week 10 Flashcards
clinical description of general anxiety disorder
For the last 6 months – “more days than not”
• Worrying excessively about common life
events or concerns
• Experiencing signs of physical tension
• Experiencing problems with attention and
concentration
• Suffering from a depressed mood
physical symptoms of GAD
muscle tension fatigue restlessness difficulty sleeping irritability edginess
example of someone with GAD who has a headache
consultsthedoctortoldthat nothing is wrong,
– stillworrythatthecausewas actually a brain tumour - doctor
missed it.
prevalence of GAD
more common in females
limbic system basis
The Limbic System
– Wraps around the brainstem and is beneath the cerebral cortex.
– Major centre for emotion formation and processing, for learning, and for
memory
– Hippocampus
– Amygdala
– The limbic structures are also connected with other major structures such as the cortex, hypothalamus, thalamus, and basal ganglia.
whats the hippocampus
• involved in memory storage and formation - also involved in complex cognitive processing
- moderate stress response
whats the amygdala
• associated with forming complex emotional responses, particularly
involving aggression
- processes emotion related stimuli (initiates behavioural response)
- formation and retrieval of emotional and fear related memories
stages of stress
stage 1: stage shock
stage 2: resistance (body fights back)
- sympathetic activiation, adrenaline is released
- adrenaline causes cortisol release, mobilise energy reserves
stage 3: (if cortisol released for too long)
- exhaustion
- impaired immune function
- chronic hypertension
- obestiy
- atherosclerosis
prefrontal cortex in GAD
less activated
response to negative words
lack of inhibition of limbic system
basal ganglia GAD
important in control movement
over activity = emotional and cognitive negativity
neurotransmitters in GAD
GABA
serotonin
noradrenaline
serotonin in GAD
hypofunction (lack inhibitory affect) limbic system (moderates activity) decrease= overactivity WORRY prefrontal cortex decrease= unable to see positive outcomes anterior cingulate gyrus decrease= unable to shift attention easily
noradrenaline in GAD
hyperfunction (excessive excitatory affect)
overactivity=arousal, stress réponse, increased basal ganglia tone, hypertension
GABA in GAD
hypofunction (lack inhibitory affect)
anterior cingulate gyrus= increased rumination
limbic sustem=overactivity, heighten fear resopnse
prefrontal cortex= unable to deliberately suppress thoughts effectively WORRY
drug therapy mental illness
Antidepressants • MAOIs - • Tricyclic Antidepressants • SSRIs – Mood stabilizers • Lithium, Valproate – Anxiolytics • Benzodiazepines • Hypnotics/sedatives – Zopiclone, Zolpidem, Busipirone, Barbiturates, Antihistamines – Antipsychotics • “Typical” antipsychotics – Flupenthixol, Haloperidol • “Atypical” antipsychotics – Risperidone, Olanzapine – Amphetamines
whats SSRIs
enhance Serotonin levels → improve mood
whats benzodiazepines
anxiolytic “GABA Facilitators.” Inhibit limbic areas
whats SSNRIS
enhance Serotonin and Noradrenaline
non pharmacological intervento
Cognitive behavioural therapy – train prefrontal cortex
Relaxation – reduce arousal Exercise
– Release of endogenous opiates – endorphins
– Reduction in circulating corticosteroid
– Stretching and relaxation of muscles
– Decrease weight gain
classifications of GAD
Generalised anxiety disorder Social anxiety. ... Specific phobias. ... Panic disorder. ... Obsessive compulsive disorder (OCD) ... Post-traumatic stress disorder (PTSD)
predisposing factors
family history of anxiety. recent or prolonged exposure to stressful situations, including personal or family illnesses. excessive use of caffeine or tobacco,
