EXAM 2 Flashcards
fear vs anxiety
fear= immediate, serious threat (jumpscare)
anxiety= vague sense of threat/danger (waiting for jumpscare)
generalized anxiety disorder (GAD)
person experiences disproportionate, uncontrollable and ongoing anxiety (worries about multiple matters) for 6+ months
at least 3 of the following: edginess, fatigue, poor concentration, irritability, muscle tension, sleep problems
social anxiety disorder (SAD)
pronounced, disproportionate, and repeated anxiety about social situations for 6+ months, fear of being negatively evaluated or offensive to others, avoidance of social situations
biological perspective- GAD
fear reactions tied to brain circuits (prefrontal cortex, anterior cingulate cortex, insula & amygdala) hyperactivity = GAD, longer and more frequent experiences of fear
low levels of GABA = less inhibition = excessive fear circuit activity
cognitive behavioral perspective- SAD
interplay of cognitive and behavioral factors (unrealistically high social standards + perfectionism)
treatment: cognitive restructuring, graded (in order of fear) exposure therapy
panic disorder
panic attack criteria: periodic, short bouts of panic that occur suddenly (out of the blue), reach a peak within minutes (<10), and gradually pass
panic disorder criteria: unforeseen panic attacks that occur repeatedly, worried about another attack coming on
cognitive behavioral perspective- panic disorder
interplay between bodily sensations, cognitions, & avoidance behaviors –> bodily sensations are misinterpreted (cognitions) as signs of medical catastrophe and controlled via avoidance
treatment: educate about cycle of panic attacks, cognitive restructuring to challenge inaccurate interpretations, graded interoceptive exposure therapy (exposure to internal bodily sensations)
agoraphobia
pronounced, disproportionate, or repeated fear about being in at least 2 of the following situations: public transportation, parking lots/bridges/open spaces, shops/theaters/confined spaces, lines or crowds, or away from home unaccompanied
belief that it would be hard to escape/get help if panic/embarrassment occurred
cognitive behavioral perspective- OCD
everyone has these intrusive thoughts, those with OCD blame themselves and expect that terrible things will happen as a result
treatment: focus on cognitive processes, exposure and response prevention (ERP): exposes client to anxiety- arousing thoughts then prevents them from performing their compulsions (50-70% improvement)
obsessive compulsive disorder (OCD)
obsessions: persistent thoughts/ideas that seem to invade a person’s consciousness (intrusive thoughts)
compulsions: repetitive and rigid behaviors that they feel must be performed to prevent/reduce anxiety (take a considerable amount of time)
dev. psych perspective- anxiety disorders
biological: genetic predisposition, hyperactive fear circuits, fearful temperament
cog-behav.: parenting style too overprotecting
sociocultural: life/stress/poverty, family disharmony/peer pressure/school difficulties
biological factors- acute stress disorder and PTSD
overlap between fear, arousal, and anxiety brain circuits
circuit: amygdala (emotional response, activates) prefrontal cortex (evaluates whether or not threat), hippocampus (forming memories + regulating stress hormones)
brain-body stress route: fight/flight, HPA axis
PTSD: overreactive amygdala + under-reactive PFC= persistent arousal
fight or flight response
controlled by hypothalamus
autonomic nervous system (ANS): involuntary activities, activates sympathetic nervous system (fight)
endocrine system: hypothalamic-pituitary- adrenal axis (HPA axis)
traumatic event
exposed to actual or threatened death, serious injury, sexual violation –>
acute stress disorder: fear/symptoms occur soon after trauma and last for less than a month (50% develop to PTSD)
PTSD: fear/symptoms occur either shortly after trauma or months/years after (25% develop 6+ months after), lasts more than 1 month
factors influencing development of PTSD
childhood experiences (assault, poverty, etc), inflexible coping style, negative worldview
severity/nature of traumatic event may determine whether or not a person will develop the disorder
PTSD treatment
exposure based treatment is the best intervention for people with PTSD, virtual reality
dissociative amnesia
person cannot recall important life-related info (personal info, not encyclopedic or procedural), typically traumatic/stressful info
localized: most common type, loss of all memory within a certain time frame
selective: loss of memory for some, but not all, events within a certain period (not emotionally intense details)
dissociative fugue
extreme version of dissociative amnesia, people not only forget personal info but also flee to a new location (may be brief or more severe)
Hannah Upp from lecture
depersonalization-derealization disorder
no memory difficulties, persistent and recurring episodes of depersonalization and or derealization
depersonalization: feeling separation from own body, dream-like, dizzy, aware of distorted perceptions
derealization: feeling external world/reality isn’t real/strange (other people as robots)
unipolar depression symptom types
emotional symptoms: sadness (miserable/empty), experiencing little pleasure (anhedonia), anger,
motivational symptoms: lacking drive/initiative/spontaneity
behavior symptoms: less active/productive, social withdrawal/isolation, slower movement/speech
cognitive symptoms: negative self views, procrastination, pessimistic
physical symptoms: headaches, dizzy spells, general pain, indigestion, constipation, sleep disturbances/fatigue
unipolar depression criteria
for a 2 week period, a person has an increased depressed mood/decrease in enjoyment or interest across most activities
major depressive disorder: presence of a major depressive episode, no pattern of mania or hypomania
persistent depressive disorder: person experiences symptoms of major/mild depression for at least 2 years (symptoms not absent for more than 2 months at a time)
biological perspective- unipolar perspective
biochemical factors: reflection of disorder or helped to produce disorder- low activity of serotonin +norepinephrine
glutamate: stimulates neurons and promotes connectivity/communication among neurons (lower levels of it amidst depression)
treatment: second gen antidepressants: increase serotonin activity (prozac, zoloft, lexapro); increase norepinephrine activity only (strattera); both
behavioral perspective- unipolar depression
Lewinsohn: number of life rewards is related to the presence or absence of depression (positive life events=feelings of happiness)
negative cognitions: Beck- unipolar depression is caused by a combination of maladaptive attitudes, cognitive traid, errors in thinking, automatic thoughts
negative cognitions perspective- unipolar depression
Beck- unipolar depression is caused by a combination of maladaptive attitudes, cognitive triad, errors in thinking, automatic thoughts
cognitive triad:negative view of experiences, oneself, and the future
Watkins- ruminative responses are linked to longer feelings of dejection, later life clinical depressions
