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Flashcards in CBT & Biological Etiology Deck (23)
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1
Q

Neurotransmitters involved in depression

A

(Carlson, 2017) (textbook)
(Sachar & Baron, 1979) (researcher)
The Monoamine Hypothesis
-Low serotonin, low norepinephrine
-supported by the efficacy of reuptake inhibitors
-supported by experiments using experimental depletion

2
Q

Neuroendocrine model of depression

A

(Carlson, 2017)
(McEwen, 2008)
-Glucocorticoid Model
-HPA axis is implicated, by way of its control of stress hormones like cortisol and other chemicals
-the hippocampus, which regulate HPA activity and mediates stress reactions, is sensitive to cortisol and vulnerable to stress, and people with depression show atrophy of the hippocampus in neuroimaging studies

3
Q

Beck’s model of depression

A

(Beck 1976)
The cognitive triad, (view of self, world, and future) is affected by a negative bias.
-This occurs due to depressogenic schemas which form due to automatic thoughts and self statements, cognitive distortions, and negative core beliefs which are activated during negative life events.

4
Q

Seligman’s Learned Helplessness model of depression

A

(Seligman, 1975)
-The person’s explanatory style has 3 components: Personalization (external vs. internal cause of events)
Pervasiveness (specific vs. global explanation)
Permanence (temporary vs. stable)
Depression’s style is Internal, Stable, Global (It’s my fault, it’ll always be this way, it’s because I’m a bad person in general)

5
Q

Heritability of depression

A

(Plomin 2001) (textbook)
(Rutter 2003) (researcher)
Monozygotic twin concordance rate 44-58%, 19-28% for dizygotic twins, making it partially heritable

6
Q

Prevalence rates of depression

A

(Kessler, 2002)
Lifetime prevalence is 6-25%
- current prevalence 2-4% for adults
comorbidity rates are 75%

7
Q

Beck’s view of anxiety

A

(Beck, 1976)

  • When a potential threat is detected in the environment, preparatory schemas are activated and this “primal mode” explains the physiological effects of anxiety (autonomic arousal, behavioral mobilization or inhibition, fear, hypervigilance)
  • When there is a cognitive bias in threat appraisal, or faulty appraisal of coping resources, excessive worry develops.
8
Q

Classical Conditioning model of anxiety

A

(Watson & Rayner 1920)

  • Little Albert
  • US, UR; US+NS=CS
  • anxieties can generalize
9
Q

Humanist view of depression

A

(Maslow 1962)

  • The most important need is self-actualization (reaching potential) which allows us to lead a meaningful life. Anything that blocks this can cause depression
  • Parents may impose conditions of worth on children
  • children may avoid this by denying the true self and making a false self to please others, however, this causes hatred of the self for living a lie
  • For adults, self-actualization can be blocked by unfulfilling jobs or relationships, unable to give and receive.
10
Q

Humanist view of anxiety

A

(Maslow 1962)
-anxiety emerges from safety needs at the 2nd from the bottom of the pyramid. Social anxiety emerges from the social needs (3rd level).

11
Q

May’s view of development

A

(May, 1969)

  • 4 stages of life:
    1) innocence: pre-egoic, pre-self conscious
    2) rebellion: childhood and adolescent ego development by contrast with adults; “no” and “no way”
    3) ordinary: normal adult ego
    4) creativity: authentic and beyond ego; self-actualizing
12
Q

May’s view of anxiety

A

(May, 1969)

  • anxiety is something we are, not something we have
  • comes from free will and being condemned to choose
  • anxiety arises from the personal need to survive and preserve our being
  • part of what it means to be human, to be grappled with in therapy
13
Q

Biological explanation of substance use

A

(Khantzian 1997) (but everyone thinks 1999)

People use substances to self medicate

14
Q

Familial risk of affective disorder

A

(Plomin 2001)

Those with a 1st degree relative with affective disorder are at increased risk

15
Q

Diathesis Stress Model

A

(Meehl 1962)
There is a biologically heritable vulnerability to develop pathology, but it requires activating circumstances in the environment to cause the disorder to develop.

16
Q

Structural Therapy view of pathology

A

(Minuchin 1974)

  • The source of pathological family systems is boundaries (marital, parental, sibling)
  • pathological systems include the disengaged family (rigid boundaries) and the enmeshed family (diffuse boundaries)
17
Q

May’s view of therapy

A

((Yolo) May, 1969)

-Importance of the here-and-now therapeutic moment (a real relationship, not transference)

18
Q

May’s view of depression

A

(May 1969)

Depression is the inability to see or construct a future

19
Q

Ellis’s view of depression

A

(Ellis, 1960)

Irrational beliefs in the form of absolute statements (musterbations)

20
Q

Lewinsohn’s behavioral view of depression

A

(Lewinsohn 1974)

Inadequate/low rate of reinforcement due to decreased potential reinforces in the environment

21
Q

Neurotransmitters involved in anxiety

A

Decreased inhibitory GABA

22
Q

Prevalence rates of GAD

A

lifetime: 5%

90% comorbidity

23
Q

Genetic risk of anxiety

A

(NIMH 1999)

6-8 times greater risk, if patient has 1st degree relative with anxiety.