CBT and Biological Etiology

Question 1

Neurotransmitters involved in depression

Answer 1

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

Question 2

Beck’s model of depression

Answer 2

(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.`

Question 3

Seligman’s Learned Helplessness model of depression

Answer 3

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)

Question 4

Heritability of depression

Answer 4

(Rutter 2003) (researcher)

Monozygotic twin concordance rate 44-58%, 19-28% for dizygotic twins, making it partially heritable

Question 5

Prevalence rates of depression

Answer 5

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

Question 6

Beck’s view of anxiety

Answer 6

(Beck, 1976)
-▪ Faulty information processing
▪ Schemas set them up for anxiety
▪ Overpredict fear and danger, overemphasize fear and dangerousness, hypervigilant to every situations and afraid of what is to come
▪ Core beliefs are due to traumatic childhood, the world is a dangerous place, I am not competent to deal with it
▪ Cognitive triad- self is helpless & worthy of punishment, world is extremely dangerous and punishing, future is terrifying

Question 7

Classical Conditioning model of anxiety

Answer 7

(Watson & Rayner 1920)

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

Question 8

Humanist view of depression

Answer 8

(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.

Question 9

Humanist view of anxiety

Answer 9

(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).

Question 10

Biological explanation of substance use

Answer 10

(Khantzian 1997)

People use substances to self medicate

Question 11

Familial risk of affective disorder

Answer 11

(Plomin 2001)

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

Question 12

Diathesis Stress Model

Answer 12

(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.

Question 13

Structural Therapy view of pathology

Answer 13

(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)

Question 14

Ellis’s view of depression

Answer 14

(Ellis, 1960)
Irrational beliefs often take the form of absolute statements (musterbations)
1. Everyone must think that I’m perfect or I will be worthless.
2. Everybody has to act the way I want them to act, and if they don’t, I will find that insufferable.
3. The universe has to give me what I want and the way I want it, and if it doesn’t, I will find that insufferable.

Question 15

Neurotransmitters involved in anxiety

Answer 15

Decreased inhibitory GABA

Question 16

Prevalence rates of GAD

Answer 16

lifetime: 5%

90% comorbidity

Question 17

Genetic risk of anxiety

Answer 17

NIMH, 1999

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

Question 18

Diathesis-Stress Model for depression/other disorders

Answer 18

Meehl, 1962

genetic predisposition (diathesis) toward depression when combined with environmental stressors produces depression

Question 19

Neuroanatomy of depression

Answer 19

Decreased tissue in prefrontol cortex (Elkis et al., 1996)

Increased activity in amygdala (Drevets, 2000)

Question 20

OCD neuroanatomy

Answer 20

deficits in orbitofrontaol cortex (Behar et al 1984)

Question 21

OCD neurophysiology

Answer 21

▪ Riggs and Foa (1993) most prevalent neurochemical implicated is 5HT as critical in expression of symptoms–low 5HT (serotonin)

▪ most of the support has come from studies of 5HT and drugs

Question 22

OCD–behavioral model

Answer 22

(Mower, 1960)

▪ person is first classically conditioned to avoid a stimulus and then secondarily experiences operant conditioning further exacerbating the fear
▪ explains the development of OCD, OCD develops as anxiety that produces distress, whereby anxiety is then reduced by an opperantly conditioned avoidant response
▪ Stage 1: neural stimulation acquires anxiety evoking properties by being paired with UCS
▪ Stage 2: aversive properties of stimulus cause avoidance responses to be developed, which are ritualistic behaviors (compulsions) that serve to reduce anxiety
▪ Stage 1 represents classical conditioning and can be used to understand etiology of anxiety from a behavioral perspective

Question 23

REBT model of Anxiety

Answer 23

Ellis, 1973

▪ Irrational belief that the world is completely dangerous
▪ People get anxious about being anxious

Question 24

Neurochemical: Anxiety

Answer 24

(Stahl, 201)

Decease in GABA; benzos increase GABA and cause anxioulytic effects

Question 25

Biological PTSD

Answer 25

Vander Kolk et al (1984) inability for certain neurotransmitters to sustain long period of changes to severe and uncontrollable stress genetic predisposition

Question 26

Cognitive Information Processing Model of PTSD

Answer 26

(Foa & Kozak, 1986 traumatic events create fear networks that are activated because of the interconnections formed through conditoning and generalizations PTSD different from other anxieties because traumatic event challenged views of safety

Question 27

Classical Conditioning PTSD

Answer 27

Keene, 1985 Two factor learning model function of both classical conditioning where fear response is learned through associative principles instrumental--individuals avoid conditioned clues that lead to anxiety

Question 28

PTSD biological

Answer 28

Delahanty et al. , 2000 people with PTSD have lower cortisol levels--people with low cortisol levels are ill equipped to handle trauma and vulnerable to the effect of stress Carlson, 2012; Stahl 2010 over activation of amygdala

Question 29

PTSD contemporary citation and explanation *think shame

Answer 29

Lansky 2000 post traumatic state--propensity to lapse into an altered ego state--fragile and at risk for fragmentation history is reactivated--think dreams trauma shatters sense of relation to self, others and the word Shame--trauma victims at high risk for same or deploy defenses that result in social isolation and withdrawal humbling, dehumanizing experience of the fragility, helpless and need to depend on others--challenges internal standards for self

Question 30

PTSD---Kernburg

Answer 30

Kernburg, 1975 splitting---good and bad (bad areas are trauma)--person can't integrate