Anxiety Disorders

Question 1

Biopsychosocial Approach To Understanding Health

Answer 1

Combination of…
Biology e.g. gender, disability
Psychology e.g. personality, past trauma, beliefs
Social context e.g. family background, socioeconomic status, education

Question 2

Anxiety Disorder

Answer 2

Anxiety interferes with day-to-day functioning
Physiological symptoms: hypertension, nausea, sleep disturbances
Lifetime prevalence: 17%
Female : male ratio - 2 : 1

Question 3

Panic Disorder

Answer 3

Frequent panic attacks, feeling of impending doom

Question 4

OCD

Answer 4

Obsessions cause anxiety/distress

Compulsions serve to neutralise anxiety

Question 5

Generalised Anxiety Disorder

Answer 5

6 months of persistent excessive anxiety

Question 6

Specific Phobias

Answer 6

Clinically significant anxiety provoked by exposure to a feared object - leads to avoidance behaviour

Question 7

Genetic contribution to anxiety disorders

Answer 7

Evidence of genetic contribution but no specific genes have been linked

Question 8

Amygdala and the fear response

Answer 8

Critical in fear response
Sensory info from the thalamus and cortex processed in basolateral nucleus of amygdala
Passed on to central nucleus
Activates HPA-axis

Question 9

HPA-axis

Answer 9

Increased stress response
H ypothalamus - releases corticotropin-release hormone (CRH)
P ituary Gland - releases adrenocorticotropic hormone (ACTH)
A drenal Gland - releases cortisol which leads to increased sympathetic activation

Question 10

Hippocampus and Stress

Answer 10

Glucocorticoid receptors in hippocampus measure cortisol levels
When levels are too high the hippocampus inhibits CRH release in hypothalamus - inhibition of HRA-axis activation

Question 11

Amygdala and Anxiety

Answer 11

Over-activated in patients with anxiety disorder

Question 12

Hippocampul Volume in Anxiety Disorders and PTSD

Answer 12

Reduced hippocampul volume
Reduced number of gluco-corticoid receptors
War Veterans with PTSD - show decreased hippocampul volume

Question 13

Stress/Stressors

Answer 13

Stress-reaction to harm or threat

Stressors-stimuli that cause stress

Question 14

Short-Term Stress

Answer 14

Stress is adaptive - acute stressors improve immune function

Question 15

Long-Term Stress

Answer 15

Stress is maladaptive - chronic stressors impair immune function

Question 16

Learned Emotional Responses

Answer 16

1. Classical fear conditioning e.g. Little Albert, 1919

2. Social referencing/imitation - seeing others emotional response leads to avoidance of previously neutral stimuli

Question 17

Amygdala and Fear Conditioning

Answer 17

Lesions of the Amygdala block fear conditioning
Amydgala receives input from all sensory systems-appears responsible for adding emotional significance to another stimuli
Lateral amygdala is the most critical in conditioned fear

Question 18

Hippocampus and Contextual Fear Conditioning

Answer 18

e.g. rat learns link between seeing a light and receiving a shock. It also links the context - the cage it is in when receiving the shock

Question 19

Ventromedial Prefrontal Cortex and Extinction

Answer 19

Conditioned stimulus repeatedly presented by itself
Conditioned emotional response disappears over time
Not gone forever just inhibited
vmPFC lesions-inhibition impaired
vmPFC stimulation-enhanced inhibition

Question 20

Behavioural Therapy in Phobias

Answer 20

Over-activation of amygdala disappears after BT

Increased activity in orbito-frontal cortex after exposure therapy: cognitive control of fear response

Question 21

Medial Prefrontal Cortex and Fear Conditioning

Answer 21

Medial PFC suppresses conditioned fear response by inhibiting lateral amygdala

Question 22

Pharmacotherapy in Anxiety Disorders

Answer 22

Gamma-aminobutyric acid (GABA) - most effective neurotransmitter
Benzodiazepine binds GABA-ergic ion-channels
This increases inhibitory efficiency and has a similar effect to ethanol

Question 23

SSRIs

Answer 23

Selective serotonin reuptake inhibitors
Serotonin is only indirectly involved in anxiety disorders
SSRIs increase density of glucocorticoid receptors in hippocampus - means better modulation of CRH release in hypothalamus - HPA axis less activated