since these increase serotonin OCD may be caused by low serotonin
- Other neurotransmitters may also play a role: GABA, dopamine, glutamate (???)

2) Brain areas:
- Orbitofrontal cortex (primitive impulses) + caudate nuclei in basal ganglia (filters the impulses and send the strongest to thalamus)
- Act on the ones that get to the thalamus
ppl think that one of these areas is too active; i.e. the need to act on something is very strong

could be mix of both of these in a circuit; serotonin (and the others) plays a role in the above brain circuit

32
Q

Evidence for bio perspective of OCD (2)

A

1) Serotonin: some have found differential serotonin activity. BUT other say that the age of onset and severity of symptoms will also affect these serotonin levels. ALSO in OCD SRIs take longer to work vs depression, suggesting = different mechanisms driving OCD pathogenesis

OVERALL: eivdence does support the role of serotonin but future research should stratify into homogenous subgroups reflecting
symptom dimensions, subtypes, and demographics

2) Brain areas:
- TBI studies suggest OFC and BG play causal role on OCD
BUT based on case reports .
- Lesions to BG/OFC reduce OCD symptoms
BUT take a while to work = suggesting neurodegen somewhere else causing the reduction

OVERALL: limitations of each see individually BUT strong convergence when looked at together

33
Q

Related disorders to panic disorder

A
  • Doesnt really occur alone
  • anxiety, depressive, alcohol misuse and bipolar = most comorbid
  • normally occurs after the others have shown
34
Q

Related disorders to social anxiety disorder (4)

A

comorbid with:

  • MDD
  • body dysmorphia
  • mood disorders
  • substance use disorders
    • often precedes other disorders EXCEPT phobia
35
Q

Related disorders to phobias

A

Rarely seen in clinical settings on its own (normally seen alone in non-clincal settings)
- normally associated (comorbid) with depression
- normally only temporarily the primary disorder
@ risk for anxiety, depressive, mood and somatic disorders.

36
Q

Related disorders to GAD

A
  • likely to meet the criteria for anxiety disorder/ unipolar depression too.
  • LESS likely to have substance use disorder
37
Q

Related disorders to OCD

A

1) Hoarding disorder
2) Trichotillomania: hair pulling out.
3) Excoriation: skin picking disorder
4) Body dysmorphic disorder
5) other anxiety disorders
6) Depressive disorders
7) Tic disorder

Accounted for by using the same kinds of explanations as in OCD